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Preventing muscle soreness: The request could not be satisfied


Stretching to prevent or reduce muscle soreness after exercise


Many people stretch before or after engaging in athletic activity. Usually the purpose is to reduce risk of injury, reduce soreness after exercise, or enhance athletic performance. This is an update of a Cochrane review first published in 2007.


The aim of this review was to determine effects of stretching before or after exercise on the development of delayed-onset muscle soreness.

Search strategy:

We searched the Cochrane Bone, Joint and Muscle Trauma Group Specialised Register (to 10 August 2009), the Cochrane Central Register of Controlled Trials (2010, Issue 1), MEDLINE (1966 to 8th February 2010), EMBASE (1988 to 8th February 2010), CINAHL (1982 to 23rd February 2010), SPORTDiscus (1949 to 8th February 2010), PEDro (to 15th February 2010) and reference lists of articles.

Selection criteria:

Eligible studies were randomised or quasi-randomised studies of any pre-exercise or post-exercise stretching technique designed to prevent or treat delayed-onset muscle soreness (DOMS). For the studies to be included, the stretching had to be conducted soon before or soon after exercise and muscle soreness had to be assessed.

Data collection and analysis:

Risk of bias was assessed using The Cochrane Collaboration’s ‘Risk of bias’ tool and quality of evidence was assessed using GRADE. Estimates of effects of stretching were converted to a common 100-point scale. Outcomes were pooled in fixed-effect meta-analyses.

Main results:

Twelve studies were included in the review. This update incorporated two new studies. One of the new trials was a large field-based trial that included 2377 participants, 1220 of whom were allocated stretching. All other 11 studies were small, with between 10 and 30 participants receiving the stretch condition. Ten studies were laboratory-based and other two were field-based. All studies were exposed to either a moderate or high risk of bias. The quality of evidence was low to moderate.There was a high degree of consistency of results across studies. The pooled estimate showed that pre-exercise stretching reduced soreness at one day after exercise by, on average, half a point on a 100-point scale (mean difference -0.52, 95% CI -11.30 to 10.26; 3 studies). Post-exercise stretching reduced soreness at one day after exercise by, on average, one point on a 100-point scale (mean difference -1.04, 95% CI -6.88 to 4.79; 4 studies). Similar effects were evident between half a day and three days after exercise. One large study showed that stretching before and after exercise reduced peak soreness over a one week period by, on average, four points on a 100-point scale (mean difference -3. 80, 95% CI -5.17 to -2.43). This effect, though statistically significant, is very small.

Authors’ conclusions:

The evidence from randomised studies suggests that muscle stretching, whether conducted before, after, or before and after exercise, does not produce clinically important reductions in delayed-onset muscle soreness in healthy adults.

Prevention & Relief of Delayed-Onset Muscle Soreness (DOMS) — Amazing-Solutions.com

Delayed-Onset Muscle Soreness (DOMS) – aka, the “all my muscles hurt” syndrome – is a normal reaction to any unfamiliar or intense exercise. Chances are, we have all experienced it (even if we did not know there was an official name for it). Maybe you attribute it to that familiar burn that comes a day after working your muscles hard at the gym. Or the achy joints and stiff muscles that come after a long day of hiking in your favorite spot.

If you wake up in the morning to find your muscles are screaming at you in agony, what you may be dealing with is DOMS.

What Causes Delayed-Onset Muscle Soreness?

If you are the type of person who likes to hit it hard at the gym or go into full-blown weekend warrior mode, you likely have experienced DOMS.

Delayed-Onset Muscle Soreness is caused by tiny, microscopic tears in the muscle fibers. Usually, those tears are from engaging in high-intensity interval exercise (HIIT). Maybe you were trying a new move or using a muscle group you previously neglected. You may feel the pain immediately as the muscle fibers tear, or it may take a few hours to a full day for the pain to kick in.

Your body perceives this kind of exercise as an attack and immediately goes into defense mode. We all know what that means: inflammation. What it means for you is double trouble. Not only are you now dealing with the muscle tears that caused the initial pain, but also the inflammation as your body works to “heal” the original injury.

There is some evidence that certain people are genetically predisposed to DOMS. Research has identified a genetic variation in people who are more prone to intense soreness following a hard workout.

Symptoms of Delayed-Onset Muscle Soreness

Muscle soreness after an intense workout is normal. Pain so bad it keeps you from moving around normally is not. Sometimes called “muscle fever,” DOMS can make your arm and leg muscles feel extremely weak. That is just one of the many signs you may be dealing with DOMS. Here are some of the other more common symptoms associated with the condition.

  • Muscles that are tender to the touch
  • Pain and stiffness that reduces the range of motion
  • Muscle swelling in affected areas
  • Muscles that feel fatigued
  • Lower back pain
  • Short-term depletion of muscle strength and control

Are Some Exercises a Higher Risk for Delayed-Onset Muscle Soreness?

We have already discussed that HIIT-style exercises often trigger DOMS. “Eccentric exercise” is another key risk factor. This is the name given to any exercise that both tenses and lengthens a muscle at the same time. Eccentric exercises are great for muscle growth and development for three reasons:

  • They require less oxygen consumption
  • They use greater force production
  • They use less energy expenditure

A perfect example of an eccentric exercise is a bicep curl. It uses a controlled, downward motion (tension) combined with the effort to straighten your forearm (lengthen). Some other common eccentric exercises include downhill running, the downward motion of squatting, and calf raises.

Other Risk Factors for Delayed-Onset Muscle Soreness

Delayed-Onset Muscle Soreness does not discriminate. From exercise newbs to elite athletes, DOMS can strike at any time. Certain risk factors make a person more susceptible.

If you are relatively fresh on the workout scene, be especially careful you do not push your muscles too hard right out of the gate. It is great you have committed to getting in shape and being healthy. Do not let that desire for a healthier you end in a painful DOMS setback. Be sure to start out slowly and give your muscles time to get used to your new routine. It might be best to avoid engaging in HIIT until you are farther along in your exercise journey.

Experienced athletes also are at risk. Just because you have exercised for years does not mean cannot fall victim to DOMS. Trying a new technique or pushing yourself too hard on a particular day is all it can take for DOMS to strike hard.

Added Risks of Home Workouts

Working out at home also is a risk factor for DOMS. Thanks to an ongoing global pandemic, many of us are avoiding public gyms and community centers. That leaves us to our own devices at home. Exercisers tend to get sloppy when they work out at home, including not wearing the proper footwear for support. Home workouts can get into a bit of a rut due to a lack of equipment, which increases the chances of injury due to complacency when working out.

If you are new to working out, go slow to avoid overuse injuries. Many trainers are offering online sessions and consults. Do not be afraid to reach out to one to have a customized home workout designed to meet your specific needs and goals.

Does Lactic Acid Build-Up Cause Delayed-Onset Muscle Soreness?

This is a common misconception. Lactic acid is the normal byproduct of muscle metabolism. When your muscles have that “I just worked out” feel to them, you can thank lactic acid. It accumulates in the muscles during a workout. When it is released, it can irritate your muscles and make them feel sore.

Lactic acid may contribute to Delayed-Onset Muscle Soreness, but it is not what makes DOMS so painful. You can thank inflammation for the extra aching that elevates post-workout “sore” to DOMS level.

The lemonade from this lemon is that as you progress in your fitness level, you can expect less tissue damage, less soreness, and faster recovery times. Your muscles will get used to your new routine and adjust accordingly. There always is a risk of DOMS with any new intense exercise you try, so be prepared to allow yourself adequate recovery time if this happens.

Delayed-Onset Muscle Soreness Prevention

The jury is still out on whether you can effectively prevent Delayed-Onset Muscle Soreness. There are several theories on things you can do to help. While none of them are a guarantee of keeping DOMS at bay, it certainly cannot hurt to try any of them.

  1. Drink more water
    Drinking water is a great healthy practice, even if Delayed-Onset Muscle Soreness prevention is not your main goal. Research suggests that dehydration is more likely to lead to muscle injury and soreness before and after a workout. Drinking water ensures richly oxygenated blood makes it to your muscles where it is needed most for recovery.
  2. Increase your circulation
    One of the best ways to increase your circulation is by exercising in a hot, humid environment. Blood flow is increased, which is crucial to getting enough oxygen to muscles during a workout. DOMS may not be totally prevented this way, but the level and duration of the pain can be greatly reduced.
  3. Cool it down. Emphasis is placed on warming up before exercising to help protect yourself from injuries. Some studies suggest that cooling down properly adds an extra layer of protection against DOMS.

Delayed-Onset Muscle Soreness Treatment & Recovery

The good news is, DOMS is not dangerous. Sure, it hurts like the dickens when you are in the throes of it. On the plus side, it is a sign your muscles are becoming stronger and more resilient. There is some truth to the “no pain, no gain” mantra where DOMS is concerned. If it strikes, do not get discouraged.

The bad news is, there is no quick fix for DOMS. It takes muscles on average 3 to 5 days to fully recover following an intense workout. There are some treatments you can use to help ease your pain during recovery from Delayed-Onset Muscle Soreness. Here are our top five recommendations:

  • Apply a topical pain reliever like Premiere’s Pain Spray Mist. It can soothe aching muscles and help you move around more freely. Over-the-counter pain relievers like ibuprofen are ineffective in helping DOMS and can even pose some dangers.
  • Take some magnesium. It helps your body use both glucose and lactic acid, which will reduce the severity of pain in your muscles. There are several top-quality magnesium supplements on the market. Foods rich in magnesium include avocados, nuts, legumes, tofu, seeds, whole grains, and some fatty fish.
  • Get a massage. Post-exercise massage can significantly reduce pain and help oxygenate the muscles more efficiently.
  • Eat some tart cherries. An interesting study published in the Scandinavian Journal of Medicine and Science in Sports found that drinking tart cherry juice five days before, the day of, and 48 hours following a marathon helped runners reduce muscle soreness.
  • Keep moving. While it is important to rest sore muscles, that is not an excuse to sit around and do nothing. Gentling moving – yoga, stretching, walking – are all great ways to ease sore muscles and keep them from stiffening up between workouts.

Is it Delayed-Onset Muscle Soreness or an Injury?

While DOMS is an unfortunate fact of life, it does not mean that all muscle pain should be ignored. Sometimes that intense, burning pain you are feeling requires the attention of a medical professional. If the pain is sharp and intense, it is most likely not DOMS. If it is lingering after 3-5 days, do not ignore it and hope it will go away. Reach out to your doctor and get it checked out. Exercising when injured can cause a prolonged setback. It is better to be safe than sorry.

Take care. Stay well.

What Is DOMS? Plus, Effective Ways To Prevent And Relieve Aches And Pains

If you’re embarking on a fitness kick for the first time, or getting back in the game after a period of inactivity, the hardest moment probably won’t come during your first workout but in the days that follow. That’s because you’ll wake up the morning after that workout to find your body is wracked with delayed onset muscle soreness (DOMS).

The optimists out there can view DOMS as an indication of a job well done. You’re challenging your body in a new way and naturally there will be some pain as your muscles rebuild themselves to adapt and become stronger. Once you get more accustomed to exercise, you’ll find that DOMS crops up less and less often, even after a particularly tough workout.

You can also reduce your chances of suffering DOMS by warming up and stretching properly before your workout, and building up the intensity of your exercise over time rather than going hell for leather on your very first try. That said, if you are trying a kind of exercise that you haven’t done before, DOMS is almost guaranteed. Sorry.

Even if you view DOMS as a marker of a good workout, no-one is going to argue that it’s an enjoyable experience in and of itself, so we sought advice on reducing and preventing the pain from Ross Preston, health advisor at the Bupa Blackpool Health Clinic.

What causes DOMS?

“DOMS occurs when you start a new exercise programme or increase the intensity [of your training],” says Preston.

“This causes microscopic damage to your muscle fibres, which results in soreness and stiffness. Exercises that really load the muscles in a lengthened position, such as Romanian deadlifts, have a tendency to increase your chances of being sore after a workout.”

It’s important to remember, though, that DOMS is only a temporary pain station en route to a stronger you.

“Don’t let DOMS put you off your workout,” says Preston.

“This discomfort is only temporary as your muscles adjust to the new exercises and grow stronger. The next time you do that activity there will be less damage to your microscopic muscle fibres, so you shouldn’t be as sore and your recovery time will be quicker than the first time.”

What are the best ways to prevent and treat DOMS?

You can read Preston’s opinion on several popular DOMS preventions and cures below, but first some general advice on how to build up your training to reduce the risk of severe muscle pain.

“There isn’t a proven formula to prevent DOMS, but you can reduce its severity by gradually introducing a new activity or slowly increasing the intensity,” says Preston.

“While stretching is a must after exercising to reduce the risk of injury, it won’t prevent DOMS.”

Fortunately while DOMS can be unavoidable at times, there are treatments to try.

“There are a few things you can do to alleviate the discomfort such as hot/cold baths, ice packs, massage, tender-point acupressure and rest,” says Preston.

“Try a couple of these options to see which one works the best for you.”

Common DOMS Cures And Whether They Work

The internet is awash with purported cures for DOMS, but – whisper this quietly – you can’t always believe everything you find on the internet (unless it’s on Coach), so we asked Preston for his opinion on some of the most common DOMS treatments.

Compression Clothing

The theory behind compression helping with DOMS seems valid, but so far it’s unproven.

“There is no conclusive evidence to suggest that compression clothing can cure or prevent DOMS,” says Preston, which is a downer. But wait! There’s more.

“When your muscle groups work hard, they become inflamed as a result of extra fluid and white blood cells rushing to the area. This inflammation can cause soreness and tightness in the muscle groups. However, people who wear compression clothing may find their muscles don’t become as inflamed as they would do if they’re wearing loose clothing.

“It’s also believed that compression garments may increase blood flow to the muscles, reducing the amount of creatine kinase, which is a chemical that builds up in your muscles and causes soreness.”

Foam Rolling

Good news for fans of self-myofascial relief: it gets the thumbs up for treating DOMS.

“While your muscle fibres are repairing themselves after a workout, they can often become knotted, reducing muscle elasticity and causing soreness and stiffness,” says Preston.

“Foam rolling, massage and active stretching can help alleviate the discomfort of DOMS.”

Pain Relief Balms

No real shock here: pain relief balms can indeed relieve pain.

“Balms like Deep Heat or Tiger Balm provide a cooling sensation on the skin, which can help reduce soreness,” says Preston.

“The menthol in the balms cause calcium ion to affect your neurons that sense temperature and inhibits your brain/pain connection in that area.”

Hot/Cold Showers And Ice Baths

The fact that subjecting yourself to hot, cold and freezing water works is good news – it’s a cheap and easy solution. (So why do we feel like it’s bad?…)

“Hot baths cause your blood vessels to expand, filling them with blood, while cold or ice baths constrict the blood vessels, forcing the blood to move on to other parts of the body,” says Preston.

“A combination of both (known as contrast hydrotherapy) flushes the nutrients carried in the blood more effectively and quicker to your muscles, which speeds up the recovery process.

BCAA Supplements

Branched-chain amino acid supplements aren’t a DOMS cure-all, but they might help with the pain.

“Amino acids are the building blocks of protein and are essential in muscle repair and growth,” says Preston.

Your body does not naturally produce all the amino acids it needs, and the ones it doesn’t produce you have to get from food or supplements, including some that are vital for muscle repair.

“Three important amino acids needed for muscle tissue repair are leucine, isoleucine and valine, which can be found in BCAA supplements. They work by helping to repair the microscopic torn muscle fibres and prevent the muscles from breaking down.

“Although they can’t help in preventing or curing DOMS, BCAAs may help reduce soreness.”


Lots of foods are reported to have DOMS-curing properties, but Preston suggest that there are three main types to look out for.

“It’s important to eat and stay hydrated after a workout, as the nutrients and protein can help your muscles recover,” says Preston. Here are his top three.

  1. Carbohydrates. “Carbs produce insulin, which is a hormone that drives muscle growth in your body. It also helps replace muscle and liver glycogen which helps refuel your energy supplies and helps the body in the recovery process.”
  2. Protein. “Protein is a nutrient that is essential for the growth, maintenance and repair of muscles and body tissue. After a workout, protein helps repair the muscle fibres that were broken down during the exercise, which helps reduce soreness and recovery time.”
  3. Antioxidants. “Foods rich in antioxidants, such as berries and cherries, help reduce inflammation and therefore soreness – and they count as one of your five a day.”

Bupa offers health assessments that give the body a full MOT. For more information head to bupa.co.uk/health-assessments

How To Avoid Muscle Soreness

To an extent, muscle soreness is to be expected from working out. However, this doesn’t mean that you just have to “deal with it”. There are ways to avoid the worst of post-workout stiffness, as well as steps you can take for relief. Here’s everything you need to know about muscle soreness and post-workout stiffness.

It’s no secret that muscles go through a lot of stress when we work out. Especially if we’re starting a new type of workout or working new muscles, soreness and tightness can occur both immediately after or 24-48 hours after a workout.

There are two types of muscle soreness: (1) pain during or immediately after a workout and (2) delayed onset muscle soreness (DOMS).

Pain and soreness during or immediately following a workout are usually caused by a build-up of lactic acid, which is a normal result of muscle use. It can irritate the muscles, causing pain and discomfort, but subsides usually within a couple of hours post-workout.

When most people say they are sore post-workout, they’re usually referring to DOMS, which occurs 24-48 hours after a workout. It’s characterized by loss of strength and reduced range of motion, not to mention tightness. Unlike the symptoms of lactic acid buildup, DOMS comes with days of soreness and tightness, coupled with lower levels of swelling and inflammation. DOMS is the result of microscopic muscle damage caused by the stress of a tough workout. Muscles repair themselves during recovery, which is why recovery is so important to proper training. The symptoms of DOMS usually subside within four days.

Is Muscle Stiffness Normal?

You’re probably no stranger to the phrase “no pain, no gain”, but there comes a point when there really is nothing to gain by the amount pain. It is normal to feel some amount stiffness after a workout. This is particularly true if you’re starting a new training program with new exercises or you’ve upped the ante in your training.

However, depending on the degree of soreness and pain, it could be a sign of bad things to come. It could mean you’re training the wrong way, either overtraining or undertraining. It could also be a symptom of oncoming sickness or, worse yet, an oncoming injury.

How can you tell when normal stiffness is abnormal? More to the point, how do you know when enough is enough?

The short answer is listening to your body. You know better than anyone else your physical limits. Pushing those limits will help you improve your fitness level, but at some point, it could be overtraining. There are certain signs and symptoms you should always be on the lookout for when it comes determining whether you’re simply sore or pushing yourself too hard:

  • Your performance is not improving, but in fact, going downhill no matter what you do.
  • You hurt even when you’re resting.
  • You have persistent soreness or localized pain that doesn’t subside after 2-3 days of rest or active recovery.
  • You’re feeling other symptoms of overtraining.

There are multiple stages to overtraining so it’s important to catch it early on before it starts setting back your hard work. Persistent muscle soreness and feeling run down are the early signs. Although stiffness can be a normal side effect of working your body, especially in ways it’s not used to, it’s important to recognize the difference between normal muscle soreness and an oncoming injury or overtraining. Furthermore, it’s important to remember that muscle soreness does not always indicate muscle growth.

Tips To Prevent Muscle Soreness

The best way to avoid muscle soreness and limit it’s impact is to take preventative measure during and immediately after your workout.

  1. Pace yourself throughout your workout. You should certainly be challenging yourself, but pushing yourself too hard too soon could not only result in muscle soreness but also injury and fatigue. Give your muscles time to adjust to the changing challenges.
  2. Rest between sets and exercises. Short breaks between sets coupled with deep breathing can help give your muscles relief from stress and allow them to shortly recover before using them again.
  3. Hydrate adequately. Many times, stiffness and soreness comes from inadequate hydration. Your muscles need water, especially to recover properly; so make sure you’re drinking enough water during your workouts, post-workout and throughout the day.
  4. Warm up and cool down properly. A proper warm up including dynamic stretching and gradual intensity increase can never be underestimated. Likewise, a cool down should include gradually decreasing intensity and stretching.
  5. Foam rolling is an effective prevention technique for muscle soreness. However, it’s important that you do it properly to avoid pain and causing an injury.

Post-Workout Stiffness Relief

Two prevailing theories of fitness wisdom are to take a break if you’re sore or, on the other end, continue to exercise. Either piece of advice is fine to follow as long as you’re listening to your body. If you feel like you should take a recovery day then take a recovery day. However, if you feel up to your next scheduled workout then you should continue with your set training program. There are also ways of combining the two sets of advice and take an active recovery day or cross-training day, which would rest the sore muscles but allow you to continue working out.

Even so, whether you decide to take a rest day or exercise, here are some tips for getting relief.

  1. Topical ointments such as over-the-counter can provide immediate although temporary relief for muscle soreness.
  2. Hot compresses or ice can also help. It’s important though to use heat and ice properly.
  3. Light stretching after getting your blood flowing with a quick warm-up can be effective for providing relief as blood circulation improves recovery speed.
  4. Getting a deep tissue massage can also relieve soreness and tightness.
  5. While foam rolling can prevent soreness it can also help relieve it.
  6. Epson salt baths are backed by science in helping muscle restoration, which can not only provide relief and prevent soreness.

In the end, if your soreness doesn’t decrease within a week or there’s persistent and localized pain, you should get yourself checked for an injury. Because, although muscles soreness can be a normal part of working out, it can also be an indication of an oncoming injury.

Prevent Muscle Soreness After Working Out

If you have been working out correctly, you have no doubt felt some muscle soreness following your exercise. If you are experiencing actual pain, now would be a good time to contact your doctor. Soreness, however, can appear anywhere from 12 to 48 hours after exercising and last about as long. And while this soreness is a good sign, it should not interfere with your daily activities. Here are some ways to prevent muscle soreness following your workout.

What Is Soreness?

First of all, what is soreness? When exercising you are creating microscopic tears in your muscle tissue. This is actually a good thing, because when your body repairs this tissue, it creates a larger muscle. However, your body’s way to tell you it is working on the tissue (and to leave it alone for a time) is DOMS (or Delayed Onset Muscle Soreness).

There is no way to entirely prevent muscle soreness, but there are several ways to effectively manage and minimize it.


Make sure to stretch. Studies show that doing so before or after exercising does not affect soreness, but does remove lactic acid from your muscles (a natural waste product your muscles create) and does keep your muscles flexible. Remaining flexible is an important way to stave off injuries and to minimize future soreness.


Taking ibuprofen is another tool to help with soreness. This painkiller works well especially with severe cases of DOMS. Taking a low dose, over-the-counter version of this medicine is an easy way to help prevent muscle soreness.

Warm Bath

A warm bath is a great post-workout routine, and a relaxing way to deal with muscle soreness. Soaking in warm water not only quiets the mind, but loosens up tight muscles. In addition, warm baths help increase blood flow. Increased blood flow promotes the circulation of blood, which in turn delivers oxygen and other vital nutrients to your recovering muscles.

Hot/Cold Packs

Hot/cold packs are another method to prevent muscle soreness. Whatever brand you choose, it is ideal to alternate from hot to cold every 15 minutes. Once again, this alternation aids in improving blood circulation and optimizing muscle regeneration.


Finally, try a massage. A firm massage is a great tool to relax and lower your heart rate. In addition, a good massage will help loosen any tight muscles and knots. Knots, which are contracted muscle fibers, can actually prevent blood flood in the muscle and increase the buildup of toxins. Massages are also great in increasing blood circulation throughout the body.

While modern medicine has not solved the issue of muscle soreness, there are several ways to ease your post workout muscles from the ache, and help prevent muscle soreness in the hours and days following your trip to the gym. With the help of experts, like those at Krav Maga, you can cultivate a workout that is tailored to your fitness level.

Reduce Muscle Soreness – 14 Proven Ways To Speed Up Recovery

Muscle pain is not exclusive to athletes. Everyone has, probably, experienced it at least once in their lifetime. Sore legs after that hiking trip to the mountains last weekend. Or maybe a push up challenge with friends the other night. Any new or strenuous activity can send people looking for ways to reduce muscle soreness in the following days.

Athletes, however, face muscle soreness on a more frequent basis than the rest of the people. They push themselves in training and racing and frequently it can be just one interval too much or too hard that causes the pain the next day.

Where does muscle soreness come from?

Muscle soreness is nothing more than an indicator of damage done to the muscle tissue. It results from micro-traumas caused by excessive lengthening of the muscle. The pain develops as the area around those micro tears gets inflamed. Symptoms might include:

  • Light swelling
  • Tenderness to the touch
  • Stiffness of the muscle or joint & reduced range of motion
  • Reduction of strength of the affected muscles

In the world of science it’s actually called Delayed Onset Muscle Soreness (DOMS), because it takes a while until inflammation develops. The strongest pain generally occurs within 24 to 48 hours after an intense exercise and can last for 2 to 3 days.

After a particularly hard session muscle soreness can occur within hours after the exercise.

Mild muscle soreness is a normal part of training process. A certain level of stress and muscle damage is required for the body to grow stronger and supercompensate.

As the athlete becomes more trained, muscle soreness should be less frequent.

In fact, for experienced and consistent athletes muscle soreness is not a good sign. It’s a signal that body was pushed too far which requires much longer time to recover from and can have bad effect on overall endurance.

How to reduce muscle soreness?

When the damage is already done there are lots of ways how to support the body and give it everything it needs to work the magic.

Some of the measures below will help to immediately reduce muscle soreness. Others are more strategic life changes that will help to reduce the overall stress placed on the body and make the body more resilient.

#1 Don’t stop exercising

When athletes experience muscle soreness the best strategy is to do a very light and short (up to 30 minutes) activity to promote blood flow. It can be as simple as a brisk walk, a veeery gentle stretch or mobility work.

Movement stimulates the heart to pump more blood to the muscles. That helps to flush out waste products (like lactic acid) and bring in minerals and nutrients required for recovery.

#2 Re-hydrate

Water is a necessary component in the process of energy production in the muscles. Without enough water the body will slow down all its functions to preserve the limited supply of energy it has.

Drinking water also helps to flush out waste products from the body quicker, which will help to recover sore muscles quicker.

#3 Get proper sleep

Our body is only able to repair the damage done to the muscle when it’s in the state of complete rest. That happens when we are asleep.

Deep sleep, in particular, is the most effective at rebuilding muscle tissue. That’s when the body fully relaxes and produces Human Growth Hormone (HGH). Moreover, in later stages of sleep the body goes into fasting state (no food for 8+ hours) and the HGH production is at its peak.

So, it’s not a good idea to eat a lot before bed. That will only disturb the quality of sleep and minimize production of HGH.

Related: The Power & Science Of Restorative Sleep For Athletes

#4 Drink a berry smoothie

Berries are packed with antioxidants and there are some studies that discuss how antioxidants help to reduce muscle soreness.

Besides that, drinking a smoothie after a hard training session may be the best thing one can do for recovery. Smoothies made of fruits, vegetables and berries provide everything that athletes need after a training session. They promote alkaline environment that reduces inflammation across the body, as well as re-stokes the supply of vitamins and minerals.

Fruits, vegetables and berries are great at minimizing inflammation across the body and reducing overall stress.

#5 Get in an ice bath or cold shower

The best way to treat acute inflammation is to reduce the body temperature. This works with injuries, bruises and muscle soreness.

The quickest way to reduce temperature is with cold exposure. Ice bath process works exactly as it sounds – fill a bath with cold water, put lots of ice there and submerge for around 15 minutes. Cold showers might provide a similar effect.

It may not be the most pleasant measure, but super effective.

#6 Reduce muscle soreness with compression clothes

A good way to stimulate blood flow and reduce muscle soreness is to wear compression clothes, like socks or pants. What compression does is help to reduce swelling, so that once socks or pants are off the blood can flow better to the muscles.

Compression socks were originally invented for travelers who sit a lot in an airplane and don’t move much. At some point runners and other athletes started to use compression clothes to aid in recovery and get the same benefits.

Heart Rate Zone Training

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#7 Drink extra virgin olive oil

Extra virgin olive oil has been used in traditional medicine to cure various diseases. Among its other nutritional and antioxidant benefits, it has also been proven to have a pain suppressing, anti-inflammatory and anti-cancer effects.

It has been estimated that 3 tablespoons of extra virgin olive oil amounts to roughly 10% ibuprofen dosage for a person.

#8 Elevate your legs to reduce muscle soreness

If you’ve done a lengthy lower-body activity (a long run, cycle or even a hike), it’s a good idea to elevate your legs to let the blood flow out from the limbs. This will help to reduce the swelling and promote blood flow afterwards – a similar effect to compression clothes.

It’s not necessary to elevate your legs all the way up on a wall, though it will be more efficient. Also, you don’t need to lie like this for the whole evening – 10 minutes here and there is enough.

#9 Use essential oils

Peppermint oil, in particular, gently massaged into the muscles will give the body a cooling effect and will aid in muscle recovery. Mix just 2 drops with a regular massage oil to create a “massage mix”.

This really helps to recover from races or long workouts when there is a lot of muscle damage and soreness.

#10 Add turmeric to your diet

Curcumin – a compound found in turmeric – is high in antioxidants. On top of that it has very powerful anti-inflammatory effects and is a great natural supplement to help reduce muscle soreness.

Turmeric can be taken in any form and is a great addition to a meal or a smoothie. In a fresh, powder or even tea kind of way.

#11 Don’t go crazy on protein

While the body needs protein for muscle repair, focusing too much on it puts a lot of stress on the body. It also requires a lot of energy to digest which can be better spent on recovery.

To process a protein-heavy meal the body requires acid environment. Since the natural state of our body is slightly alkaline, kidneys try to balance the acidic environment by using glutamine. This is where it gets interesting, because the body sources glutamine by breaking down our muscles.

So, by eating a protein-heavy meal we force our body to break down muscle tissue, instead of growing new one.

It’s much better to incorporate a bit of protein into every meal or snack than eat a lot in one sitting.

#12 Try a vegetarian or plant-based diet to reduce muscle soreness

Vegetarian and plant-based diets tend to be more focused on fruits, vegetables and legumes. These foods are much easier to digest, so the body spends less energy on that. Also, such meals promote alkaline environment in the body that reduces overall inflammation.

The less energy the body has to spend on digestion and dealing with inflammation, the more it can use for recovery.

Vegetarian and plant-based diets provide a high variety of vitamins and minerals that are so important for athlete’s recovery.

#13 Reduce alcohol consumption

Alcohol has a lot of different impacts on our bodies. The most important one is that it’s a toxin. And, as with any toxin, the body fights hard to process it and get rid of it.

While fighting the toxin the body doesn’t have too much energy to work on repairing muscle damage or re-stocking mineral, nutrient and water supply. So, the process of complete recovery takes much longer.

#14 Prevent muscle soreness in the first place

By far the best strategy to reduce muscle soreness is to prevent it.

When we incur too much muscle damage and accumulate fatigue we compromise our future training sessions. It’s much better to have a consistent schedule of good training sessions than one very hard one.

So, build fitness gradually. Start slow by sticking to a consistent schedule and creating a solid aerobic base first. Make sure that the volume and intensity don’t increase too fast. Finally, include enough recovery to allow the body to gradually grow stronger.

How To Prevent Post-Workout Soreness – SWEAT

Starting a new training program can be hard. If you’re new to working out or are returning to exercise after an injury, you may have experienced a fitness hangover or felt the effects of delayed onset muscle soreness (DOMS).

When you try a new training style or add new exercises into your workouts, it can take time for your muscles to adapt. This might mean that you feel stiff and sore — that sore feeling is an indication that your muscles have been challenged, and you are getting stronger. 

If you have experienced DOMS, here’s why you feel sore and what you can do to recover faster.

What is DOMS?

Delayed-onset muscle soreness is pain and stiffness that occurs 24 to 48 hours after a workout. This can happen when you’ve worked the muscle harder than you are used to by increasing the intensity of your workout. 

This might be because you’ve trained at a higher rate of perceived exertion, or perhaps done a type of exercise you haven’t tried previously. During your workouts, small tears, called “micro-tears”, occur within the muscle tissue, causing you to feel achy and sore. 

According to a 2008 study by Southampton Solent University in the UK, and published in the Clinical Journal of Sports Medicine, DOMS results from eccentric muscle contraction — this is when the muscle tenses as it lengthens. A bicep curl is one example of an eccentric contraction. As you lower the dumbbell, the bicep muscle engages to support the weight. 

Muscle vibration can also contribute to muscle damage and soreness — that means DOMS can occur after high-intensity training as well as after a strength workout. 

Delayed onset muscle soreness can occur when your overall training load increases as you work towards your fitness goals. You might have increased your number of workouts or the length of your workouts, lifted a heavier weight or increased your number of repetitions. 

What are the symptoms of DOMS?

Signs that you have delayed onset muscle soreness include: 

  • Muscles worked feel tender to touch
  • Stiffness and reduced range of motion when moving
  • Short term loss of muscle strength
  • Muscle fatigue

If you find that you are sore the next day after a workout, there are ways that you can speed up your muscle recovery and get back to your training. 

It’s important to note that if you don’t experience delayed onset muscle soreness, this doesn’t necessarily mean that you’ve reached a workout plateau. There are other ways to track your fitness progress to ensure you’re moving towards your health goals. 

Should you train with sore muscles?

This is a question that is often asked by the Sweat Community. 

Delayed onset muscle soreness shouldn’t prevent you from training for long. However, you might need to adjust the intensity of your workouts for a few days to allow your body to recover and adapt. 

Rest and good nutrition are a very important part of any workout program. When you rest and eat a balanced diet that includes carbohydrates and high protein foods, you give your body the building blocks it needs to repair and become stronger for your next workout.  

When feeling very sore, you should reduce the intensity of your workouts to allow your body to fully recover. Try yoga or low-intensity cardio instead of a tougher workout to allow your body time to adapt. 

When you first start working out, aim to schedule your resistance workouts every second day to give yourself a day to recover between workouts. 

What training can you do with DOMS?

If you are experiencing delayed onset muscle soreness, it can be tempting to stop moving altogether until you recover. However, by continuing to gently move your body, you can speed up your recovery time. 

Active recovery such as a swim, a walk or some yoga can help to reduce muscle soreness. 

If you do want to do a resistance workout, consider training a different area of your body. For example, if your legs are feeling sore from your last workout, do an upper body workout and allow your leg muscles more time to recover. 

It’s also okay to take a rest day — rest is just as important as your workout. Establishing healthy sleep habits or making time for mindfulness and meditation can help you to develop a better mind-body relationship so that you can get more out of your workouts.   

The Sweat programs balance resistance training with recovery and low-intensity cardio to ensure that muscle soreness won’t prevent you from making working out into a habit.

How to reduce DOMS

Here are a few things that you can do to reduce the discomfort of delayed-onset muscle soreness, or to prevent it altogether.

Increase intensity gradually

When you start a new exercise regime, look for a training program that incorporates “progressive overload”. This is a training principle that gradually progresses your fitness by increasing the amount of weight you lift or the number of reps or circuits you do. 

While you definitely should be challenging your body, it’s important to do so gradually. This will help to prevent DOMS, and it will also help to keep you moving towards your fitness goals.

When you start a new workout program or training style, adjust the intensity of your training to ensure that you can complete the recommended number of repetitions easily. 

Focus on maintaining proper form and ensure that you do each exercise correctly so that you get the maximum training benefits. As you gain confidence, you can increase the weight or number of reps to start pushing your body. 

Drink plenty of water

Staying hydrated before, during and after your workout can help to reduce muscle soreness. 

Carrying a water bottle during the day can help to remind you to take regular sips so that you maximise your workouts and stay hydrated. 

Take time to cool down

Making time for low-intensity movement at the end of each resistance training session can help to reduce delayed-onset muscle soreness. You can include static stretching in your cool down to boost your flexibility too. 

There’s a guided cool down at the end of each resistance training workout in the Sweat app that you can use to help ease any post-workout tension. 

Do a foam rolling session

Foam rolling is essentially a form of self-massage that can help to reduce post-workout muscle soreness. You can use a foam roller right after a workout to help to reduce the symptoms of DOMS and perceived fatigue by stimulating blood flow to the muscles used in your workout.

Swap a workout for active recovery

If you are really too sore to work out, try switching your scheduled workout for low-intensity cardio or active recovery instead. A 2018 review by the University of Poitiers, France, and published in Frontiers of Physiology, found that short bursts of low-intensity movement can help to reduce DOMS. 

Active recovery helps to enhance blood flow to the muscle tissue which assists with the removal of metabolic waste, including lactate. 

Get a massage

A 2017 literature review by Shanghai University of Sport and Wenzhou Medical University in China, and published in Frontiers In Physiology, found that massage was the most effective method for reducing DOMS and perceived fatigue. 

Massage helps to reduce the inflammatory proteins circulating in the blood after a workout and increases blood and lymph flow. 

Wear compression garments

The same 2017 review found that compression clothing can help to reduce delayed-onset muscle soreness for up to four days after a workout. Compression can also help with your perception of fatigue, so you’ll feel less tired and sore. 

Immerse your sore muscles in cool water

A 2015 review of nine studies by São Paulo State University, Brazil, and published in Sports Medicine, found that immersion in cold water with a temperature of 11-15 degrees Celsius (52-59 degrees Fahrenheit) for 10-15 minutes following exercise can effectively reduce post-workout soreness.

Use these tips to reduce delayed onset muscle soreness

If you’ve pulled up sore after a tough workout, don’t be discouraged — if you stick with a consistent workout program, your body will adapt to the exercise you are doing.

Use your rest days effectively to help your body to recover faster from your workouts and focus on listening to your body. Being fit and healthy isn’t something that you can achieve overnight — it’s a life-long process that you will keep working on!

90,000 Myofascial pain. Treatment of myofascial pain

Definition of myofascial dysfunction.

Back pain, however, like any muscle pain, is often the main complaint with which a patient seeks a doctor for myofascial pain dysfunction. Myofascial pain dysfunction is a violation of the function of a particular muscle, arising in connection with its overload and manifested by muscle spasm, the presence of painful muscle seals in tense muscles or local muscle hypertonia and trigger points.

Prevalence of back pain.

Back pain, according to the WHO recommendation, since 2000, is included in the list of priority studies. Since muscle pain is not a definite nosological form, it attracts the attention of neurologists, vertebrologists, rheumatologists and doctors of other specialties. This is primarily due to the incidence of chronic pain syndrome, leading to long-term disability in young people.

According to the estimates of most of the researchers, the prevalence of muscle pain in the back and limbs among the population in the epidemiological studies conducted is up to 64%.The highest prevalence of pain of musculoskeletal origin reaches in middle age and decreases in subsequent years. So, according to A.A. Skoromtsa (1997), patients from 30 to 59 years old accounted for 75% of all age groups.

In addition to prevalence, a medical and social problem is significant disability and high cost of treating patients with musculoskeletal pain. For example, in the UK, 90 million were lost due to back pain.working days, which was second only to respiratory and circulatory diseases.

Based on the 8th World Pain Congress (Vancouver, 1996), back pain is the second most common cause of medical visit after respiratory illness and the third most common cause of hospitalization.

The International Congress on Musculoskeletal Pain, held in 1995, was also devoted to the problem of myofascial pain syndrome. in San Antonio (USA), which emphasized that myofascial pain syndrome was detected in 100% of cases when examining patients with vague pelvic pain who did not suffer from any pathology of the pelvic organs.Myofascial dysfunction is revealed in 2/3 of patients with pain syndromes in the trunk and extremities.

History of the development of views on myofascial pain

For a long time, there was, and still is, terminological confusion regarding muscle pain, associated primarily with the presence of palpable painful muscle areas.

In the nineteenth century. in English-speaking and German-speaking countries, the term “muscular rheumatism” arose in connection with this. But at the same time, inflammatory changes in the blood characteristic of connective tissue diseases were not revealed.

The subjective sensation of pain in the muscles was defined by some authors as “idiopathic”, “traumatic” or “rheumatic” myalgia.

The term “myofascitis”, or “myofasciitis” also turned out to be insufficiently correct, since there is no inflammatory process in myofascial pain syndrome.

The term myogelosis arose from the theoretical assumptions that muscle tightness is the result of the transition of muscle protein into the gel phase. Although further morphological studies did not confirm this assumption.

Nevertheless, at a certain stage of the disease, structural changes were revealed in the zones of painful muscle compaction. Were found groups of atrophied muscle fibers, endomysial fibrosis, and in later stages – pronounced fibrosis. From the standpoint of morphological data, two stages of induration formation can be distinguished – painful (no changes are detected with light microscopy) and trigger (vasomotor, autonomic shifts are determined, clinically reversible).

To designate local areas of increased muscle tone G.A. Ivanichev proposed the term “painful muscle compaction”, which is identical to the concept of “myofascial trigger point”.

But, according to V.A. Karlova, is the term “painful muscle-fascial dysfunction.”

The Kazan school of neurologists made a great contribution to the development of the modern concept of trigger points. It was shown that the biochemical basis for the formation of muscle seals is an excess of calcium with a deficiency of high-energy compounds, which causes an increase in the contractility of muscle fibers and a decrease in blood flow in them.
A vertebrogenic concept of the onset of myofascial dysfunction has also been proposed. But, according to V.A. Karlova and A.M. Wein, in general medical practice today there is an overdiagnosis of osteochondrosis of the spine as a cause of musculoskeletal pain. Thus, according to L.A. Bogacheva (1996, 1998), in a study of 4000 patients with pain in the muscles of the back, only 5% had radiculopathy and tunnel neuropathies, while 95% of the examined patients had musculoskeletal dysfunction.

Therefore, if we talk about back pain of a vertebrogenic nature, but without radicular disorders, then the most common cause of myofascial pain is associated not with morphological changes in the spine, but with functional disorders that can be combined with morphological ones. We are talking about limiting the mobility of the spine in the motor segment, or about reversible blockage localized in the intervertebral joints, leading to strong reflex changes. Blocking in one part of the spine causes functional changes in adjacent areas in the form of compensatory hypermobility in distant areas.

Thus, muscle pain in the back and extremities is a syndrome, the origin of which is associated with the irritation of the receptor apparatus in the area of ​​the affected spinal motion segments or large joints with painful reactions of the muscles of the spine and extremities. Constant painful stimuli are fixed by the central nervous system, which leads to long-term dysfunction of the corresponding muscle groups. A vicious circle is formed: pain – muscle spasm – pain – muscle spasm.

Clinical picture of myofascial pain syndrome

Myofascial pain dysfunction has a clear clinical picture, consisting in the occurrence of muscle spasm, the presence of painful muscle seals in tense muscles (trigger points), a decrease in the range of motion of the affected muscle and the presence of zones of reflected pain.

The basis of musculoskeletal pain is the myofascial trigger point – an area of ​​increased irritability within the tense bundles of skeletal muscles or muscle fascia. Active trigger points are distinguished – foci of hyper-irritability in the muscle, manifested in the form of pain in the place of localization of the point, as well as in distant, characteristic areas for it. The pain can be observed both at rest and during movement. Each point has a specific point of reflection of pain within the same sclerotome.Moreover, in the zone of reflected pain, vegetative manifestations can also occur in the form of changes in sweating, skin color, hypertrichosis. In response to stimulation of trigger points, a local convulsive response (“jump symptom”) occurs with muscle contraction and increased pain.

In addition to active, there are latent trigger points that are more common than active ones. Palpation of latent triggers reveals local soreness without pain reflection in distant zones.

Latent trigger points can be activated under the influence of the provoking factors mentioned above (hypothermia, postural overstrain, physical exertion, emotional stress, anxiety, etc.).etc.). And, conversely, under the influence of short-term rest, warmth, adequate therapy, the active trigger point can go into a latent state.

V.A. Karlov distinguishes three phases of the course of myofascial pain syndrome:

  • I phase – acute. It is characterized by constant excruciating pain from especially active trigger points.
  • II phase – characterized by the onset of pain only during movement and absence at rest.
  • III phase – chronic. At the same time, the patient retains some dysfunction, a feeling of discomfort in the corresponding zone.There are only latent trigger points that retain the ability to reactivate. Moreover, emotional stress, the presence of asthenic, anxious, depressive syndromes are of great importance in their reactivation.

Studying the state of the autonomic nervous system in patients with myofascial pain of the cervicothoracic localization, in 85% of patients we revealed the syndrome of vegetative dystonia and permanent and paroxysmal types, and its frequency increased with the transition of the disease from the acute phase to the chronic one, which was accompanied by an increase in the dysfunction of nonspecific systems brain.Moreover, 2/3 of patients testified to the presence of complaints from the autonomic nervous system even before the development of myofascial syndrome and its intensification after the onset of the latter.

Segmental and suprasegmental disorders were distinguished in the structure of vegetative-vascular dystonia. At the segmental level, autonomic disorders were characterized by vascular-algic trophic disorders in the form of burning pain in the occiput, both independently and in the structure of the posterior cervical sympathetic Barre-Lieu syndrome, as well as the anterior sympathetic Glaser syndrome.Similar syndromes were associated with tension of the oblique or belt muscles of the head, causing compression of the vertebral artery, in the first case, and tension of the sternocleidomastoid muscle with irritation of the sympathetic plexuses surrounding the carotid artery in the second.

The presence of dysfunction in the upper trapezius muscle causes a throbbing headache in the temporal regions. In some of our patients (12%), we observed the phenomenon of humeral-scapular periarthrosis, in the form of pain and limitation of mobility in the shoulder joint, and in 10%, an anterior scalene syndrome, characterized by parasthesia, marbling and swelling of the hand, was recorded.

Suprasegmental autonomic disorders were manifested in the form of psychovegetative syndrome in the structure of vegetative dystonia syndrome. Moreover, the most frequent manifestations were in the cardiovascular and muscular systems. The most common complaints were tension headaches, vasomotor and venous cephalalgias, and cardialgic (senestopathic) syndrome (in 47% of patients).

In 45% of patients, there were dyssomnic disorders in the form of falling asleep disorder and early awakening, and only 15% of patients had insomnia associated with pain, the rest – with anxiety and emotional stress in the absence of pain.

28% developed vegetative paroxysms with vegetative-visceral manifestations, as well as syncope and vegetative-vestibular crises. Moreover, in a quarter of patients, vegetative crises occur immediately after the onset of acute myofascial pain phenomena, then in 30% – against the background of chronic myofascial pain, and in 45% of patients, paraxisms were observed before the onset of musculoskeletal pain and with its manifestation became more frequent. The formation of the syndrome of autonomic dystonia is, apparently, on the one hand, a reaction to chronic pain, and on the other, contributes to the formation of an anxious painful personality.

Causes of myofascial pain

Myofascial pain occurs when a combination of predisposing and provoking factors.

First of all, this is a violation of the motor pattern, in which overstrain of various muscle groups develops. Most often, in patients with myofascial pain syndrome, posture and gait disorders are detected (scoliosis, combined with kyphotic deformity of the chest and short leg syndrome, flat feet, long second metatarsal bone with shortening of the first).

Short leg syndrome is often ignored by doctors, since patients with this syndrome do not experience any difficulty in walking and do not feel unstable. However, according to D. Travel, V. A. Karlov, the difference in leg length even in 3 – 4 mm in children leads to twisting (distortion) of the pelvis and the development of S-shaped scoliosis. In turn, this leads to the development of functional blockages of the vertebral motor segments and the formation of latent trigger points in the muscles of the back and neck. The uncorrected difference in leg length increases with age, impairing the biomechanics of the spine and maintaining myofascial dysfunction.According to our research, the difference in leg length among 141 patients with musculoskeletal pain in the neck and shoulder girdle was 1.2+ 0.4 cm.

Slouching (kyphotic deformity of the thoracic spine) also leads to an overload of the muscles of the neck, shoulder girdle and the occurrence of myofascial pain syndrome, the most common causes of which are Scheuermann-Mau disease, the consequences of rickets, heredity.

Among the reasons for the development of myofascial pain can be called short shoulders with an elongated torso, causing tension in the muscles of the shoulder girdle and activation of trigger points located in the trapezius muscle and in the muscle lifting the scapula.

One of the risk factors can be called postural tension arising from an incorrect posture and, accordingly, a non-optimal balance of the load on the muscles or the forced maintenance of a monotonous posture for a long time due to the nature of their work.

Trigger points can also activate long-term maintenance of a monotonous posture during deep sleep. Long-term immobilization of the limbs after fractures leads to a violation of the stereotype of movements of the whole body and the appearance of asymmetries of the body.

Prolonged activity of myofascial trigger points promotes prolonged muscle compression by belts of a bag, a heavy coat, a tight collar, corsets, and a belt.
The provoking factors include general and local muscle hypothermia, often combined with physical overstrain.

We must not forget about the role of acute and chronic emotional stress in the development of muscle pain. Emotional tension is always accompanied by muscle tension. In anxious individuals, even after the cessation of stressful effects, the muscles continue to be in a contracted state, and in a state of chronic stress this leads to a change in the stereotype of movements.A change in posture leads to muscle overload and the appearance of pain, a vicious circle is formed: emotional stress – a change in the motor stereotype – muscle tension – pain – increased stress.

In addition, with emotional disturbances, the descending antinoceptive impulses to the posterior horns are weakened, which leads to a decrease in the pain threshold and an increase in pain sensations. In anxious individuals, even non-painful impulses from the muscles are perceived as pain, which causes muscle tension, which in turn aggravates the pain.

One of the risk factors for myofascial pain is a weak muscle corset. Unaccustomed prolonged work of untrained muscles leads to the development of painful muscle tension and activation of trigger points. This is especially true for people of mental labor.

A common cause of the development of myofascial pain dysfunction is somatic pathology, accompanied by impulses from the affected internal organ and leading to a protective tension of the corresponding muscles.So, coronary pathology can be accompanied by the appearance of tension and pain in the scalene muscles, small and pectoralis major, subclavian muscles. And already from the trigger points in these muscles, the pain radiates to the supra-, sub- and interscapular regions.

In gynecological pathology, pain caused by muscle tension appears in the lower abdomen, in the lower back, in the region of the sacrum.

Gastroenterological pathology is accompanied by myofascial pain in the paravertebral regions. It should be remembered that half of patients with chronic myofascial pain have vitamin deficiency, especially vitamins of the “B” group, folic, ascorbic acid.

Thus, the predisposing and provoking factors for the development of myofascial pain syndrome are the following:

1. Violation of posture and gait, as well as developmental abnormalities:

  • body asymmetry due to different leg lengths;
  • S-shaped scoliosis;
  • reduced size of one half of the pelvis;
  • kyphotic deformity of the thoracic spine;
  • flat feet;
  • short shoulders with an elongated body;
  • Long second metatarsal bone with a shortened first.

2. Functional blockages in the vertebral motor segments.

3. Postural tension in a non-physiological position or prolonged immobilization.

4. Overload of untrained muscles.

5. Compression or stretching of muscles.

6. Emotional stress, asthenic, anxious, depressive syndromes.

7. Diseases of internal organs.

Thus, having a patient with muscle pain in front of him, the doctor needs to identify the presence of these risk factors, as well as the causes leading to the onset of pain, which is important for adequate therapeutic correction.

It should also be remembered that myofascial pain syndrome occurs independently of osteochondrosis of the spine, but can occur as a complication of vertebrogenic reflex muscle-tonic syndrome. In this case, against the background of painful muscle spasm, active trigger points appear, characteristic of myofascial pain.

Diagnosis of myofascial pain syndrome

The presence of muscle pain requires, first of all, the exclusion of inflammatory etiology, as well as the exclusion of vertebral compression radicular and spinal pathology.
Diagnosis of myofascial pain syndrome requires correct palpation technique to identify trigger points. It is recommended to stretch the muscles along the length on the verge of pain stimulation, while among the relaxed muscles a cord in the form of a tight cord is palpated, along which the point of maximum pain is revealed, the pressure on which causes reflected pain.

There are methods of deep palpation, when the fingertips follow across the muscle fiber, and tick-borne palpation, in which the abdomen of the muscle is grasped by the thumb and other fingers and rolled between them in order to identify the cords.When making a diagnosis, you can focus on the following criteria (Trevell D.G., Simons D.G., 1989):

  1. The connection of pain with physical overload, postural tension or direct hypothermia is characteristic;
  2. Dense painful bands are defined in the muscles. There is no muscle hypo- or atrophy;
  3. Pain extends to areas distant from the tense muscle;
  4. Within the limits of the tense muscles, areas of even greater muscular compaction are palpated, the pain of which sharply increases with pressure – a “jump symptom”;
  5. Reflected pain is reproduced when the trigger points are compressed or punctured;
  6. Elimination of symptoms with a specific local effect on a tense muscle.

Among these criteria, one of the decisive points of diagnosis is finding an active trigger point and pain reproducibility.

Treatment of myofascial pain

Treatment of myofascial pain consists of several directions. The first direction is the elimination of the causes of pain, it is also a means of preventing musculoskeletal pain dysfunction.

Impaired posture requires orthopedic correction and the creation of the correct motor stereotype and muscle corset using a pathogenetic set of exercises.

In case of the syndrome of the shortened half-pelvis, patients are advised to place a pillow under the buttocks in a sitting position, designed to compensate for the difference in the height of the sides of the pelvis.
To correct the imbalance of the I and II metatarsal bones (Morton’s foot), it is recommended to wear special insoles with a 0.3 – 0.5 cm thickening under the head of the I metatarsal bone.
When functional blockages of joints are detected, manual therapy is used to restore normal mobility (mobilization) of the blocked joint.

The second direction is the treatment of pain syndrome associated with myofascial dysfunction. It can be divided into non-drug and drug methods, used both independently and in combination. The most effective is post-isometric relaxation of the affected muscle. The essence of the method lies in the initial stretching of the affected muscle, and then in the isometric mode for 10 s. Subsequent further stretching and repetition of isometric tension.Reception is repeated 3-5 times, depending on the severity of muscle tension.

D. Trevell and D. Simons proposed puncture of trigger points with an injection needle with or without novocaine (dry puncture). After piercing the trigger point, the main symptoms (local convulsive response, reflected pain, local soreness) disappear, and the muscle cord relaxes.

A correctly performed so-called ischemic compression of the trigger point with a finger (acupressure) has a similar effect.As the pain decreases, the pressure on the point increases. The acupressure process continues individually in each case.

The complex of treatment should include massage, physiotherapy procedures.

At the present stage, special acupuncture techniques have been developed for the treatment of myofascial pain syndromes, which are one of the most promising areas. Acupuncture works well with any other treatment and can enhance the effect of drug therapy.In addition, in the course of treatment, other therapeutic effects characteristic of acupuncture are manifested. For example, a powerful anti-stress effect and a vasoregulatory effect.

Drug therapy of myofascial pain syndrome has, in turn, two directions:

  1. Effects on the vicious circle: muscle spasm – pain – muscle spasm. Pathogenetically justified is the appointment of muscle relaxants, which reduce the flow of pain impulses from the periphery. In the arsenal of doctors, there are currently muscle relaxants – sirdalud, baclofen, mydocalm.
  2. Influence on the functional state of the limbic-reticular structures, on which the transition of pain to chronic pain depends to a certain extent during the formation of vegetative dystonia syndrome with the development of anxious, depressive and asthenic reactions.

For this purpose, GABA is prescribed – ergic drugs (Noofen, picamion, adaptol), sedatives, tricyclic antidepressants and serotonin reuptake inhibitors, as well as vegetotropic drugs such as bellaspon.Such therapy enhances the central antinociceptive effects, which contributes to a more rapid relief of pain syndrome. In addition, it is advisable to include acupuncture in the complex of treatment using points used for vegetative dystonia. The complex of treatment may include B vitamins in this category of patients.

The third direction is the rehabilitation of patients with myofascial pain dysfunction. The main task of rehabilitation is to create a new correct motor stereotype, to teach the patient the ability to control his body, to control the condition of his muscles, to create or strengthen a muscle corset.At the same time, the main attention is paid to the pathogenetic complex of corrective (including the use of post-isometric relaxation and acupressure) and general strengthening exercises, which, if performed correctly, lead to the correction of posture defects.

An important task of the doctor is also to improve the medical culture of the patient, who must understand the causes of muscle pain and know how to prevent them.

In our practice, we try to combine all these principles in the treatment of myofascial pain syndromes.This makes it possible to obtain a pronounced positive trend in the treatment of patients with advanced myofascial dysfunctions.

90,000 Treatment Subacromial conflict syndrome (impingement syndrome)


Shoulder impingement syndrome is based on improper collision (conflict) between the acromion and the head of the humerus, which leads to compression and chronic trauma to the tendons of the muscles of the rotator cuff of the shoulder during movement.The rotator cuff of the shoulder is located in the space between the acromial process of the scapula and the head of the humerus (Fig. 1). The height of this space is 6-7 mm, while the thickness of the rotator cuff is slightly less – 5-6 mm, which provides normal conditions for its sliding and prevents compression.

Subacromial conflict syndrome (impingement syndrome)

Normally, no collision occurs between the acromion and the head of the humerus. However, with a decrease in the height of the space, the reasons for which may be different, collision becomes possible, due to which, during movement, the muscles of the rotators are compressed by the above structures, their chronic trauma, and then damage.

impingement syndrome treatment

The most common reasons for the decrease in the height of the space and the development of subacromial impingement syndrome are the structural features of the acromial process – curved or hook-shaped types of processes, incorrectly fused fractures of the greater tubercle of the humerus or acromion, osteophytes 9000


The clinical manifestations of shoulder impingement syndrome are pain and limitation of movement in the shoulder joint during shoulder abduction and flexion.

The maximum pain is observed when the arm is abducted at an angle of 70 – 120 °, i.e. in a position where the head of the humerus, with the muscles attached to it, comes as close as possible to the lower edge of the acromion and clamps the muscles of the rotators.

With further abduction, the pain decreases. This dynamics of pain in shoulder abduction is called “painful middle arch of abduction.”

What are the symptoms of impingement of the shoulder syndrome?


Clinical tests
To diagnose impingement syndrome, special tests are used in which the doctor, bringing the patient’s hands to a certain position, artificially causes compression of the subacromial structures (causes additional pressing of the head of the humerus against the lower surface of the acromion) and looks to see if a characteristic pain syndrome appears or not.The diagnostic value of these tests is extremely high, the information content of some of them is at the level or even higher than that of MRI studies of the shoulder.

Clinical tests

The simplest and most informative diagnostic method that allows you to reliably distinguish subacromial conflict from other shoulder diseases is the NIRA test – the essence of which is a temporary decrease in the intensity of pain in a patient after injection of lidocaine into the subacromial bursa.

Ultrasound diagnostics
MRI – diagnostics
X-ray diagnostics

Arthroscopic diagnostics is the most reliable diagnostic method.With the help of a modern device – an arthroscope, the doctor can examine all structures of the joint from the inside and reveal even the smallest damage.

Treatment for shoulder impingement syndrome depends on the severity of the symptoms and the stage of the process. As a rule, at the initial stages of the disease, treatment begins with conservative measures:

Anti-inflammatory and therapy – taking non-steroidal anti-inflammatory drugs (NSAIDs).

Subacromial administration of glucocorticosteroids (blockade) – recommended for persistent pain syndrome. It is performed once a week, but no more than 3 injections during the year.

Physiotherapy – ultrasound, magnetotherapy, electrotherapy.

Physiotherapy – aimed at restoring the balance of the shoulder muscles, preventing the development of contractures – muscle spasms and tightness.

In the absence, within 3-4 months, of a positive effect from conservative therapy, surgical treatment is indicated.

The most modern and low-traumatic method of surgical treatment for shoulder impingement syndrome is shoulder arthroscopy. Arthroscopy allows you to perform acromion plastics (in the case of hook-shaped or bent variants of the structure), remove osteophytes on the lower surface of the acromion, often located in the area of ​​the articular surfaces of the clavicular-acromion joint, eliminate compression of muscles and tendons, and restore their integrity.

To perform high-quality arthroscopy of the shoulder joint and obtain the most successful results from the operation, 3 conditions are required:

Experienced orthopedic surgeon
Shoulder arthroscopy is a technologically more complex operation than, for example, knee arthroscopy. We can say that this is aerobatics, even for an experienced orthopedic surgeon dealing with joint arthroscopy.By international standards, a surgeon who practices shoulder arthroscopic surgeries can be considered experienced if he has performed at least 1000 such surgeries, which is a rather difficult task.

Sufficient equipment for arthroscopy
It is necessary to have a full set of expensive high-tech equipment: a monitor, a digital video camera, an optical device (astroscope with a diameter of 4 4.5 mm), a source of xenon illumination with a power of at least 150 W, a device for supplying a solution that flushes the joint during an operation (arthroscopic pump), a device for coagulation and cutting of tissues in solution (vaporizer), installation for mechanical removal of soft and bone tissues.(shaver), a special set of instruments for carrying out different types of restorative interventions. The absence of at least one of the above makes it impossible to perform high-quality shoulder arthroscopy.

Adequate anesthetic management


Correctly performed surgery allows you to start active rehabilitation quickly enough to prevent the development of complications and optimize the timing of recovery.

After shoulder arthroscopy, the arm is immobilized in the abduction position for several weeks using a special splint. Such immobilization reduces the tension of the tendons and reduces the risk of re-rupture, creates favorable conditions for better healing of the tendon. The duration of immobilization is determined by the surgeon who performed the operation, since only he can assess the condition of the tendons and the strength of the suture.

From the first weeks after shoulder arthroscopy, patients are advised to perform special exercises aimed at developing movements in the shoulder joint.However, their intensity and sequence should be selected by the operating physician and an experienced rehabilitation therapist.

In our Medical Center, patients after shoulder arthroscopy are offered a whole range of rehabilitation measures. The rehabilitation program is selected individually and includes:

Special exercises and exercise therapy at the rehabilitation therapists of our Medical Center using the kinesiotherapy method. Exercises are aimed at improving the range of motion in the shoulder joint, preventing the development of contractures, increasing strength and endurance in the muscles of the shoulder girdle.Exercises are selected on an individual basis and performed on professional equipment in the rehabilitation room, under the supervision of experienced instructors – rehabilitation therapists. Some of the exercises are prescribed for the patient to be carried out at home.

Physiotherapy using professional BTL equipment: magnetotherapy, ultrasound therapy with the introduction of drugs, electrotherapy – reduce pain and swelling in the operated shoulder, prevent the formation of adhesions and scars, promote better healing, restore muscle tone.

90,000 Does stretching reduce soreness? | TipTar

Exercise-induced muscle pain is commonly known as “soreness” (DOMS), but must be distinguished from muscle fatigue pain immediately after muscle use. All of the studies presented in this article investigate muscle pain caused by rigidity. Do you still think static stretching can help combat soreness? Maybe it’s time, of course, to rethink this, with scientific evidence .

When and how shoelaces occur

Stiffness usually occurs during exercise that you are not used to, especially if it involves eccentric muscle action. Eccentric action (or negative phase of movement) occurs when a muscle generates tension to control the speed at which it is stretched. A perfect example of this is the negative phase of the squat (when we descend), the quadriceps muscle begins to stretch, and the tension that is created in the muscle helps to avoid lengthening too quickly or excessively.

They usually appear the day after training and peak intensity after about 48 hours (Balnave 1993; Bobbert 1986; Wessel 1994). However, the exact manufacturing process for the laces is unknown. The theory is currently being developed partial rupture of sarcomeres , which causes muscle fiber swelling and triggers an anti-inflammatory response that can excite nociceptors (pain receptors; Lieber 2002), but this inflammation is not enough to cause pain as the muscle needs to stretch or contract. to feel typical aches and pains (punctures).For the curious and the most diligent, Weerekkody 2001 points out that the excitation of larger-diameter muscle afferents, especially the neuromuscular spindle (a sensory receptor located in the abdominal part of a muscle that detects changes in muscle lengthening), is involved in the sensation of pain. …

Research Analysis

Herbert RD, de Noronha M, Kamper Sj in the article “Stretching to Prevent or Reduce Muscle Soreness after Exercise (Review)” provides a full analysis of various studies conducted previously on whether stretching is beneficial for pain relief. caused by laces.

A total of 12 studies were included : Buroker 1989; Dawson 2005; Gulick 1996; Height 1989; Jamtvedt 2010; Johansson 1999; Marques 2006; Maxwell 1988; McGlynn 1979; Terry 1985; Wessel 1994a; Wessel 1994b. In particular, the Jamtvedt 2010 is of great importance, in which 2377 people took part, and the average age of the participants was “adult” (39.9 years).

Three studies looked at pre-workout stretching (Hight 1989; Johansson 1999; Wssel 1994a) Seven studied post-workout stretching (Dawson 2005; Gulick 1996; Hight 1989; Maxwell 1988; McGlynn 1979; Terry 1985; Wessel 1994b), one study examined the effects of stretching before and after exercise (in selected groups) (Marques 2006), and only one study examined the effects of stretching before and after exercise (in one group) (Jamtvedt 2010).The different studies do not look at the same muscle, but all but one use the same technique: static stretching (standing). The length of these segments ranges from 40 seconds to 900 seconds.

Study Results

This analysis is an update of the previous one (Hebbert 2007), which adds two more vital studies. In a previous review, the results were unequivocal: ” The data from these studies show that stretching immediately before or immediately after training does not significantly reduce muscle pain in the first days after training. “. In this new update (Hebbert 2011), the conclusion remains the same.

According to the analysis, the reduction in pain caused by soreness after stretching before and / or after exercise is 4 out of 100 points. This analysis suggests that it has no effect on reducing pain. , because only an assumption of 6 out of 100 would have a small positive effect.

Likewise, these studies are carried out under ideal laboratory conditions.It should be assumed that in any other case (in the absence of control over the optimal result) the effects will be even less than .

Where did the idea come from that stretching reduces soreness?

It is possible that this idea stems from a false belief that prevailed in the 60s and 70s about how muscle pain occurs. At the time, muscle pain was thought to be caused by muscle spasms (de Vries 1961), although this idea was later rejected (Bobbert 1986).

So … should we stretch?

After reading this article, you may have some misconceptions, as many people associate stretching with a warm-up, although they are not the same thing. These studies have shown that static stretching does not reduce soreness, which does not mean that other types of stretching do not have a beneficial effect.

In fact, dynamic stretching has been shown to have great benefits for athletic performance .If you want to learn how to warm up properly, this is your article: How to warm up and stretch before training?


  • Balnave 1993
    CD Balnave, Thomson M.V. Effect of training on muscle damage caused by eccentric exercise. Journal of Applied Physiology 1993; 75 (4): 1545-51.
  • Bobbert 1986
    Bobbert M.F., Hollander A.P., Huijing PA. Factors of delayed onset of muscle pain in men. Medicine and Science in Sports and Exercise 1986; 18 (1): 75–81.
  • Wessel 1994
    Wessel J, Wan A. Effect of stretching on the intensity of delayed muscle soreness. Clinical Journal of Sports Medicine 1994; 4 (2): 82-7.
  • Dear 2002
    Lieber RL, Frieden J. Morphological and mechanical bases of delayed muscle soreness. Journal of the American Academy of Orthopedic Surgeons 2002; 10 (1): 67–73.
  • Weerakkody 2001
    Weerakkody NS, Whitehead NP, Canny BJ, Gregory JE, Proske W. Large fiber mechanoreceptors contribute to muscle soreness after eccentric exercise.Pain Journal 2001; 2 (4): 209-19.
  • Buroker 1989
    Buroker KC, Schwane JA. Does post-exercise static stretching relieve delayed muscle soreness? Physician and Sports Medicine 1989; 17 (6): 65–83.
  • Dawson 2005
    Dawson B., Gough S., Modra S., Bishop D., Stewart G. Effect of immediate post-play recovery procedures on muscle soreness, strength, and flexibility over the next 48 hours. Journal of Science and Medicine in Sports 2005; 8 (2): 210–21
  • Gulik 1996
    Gulik D.T., Kimura I.F., Sitler M., Paolone A., Kelly D.D. Various treatments for the signs and symptoms of delayed muscle soreness. Sports Training Journal 1996; 31 (2): 145–52.
  • High 1989
    High DM, Howley ET, Franks BD. Effects of static stretching and warm-ups on the prevention of delayed muscle soreness. Exercise and Sports Quarterly Report 1989; 60 (4): 357–61.
  • Jamtvedt 2010
    Jamtvedt G, Herbert RD, Flottorp S, Odgaard-Jensen J, Havelsrud K, Barratt A, et al.A pragmatic randomized trial of stretching before and after physical activity to prevent injury and pain. British Journal of Sports Medicine 2010; Vol. 44, no. 14: 1002-9.
  • Johansson 1999
    Johansson PH, Lindström L, Sundelin G, Lindström B. Effect of pre-workout stretching on muscle soreness, soreness and loss of strength after heavy eccentric exercise. Scandinavian Journal of Medicine and Sports Science, 1999; 9 (4): 219-25.
  • 2006 Brands
    Marques DB, Valentini L, Penoni AC, Abe PT, Alvarenga NM.Effects of stretching on the prevention of delayed muscle soreness. Proceedings of the International Congress on Rehabilitation Neuromusculoskeletica e Esportiva, Rio de Janeiro. 2006
  • Maxwell 1988
    Maxwell S., Cohn S., Watson A., Balnav R.J. Is stretching effective in preventing or reducing delayed-onset muscle soreness? In: Editor (s) Torode M. Maximizing Athlete Participation and Minimizing Risk. Sydney: Cumberland College of Health Sciences, 1988: 109–18.
  • McGlynn 1979
    McGlynn GH, Laughlin NT, Rowe V.Effect of electromyographic feedback and static stretching on
    artificially induced muscle soreness. 1979 American Journal of Physical Medicine; 58 (3): 139–48.
  • Terry 1985
    Terry L. Muscle sprains and soreness. Study of the effect of retention-relaxation on delayed soreness of the quadriceps muscle after exercise – a pilot study [thesis]. Adelaide
    (Australia): South Australian Institute of Technology, 1985.
  • Wessel 1994a
    Wessel J, Wan A.Effect of stretching on the intensity of delayed muscle soreness. Clinical Journal of Sports Medicine 1994; 4 (2): 83-7.
  • Wessel 1994b
    Wessel J, Wan A. Effect of stretching on the intensity of delayed muscle soreness. Clinical Journal of Sports Medicine 1994; 4 (2): 83–7
  • Herbert 2007
    Herbert RD, Noronha M. Stretching to prevent or reduce muscle soreness after exercise. Cochrane Database of Systematic Reviews 2007, Issue 4.[DOI: 10.1002 / 14651858.CD004577.pub2]
  • de Vries 1961
    de Vries HA. Prevent muscle stress after exercise. Research Quarterly 1961; 32: 177-85.
  • Hebert 2011
    Herbert R.D., de Noronha M., Camper S.J. Stretching to Prevent or Reduce Muscle Soreness After Exercise (Review) Cochrane Library 2011 Issue 7


A problem such as knee pain is faced by people of all ages for their own reasons.Knees can hurt both in young people, especially in athletes, and in old people due to the deterioration of recovery processes in the knee joint and for some other reasons. Soreness in the knee can “show itself” suddenly, abruptly, or it can develop gradually.

They usually get used to constant knee pain (not intense) and do not seek help for a long time, which is very dangerous, because such pain can be a signal of the development of a pathological process in the knee joint.In this case, it is important not to skip the stage at which it will still be possible to effectively cope with the disease.

In general, knee pain can be considered any painful sensation in the area of ​​the knee joint that causes discomfort and sometimes suffering to a person.


Symptoms knee pain are very diverse and depend, first of all, on the cause of it. Now let’s look at the symptoms by which you can determine the presence of pain in the knee:

  • Most importantly, a painful condition or a feeling of discomfort is localized in the area of ​​the knee joint.
  • Soreness can be both less intense, but more constant, as well as more noticeable, but only appear under certain circumstances (for example, while running).
  • For knee pain , a gradual increase in pain symptoms with a gradual limitation of the joint’s motor ability is characteristic. At first, the movements become more difficult, and then it is more impossible to calmly step on the foot and up to the complete immobilization of the joint.
  • Periods of remission are also characteristic, that is, there was pain, maybe even significant and with limited movement, then everything calmed down for a while, and then the pain returned again.
  • A fairly common feature is that in the absence of loading of the joint, the pain disappears, although it can intensify at night.
  • After some time, contracture (irreversible change in configuration) may develop on the injured limb, that is, in this case, the lower limb may acquire a bent position with its lower part turned to the right or left.It is impossible to get out of this situation on your own. It can be deformed in the form of the letter O (varus deformed) or the letter X (valgus).
  • Many people find it difficult to walk in the morning, after a while such patients “walk around”.
  • To palpate (feel) such a joint is also painful.
  • The area of ​​the knee joint may be inflamed, enlarged due to edema, and the skin may also acquire a red tint (hyperemia occurs).
  • A painful joint can crackle when walking, standing up, and any load, and such a crunch will be pathological.
  • There may be a constriction sensation below the knee.
  • The knee joint may be sharply contoured.
  • Feeling of a “heavy joint” that prevents normal movement.
  • “Unstable joint” – patients feel uncertain that such a joint will withstand the usual load.

Soreness of the knee joints can cause any “detrimental” incident for them, therefore, the causes of knee pain are many and varied:

  • Injury of the ligamentous apparatus of the knee joint.The knee joint plays an important role in the implementation of motor function, therefore, trauma to this ligamentous apparatus will not have very pleasant consequences. There are four ligaments in the knee joint. It is thanks to them that the upper and lower parts of the lower limb are united, that is, the femur and fibula. There are accompanying and cruciate ligaments. The first two (outer) are located on the inner and outer sides of the knee joint, middle and lateral, respectively. Their rupture usually occurs in athletes with a sharp movement, in which case soreness appears instantly and persists for a long time after their healing.The other two (internal) intersect, forming a cross, which is why they are named so. If the ligaments located in the front are torn, this is immediately noticeable by the appearance of intense pain and swelling of the joint. In this case, it is important to stop immediately so as not to worsen the condition. If the ligament located behind is torn, then there will be soreness and swelling in the fossa under the knee (popliteal), the injury is less serious than in the previous version.
  • Injury to tendons (tendinitis). Tendinitis refers to any damage or inflammation in the tendons through which muscles are able to attach to the tendons, they are made up of fibers.Tendons are also damaged most often in athletes, people who are involved in cycling, jogging, skiing are especially susceptible to such damage. The most vulnerable tendon is the quadriceps muscle. One knee can be affected, or both. In this case, the knee hurts in front and there may be swelling. A damaged tendon at rest usually does not hurt, but physical exertion such as climbing stairs, squatting, or jogging causes soreness. If there is an incomplete rupture of the tendon of the quadriceps muscle, then the maximum pain will be when the leg rotates in the knee.A complete rupture of the tendons completely restricts movement.
  • Lesion of the menisci. The meniscus is a special cartilaginous formation capable of bending in the area of ​​the knee joint. A feature of damage to the meniscus is that various parts of it can be injured (torn). If there is a gradual rupture of the structures of the meniscus, then the soreness may not appear immediately and grows over time, usually over one or two days, and the joint slowly increases in size due to swelling.”Knee closure” may occur, that is, the torn off fibrous parts of the cartilage end up among the bones, thus disrupting the knee joint to function fully, “closing” it. In this case, the pain will be quite intense, and the treatment will only be surgical. Mild cases are amenable to non-surgical treatment.
  • Inflammation of the bursa (bursitis). All joints have special bags that contain the fluid necessary for the smooth functioning of the joint. It is these articular bags that are exposed to inflammation.When such inflammation occurs, the joint swells, increases in size and is outwardly hyperemic (redness occurs). The soreness is quite strong, a special peak of such soreness is caused by squatting, as well as sitting on your knees. If the area in front of the knee cap becomes inflamed, especially when an infection is attached, this can lead to a general intoxication syndrome, that is, an increase in the general body temperature, malaise.
  • Free body symptom. This condition may result from any damage or degeneration process and consists in the fact that a piece of bone or cartilage tissue is torn off, which leads to its free “floating”.Such a piece can fall between other structures of the joint, thereby disrupting free movements in it.
  • Moving the knee cap. The patella has a special bone called triangular and located on its front surface. Under some circumstances (for example, injuries), it is capable of displacement. Such a displacement is noticeable immediately and this bone takes a perpendicular position. The soreness will be extremely severe, and the anterior surface of the joint will become edematous, and it will become difficult to walk and stretch the leg.Such a displacement rarely happens once, usually such an incident is repeated at least several times. Each subsequent displacement will be painful and accompanied by swelling. To prevent re-displacement, a set of special exercises can help strengthen the muscles surrounding the knee.
  • Defeat of osteochondrosis of a tuberous formation (tuberosity) of the tibial bone, also called Osgood-Schlatter’s disease. This disease is characteristic of young athletes.The disease mainly affects the tibia slightly below the knee cap. A tumor forms in this place. Soreness can be of varying intensity, depending on the presence or absence of physical activity. More often, the disease has one-sided localization and disappears after the child grows up.
  • Syndrome of the tibial-iliac tract. This syndrome “affects” the ligament that runs along the outside of the leg from the pelvic bones to the lower leg. If this ligament is strongly stretched, then it begins to rub against the underlying bones.This syndrome is typical for runners and it manifests itself during the first 10 minutes of running, and after rest it usually goes away.
  • Extended knee joint. This happens as a result of injury. In this case, the knee joint expands, swells and is capable of partial posterior bending. Even if the damage is not very serious, soreness and swelling will be uncomfortable. Damage to the ligamentous apparatus of the knee joint is also possible.
  • Infectious lesion of the knee joint.Any inflammation leads to soreness, especially when it comes to joints. This can also increase the overall body temperature.
  • Overweight. Excess weight also puts an extra load on the body, in this case, on the knee joint, which can lead to damage and inflammation, and pain.
  • Significant physical activity. Our joints, unfortunately, do not last forever and have their own limit of loads. In addition, over time, they become depleted and weak.
  • Developmental anomalies of the knee joint.
  • Age-related changes.

Diseases such as gonarthritis and gonarthrosis should be separately mentioned:

  • Gonarthritis. Literally, gonarthritis translates as “inflammation of the knee joint”, while the inflammatory process includes the following structures of the knee joint: muscles surrounding the joint, its ligamentous apparatus, capsules, synovial membranes, as well as soft tissues surrounding the joint, as well as its cartilage, which are always affected …
    It is gonarthritis that is the most common reason due to which the patient experiences soreness of the knee joints. Gonarthritis is absolutely not dangerous for life, but significantly worsens its quality. It is much more difficult for patients with gonarthritis to move and perform everyday work.
    The affected joint hurts, while the soreness can be of varying intensity, and its physical activity increases. Initially, gonarthritis is characterized by periods of exacerbation, that is, pain appears under certain circumstances.If untreated, gonarthritis becomes chronic and constantly bothers the patient. Gradually, joint pains appear more and more often and begin to bother the patient more and more, and more and more the joint loses its mobility.
    In case of suspicion or already established presence of gonarthritis, it is important not to miss the stage at which it is possible to return the joint to its full life, and to urgently begin treatment, which in the first stages will be conservative.
  • Gonarthrosis, – compared with gonarthritis, is a more serious disease, because dystrophic and degenerative changes in all articular structures occur in the joint, as well as the muscles that surround the diseased joint are affected.
    Gonarthrosis is considered to be an idiopathic disease, that is, one in which it is not possible to find a clear cause of its occurrence. The disease begins with some kind of articular section, whether it be its outer, inner or front part. The clinical picture, in principle, does not differ from that in gonarthritis (pain during movement, swelling of the knee joint, limited movements in it, its stiffness and instability), except that the joint is also deformed in the form of the letter O (varus) or X (valgus ).
    Over time, the symptoms increase and the condition of the joint worsens. Depending on the stage of the process, treatment can be either conservative or operative.

The main risk factors include:

  • Age. Moreover, there are joint diseases, the risk group of which is elderly people, and there are those who have not yet reached the age of majority.
  • Women, because they most often suffer from diseases of the knee joints.
  • Excessive body weight.
  • Injured joint.
  • Heredity.
  • Previously removed articular meniscus.
  • Athletes who play sports professionally, especially if the load on the knee joints is significant, especially runners and jumpers.
  • Work involving heavy physical exertion.
  • Long walks (more than 3 kilometers daily).
  • Sitting on your knees or squatting for extended periods.
  • Climbing stairs.

Basic prevention measures knee pain are simple:

  • Constant moderate physical activity. Such loads include morning exercises, which are 100% useful and are the key to the health of your joints and the whole body as a whole. Do it daily for 15 to 20 minutes.
  • Maintain the optimal weight for your body.Naturally, people are individual and the concept of “ideal” weight is different for everyone. Just do not forget that the knee joints bear a huge load on themselves and play a vital role in the implementation of movements by our body, so eat right, play sports and fight excess weight so as not to destroy your joints.
  • If you are involved in sports in which injuries occur frequently, try to protect your joints with, for example, knee pads, wristbands, and so on.
  • It is better, of course, to choose the sport in which joint injuries are the least dangerous, for example, swimming or yoga, especially if there are hereditary predispositions or developmental abnormalities.
  • Do not torment your joints with long climbs up stairs, or constant squatting or kneeling.
  • If a child has flat feet, it should be treated by wearing orthopedic shoes.

There are many reasons why the knee joint may hurt and the treatment will also be different in some way, so a very important (most important!) Step will be to find the reason why the patient consulted a doctor.

First, the doctor interrogates the patient, while the patient should describe as clearly as possible what exactly he is complaining about, describe the characteristics of the pain syndrome, what may have caused it and whether any of the relatives has a similar disease. You should also inform your doctor about the peculiarities of your work and sports.

This is followed by a manual examination, that is, examination with the help of hands. In this way, the doctor can detect a more accurate localization of the lesion, joint deformity, swelling, possible slipping of the patella, and so on.

The doctor may ask the patient to share with him previous studies, if, of course, he underwent them, such as CT (computed tomography), MRI (magnetic resonance imaging), X-ray diagnostics to clarify the cause of the condition. If necessary, she will write out a referral for the necessary examination.

Group Stretching


Regular stretching provides health benefits.However, without control from the outside, this type of physical activity is quite traumatic. Therefore, it is better to study in a group under the guidance of an experienced coach. Stretching (Stretching) is a system of movements performed with the aim of stretching the ligaments and muscles, increasing flexibility.

What is stretching training for?

Stretching not only improves health, but also increases the physical capabilities of a person, and also enhances his visual appeal.

What do you need for the lesson?

You will need sportswear that does not hinder your movements, preferably made of “stretching” material.You should also bring elastic bandages to class to prevent injury.

Important: do not try to immediately sit on the split and show other miracles of flexibility. Start slowly at a low intensity. To avoid injury, stretch only after warm-up.

Top five reasons to start stretching

  1. Stretching can improve your posture.
    – Many of us spend at least part of the day sitting at a computer or looking at our phone or tablet.The posture typical of these activities (rounded shoulders and head forward) contributes to poor posture. This can be corrected by stretching the pectoral and upper trapezius muscles, hamstrings, etc.

  2. Stretching increases the range of motion.
    – As we age, our joints lose their mobility. We can counteract this by stretching regularly. Even if the range of motion in some joints is limited, stretching can help increase it.

  3. Stretching reduces back pain.
    – This goes hand in hand with posture to some extent. If we have poor posture in the upper back, the lower back compensates for the disturbance, pain may develop. In addition, if we have tight hamstrings, the lower back compensates for this and often hurts. Stretching the muscles in the legs and muscles needed to maintain posture relieves and eliminates back pain.

  4. Stretching helps prevent injury.
    – If you stretch and increase the range in which a muscle can move, the likelihood of injury is reduced. Stretching before exercise especially helps prevent injury by allowing blood to flow to the muscles, warming them up, and relieving any tightness that may arise.

  5. Stretching reduces muscle soreness.
    – If you have soreness in a muscle or muscle group due to a recent workout, stretching will eliminate that discomfort.Often when we are injured, the muscles around the injured area tense up as a defensive reaction. By stretching these tense muscles, pain and soreness can be relieved.

Basic stretching exercises

  • Kneel down and extend one leg between your arms, straighten your back, keeping the load on your torso. Hold this pose for 30 seconds, focusing on your breathing. Then switch to the other leg and hold for 30 seconds.

  • Start with a lunge with one foot on the floor. Next, you need to tighten the pelvis and raise the chest high. Lean forward and you can feel the hip stretch. Hold for 30 seconds and then repeat on the other leg.

  • Starting from the same position as above, place your hands on the floor and lift your back leg off the floor. Rotate your upper body to the right side. Engage the body while rotating.Hold for 30 seconds and repeat on the other side.

  • Lie on your back. Raise your legs into the air at a 90 degree angle. Bend one knee outward. Place your hands behind your straightened knee and bring it closer to you. Hold the pose for 30 seconds and then switch legs.

  • Sit on the ground with your legs apart. Stretch and reach with your right hand to your left leg, hold for 30 seconds. Repeat on the other side for 30 seconds.

Recommendations and contraindications for stretching

Stretching in general is very beneficial for the body. There are states when it is necessary to eliminate a number of problems. But since stretching is intense physical activity, be careful with contraindications.

The indications are:

  • Weakness of muscles, especially with their shortening due to imbalance.

  • Prevention of injuries of the musculoskeletal system.

  • Soreness on natural movements.

  • Posture defects.


  • Recent fracture with incomplete bone union.

  • Acute inflammation or infection, recent surgery with early tissue healing.

  • Hematoma or other sign of tissue injury.

Stretching in general is very beneficial for the body.There are states when it is necessary to eliminate a number of problems. But since stretching is intense physical activity, be careful with contraindications.

News of the Department of Vascular Surgery №1

In the summer season, there is a tendency for exacerbation of cardiovascular diseases. Due to the heat at this time, the human body is dehydrated and becomes prone to thrombosis.This leads to an increase in hospitalizations in the department of vascular surgery of patients with thromboembolic lesions of the great vessels of the arterial and venous bed.

Clinical case from the practical experience of the Department of Vascular Surgery.

Patient K., 83 years old, was taken to the admission department of the GBUZ GKB No. 3 of the Ministry of Health of the Republic of Kazakhstan by the ambulance team, with complaints of pain in the right lower extremity, a feeling of cold snap and numbness, aggravated with minimal physical exertion, arising acutely, about three hours back.Since the onset of the above complaints, the patient’s condition worsened. At the initial examination, the pale cyanotic color of the skin of the right lower extremity attracted attention, there was a pronounced thermal asymmetry. A sharp soreness of the muscles of the lower leg of the affected limb, the absence of pulsation in the popliteal artery and tibial arteries is also determined. According to the patient, for a long time suffers from heart rhythm disturbances: a constant form of atrial fibrillation.

The preliminary diagnosis was made: “Thromboembolism of the popliteal artery.Acute arterial insufficiency 1B-2A according to V.S. Savelyev. ” An ultrasound scan of the arteries of the lower extremities was performed, according to which the diagnosis was confirmed.

In order to save a limb and prevent life-threatening toxicometabolic syndrome, it was decided to perform an emergency surgery.

In the operating room under the MCA medial access in / 3 tibia, the popliteal artery (RCA) and its trifurcation (the proximal segment of the PBBA, MCA and ZBBA) were isolated, taken on turnstiles.After systemic heparinization, the patient is administered intravenously with 5 thousand units. A combined RCA and BBA embolthrombectomy was performed. A good retrograde blood flow was obtained from the tibial arteries. However, questionable central blood flow was obtained from the RCA. With careful revision, a stenosing atherosclerotic plaque is visualized in the lumen of the artery. The lack of adequate pulsating arterial flow and the presence of convincing retrograde blood flow were the reason for the decision to perform reconstructive surgery.Performed femoropopliteal autovenous shunting (v. Sapfena magna). The postoperative period was uneventful and uneventful. Signs of limb ischemia regressed: the leg acquired a physiological coloration, warmed up, a pulse appeared on the arteries of the foot, and the veins filled.

The limb function was fully restored. Due to the presence of concomitant cardiac pathology, constant anticoagulant therapy was prescribed.

Discharged in satisfactory condition, on the 12th day after removal of stitches, under the supervision of a surgeon and therapist at the place of residence.

Summarizing the presented case, I would like to draw your attention to the fact that in order to prevent such situations, people with chronic cardiovascular diseases should pay attention to the amount of fluid they consume and be monitored by a therapist or cardiologist to correct the received therapy.


Osteomalacia in the practice of an endocrinologist: etiology, pathogenesis, differential diagnosis with osteoporosis | Golounina


Osteomalacia is a systemic skeletal disease characterized by impaired mineralization or defective mineralization of the newly formed bone matrix in adults.Unlike osteoporosis, in osteomalacia, excessive accumulation of non-mineralized osteoid comes to the fore, which contributes to the development of secondary deformities and bone fractures [1].

Bone minerals are formed by small imperfect hydroxyapatite crystals [Ca 10 (PO 4 ) 6 (OH) 2 ]. Calcium, phosphate and alkaline phosphatase (ALP) are required for full bone mineralization. This process is disrupted by a deficiency of vitamin D, a decrease in calcium absorption in the intestine, hypophosphatemia, a mutation in the gene ALPL , which encodes a nonspecific tissue alkaline phosphatase (TNSALP) isozyme.A characteristic sign of insufficient mineralization in bone biopsy is an increased content of osteoid – newly synthesized non-mineralized collagen on the bone surface. The most pronounced lack of mineralization is observed in hypophosphatasia, which is associated with the complete absence of TNSALP [2].


Diagnosis of osteomalacia in most cases is based on the results of clinical, laboratory and X-ray studies.At the same time, the similarity of osteomalacia symptoms with other metabolic osteopathies, as well as with conditions not associated with skeletal pathology, often complicates the diagnosis (Table 1).

Table 1. Differential diagnosis of osteomalacia



Decrease in IPC

Osteoporosis, renal osteodystrophy, primary hyperparathyroidism

Skeletal deformities

Osteochondrodysplasia, hypophosphatasia

Bone pain

Rheumatic polymyalgia, ankylosing spondyloarthrosis, hypophosphatasia

Muscle weakness

Neuromuscular diseases

ALP increase

Primary hyperparathyroidism, renal osteodystrophy, bone metastases

Based on the clinical picture of the disease, two forms of osteomalacia are distinguished – asymptomatic and manifest.The asymptomatic form is characterized by the absence of obvious signs and complaints, but the results of X-ray studies reveal a decrease in bone mineral density (BMD) [3].

One of the features of the clinical manifestation of the manifest form of osteomalacia is pronounced muscle weakness due to a deficiency of calcium or phosphorus, which are directly involved in the transmission of neuromuscular impulses, as well as a pronounced deficiency of vitamin D [4, 5]. Muscle weakness, characteristic of the manifest form of osteomalacia, determines the violation of the gait, which is described by patients as “cotton”.”Duck gait” when walking due to muscular hypotension and atrophy is a serious clinical sign that allows one to suspect a diagnosis.

Generalized diffuse bone pain resulting from stretching of the periosteum during bone deformity, especially in the lumbar spine, pelvic bones and lower extremities, is another common complaint of patients with a manifest form of osteomalacia. Examination reveals pain on palpation in the areas of bone projections, curvature of the spine, deformity of the chest and pelvis, especially with a long course of the disease [3].

The etiological classification of osteomalacia in adults and the main laboratory signs of differential diagnosis are summarized in Table. 2.

Table 2. Etiological classification of osteomalacia in adults and the main laboratory signs of differential diagnosis (adapted from [68])

Ca 2+


25 (OH) D

1.25 (OH) 2 D 3



Hypocalcemia (vitamin D-related causes)

Vitamin D deficiency

(insufficient insolation, malabsorption syndromes, including in patients after bariatric surgery, low vitamin D content in food)




# / N / $


Liver pathology





N / #

Kidney pathology



N / $



Vitamin D-resistant rickets and osteomalacia type I (violation of 1α-hydroxylation of 25 (OH) D)






Vitamin D-resistant rickets and osteomalacia type II (target organ resistance to 1.25 (OH) 2 D 3 )






Hypophosphatemia associated with overproduction of FGF23

Autosomal dominant hypophosphatemia and osteomalacia (point missense mutations in the FGF23 gene)

N / $




N / #

# FGF23

Autosomal recessive hypophosphatemic rickets and osteomalacia (mutations in the DMP1 gene)

N / $




N / #

# FGF23

X-linked dominant hypophosphatemic rickets (mutations in the PHEX gene)

N / $




N / #

# FGF23

Tumor-induced osteomalacia (secretion of FGF23)

N / $




N / #

## FGF23

McCune-Albright-Braitsev syndrome (polyostous fibrous dysplasia)

(mutations in the GNAS gene)





N / #

## FGF23

Skin-skeletal hypophosphatemic syndrome, or epidermal nevus syndrome (mutations in the RAS-chain genes: HRAS, KRAS, NRAS)

N / $




N / #

# FGF23

Hypophosphatemia (other disorders leading to a decrease in phosphorus)

Hereditary recessive hypophosphatemic rickets with hypercalciuria (mutations in the SLC34A3 (NaPi-IIc) gene)






# Ca 2+ and # phosphorus in urine

Loss of phosphorus with urine

(X-linked recessive hypophosphatemic rickets with hypercalciuria (Dent’s disease), Fanconi’s syndrome, heavy metal poisoning, cadmium poisoning)






Excessive consumption of antacids






Toxic osteomalacia







Aluminum (parenteral)












Other causes of osteomalacia

Hypophosphatasia (adult)






$$ ALF

Metabolic acidosis







Most often, osteomalacia develops as a result of severe vitamin D deficiency (<10 ng / ml) of any etiology, as well as disorders of its metabolism, which leads to a decrease in calcium absorption in the intestine and is accompanied by constant or transient hypocalcemia [6].Today, insufficient supply of vitamin D is typical for the bulk of the population in temperate geographic latitudes, and in some countries, vitamin D deficiency is recognized as a pandemic condition.

In normal kidney function, hypocalcemia due to vitamin D deficiency, in contrast to hypoparathyroidism, is accompanied by hypophosphatemia and increased renal phosphate clearance. Such an increase in phosphate clearance is a direct consequence of compensatory (secondary) hyperparathyroidism (SHPT) due to hypocalcemic stimulation of parathyroid hormone (PTH) secretion, PTH gene expression, and proliferation of parathyroid gland (PTG) cells [7].Determination of the content of phosphates and PTH in blood serum is necessary for the differential diagnosis of such disorders with hypoparathyroidism. In turn, VHPT leads to increased mobilization of calcium from bones, increased reabsorption of calcium in the kidneys, and increased hydroxylation of 25 (OH) D to 1.25 (OH) 2 D 3 1α-hydroxylase (CYP27B1). Severe vitamin D deficiency (<10 ng / ml) is usually accompanied by a low level of 1.25 (OH) 2 D 3 , while against the background of moderate vitamin D deficiency (<20 ng / ml), stimulation of CYP27B1 under the action of PTH can lead to normal or even elevated levels of 1.25 (OH) 2 D 3 [8].

In the vast majority of cases, osteomalacia, which develops due to vitamin D deficiency, proceeds without clinical symptoms or manifests itself as proximal myopathy and bone pain, but these symptoms can be subtle and often go unnoticed at the initial stage of the disease.

Interestingly, cases of the development of rickets in children as a result of vitamin D deficiency with adequate calcium intake and calcium deficiency under conditions of sufficient supply of the body with colecalciferol [9] are described in all countries of the world, while in adults osteomalacia associated only with insufficient intake calcium with food was not observed.It is known that restriction of dietary calcium intake leads to an increase in the efficiency of calcium absorption in the intestine due to the activation of PTH secretion, which, in turn, induces the synthesis of 1α-hydroxylase (CYP27B1) in the proximal convoluted and rectal tubules of the kidneys with the subsequent formation of 1.25 (OH ) 2 D 3 [10]. The biological effect of 1,25 (OH) 2 D 3 is mediated through the nuclear vitamin D receptor (VDR) [11]. Interaction of VDR with 1,25 (OH) 2 D 3 leads to protein hyperphosphorylation with subsequent conformational changes [12, 13] and activation of VDR on the apical membrane of intestinal cells.As a result, the expression of genes for highly selective calcium channels TRPV6 (transient receptor potential cation channel, subfamily V, member 6, TRPV6), genes for calcium-binding proteins (calbidin D28k, calbidin D9k) and other genes involved in transcellular calcium transport from its subsequent absorption in the intestine [13-15]. In addition, PTH together with 1,25 (OH) 2 D 3 stimulate the reabsorption of calcium in the renal tubules, regardless of the calcium concentration in the glomerular filtrate, reduce its excretion in the urine, thereby increasing the extracellular concentration.This effect is enhanced by increased release of calcium-binding proteins – calbidin D28k and calbidin D9k, which is stimulated by 1.25 (OH) 2 D 3 [14]. Calcium reabsorption is also directly enhanced by any tendency towards hypocalcemia, which is captured by calcium-sensitive receptors (CaSRs), followed by modulation of PTH synthesis and secretion. The effect of calcium deficiency in the diet is reduced by about 15% due to the release of calcium from bone tissue in response to the action of PTH and 1,25 (OH) 2 D 3 .As a result of the homeostatic mechanisms described, people with insufficient calcium intake maintain near-normal levels of total and ionized serum calcium, but there is an increased absorption of calcium in the intestine, increased bone resorption and progressive osteopenia, increased calcium reabsorption and decreased phosphate reabsorption in the renal tubules, low calcium excretion and increased urinary phosphate excretion; and high serum PTH concentration.


Clinically, severe vitamin D deficiency resulting from liver disease is rare because the degree of liver destruction required to disrupt CYP2R1 hydroxylation of vitamin D at C25 to form 25 (OH) D is incompatible with long-term survival. Families have been described in which clinical and biochemical signs indicated a hereditary defect in 25-hydroxylation [16-18].However, genetic analysis of unrelated people did not reveal mutations either in the coding region or in the splicing points of the CYP2R1 gene [19]. The obtained data, together with observations according to which mice with the genotype Cyp2r1 – / – had a decrease in 25 (OH) D level only by 50%, indicate that CYP2R1 is not the only enzyme capable of 25-hydroxylation of vitamin D [twenty].


There are two groups of kidney diseases that have a significant effect on the state of bone tissue: chronic kidney disease (CKD) and diseases associated with a predominant lesion of renal tubular functions – de Toni – Debre – Fanconi syndrome, renal tubular acidosis.

The final stage of vitamin D activation is hydroxylation by 1α-hydroxylase in 1,25 (OH) 2 D 3 in the proximal convoluted tubules of the kidneys [21]. In chronic kidney disease, all links in the regulation of mineral metabolism are disrupted, which are manifested already in the early stages of the disease by a decrease in the synthesis of calcitriol, which controls the active reabsorption of calcium in the intestine, an increase in the production of fibroblast growth factor 23 (FGF23), which normally prevents the development of hyperphosphatemia, an increase in expression of the sclerostin and Dickkopf-1 genes [22, 23].

The primary increase in FGF23, which reduces the activity of 1α-hydroxylase, is the main cause of calcitriol deficiency, predetermining the further development of bone mineral disorders in patients with CKD [24]. At normal serum phosphorus levels, intracellular phosphate and the accumulation of phosphate in the proximal renal tubules act as a signal to enhance FGF23 production. Since the drop in α-Klotho synthesis, detected even in patients with stage I CKD, outpaces the increase in FGF23, there is reason to assume that Klotho deficiency is the primary event in the development of renal osteodystrophy [25, 26].

In the early stages of kidney disease (CKD stage II), even in the absence of changes in mineral metabolism under the influence of proinflammatory cytokines, transforming growth factor beta (TGF-β), toxins (indoxyl sulfate), the expression of sclerostin in osteocytes and its level in blood serum increases, causing disturbances in the Wnt signaling pathway, which inhibits the maturation and differentiation of osteoblasts, but inhibits the production of PTH [27]. Simultaneously, α-Klotho deficiency develops and the secretion of FGF23 by osteocytes and osteoblasts increases, preventing hyperphosphatemia [24].As CKD progresses, the inhibitory effect of FGF23 on PTH secretion is overcome and the level of Dickkopf-1 and SFRP1 (secreted-frizzled related protein 1) in the serum of patients increases [28]. In this case, the production of sclerostin decreases, and Dickkopf-1 aggravates the impairment of the Wnt signaling pathway and bone mineralization, which ultimately induces the development of IHPT [27].

De Toni – Debreu – Fanconi syndrome is a generalized proximal tubulopathy characterized by a nonselective defect in the systems of transport and reabsorption of amino acids, glucose, phosphates, bicarbonates, uric acid, citrates, and proteins with a low molecular weight [29].In this syndrome, calcium, magnesium, sodium, potassium and water are also excreted in large quantities. Distinguish between hereditary and acquired variants of this disease.

Acquired Fanconi syndrome occurs when poisoning with salts of heavy metals (lead, cadmium, mercury), toxic effects of drugs, various chemicals, compounds that damage the proximal renal tubules and, as a result, reduce phosphate reabsorption and increased loss of phosphorus in the urine [30 ].The developing hypophosphatemia disrupts normal bone mineralization, and metabolic acidosis leads to a decrease in alkaline phosphatase activity. In addition, in patients with Fanconi syndrome, a relative decrease in the level of vitamin D in the blood serum is often observed [31].

Renal tubular acidosis is another group of tubular renal diseases characterized by impaired reabsorption of bicarbonate, secretion of hydrogen ions, or a combination of both defects. Due to impaired reabsorption of bicarbonates in the proximal tubule, bicarbonaturia develops at a normal concentration of bicarbonates in the blood plasma, which leads to metabolic acidosis, despite the intact mechanisms of distal secretion of hydrogen ions.As soon as the plasma bicarbonate concentration falls below the threshold value, the filtered bicarbonate begins to be completely reabsorbed [32]. On the part of the bone tissue, there are also changes in the type of rickets in children and osteomalacia in adults.


Serum phosphate concentration is regulated by sodium-dependent cotransporters NaPi-IIa and NaPi-IIc, expressed in proximal renal tubules. A decrease in tubular reabsorption, for example, with a pathological increase in the level of PTH in the serum against the background of primary or secondary hyperparathyroidism, with PTHP-associated / dependent hypercalcemia against the background of malignant tumors is accompanied by the development of hypophosphatemia.

Other causes of impaired phosphate reabsorption in the renal tubules include osmotic diuresis associated with poorly controlled diabetes mellitus, alcoholism, hyperaldosteronism and exposure to a number of drugs or toxins such as acetazolamide, ifosfamide, high doses of glucocorticoids, cisplatin, and others.

Overproduction of FGF23 becomes a somewhat less common cause of osteomalacia in adults. Linkage analysis in susceptible relatives revealed a gene mutation FGF23 as the main cause of autosomal dominant hypophosphatemia and osteomalacia [33].Point missense mutations in the gene FGF23 change the amino acid sequence at the site of FGF23 cleavage by a furin-like protease (R176XXR179 / S180), which is accompanied by an increase in the concentration of the active form of FGF23 in the blood [34]. An increased level of FGF23 is also noted in autosomal recessive hypophosphatemia caused by mutations in the genes encoding dentin matrix protein-1 (DMP1) and FAM20C. DMP1 is expressed in osteocytes and, presumably, regulates the local synthesis of FGF23 [35].FAM20C is a secreted kinase that phosphorylates FGF23 near the furin cleavage site. Such phosphorylation is required to inactivate cleavage by furin-like protease [36]. High levels of FGF23 in the blood are also observed in X-linked dominant hypophosphatemic rickets caused by inactivating mutations in the gene PHEX [37,38], in osteomalacia induced by a tumor secreting FGF23, epidermal nevus syndrome [39], as well as in approximately 50% of patients with McCune – Albright – Braitsev syndrome [40].

Renal phosphate clearance may also be impaired by inactivating mutations in the NaPi-IIc cotransporter, which cause a rare disorder known as hereditary recessive hypophosphatemic rickets with hypercalciuria. In this disease, the loss of phosphate through the renal tubules causes a concomitant increase in serum 1.25 (OH) 2 D 3 , causing hypercalciuria [41].

It is believed that therapy with the use of protein tyrosine kinase inhibitors – imatinib and nilotinib causes the development of hypophosphatemia due to inhibition of the formation of both osteoblasts and osteoclasts, a decrease in serum calcium, stimulating the development of IHPT [42–44].


It is extremely rare that the cause of osteomalacia is hypophosphatasia, a rare hereditary metabolic disease caused by mutations in the gene ALPL [2]. In hypophosphatasia, excessive accumulation of inorganic pyrophosphate, pyridoxal-5′-phosphate and phosphoethanolamine disrupts the processes of bone mineralization and the formation of hydroxyapatite crystals [45]. Some of the symptoms of hypophosphatasia found in adults may indicate rickets experienced in childhood.The main laboratory sign of hypophosphatasia, which allows differential diagnosis with other metabolic diseases of the skeleton, is a pronounced decrease in alkaline phosphatase in the blood [46].

Rarely, mutations in both alleles of the gene CYP27B1 , which encodes 1α-hydroxylase, can cause resistance to vitamin D. From a biochemical point of view, this disease, called pseudo-vitamin D-deficient rickets, is characterized by hypocalcemia and VHPT. The only metabolic disorder that distinguishes disease from vitamin D deficiency in the diet is normal or elevated serum 25 (OH) D levels, accompanied by a low concentration of 1.25 (OH) 2 D 3 [47].Pseudo-vitamin D-deficient rickets is inherited in an autosomal recessive manner and manifests itself as rickets, osteomalacia, and seizures. Timely detection of this disease, the appointment of active metabolites of vitamin D leads to clinical remission.

Mutations in the gene VDR cause the development of another rare hereditary disease with an autosomal recessive mode of inheritance – vitamin D-resistant rickets and osteomalacia, characterized by resistance to the biological effect of 1.25 (OH) 2 D 3 .The biochemical picture of this disease coincides with the picture of vitamin D deficiency and includes hypocalcemia, hypophosphatemia and VHPT, however, in contrast to vitamin D deficiency, an increased content of 1.25 (OH) 2 D 3 is observed [48]. In most patients, the disease manifests itself in early childhood in the form of rickets, hypophosphatemia, seizures and alopecia; however, there are reports in the literature on the manifestation of the disease in late adolescence and even in adults [49–51].Due to the resistance of target organs to the active metabolite of vitamin D, the only therapeutic option is the administration of active metabolites of vitamin D and calcium in supraphysiological doses or parenteral infusions of calcium preparations to correct osteomalacia lesions [52,53]. Studies on mice with a blocked gene Vdr – / – have shown that maintaining normal homeostasis of mineral ions prevents all complications of the disease, with the exception of alopecia [54].

A number of works by foreign researchers present clinical cases describing patients with osteomalacia against the background of chronic fluoride intoxication [55–57]. An interesting fact is that, despite the severity of clinical manifestations, osteomalacia was detected only during a detailed examination of patients for existing bone disorders, pain in the joints and muscles.


The gold standard for differential diagnosis of bone disorders in CKD is tetracycline-labeled bone biopsy.An important aspect of drug therapy for low-turnover bone pathology is the limitation of the prescription of bisphosphonates.

A histomorphometric study is the most accurate method for establishing the diagnosis of osteomalacia, allowing to assess the rate of bone formation and calcification. The level of mineral apposition, the rate of osteogenesis, and the volume of osteoid / bone tissue can be determined from the results of a single biopsy, but only after sequential tetracycline labeling, which is necessary to measure the distance between the two fronts of mineralization [58, 59].The labeling intervals vary somewhat, however, as a rule, they are 3 days at the beginning (1-3 days) and then 3-21 days using 250 mg of tetracycline 3-4 times a day. Fluorescent tetracycline makes it possible to determine the rate of bone tissue renewal, which is normally about 1 µm / day, while complete mineralization of osteoid in normal bone takes 10–21 days [60]. The thickness of the osteoid layer usually does not exceed 15 µm, and the bone surface covered by the osteoid is less than 20% [61].In osteomalacia, the distance between two tetracycline labels decreases, and a non-mineralized matrix appears in the form of an osteoid strip> 15 μm wide and a delay in mineralization> 100 days [62].

Radiological signs of the disease are an increase in the transparency of the bone, blurring of the trabecular pattern of the vertebral bodies due to inadequate mineralization of the osteoid, devoid of calcium, and resorption of secondary trabeculae. With a long course of the disease, deformation of the endplates of the vertebral bodies occurs in the form of their depression (“fish vertebrae”), kyphoscoliosis, a deformed triangular pelvis with protrusion of the sacral promontory, and deformation of long bones are noted [63].The most characteristic X-ray symptom of osteomalacia is narrow transverse lines 2–5 mm wide, located bilaterally and symmetrically, and are fractures of the cortical bone layer due to stress-induced overload (Loozero transformation zones, Loozero pseudofractures) [64]. Such lines are mainly located in the region of the neck and medial part of the diaphysis, near the greater trochanter of the femur, in the pubic articulation and ischial tubercles, less often in the shoulder blades, clavicles, ribs, ulna and metatarsal bones.On bone scintigraphy, Loozero pseudo-fractures appear as “hot” spots [65]. Looser’s multiple transformation zones are described in the literature as Milkman syndrome.

Due to the similarity of radiological signs, osteomalacia must be differentiated from systemic osteoporosis. Osteoporotic changes in the trabecular part of the peripheral skeleton are expressed by a similar resorption of trabeculae, which is radiographically manifested by a rarefaction of their pattern.However, in osteomalacia, in contrast to osteoporosis, cortical and trabecular structures are practically not differentiated, which is clearly noticeable in the lateral projection. In addition, it should be noted that radiography does not serve as a method for diagnosing osteoporosis and is used only if there is a suspicion of the presence of compression fractures of the vertebral bodies and osteoporotic fractures of other localizations. An increase in the transparency of bone tissue on X-ray images is a nonspecific symptom that largely depends on the technical conditions of the shooting and the quality of the appearance of the X-rays.

To date, the most popular method for assessing BMD is dual-energy X-rays absorptiometry (DXA). Despite all the advantages of this diagnostic method, DXA does not allow assessing the bone volume and structure of bone tissue, as well as conducting differential diagnostics and establishing the cause of the decrease in bone mass, since low BMD values ​​can be observed in both osteoporosis and osteomalacia. Thus, in the case of newly diagnosed osteoporosis based on DXA results, it is necessary to carry out differential diagnosis and exclude other metabolic diseases of the skeleton, in which a decrease in BMD and / or low-traumatic fractures are the main manifestations [66].


Along with instrumental diagnostics, it is necessary to conduct a number of biochemical studies characterizing the state of phosphorus-calcium metabolism and bone metabolism. Laboratory changes in osteomalacia include an increase in the activity of alkaline phosphatase, PTH, a slight decrease in calcium and phosphorus in the blood serum, and a decrease in 25 (OH) D <15 ng / ml (Table 3).

Table 3. Changes in laboratory parameters for alimentary causes of osteomalacia according to the data of a retrospective study Basha B.[69], Bhambri R. [70]



Frequency of occurrence,%










Alkaline phosphatase



25 (OH) D, ng / ml



Excretion of calcium in the urine




When analyzing laboratory data, depending on the results obtained, one or another form of osteomalacia can be assumed (see.tab. 1). However, the main task in the treatment of osteomalacia of any etiology is to eliminate vitamin D deficiency, hypocalcemia, hypophosphatemia, and prevent the progression of bone deformities and muscle hypotension.

Elemental calcium is required in all cases of hypocalcemia. When a vitamin D deficiency or resistance to it is detected, the vitamin D metabolite is selected depending on the disease. For example, in CKD, vitamin D-resistant rickets, metabolites are prescribed that do not require appropriate modification (calcitriol or alfacalcidol at a dose of 0.25 to 1 μg / day, in some cases up to 3-4 μg / day).In patients with osteomalacia associated with a deficiency in vitamin D and calcium intake, the use of therapeutic doses of cholecalciferol is optimal [67].

All patients taking vitamin D metabolites and calcium supplements should be aware of potential therapeutic complications and be monitored by an endocrinologist.


Osteomalacia, like osteoporosis, is of great socio-economic importance due to the increased risk of low-traumatic fractures.Unfortunately, most of the works are a description of individual or small series of cases, which makes it impossible to assess the true prevalence of osteomalacia in the population. To exclude a diagnostic error, in the case of a pronounced decrease in bone mass according to the results of DXA, before the appointment of anti-osteoporotic therapy, it is recommended to conduct additional laboratory tests and, in some cases, a histomorphometric study of an iliac biopsy for the purpose of differential diagnosis of osteoporosis and osteomalacia.


Funding source . The search and analytical work and preparation of the article were carried out at the personal funds of the group of authors.

Conflict of interest . The authors declare no obvious and potential conflicts of interest related to the publication of this article.

Contribution of Authors . All authors made a significant contribution to the search and analytical work and preparation of the article, read and approved the final version before publication.

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