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. Cause
ER is more likely to occur when strenuous exercise is performed under high temperatures and humidity. Poor hydration levels before, during, and after strenuous bouts of exercise have also been reported to lead to ER. 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.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. Eccentric contraction of muscles can result in ER more often than concentric contraction. Dehydration is one of the biggest factors that can give almost immediate feedback from the body by producing very dark-colored urine. 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. Damage to the sarcolemma and sarcoplasmic reticulum from direct trauma or high force production causes a high influx of calcium into the muscle fibers increasing calcium permeability. Calcium ions build up in the mitochondria, impairing cellular respiration. The mitochondria are unable to produce enough ATP to power the cell properly.
Hypertonic saline and mannitol are the main osmotic agents in use, while loop diuretics can aid in the removal of the excess fluid pulled out of the brain. Hypertonic saline is a highly concentrated solution of sodium chloride in water and is administered intravenously. It has a rapid-onset, with reduction of pressures within 5 minutes of infusion, lasting up to 12 hours in some cases, and with negligible rebound pressure. The exact volume and concentration of the hypertonic saline varies between clinical studies. Bolus doses, particularly at higher concentrations, for example 23.4%, are effective at reducing ICP and improving cerebral perfusion pressure. In traumatic brain injuries, a responsiveness to hypertonic saline lasting greater than 2 hours was associated with decreased chance of death and improved neurologic outcomes. The effects of hypertonic saline can be prolonged with combination to agents such as dextran or hydroxyethyl starch, although their use is currently controversial. When compared to mannitol, hypertonic saline has been shown to be as effective as mannitol in decreased ICP in neurocritical care and is more effective in many cases. Hypertonic saline may be preferable to mannitol in persons with hypovolemia or hyponatremia. Mannitol is an alcohol derivative of simple sugar mannose, and is historically the most commonly used osmotic diuretic. Mannitol acts as an inert solute in the blood, decreasing ICP through osmosis as discussed above. Additionally, mannitol decreases ICP and increased cerebral perfusion pressure by increasing reabsorption of cerebrospinal fluid, dilutes and decreased the viscosity of the blood, and can cause cerebral vasoconstriction.