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Stumbling upon this blog entry on DOMS was like a flashback to one of Dr. Squat's classic bodybuilding books. Can anyone guess which one? I lost my old copy, and since the book is out-of-print, it's nice to see bloggers reposting it and keeping it alive.

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Delayed-Onset Muscle

Delayed-Onset Muscle Soreness
Delayed onset muscle soreness (DOMS) – sometimes called post-exercise muscle soreness -- involves muscle pain, soreness or stiffness that is not felt until 12-48 hours after exercise. It is commonly experienced when beginning an exercise program after a prolonged layoff or as a raw beginner in weight training or other forms of exercise. It is also common following a change in sports activities, or following a dramatic increase in the duration or intensity of exercise.
Minor, non-debilitating muscle pain is normal and quite ubiquitous. It is a response to strenuous exertion and is part of the adaptation process that leads to greater muscle size, stamina or strength as the muscles recover and supercompensation occurs. The delayed soreness is generally at its worst within the first 2 days following the activity and subsides over the next few days.
DOMS is quite common and quite annoying, particularly for those beginning an exercise program or adding new activities. For example, a beginning exerciser who bikes 10 miles, followed by push-ups and sit-ups is likely to experience muscle pain and soreness in the next day or two.
Causes of DOMS
Delayed onset muscle soreness is thought to be a result of microscopic tearing of the muscle fibers. The amount of tearing (and soreness) depends on how hard and how long you exercise and what type of exercise you do. Any movement you aren't used to can lead to DOMS, but eccentric muscle contractions (movements that cause muscle to forcefully contract while it lengthens) seem to cause the most soreness.
Examples of eccentric muscle contractions include going down stairs, running downhill, lowering weights and the downward motion of squats and push-ups. In addition to small muscle tears there can be associated swelling in a muscle which may contribute to soreness.
Treatment
There is no one simple way to treat delayed onset muscle soreness. In fact, there has been an ongoing debate about both the cause and treatment of DOMS. In the past, gentle stretching was one of the recommended ways to reduce exercise related muscle soreness, but a study by Australian researchers published in 2007 found that stretching is not effective in avoiding muscle soreness.
Does anything work to reduce delayed-onset muscle soreness? Some people have found the following advice helpful, but it's best for an individual to try a few things to see what works for them. Ultimately, the best advice for treating DOMS is to prevent it or at least minimize it in the first place.
Here are some tips you should provide your client with for dealing with DOMS:
• DOMS will go away in 3 to 7 days with no special treatment. You may wish to exercise a muscle after 3-4 days despite mild stiffness or pain. Some people claim that this helps in speeding the recovery process. Just don’t overdo it.
• You may still exercise other (non-affected) muscles. A complete cessation of working out is not necessary or fruitful.
• Try an ice bath or contrast water bath. Although no clear evidence proves they are effective, many pro athletes use them and claim they work to reduce soreness.
• Use active recovery techniques. This strategy does have some support in the research. For example, perform some easy low-impact aerobic exercise to increase blood flow. This may help diminish muscle soreness.
• Although research doesn't find that stretching reduces soreness, some say they like it because it simply feels good. It’s a temporary fix at best.
• Gently massage the affected muscles. Some research has found that massage was effective in alleviating DOMS by approximately 30% and reducing swelling, but it had no effects on muscle function.
• Try using a nonsteroidal anti-inflammatory drug (NSAIDs such as aspirin or ibuprofen) to reduce the soreness and inflammation.
• Avoid any vigorous activity that increases pain in the affected muscle(s).
• Don't forget to warm up completely before your next exercise session. There is some research that supports that a warm-up performed immediately prior to unaccustomed eccentric exercise produces small reductions in DOMS, while a cool-down performed after exercise does not.
• If your pain persists longer than 7 days, or reaches an intolerable pain level despite these measures, or if you notice a brownish tint in your urine, consult your physician. This may be a sign of rhabdomyolysis (explained below).
Preventing DOMS
While DOMS is common and annoying, it is not necessary for it to be so painful as to become disruptive or debilitating. There are many things you can do to ameliorate the debilitating effects of DOMS:
• Warm up thoroughly before activity and cool down completely afterward.
• Be sure to hydrate before exercise and rehydrate during and after exercise.
• When beginning a new activity start gradually and build up your time and intensity.
• Start a new weight training routine with a weight that yu can easily perform 10-12 with, but do only 5-6 reps with that weight at first. Gradually increase the amount you lift as well as the number of reps and sets you perform over several weeks.
• Avoid making sudden major changes in the type of exercise you do.
• Avoid making sudden major increases in the frequency, intensity or duration of your exercises.
• Avoid making sudden major increases in the amount of time that you exercise.
At this point, we will segue to the extreme case of DOMS, a condition that is referred to among medical professionals as rhabdomyolysis.

Rhabdomyolysis
While not clinically proven, it appears that rhabdomyolysis is on a continuum with DOMS. Like DOMS, rhabdomyolysis is caused by the breakdown of skeletal muscle tissue due to injury, but it is far more severe. Unlike DOMS, rhabdomyolysis is a potentially life-threatening syndrome resulting from the breakdown of skeletal muscle fibers with leakage of muscle contents into the circulation. While muscle injury due to exercise stress is the most common among gym-goers, muscle damage may be caused by physical, chemical, or biological factors. The destruction of the muscle leads to the release of the constituents of damaged muscle cells into the bloodstream. Some of these muscle constituents, such as myoglobin, are harmful to the kidney and may lead to acute kidney failure.
One of the reasons that a thorough medical history on your client is vital is that rhabdomyolysis can be caused by several other common factors besides intense physical activity. As always, if any factors appear on your client’s history that you are unsure about, or which match the physical or non-physical causes listed below, you must discuss them with your client’s physician.
Signs and symptoms
Most cases of rhabdomyolysis develop as a result of muscle injury or strain, or other external causes (such as medication or intoxication). However, the cause is not always directly evident. Pain, tenderness, weakness and edema (swelling) of the affected muscles is usually present. If the swelling is very rapid, low blood pressure and shock may be present due to depletion of fluid from the bloodstream. Other symptoms are nonspecific and result either from the consequences of the breakdown in muscle tissue, or from the condition that caused the muscle breakdown.
Swelling of the damaged muscle occasionally leads to compartment syndrome, the compression by swollen muscle of surrounding tissues in the same fascial compartment (such as nerves and blood vessels), leading to damage or loss of function in the part of the body supplied by these structures. Symptoms of this complication include decreased blood supply, decrease in sensation, or pain in the affected limb.
Release of the components of muscle tissue into the bloodstream leads to disturbances in electrolytes, causing nausea, vomiting, confusion, coma and cardiac arrhythmias (abnormal heart rate and rhythm). Furthermore, damage to the kidneys may lead to dark (tea-colored) urine or a marked decrease or absence of urine production, usually about 12–24 hours after the initial muscle damage. Finally, disruptions in blood clotting may lead to the development of a state called disseminated intravascular coagulation.

This chart shows how DOMS and rhabdomyolysis represent overlapping ends of the continuum.

Severity

1
No tissue damage (sub-Acute Exercise; This form of training is used with new clients who have not exercised in years, and must learn the exercise movements and to overcome the ill effects of sarcopenia -- sedentary lifestyle )
2
Mild (normal and beneficial) tissue damage resulting in mild DOMS (this form of training is used with beginning clients who have just begun exercising after years of sedentary lifestyle
3

4
Moderate (normal and beneficial) tissue damage resulting in moderate DOMS (this is the effect which most fitness enthusiasts and athletes experience upon beginning a new regimen or exercise that is mildly taxing)
5

6
Heightened (moderately excessive but potentially beneficial) tissue damage resulting in heightened DOMS (this form of training is often used by bodybuilders attempting to effect fiber fusion/hypertrophy; When performed repeatedly over time, usually leads to overreaching/overtraining)
7

8
Strenuous and exhaustive exercise prompting heightened-to-severe tissue damage resulting in non-traumatic (asymptomatic) rhabdomyolysis, which generally is not accompanied by visible changes in urine color or elevated CK. Often experienced by marathoners, soldiers and poorly supervised athletes.
9

10
Severe tissue damage resulting in traumatic rhabdomyolysis, signaled by release of muscle cell content into the plasma, causing myoglobinuria (red or brown urine) and elevated serum aldolase and CK. Beginners pushed by unqualified personal trainers to exceeding levels of exercise intensity for a prolonged period are often victims. Often experienced by marathoners, soldiers and poorly supervised athletes. Hospitalization required.
11

12
Severe tissue damage resulting in traumatic rhabdomyolysis, signaled by release of muscle cell content into the plasma, causing myoglobinuria (red or brown urine) and elevated serum aldolase and CK, and/or compartment syndrome, and hospitalization is required.
13

14

15 Massive and severe tissue damage resulting in dialysis-dependent acute renal failure. Hospitalization required.

Traumatic rhabdomyolysis resulting in acute renal failure and (possibly) death.

Local features
• Muscle pain
• Tenderness
• Swelling
• Bruising
• Weakness
Systemic features
• Tea-colored urine
• Fever
• Malaise
• Nausea
• Emesis
• Confusion
• Agitation
• Delirium
• Anuria

Causes
Anything that destroys muscle tissue can cause rhabdomyolysis. The causes of rhabdomyolysis can be classified as either physical or non-physical. Physical rhabdomyolysis is in some situations confined to a particular area of the body, while rhabdomyolysis due to other causes tends to affect all muscles simultaneously.
Physical causes
Recognized physical causes for rhabdomyolysis are:
• Traumatic compression of muscles: crush syndrome (e.g. in earthquakes), car accident, confinement in a fixed position (e.g. after a stroke, due to drunkenness or in prolonged surgery),
• Obstruction of blood supply to muscles
• Excessive muscle strain or activity: extreme physical exercise (particularly when poorly hydrated),
• Electrical: lightning, high-voltage electric shock, including electroshock weapon injuries
Non-physical causes
Non-physical causes reported to cause rhabdomyolysis include:
• Disorders of muscle energy supply (usually hereditary enzyme problems): Poisons such as heavy metals and venom from insects or snakes
• Foodborne toxins,
• Drugs of abuse, such as Ecstacy, ethanol, methamphetamines, cocaine, heroin, PCP
• Medications:
o statins,
o anti-psychotic medications,
o neuromuscular blocking agents
o diuretics
• Infections
• Electrolyte and metabolic disturbances
• Autoimmune muscle damage

Diagnosis
The most reliable test in the diagnosis of rhabdomyolysis is the level of creatine kinase (CK) in the blood. This enzyme is released by damaged muscle, and levels above 5 times the upper limit of normal (ULN) indicate rhabdomyolysis. Normal values are usually between 25 and 200 U/L. Depending on the extent of the rhabdomyolysis, levels up to 100,000 units are not unusual. Initial and peak CK levels have a linear relationship with the risk of acute renal failure: the higher the CK, the more likely it is that kidney damage will occur. CK levels rise after 12 hours of the initial damage, remain elevated for 1–3 days and then fall gradually. Myoglobin has a short half-life, and is therefore less useful as a diagnostic test in the later stages.
Compartment syndrome is a clinical diagnosis (i.e. no tests conclusively prove its presence or absence), but direct measurement of the pressure in a fascial compartment may be used to assess its severity. Values of 30–50 mmHg indicate severe compartment syndrome and possible need for fasciotomy, which is an incision to relieve increased pressure.

Complications of Rhabdomyolysis
Early complications
• Hyperkalemia
• Hypocalcemia
• Hepatic inflammation
• Cardiac arrhythmia
• Cardiac arrest
Late complications
• Acute renal failure
• Disseminated intravascular coagulation
Early or late complication
• Compartment syndrome

Various consequences of muscle swelling and breakdown together may cause renal failure. The swelling of large areas of muscle tissue leads to depletion of fluid from the circulation, causing relative lack of blood flow to the kidney. Uric acid may precipitate in the tubules, causing obstruction. Finally, the most important problem is the accumulation of myoglobin in the tubules. Myoglobinuria (the appearance of myoglobin in the urine) occurs when the levels in plasma exceed 1.5 mg/dl. As the kidneys reabsorb more water from the filtrate, myoglobin forms casts that obstruct the normal flow of fluid through the nephron; the condition is worsened by high levels of uric acid and acidification of the filtrate. Iron released from the myoglobin generates reactive oxygen species, damaging the kidney cells. Acute tubular necrosis (destruction of the cells of tubules) occurs, preventing the kidney from performing its normal excretory functions (hence the fall in glomerular filtration rate), electrolyte regulation (hence worsening potassium levels) and hormone production (hence decreased vitamin D processing, further worsening the low calcium levels).
Treatment
Fluid therapy
The main goal of treatment is to treat shock and preserve kidney function. Initially this is done through the administration of generous amounts of intravenous fluids, usually saline (0.9% weight per volume sodium chloride solution). Amounts of 6 to 12 liters over 24 hours are recommended.
Prognosis
The prognosis depends significantly on the underlying cause and whether any complications occur. Rhabdomyolysis patients who experience acute renal failure (ARF) may have a mortality rate as high as 20%.
Case Reports
•Case #1: A 19-year old college freshman experienced 2 episodes of rhabdomyolysis while playing competitive ultimate frisbee. The first episode occurred following a 5-hr frisbee tournament (her actual playing time was estimated to be 3 hours). At the end of the tournament, she developed severe, diffuse muscle soreness. She was unable to straighten her elbows and knees and had difficulty standing because of soreness in her back muscles. Her urine became brown-colored but she did not seek medical attention. The muscle soreness resolved after 3 days. Her second episode of rhabdomyolysis occurred 2 weeks later. This time, she participated in a 2-hr frisbee scrimmage followed by a 2-hr karate class. Shortly thereafter, she experienced severe muscle cramping and sought medical attention. The following day, her CK (creatine kinase, an enzyme found in muscle cells) levels peaked at 59,000 U/L. Over the following week, the CK level fell to 266. She did not recall any illness or fever preceding these 2 episodes and was not taking any medication. Until this point in her life, this young woman had no history of rhabdomyolysis. In high school, she played tennis and ran track. She tolerated workouts of up to 2 hours without difficulty. She was a sprinter, but could run 2 miles with no problem. It was subsequently determined that she had a genetic predisposition for rhabdomyolysis (Krivickas LS. 2006).
•Case #2: A 40-year old black male developed rhabdomyolysis in his biceps after doing several sets of "negative curls". These are exercises where a spotter helps lift a heavy barbell up to the ready position (concentric phase), and then the weight-lifter lowers the barbell (without assistance) until his arms are in an extended position (eccentric phase). Roughly 18 hours after doing negative curls, this athlete experienced severe biceps pain and could not fully extend his arms. His CK levels reached 76,000 U/L (normal range: 60-320 U/L) (Bolgiano EB. 1994).
•Case #3: A 21-year old inmate participated in a prison hazing ritual where he had to move 10 chess pieces on the floor. (I won't mention which part of his anatomy was used to pick up the chess pieces, but, suffice to say it wasn't his hands!) The chess pieces were lined up on the floor and the prisoner had to squat to first pick them up, then had to squat again to put them down. This required approximately 110 deep knee bends. Within 12 hours, he was unable to leave his bed because of severe pain in his anterior thighs. Three days later, he was taken to the hospital with complaints of brown urine and nocturia. On physical exam, his thighs were mildly swollen and his quadriceps were exquisitely tender. He was unable to flex his knees. He had protein in his urine, and his CK level was greater than 160,000 U/L. With treatment, the CK levels returned to normal after 12 days (Frucht M. 1994).
•Case #4: During a 6-month Amphibious Task Force deployment to the Mediterranean Sea, five sailors and Marines developed severe arm pain. Each patient had begun a vigorous upper-extremity work-out program in the ship's weight room 1-3 days prior to the onset of these symptoms. A medical exam revealed elevated serum muscle enzymes and the presence of blood in the urine. All subjects responded to IV fluids, alkalinization of the urine, and rest (Brown JA, et al. 1994).
•Case #5: In Greece, there is a race called the "Spartathlon" that requires running from Athens to Sparta in under 36 hours. (The distance is 152 miles!) After one of these events, blood levels of CK were measured in 39 athletes within 15 minutes after completing the race. It was found that the average post-exercise CK level was 43,763 +/-6,764 IU/L. Although this is a very high CK value, none of the runners required medical attention during or after the race (Skenderi KP, et al. 2006).
Summary
All strenuous exercise results in some degree of muscle fiber breakdown. The extent of muscle fiber breakdown is dependent upon several factors, all of which are under the control of the person in charge (e.g., the exerciser himself/herself, or their coach, teacher, drill instructor or personal fitness trainer). ISSA categorizes the damage thusly along a continuum:
• Normal and beneficial muscle fiber breakdown resulting in an array of physical and metabolic circumstances which cause little or mild muscle soreness
• Supernormal muscle fiber breakdown resulting in an array of physical and metabolic circumstances which cause severe muscle soreness that can hamper normal movement, activity and flexibility
• Major (severe) muscle damage resulting in an array of physical and metabolic circumstances which threaten the long-term well-being or life of the individual.
The first two syndromes are widely referred to as “delayed onset muscle soreness” (DOMS), and most people who have exercised strenuously have experienced it to one degree or another. If the continuum were numbered in a fashion similar to the Borg scale of perceived exertion, the first may be rated between 1 – 5, the second between 6 – 10, and the third, referred to by the medical community as “exertional rhabdomyolysis,” between 11 – 15. It is the third degree of the continuum which concerns ISSA greatly, as the incidence of this syndrome appears to either be increasing or more frequently reported. It can result in kidney failure and death. There are instances in which personal fitness trainers were found culpable.
Exertional rhabdomyolysis is characterized by hypokalemia, intravascular coagulation, hyperuricemia, myoglobinuria, myalgia, and lactic acidosis. Exertional rhabdomyolysis may occur after an individual performs unaccustomed, exhaustive exercise in the heat and/or may be exacerbated when the individual is dehydrated. Some people appear more susceptible to exertional rhabdomyolysis than others. Heat stress and dehydration appear to exacerbate rhabdomyolysis, making it even more dangerous in an exercise setting, particularly among new detrained clients. Clearly, owing to the markers which describe the condition, exertional rhabdomyolysis can only be diagnosed by a physician with a sophisticated laboratory at his/her disposal.
Exertional rhabdomyolysis develops from both exercise and nonexercise risk factors. The amount of cellular damage may be affected by a subject's 1) fitness level. 2) the intensity of exercise, 3) the duration of exercise, and 4) the type of exercise.
• Fitness level. Muscle tissue adapts to exercise, allowing the tissue to perform more work, resist damage, and repair at a faster rate. Thus, an experienced athlete would be less likely to develop exertional rhabdomyolysis, while a new client in a detrained state would be more likely to show signs of exertional rhabdomyolysis.
• Intensity and duration. Studies show that increasing the intensity of an activity (eg, lifting heavier weight, pedaling faster) results in higher creatine kinase levels (widely regarded as the most important marker of exertional rhabdomyolysis) when compared with increasing the duration (eg, more repetitions with less weight, longer bicycling with slower pedaling).
• Type of exercise. Different amounts of cellular destruction occur between concentric exercise and eccentric exercise. Eccentric activities cause more destruction, resulting in higher levels of intracellular contents in the bloodstream.
Minimizing Risk
The only real solution for rhabdomyolysis is prevention. Participants in exercise programs should increase the intensity of their exercise programs at a pace that will allow muscle tissue time to adapt. Limiting or avoiding exercise during high temperature and humidity conditions, and limiting exercise during times of illness are also advised. Clients who have predisposing risk factors, such as metabolic myopathies, sickle cell trait, or certain viral infections, should be instructed by their physician to observe precautions when exercising. In such instances, if a personal trainer is involved, his/her job requires that consultation with the client’s physician is carried out.
Personal fitness trainers should never begin training a new client using repetitive or strenuous, unaccustomed exercises. All exercise training should begin with mild intensity exercise, which is gradually increased to an appropriate level. This practice will ensure safety. Moreover, preventing even moderate muscle soreness will benefit training because working with sore muscles (which also are weaker) will compromise the quality of the practice sessions.
Because dehydration is implicated in rhabdomyolysis, adequate fluid should be available and ingested before and during exercise. During strenuous exercise in the heat, precautions such as adequate fluid intake and acclimatization are critical.
In summary, exertional rhabdomyolysis and its serious consequences can be avoided by maintaining adequate hydration, avoiding heat stress, not performing strenuous repetitive exercise for which a person is not trained and increasing exercise intensity in a gradual manner. These safeguards will prevent subsequent muscle pain and optimize performance, but more importantly, they may save a life.

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