Acute Quadriceps Compartment Syndrome and Rhabdomyolysis in a Weight Lifter Using High-Dose Creatine Supplementation

Stacey J. Robinson, CAPT, USAF MC, Department of Family Practice, 6th Medical Group, MacDill Air Force Base, Fla.

J Am Board Fam Med. 2000;13(2) 

In This Article

Discussion

Creatine functions as a high-energy phosphate carrier, donating a phosphate for the recycling of adenosine triphosphate (ATP) from adenosine diphosphate (ADP), providing energy for muscle contraction. The daily requirement of creatine for a 70-kg person is 2 g. Creatine is obtained from dietary consumption of meat and fish as well as synthesis from endogenous amino acids. There is approximately 1 g of creatine contained in 8 ounces of lean beef.

In theory, oral supplementation with creatine will increase muscle creatine stores, providing higher rates of ATP recycling and better performance. In 1992 Harris et al[5] were the first to show an increase (20%) in total muscle creatine after an oral creatine load (20 to 25 g for 5 to 7 days). Results of numerous studies investigating the performance-enhancing effects of creatine have not been as consistent. In a 1998 review of the performance-enhancing effects of creatine, Juhn and Tarnopolsky[6] reported that creatine has consistently been shown to improve only repeated 6- to 30- second bouts of stationary cycling with recovery of 20 seconds to 5 minutes. Effects of creatine on single cycling sprints and single or repeated swimming and running sprints have been too inconsistent to draw any conclusion. They also report that creatine does not benefit submaximal or endurance exercise. Of note, most studies were performed in a laboratory setting; therefore, effects on actual competition are unknown.

Hultman et al[2] also state that lean body mass is increased by creatine supplementation. Although the mechanism is unclear, it is believed that short-term gains in body mass are secondary to fluid retention, because creatine draws free water into the muscle cells. This cellular hydration could stimulate protein synthesis, leading to a long-term increase in true muscle mass.[7]

Doubts about the safety of creatine were first raised when three college wrestlers, who were reportedly taking creatine, died within a 2-month period in 1997.[8] Dehydration was evident in all three cases, and causes of death were documented as unknown, hyperthermia, and rhabdomyolysis, respectively. They had all been participating in rapid weight-loss techniques, including intensive exercise in rubber suits and saunas, in an attempt to qualify for a lower weight class. Although wrestlers have been using rapid weight-loss techniques for decades, these are the first documented cases of deaths in collegiate wrestling. Although the Centers for Disease Control and Prevention and the FDA has not implicated creatine in the wrestlers' deaths, it is difficult to ignore that creatine was a new factor common to these wrestlers and might have been the additional contributor leading to fatal effects of severe dehydration.

Anecdotal reports of side effects include gastrointestinal symptoms, muscle cramps and strains, dehydration, renal and liver dysfunction, and seizures. None of these potential side effects has been substantiated, although studies have involved relatively few subjects. A review of the literature found only two cases involving adverse effects of creatine use. A 25-year-old male soccer player with a history of focal segmental glomerulosclerosis, who had maintained normal renal function on cyclosporin, had serious worsening of renal function after taking a creatine load of 15 g/d for 1 week then 2 g/d for 6 weeks. Renal function normalized when the creatine was discontinued.[9] The second case report described a previously healthy 20-year-old man who, after taking 20 g of creatine daily for 4 weeks, developed interstitial nephritis that also resolved when creatine was discontinued.[10] Two in vitro studies from the 1970s might link creatine use with cardiac muscle hypertrophy.[11,12]

As do many other athletes, this patient was taking long-term, high-dose creatine. He developed acute compartment syndrome after a lower extremity workout similar to his previous workouts. Based on what is known about its effects on the distribution of total body water, creatine could have predisposed this patient to compartment syndrome by increasing water content in the muscle cells and thus increasing baseline compartment pressures. Another contributing factor could have been the 8-day rest period preceding the event, which brings into question the safety of taking a loading dose of creatine in the absence of exercise. Furthermore, creatine could have predisposed this patient to dehydration, contributing to the development of acute renal failure by causing intravascular volume depletion. Without a baseline echocardiogram for comparison, it is unclear whether creatine contributed to left ventricular hypertrophy and cardiac decompensation.

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