Muscle Cramping in the Marathon : Aetiology and Risk Factors

The aetiology of exercise-associated muscle cramps (EAMC), defined as 'painful, spasmodic, involuntary contractions of skeletal muscle during or immediately after physical exercise', has not been well investigated and is therefore not well understood. This review focuses on the physiological basis for skeletal muscle relaxation, a historical perspective and analysis of the commonly postulated causes of EAMC, and known facts about EAMC from recent clinical studies. Historically, the causes of EAMC have been proposed as (1) inherited abnormalities of substrate metabolism ('metabolic theory') (2) abnormalities of fluid balance ('dehydration theory'), (3) abnormalities of serum electrolyte concentrations ('electrolyte theory') and (4) extreme environmental conditions of heat or cold ('environmental theory'). Detailed analyses of the available scientific literature including data from recent studies do not support these hypothesis for the causes of EAMC. In a recent study, electromyographic (EMG) data obtained from runners during EAMC revealed that baseline activity is increased (between spasms of cramping) and that a reduction in the baseline EMG activity correlates well with clinical recovery. Furthermore, during acute EAMC the EMG activity is high, and passive stretching is effective in reducing EMG activity. This relieves the cramp probably by invoking the inverse stretch reflex. In two animal studies, abnormal reflex activity of the muscle spindle (increased activity) and the Golgi tendon organ (decreased activity) has been observed in fatigued muscle. We hypothesize that EAMC is caused by sustained abnormal spinal reflex activity which appears to be secondary to muscle fatigue. Local muscle fatigue is therefore responsible for increased muscle spindle afferent and decreased Golgi tendon organ afferent activity. Muscles which cross two joints can more easily be placed in shortened positions during exercise and would therefore decrease the Golgi tendon organ afferent activity. In addition, sustained abnormal reflex activity would explain increased baseline EMG activity between acute bouts of cramping. Finally, passive stretching invokes afferent activity from the Golgi tendon organ, thereby relieving the cramp and decreasing EMG activity.

To determine whether acute exercise associated muscle cramping (EAMC) in distance runners is related to changes in serum electrolyte concentrations and hydration status. A cohort of 72 runners participating in an ultra-distance road race was followed up for the development of EAMC. All subjects were weighed before and immediately after the race. Blood samples were taken before the race, immediately after the race, and 60 minutes after the race. Blood samples were analysed for glucose, protein, sodium, potassium, calcium, and magnesium concentrations, as well as serum osmolality, haemoglobin, and packed cell volume. Runners who suffered from acute EAMC during the race formed the cramp group (cramp, n = 21), while runners with no history of EAMC during the race formed the control group (control, n = 22). There were no significant differences between the two groups for pre-race or post-race body weight, per cent change in body weight, blood volume, plasma volume, or red cell volume. The immediate post-race serum sodium concentration was significantly lower (p = 0.004) in the cramp group (mean (SD), 139.8 (3.1) mmol/l) than in the control group (142.3 (2.1) mmol/l). The immediate post-race serum magnesium concentration was significantly higher (p = 0.03) in the cramp group (0.73 (0.06) mmol/l) than in the control group (0.67 (0.08) mmol/l). There are no clinically significant alterations in serum electrolyte concentrations and there is no alteration in hydration status in runners with EAMC participating in an ultra-distance race.