Exertional rhabdomyolysis

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Exertional rhabdomyolysis
Other namesexercise-induced rhabdomyolysis

Exertional rhabdomyolysis (ER) is the breakdown of muscle from extreme physical exertion. It is one of many types of rhabdomyolysis that can occur, and because of this, the exact prevalence and incidence are unclear.

Contents

Cause

ER is more likely to occur when strenuous exercise is performed under high temperatures and humidity. [1] Poor hydration levels before, during, and after strenuous bouts of exercise have also been reported to lead to ER. [2] This condition and its signs and symptoms are not well known amongst the sport and fitness community and because of this it is believed that the incidence is greater but highly underreported. [2]

Risks that lead to ER include exercise in hot and humid conditions, improper hydration, inadequate recovery between bouts of exercise, intense physical training, and inadequate fitness levels for beginning high-intensity workouts. [3] Eccentric contraction of muscles can result in ER more often than concentric contraction. [4] Dehydration is one of the biggest factors that can give almost immediate feedback from the body by producing very dark-colored urine. [5]

Mechanism

Anatomy

Exertional rhabdomyolysis results from damage to the intercellular proteins inside the sarcolemma. Myosin and actin break down in the sarcomeres when ATP is no longer available due to injury to the sarcoplasmic reticulum. [6] Damage to the sarcolemma and sarcoplasmic reticulum from direct trauma or high force production causes a high influx of calcium ions into the muscle fibers increasing calcium permeability. Calcium ions build up in the mitochondria, impairing cellular respiration. [7] The mitochondria are unable to produce enough ATP to power the cell properly. Reduction in ATP production impairs the cells' ability to extract calcium from the muscle cell.

Motor endplate of a person with rhabdomyolysis Motor End Plate of Rhabomyolysis.png
Motor endplate of a person with rhabdomyolysis

The ion imbalance causes calcium-dependent enzymes to activate which break down muscle proteins even further. [8] A high concentration of calcium activates muscle cells, causing the muscle to contract while inhibiting its ability to relax.

Actin, and myosin Actin and Myosin filament breakdown with Rhabdomyolysis.png
Actin, and myosin

The increase of sustained muscle contraction leads to oxygen and ATP depletion with prolonged exposure to calcium. The muscle cell membrane pump may become damaged allowing free form myoglobin to leak into the bloodstream. [9]

Physiology

Rhabdomyolysis causes the myosin and actin to degenerate into smaller proteins that travel into the circulatory system. The body reacts by increasing intracellular swelling to the injured tissue to send repair cells to the area. This allows creatine kinase and myoglobin to be flushed from the tissue where it travels in the blood until reaching the kidneys. [10] In addition to the proteins released, large quantities of ions such as intracellular potassium, sodium, and chloride find their way into the circulatory system. Intracellular potassium ion has deleterious effects on the heart's ability to generate action potentials leading to cardiac arrhythmias. [11] Consequently, this can affect peripheral and central perfusion which in turn can affect all major organ systems in the body.[ citation needed ]

When the protein reaches the kidneys it causes a strain on the anatomical structures reducing its effectiveness as a filter for the body. The protein acts as a dam as it forms into tight aggregates when it enters the renal tubules. [11] In addition, the increased intracellular calcium has greater time to bind due to the blockage allowing for renal calculi to form. [12] As a result this causes urine output to decrease allowing for the uric acid to build up inside the organ. The increased acid concentration allows the iron from the aggregate protein to be released into the surrounding renal tissue. [13] Iron then strips away molecular bonds of the surrounding tissue which eventually will lead to kidney failure if the tissue damage is too great.[ citation needed ]

Renal tubules of exertional rhabdomyolysis Renal Tubules of Exertional Rhabdomyolysis.png
Renal tubules of exertional rhabdomyolysis

Mechanical consideration

Muscle degeneration from rhabdomyolysis destroys the myosin and actin filaments in the affected tissue. This initiates the body's natural reaction to increasing perfusion to the area allowing for an influx of specialized cells to repair the injury. However, the swelling increases the intracellular pressure beyond normal limits. As the pressure builds in the muscle tissue, the surrounding tissue is crushed against the underlying tissue and bone. [14] This is known as compartment syndrome which leads to greater death of the surrounding muscle tissue around the injury. [14] As the muscle dies this will cause pain to radiate from the affected area into the compartmentalized tissue. A loss of range of motion from swelling will also be seen in the affected limb. Along with muscle strength weakness associated with the muscles involved from loss of filament interaction. [15]

Compartment syndrome in muscle Compartment Syndrome in Muscle (cleaned up) (annotated).jpg
Compartment syndrome in muscle

Dehydration is a common risk factor for exertional rhabdomyolysis because it causes a reduction of plasma volume during exertion. This leads to a reduction of blood flow through the vascular system which inhibits blood vessel constriction. [16]

Diagnosis

Exertional rhabdomyolysis, the exercise-induced muscle breakdown that results in muscle pain/soreness, is commonly diagnosed using the urine myoglobin test accompanied by high levels of creatine kinase (CK). Myoglobin is the protein released into the bloodstream when skeletal muscle is broken down. The urine test simply examines whether myoglobin is present or absent. When results are positive the urine normally obtains a dark, brown color followed by serum CK level evaluation to determine the severity of muscle damage. Elevated levels of serum CK greater than 5,000 U/L that are not caused by myocardial infarction, brain injury or disease, generally indicate serious muscle damage confirming the diagnosis of ER. [17] Urine is often a dark "cola" color as a result of the excretion of muscle cell components.[ citation needed ]

Prevention

Military data suggest that the risk of exertional rhabdomyolysis can be lowered by engaging in prolonged lower-intensity exercise, as opposed to high-intensity exercise over a shorter time period. In all athletic programs, three features should be present: (1) emphasizing prolonged lower-intensity exercise, as opposed to repetitive max intensity exercises; (2) adequate rest periods and a high-carbohydrate diet, to replenish glycogen stores; and (3) proper hydration, to enhance renal clearance of myoglobin. [18] Also, exercise in above-average temperature and humidity can increase risk for ER. [19] ER can be avoided by gradually increasing intensity during new exercise regimens, properly hydrating, acclimatization, and avoidance of diuretics during times of strenuous activity. [20]

Treatment

After ER is diagnosed, treatment is applied to 1) avoid renal dysfunction and 2) alleviate symptoms. This should be followed by recommended rehabilitation program, exercise prescription (ExRx). Treatment involves extensive hydration normally done through IV fluid replacement with administration of normal saline until CK levels reduce to a maximum of 1,000 U/L. [21] Proper treatment will ensure hydration and normalize muscle discomfort (pain), flu-like symptoms, CK levels, and myoglobin levels for patient to begin ExRx.[ citation needed ]

Although sufficient evidence is currently lacking, supplementation with a combination of sodium bicarbonate and mannitol is commonly utilized to prevent kidney failure in rhabdomyolysis patients. Sodium bicarbonate alkalizes urine to stop myoglobin from precipitating in renal tubules. Mannitol has several effects, including vasodilatation of the renal vasculature, osmotic diuresis, and free-radical scavenging. [22]

Recovery

Before initiating any form of physical activity, the individual must demonstrate a normal level of functioning with all previous symptoms absent. Physical activity should be supervised by a health care professional in case of a recurrence. However, in some low-risk individuals, supervision by a medical professional is not required as long as the individual follows up with weekly checkups. [23] Proper hydration prior to performing physical activity and performing exercise in cool, dry environments may reduce the chances of developing a reoccurring episode of ER. [23] Lastly, it is imperative for urine and blood values to be monitored along with careful observation for the redevelopment of any signs or symptoms.[ citation needed ]

The recovery program focuses on progressive conditioning/reconditioning the individual and improving functional mobility. However, special considerations prior to participating in the rehabilitation program include the individual's 1) extent of muscle injury, if any 2) level of fitness before the incident and 3) weight training experience. [19] These special considerations collectively are a form of assessing the individual's capacity to perform physical activity, which is ultimately used to specify the ExRx design.[ citation needed ]

Costs

The actual cost for this condition is unknown and also dependent on the level of the condition. In some cases ER can lead to acute kidney failure and bring medical costs up due to the need for hemodialysis for recovery/treatment. [5]

Related Research Articles

<span class="mw-page-title-main">Myoglobin</span> Iron and oxygen-binding protein

Myoglobin is an iron- and oxygen-binding protein found in the cardiac and skeletal muscle tissue of vertebrates in general and in almost all mammals. Myoglobin is distantly related to hemoglobin. Compared to hemoglobin, myoglobin has a higher affinity for oxygen and does not have cooperative binding with oxygen like hemoglobin does. Myoglobin consists of non-polar amino acids at the core of the globulin, where the heme group is non-covalently bounded with the surrounding polypeptide of myoglobin. In humans, myoglobin is only found in the bloodstream after muscle injury.

<span class="mw-page-title-main">Adenosine monophosphate deaminase deficiency type 1</span> Medical condition

Adenosine monophosphate deaminase deficiency type 1 or AMPD1, is a human metabolic disorder in which the body consistently lacks the enzyme AMP deaminase, in sufficient quantities. This may result in exercise intolerance, muscle pain and muscle cramping. The disease was formerly known as myoadenylate deaminase deficiency (MADD).

<span class="mw-page-title-main">Glycogen storage disease type V</span> Human disease caused by deficiency of a muscle enzyme

Glycogen storage disease type V, also known as McArdle's disease, is a metabolic disorder, one of the metabolic myopathies, more specifically a muscle glycogen storage disease, caused by a deficiency of myophosphorylase. Its incidence is reported as one in 100,000, roughly the same as glycogen storage disease type I.

<span class="mw-page-title-main">Rhabdomyolysis</span> Human disease (condition) in which damaged skeletal muscle breaks down rapidly

Rhabdomyolysis is a condition in which damaged skeletal muscle breaks down rapidly, often due to high intensity exercise over a short period of time. Symptoms may include muscle pains, weakness, vomiting, and confusion. There may be tea-colored urine or an irregular heartbeat. Some of the muscle breakdown products, such as the protein myoglobin, are harmful to the kidneys and can cause acute kidney injury.

<span class="mw-page-title-main">Kidney failure</span> Disease where the kidneys fail to adequately filter waste products from the blood

Kidney failure, also known as end-stage kidney disease, is a medical condition in which the kidneys can no longer adequately filter waste products from the blood, functioning at less than 15% of normal levels. Kidney failure is classified as either acute kidney failure, which develops rapidly and may resolve; and chronic kidney failure, which develops slowly and can often be irreversible. Symptoms may include leg swelling, feeling tired, vomiting, loss of appetite, and confusion. Complications of acute and chronic failure include uremia, hyperkalaemia, and volume overload. Complications of chronic failure also include heart disease, high blood pressure, and anaemia.

<span class="mw-page-title-main">Urinalysis</span> Array of tests performed on urine

Urinalysis, a portmanteau of the words urine and analysis, is a panel of medical tests that includes physical (macroscopic) examination of the urine, chemical evaluation using urine test strips, and microscopic examination. Macroscopic examination targets parameters such as color, clarity, odor, and specific gravity; urine test strips measure chemical properties such as pH, glucose concentration, and protein levels; and microscopy is performed to identify elements such as cells, urinary casts, crystals, and organisms.

Tumor lysis syndrome (TLS) is a group of metabolic abnormalities that can occur as a complication from the treatment of cancer, where large amounts of tumor cells are killed off (lysed) from the treatment, releasing their contents into the bloodstream. This occurs most commonly after the treatment of lymphomas and leukemias and in particular when treating non-Hodgkin lymphoma, acute myeloid leukemia, and acute lymphoblastic leukemia. This is a potentially fatal complication and patients at increased risk for TLS should be closely monitored while receiving chemotherapy and should receive preventive measures and treatments as necessary. TLS can also occur on its own although this is less common.

<span class="mw-page-title-main">Hyperkalemia</span> Medical condition with excess potassium

Hyperkalemia is an elevated level of potassium (K+) in the blood. Normal potassium levels are between 3.5 and 5.0 mmol/L (3.5 and 5.0 mEq/L) with levels above 5.5 mmol/L defined as hyperkalemia. Typically hyperkalemia does not cause symptoms. Occasionally when severe it can cause palpitations, muscle pain, muscle weakness, or numbness. Hyperkalemia can cause an abnormal heart rhythm which can result in cardiac arrest and death.

<span class="mw-page-title-main">Creatine kinase</span> Class of enzymes

Creatine kinase (CK), also known as creatine phosphokinase (CPK) or phosphocreatine kinase, is an enzyme expressed by various tissues and cell types. CK catalyses the conversion of creatine and uses adenosine triphosphate (ATP) to create phosphocreatine (PCr) and adenosine diphosphate (ADP). This CK enzyme reaction is reversible and thus ATP can be generated from PCr and ADP.

Overtraining occurs when a person exceeds their body's ability to recover from strenuous exercise. Overtraining can be described as a point where a person may have a decrease in performance and plateauing as a result of failure to consistently perform at a certain level or training load; a load which exceeds their recovery capacity. People who are overtrained cease making progress, and can even begin to lose strength and fitness. Overtraining is also known as chronic fatigue, burnout and overstress in athletes. It is suggested that there are different variations of overtraining, firstly monotonous program over training suggest that repetition of the same movement such as certain weight lifting and baseball batting can cause performance plateau due to an adaption of the central nervous system which results from a lack of stimulation. A second example of overtraining is described as chronic overwork type training where the subject may be training with too high intensity or high volume and not allowing sufficient recovery time for the body. Up to 10% of elite endurance athletes and 10% of American college swimmers are affected by overtraining syndrome.

<span class="mw-page-title-main">Equine exertional rhabdomyolysis</span>

Equine exertional rhabdomyolysis (ER) is a syndrome that affects the skeletal muscles within a horse. This syndrome causes the muscle to break down which is generally associated with exercise and diet regime. Depending on the severity, there are various types of ER, including sporadic and chronic.

<span class="mw-page-title-main">Crush syndrome</span> Medical condition

Crush syndrome is a medical condition characterized by major shock and kidney failure after a crushing injury to skeletal muscle. Crush injury is compression of the arms, legs, or other parts of the body that causes muscle swelling and/or neurological disturbances in the affected areas of the body, while crush syndrome is localized crush injury with systemic manifestations. Cases occur commonly in catastrophes such as earthquakes, to individuals that have been trapped under fallen or moving masonry.

<span class="mw-page-title-main">Myoglobinuria</span> Medical condition

Myoglobinuria is the presence of myoglobin in the urine, which usually results from rhabdomyolysis or muscle injury. Myoglobin is present in muscle cells as a reserve of oxygen.

<span class="mw-page-title-main">Sickle cell trait</span> Medical condition

Sickle cell trait describes a condition in which a person has one abnormal allele of the hemoglobin beta gene, but does not display the severe symptoms of sickle cell disease that occur in a person who has two copies of that allele. Those who are heterozygous for the sickle cell allele produce both normal and abnormal hemoglobin.

The actions of vasopressin are mediated by stimulation of tissue-specific G protein-coupled receptors (GPCRs) called vasopressin receptors that are classified into the V1 (V1A), V2, and V3 (V1B) receptor subtypes. These three subtypes differ in localization, function and signal transduction mechanisms.

<span class="mw-page-title-main">Nephrocalcinosis</span> Medical condition caused by the deposition of calcium salts in the kidneys

Nephrocalcinosis, once known as Albright's calcinosis after Fuller Albright, is a term originally used to describe the deposition of poorly soluble calcium salts in the renal parenchyma due to hyperparathyroidism. The term nephrocalcinosis is used to describe the deposition of both calcium oxalate and calcium phosphate. It may cause acute kidney injury. It is now more commonly used to describe diffuse, fine, renal parenchymal calcification in radiology. It is caused by multiple different conditions and is determined by progressive kidney dysfunction. These outlines eventually come together to form a dense mass. During its early stages, nephrocalcinosis is visible on x-ray, and appears as a fine granular mottling over the renal outlines. It is most commonly seen as an incidental finding with medullary sponge kidney on an abdominal x-ray. It may be severe enough to cause renal tubular acidosis or even end stage kidney disease, due to disruption of the kidney tissue by the deposited calcium salts.

<span class="mw-page-title-main">Lactate dehydrogenase</span> Class of enzymes

Lactate dehydrogenase (LDH or LD) is an enzyme found in nearly all living cells. LDH catalyzes the conversion of pyruvate to lactate and back, as it converts NAD+ to NADH and back. A dehydrogenase is an enzyme that transfers a hydride from one molecule to another.

<span class="mw-page-title-main">Metabolic myopathy</span> Type of myopathies

Metabolic myopathies are myopathies that result from defects in biochemical metabolism that primarily affect muscle. They are generally genetic defects that interfere with muscle's ability to create energy, causing a low ATP reservoir within the muscle cell.

A crush injury is injury by an object that causes compression of the body. This form of injury is rare in normal civilian practice, but common following a natural disaster. Other causes include industrial accidents, road traffic collisions, building collapse, accidents involving heavy plant, disaster relief or terrorist incidents.

Crystallopathy is a harmful state or disease associated with the formation and aggregation of crystals in tissues or cavities, or in other words, a heterogeneous group of diseases caused by intrinsic or environmental microparticles or crystals, promoting tissue inflammation and scarring.

References

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  12. ↑ Rodríguez E, Soler MJ, Rap O, Barrios C, Orfila MA, Pascual J (2013). "Risk factors for acute kidney injury in severe rhabdomyolysis". PLOS ONE. 8 (12): e82992. Bibcode:2013PLoSO...882992R. doi: 10.1371/journal.pone.0082992 . PMC   3867454 . PMID   24367578.
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  14. 1 2 Davis DE, Raikin S, Garras DN, Vitanzo P, Labrador H, Espandar R (October 2013). "Characteristics of patients with chronic exertional compartment syndrome". Foot & Ankle International. 34 (10): 1349–54. doi:10.1177/1071100713490919. PMID   23669162. S2CID   25833426.
  15. ↑ "Compartment Syndrome". The Lecturio Medical Concept Library. Retrieved 2021-06-25.
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  18. ↑ Line RL, Rust GS (August 1995). "Acute exertional rhabdomyolysis". American Family Physician. 52 (2): 502–6. PMID   7625324.
  19. 1 2 Cleary M, Ruiz D, Eberman L, Mitchell I, Binkley H (August 2007). "Dehydration, cramping, and exertional rhabdomyolysis: a case report with suggestions for recovery". Journal of Sport Rehabilitation. 16 (3): 244–59. doi:10.1123/jsr.16.3.244. PMID   17923731.
  20. ↑ Hamer R (May 1997). "When exercise goes awry: exertional rhabdomyolysis". Southern Medical Journal. 90 (5): 548–51. doi:10.1097/00007611-199705000-00019. PMID   9160079.
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  22. ↑ Brown CV, Rhee P, Chan L, Evans K, Demetriades D, Velmahos GC (June 2004). "Preventing renal failure in patients with rhabdomyolysis: do bicarbonate and mannitol make a difference?". The Journal of Trauma. 56 (6): 1191–6. doi:10.1097/01.ta.0000130761.78627.10. PMID   15211124.
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