Treatment of Exercise-Induced Rhabdomyolysis

Kirstie B. Pistner
California University of Pennsylvania


Rhabdomyolysis is a disorder that causes rapid destruction to the sarcolemma, or cell membrane, of skeletal muscles. Such damage results in leakage of myoglobin and muscle protein into the urine. Complications of rhabdomyolysis can include compartment syndrome of the damaged muscles in the same fascial compartment, kidney failure, and, in extreme cases, death. The rapid detection of myoglobin, the cell's store of oxygen, into the urine is paramount in the diagnosis and treatment of rhabdomyolysis in order to avoid severe complications and continued digression of the patient. A systemic review of online databases such as SPORTDiscus, MEDLINE, and CINAHL were utilized to conduct this research. Current clinical research suggests that electrolyte replacement through intravenous fluids and monitoring muscle enzyme levels are acceptable means for managing this skeletal muscle pathology.


Rhabdomyolysis is a condition that causes rapid destruction to the sarcolemma, or cell membrane, of skeletal muscles resulting in leakage into the urine of the muscle protein, myoglobin. Myoglobin is a muscle protein that is released into the bloodstream following the onset of this condition. Research has shown the vast improvements in terms of effective treatment options that have been made over the years regarding such a rare condition. This topic is equally important to all health care professionals as it is prevalent in athletes and the general population. However, additional research must be conducted in order to fully avoid severe complications and administer the correct treatment for rhabdomyolysis. The purpose of this paper is to provide further insight into the research topic, including historical perspective, etiological information, diagnosis, treatment, return to play, and summary.

Historical Perspective

The first description of rhabdomyolysis was famously made by two physicians, Bywaters and Beall in Sicily in 1908, who first observed the sequence of symptoms. They identified the role of myoglobin in its pathogenesis and promoted the use of intravenous bicarbonate solutions as a form of treatment (Ismaili, Piccioni, & Zappitelli, 2011). They further noted that myoglobin released into the bloodstream was responsible for kidney failure, which resulted in high rates of mortality associated with this condition. During this time, Bywaters and Beall identified the first cause and effect relationship between acute renal failure and rhabdomyolysis. In 1941, this medical condition was accurately described in the victims of the London Blitz. The incidence in war victims remained high until the Vietnam War, when more rapid field evacuations and prompt administration of intravenous fluid therapy led to a significant drop in mortality rates (Ismaili, Piccioni, &Zappitelli, 2011).

Etiological Information

Rhabdomyolysis is a condition that causes rapid destruction to the sarcolemma of skeletal muscles resulting in leakage into the urine of the muscle protein, myoglobin (Cerevillin et al., 2010), which may arise from a wide variety of signs and symptoms ranging from an escalation in plasma creatine kinase levels, an increase in enzyme level activity, and alterations in electrolyte disturbances. Although an extreme level of creatine kinase has no toxic effects, it is significant to note that these standards are pathognomonic for this condition as no other disorder will cause such dangerous creatine kinase level.
Understanding rhabdomyolysis requires cognizance of standard intracellular and extracellular distribution of ions and what may occur when these balances are disrupted. Sodium, calcium, chloride, and bicarbonate ions are extracellular ions, whereas potassium, magnesium, and phosphate ions are categorized as intracellular (Criddle, 2003). In order for the body to function properly, balance between these ions inside and outside of the muscle cells must be maintained. Three causes may disrupt the balance between extracellular and intracellular ions. The first cause is direct injury to the cell membrane. Damage to this structure causes intracellular molecules to escape and extracellular molecules to enter, creating potential imbalance. Injury to the cellular membrane has distinct mechanisms such as crushing, tearing, burning, pounding, poisoning, and dissolving. The second cause is muscle cell hypoxia, or lack of sufficient oxygen, leading to depletion of adenosine triphosphate (ATP). The sodium-potassium pump plays a crucial role in preserving extracellular and intracellular electrolyte balances. This pump is dependent upon energy in the form of ATP. Without a steady supply of oxygen, the pump is unable to produce ATP. Mechanisms that induce muscle cell hypoxia include shock states, vascular occlusion, tissue compression, or any other anaerobic condition. Muscle cell hypoxia is also linked to excessive energy use due to seizures, hyperthermia, strenuous exercise, and prolonged sympathetic stimulation. This causes oxygen and ATP production to diminish and in turn causes the pump to dysfunction. The third cause of cellular destruction in rhabdomyolysis is severe electrolyte disturbances disrupting the sodium-potassium pump. Two mechanisms reportedly trigger such electrolyte imbalances, hypokalemia, which involves vomiting, diarrhea, and extensive dieresis, and hyponatremia, also known as water intoxication (Criddle, 2003).

Not only do intracellular and extracellular ions play a large role in the development of rhabdomyolysis, but many other key factors may contribute to the onset of this condition such as infections, hot/humid environments, toxic muscle injury, neuroleptic malignant syndrome, muscle exertion, repetitive muscle injury, drug overdoses, extended periods of muscle exposure, extreme lithotomy positions for extended periods of time, carcinoma, diabetes mellitus, trauma, and status epilepticus (Russell, 2005).


With many etiological factors that may produce the onset of rhabdomyolysis, proper diagnosis is important in order to determine appropriate forms of treatment. Rhabdomyolysis can be confused with various typical problems reported by athletes and those involved in regular and exertional exercise such as muscle cramping, dehydration, or heat related illness. Although the diagnosis of rhabdomyolysis can be hypothesized thorough history and physical examination, it must be confirmed with laboratory testing of the blood and urine. Many muscular signs and symptoms will present themselves in individuals with this condition during a physical examination. Most patients will present with an obvious muscle deformity that shows reddening over the skin along with swelling. Although symptoms will vary on a case-by-case basis, the most common symptoms presented are muscle pain, weakness, tenderness, stiffness, and contractures predominately during and after exercise. Paralysis may occur due to severe necrosis or hyperkalemia. Nearly fifty percent of patients will present with symptoms that involve the lower extremities, which are also tender to palpation (Ismaili et al., 2011).
A urinalysis is the first clinical sign of rhabdomyolysis with tea-colored urine. This is caused by the release of myoglobin from the injured muscle into the bloodstream, which is then detached from the plasma by the kidneys and expelled into the urine. Myoglobin can accrue, and in turn cause a barrier in the kidney that can lead to a life-threatening complication of kidney failure. Urinalysis will confirm the diagnosis of rhabdomyolysis by using a simple dipstick procedure to determine the presence of myoglobin. A microscopic urinalysis will also be used in determining the diagnosis of rhabdomyolysis. Microscopic urinalysis is used to determine the existence of casts that are tube shaped particles that develop in the kidneys. These casts consist of particles including fatty particles, red blood cells, white blood cells, and kidney cells. Individuals with rhabdomyolysis are known to have brown casts, as well as uric acid crystals present in their urine during a microscopic urinalysis (Olerud et al., 1976).

Blood tests involve the measuring of creatine kinase levels, myoglobin, and blood potassium levels. The creatine kinase levels will increase significantly within the first twelve hours of onset of rhabdomyolysis. The levels will remain high and peak within a three-day period before falling back into the normal range following treatment. In individuals with this condition, their creatine kinase levels will be around five times higher than those who do not have this condition. Myoglobin will show positive in the blood with higher levels than normal. Each laboratory has different normal values of how much myoglobin should be in the bloodstream; however, in individuals with rhabdomyolysis, the levels will be significantly higher. Typical myoglobin levels in males are 10-95 ng/mL whereas in females it is 10-65 ng/mL. Blood potassium levels are also an important piece of information in the diagnosis of rhabdomyolysis. The increase of potassium levels in the blood, also known as hyperkalemia, is a substantial complication of rhabdomyolysis. Due to the muscle tissue breaking down, the cell membranes become permeable, which allows too much sodium to enter and too little potassium to exit the skeletal muscle cell. Blood tests will reveal a large increase in potassium levels in comparison to normal values. Determining blood potassium levels is essential due to the fact that an increased level can lead to cardiac arrhythmias or cardiac arrest (Olerud, Homer, & Carroll, 1976).


The treatment of rhabdomyolysis is determined on an individual basis that is constructed on the severity and identified cause of this condition. Once the cause is identified, the treatment will be specific to the case presented. For example, treatment can include discontinuing a toxic medication, replacing electrolytes through intravenous fluids, and/or treating underlying muscle pathologies. Cryotherapy, stretching, and electrolyte replacement are the three most common forms of treatment for individuals with rhabdomyolysis in an athletic environment (Eberman, Kahanov, Alvey, & Wasik, 2011). In mild cases of rhabdomyolysis, the typical form of treatment will consist of rehydration and discontinuing exercise until approved by a physician. In severe cases, hospitalization may be required to properly treat the individual. Immediate initiation of hydration with intravenous fluids is essential as well as the removal of the aggravating factors (Rosenberg, 2008). The monitoring and managing of kidney dysfunctions, along with correcting disturbances in electrolyte levels as well as monitoring muscle enzyme levels are most efficiently done in the hospital setting when rhabdomyolysis is severe. Again, without proper treatment of rhabdomyolysis that consists of a urinalysis, blood tests, and electrolyte replacement through intravenous fluids, it is possible for the individual to later develop severe complications such as compartment syndrome of the damaged muscles in the same fascial compartment, kidney failure, and in extreme cases, death. There is no evidence that suggests if once diagnosed with rhabdomyolysis, that a reoccurrence of this condition will follow.

Return to Play

A well-defined standard for return-to-play decisions is not currently available in the literature for individuals treated for rhabdomyolysis (O'Connor, Brennan, Campbell, Heled, & Deuster, 2008). Typically, the return to play ranges from one day to one month following the onset of symptoms. Also, no timeline has been established in terms of a follow-up evaluation for biological markers related to rhabdomyolysis (O'Connor, Brennan, Campbell, Heled, & Deuster, 2008). No timeline has been established for rhabdomyolysis due to each individual needing to be treated on a separate basis. However, the following five guidelines have been recommended, but not validated, for return to play of individuals who have been diagnosed with this disorder (O'Connor, Brennan, Campbell, Heled, & Deuster, 2008).
The first guideline states that each return-to-play decision should be on an individual basis. Individuals who have rhabdomyolysis often have other associated conditions; therefore, numerous variables will play into the return-to-play decision. It is best to have the individual monitored and have sport-specific drills in place to determine readiness.

The second guideline recommends that the individual obtains a normal range in creatine kinase level along with a myoglobin reading that may be compared to future episodes. Each patient should be returned individually because normal levels vary among individuals.

The third guideline states that a period of acclimatization, adaptation to a new climate, is essential for individuals participating in hot, humid environments. This is the type of climate that may trigger more episodes involving rhabdomyolysis.

The fourth guideline states that athletic trainers should monitor hydration levels before, during, and after exercise. A documentation of urine color along with a change in weight indicated dehydration should be noted. It is recommended that the fluid replacement should match the volume lost throughout exercise.

The fifth guideline states that if there is evidence of muscular fasciculation or muscle twitches that all types of activity should be stopped immediately. Eccentric muscle contractions should also be limited as they cause the muscle to quickly fatigue and therefore release more myoglobin into the bloodstream.

Again, there is no definitive set of guidelines in place for the return-to-play decision involving those with this condition (O'Connor, Brennan, Campbell, Heled, & Deuster, 2008), which requires additional research. It is important for guidelines to be set in place for return-to-play decisions due to the severity of this condition.


Due to the rapid destruction of sarcolemma, or cell membrane, of skeletal muscles, resulting in leakage into the urine of the muscle protein myoglobin, it is essential for the athlete to be properly treated to avoid severe complications as a result of rhabdomyolysis. Research suggests that electrolyte replacement through intravenous fluids and monitoring muscle enzyme levels are acceptable means for managing this skeletal muscle pathology. The research shows that with intravenous fluid replacement that creatine kinase levels significantly decreased along with myoglobin levels in the bloodstream. It is clear that if each case is caught and treated on an individual basis detrimental results may be avoided. However, extensive research shows that guidelines are not set in place for return-to-play decisions and the particular pathogenesis for this condition is still not clearly understood, which leaves room for improvements.


Cerevillin, G., Comelli, I., & Lippi, G. (2010). Rhabdomyolysis: Historical background, clinical, diagnostic and therapeutic features. Clinical Chemistry and Laboratory Medicine, 48(6), 749-756. Retrieved October 8, 2012, from the MEDLINE database.

Criddle, L. (2003). Rhabdomyolysis: Pathophysiology, recognition, and management. Critical Care Nurse, 23(6), 1-16. Retrieved October 3, 2012, from the CINAHL database.

Eberman, L., Kahanov, L., Alvey, T., & Wasik, M. (2011). Exertional rhabdomyolysis: Determining readiness to return to play. International Journal of Athletic Therapy & Training, 16(4), 1-5. Retrieved October 1, 2012, from the SPORTDiscus database.

Ismaili, A., Piccioni, M., & Zappitelli, M. (2011). Rhabdomyolysis: Pathogenesis of renal injury and management. Pediatric Nephrology, 26(10), 1781-1788. Retrieved October 4, 2012, from the MEDLINE database.

O'Connor, F., Brennan, F., Campbell, W., Heled, Y., & Deuster, P. (2008). Return to physical activity after exertional rhabdomyolysis. American College of Sports Medicine, 7(6), 1-5. Retrieved October 2, 2012, from the SPORTDiscus database.

Olerud, J., Homer, L., & Carroll, H. (1976). Incidence of acute exertional rhabdomyolysis. Serum myoglobin and enzyme levels as indicators of muscle injury. Archives of Internal Medicine, 136(6), 692-697. Retrieved October 1, 2012, from the MEDLINE database.

Rosenberg, J. (2008). Exertional rhabdomyolysis: Risk Factors, presentation, and management. Athletic Therapy Today, 13(3), 1-3. Retrieved October 7, 2012, from the SPORTDiscus database.

Russell, T. (2005). Acute renal failure related to rhabdomyolysis: Pathophysiology, diagnosis, and collaborative management. Nephrology Nursing Journal, 32(4), 1-12. Retrieved October 4, 2012, from the CINAHL database.


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