Testing electrolyte supplementation for muscle cramp

Abstract

The occurrence of muscle cramp, consisting of painful hypercontraction of a muscle, part of a muscle, or even a group of functionally related muscles during exercise is a well-known and common experience among both casual and professional athletes. It is especially frequent in runners in long distance events, such as marathons, and in soccer players, who may run many kilometers during a match. Although it is subjectively associated with fatigue and with nearmaximal exercise in hot, humid environments these factors are by no means invariable. For example, leg cramp in bed, even in sleep, is especially frequent in the elderly. Cramp is particularly associated with neurogenic disorders, such as motor neuropathies, and especially with amyotrophic lateral sclerosis and in cramp-fasciculation syndrome, regardless of exercise. It is associated with hypocalcemia, hypomagnesemia, and hypokalemia, and with leg ischemia and hypothyroidism. Individual susceptibility in otherwise healthy individuals is also recognized. Exercise-associated muscle cramp (EAMC) is, therefore, one of several clinical associations of muscular cramp. Muscle cramps often seem to be induced during slight contraction of an already partially contracted muscle, and environmental cold or contact with a cold surface are also common triggers. Forced, passive muscle stretch will relieve cramp after a few seconds, but not immediately, probably due to increased Golgi tendon organ activation and/or unlocking of actin-myosin bridges in hypercontracted muscle fibers. Without such a maneuver cramp may persist for several minutes. Cramp is characteristically painful. Pain is probably myofascial in origin, from activation of pain receptors in intramuscular fascia and arterioles. Cramp-associated muscle pain is sometimes ascribed to local lactate accumulation in over-contracted muscle fibers, but this explanation lacks experimental verification and does not account for the immediate co-occurrence of cramping contraction and pain. During cramp, motor unit firing rates are unusually rapid, approaching 50–60 Hz. The discharge rate slowly decreases as the cramp resolves. Muscle cramp is induced and modulated by motor neuronal activity at the spinal level, perhaps associated with plateau potentials triggered by increased synaptic input to motoneurons during prolonged exercise. Because this plateau potential is close to threshold for motor unit firing increased synaptic activity, or sensory input, can induce repetitive firing. However, in peripheral neuropathies, a peripheral nerve origin associated with channel dysfunction is more likely as a primary event with back-firing to anterior horn cells. Cramp and muscle pain are also characteristic of hereditary myopathy associated with tubular aggregates. EAMC has been attributed to two main causes: increased motor neuronal excitability consequent on vigorous exercise, that may persist for up to an hour afterward, and sweat-related dehydration with electrolyte depletion. The latter is presumed also to induce increased motor neuron excitability. However, the roles of these possible factors are controversial and no exercise-related changes in blood electrolytes have been reported. Thus, it is likely that increased motoneuronal excitability is the initiating factor, as in cramp-fasciculation syndrome, although several physiological factors can induce this hyperexcitable state. In a report in this issue of the Journal, cramp susceptibility was studied using the nerve stimulation cramp threshold frequency (TF) test. In this test, 2-s trains of biphasic 80 mV electrical stimuli were applied to the tibial nerve at increasing frequencies (8–30 Hz) until cramp was induced in the flexor hallucis brevis (FHB) muscle, as reported by the subject andmeasured by great toe flexion load. Electromyographic (EMG) activity in the FHB was assessed using a root mean square calculation from the surface EMG signal compared with the maximum voluntary activity assessed before the electrical test. This experimental setup was used to assess the effect of a commercial electrolyte-supplemented beverage, marketed for athletes, compared with a commercially available low-calorie beverage in 500-cc doses, taken 15 min before TF testing, in 12 cramp-prone subjects. Before the study, five of the subjects reported cramp susceptibility in many muscles, including abdominal, feet, calves, and hamstrings, but none had a diagnosis of any specific neuromuscular disease and none complained specifically of EAMC. Four reported cramping while sleeping. TF induced cramp in only 9 of these 12 subjects. Urine specific gravity (< 1.020) and total and compartmental body water studies were similar before testing, and there were no significant dietary differences in electrolyte intake. In this admittedly small study of nine cramp-prone subjects, the investigators found that, in five subjects, consumption of the electrolytereinforced drink resulted in a large increase in TF compared with consumption of the low-calorie drink, indicating that the effect was not due to a hydration effect of the beverages. However, the remaining four of the nine subjects showed no difference in TF between the two experimental trials. Pain was subjectively less severe in six of nine of the electrolyte-treated group. The authors recognize that the electrolytereinforced drink also contained a large carbohydrate load and were unable to exclude this as a factor affecting their results. They discounted flavor differences and excluded failed test blinding of the study by questionnaire at the conclusion of the study. Received: 21 August 2019 Revised: 25 August 2019 Accepted: 26 August 2019