Aetiology of skeletal muscle 'cramps' during exercise: a novel hypothesis.

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.

[1]  J. D. Riley,et al.  Leg cramps: differential diagnosis and management. , 1995, American family physician.

[2]  S. Heller,et al.  Exercise and recovery ventilatory and VO2 responses of patients with McArdle's disease. , 1990, Journal of applied physiology.

[3]  S. McGee.  Muscle cramps. , 1990, Archives of internal medicine.

[4]  J. Robertson.  Medical Problems in Mass Participation Runs , 1988, Sports medicine.

[5]  D. Arnold,et al.  Ca2+-ATPase deficiency in a patient with an exertional muscle pain syndrome. , 1988, Journal of neurology, neurosurgery, and psychiatry.

[6]  M. O'Toole,et al.  Medical and physiological considerations in triathlons , 1987, The American journal of sports medicine.

[7]  T. Yuasa,et al.  31P‐NMR Studies on an animal model of human defective muscle glycolysis , 1986, Muscle & nerve.

[8]  R. Hutton,et al.  Stretch sensitivity of Golgi tendon organs in fatigued gastrocnemius muscle. , 1986, Medicine and science in sports and exercise.

[9]  R. Maughan.  Exercise-induced muscle cramp: a prospective biochemical study in marathon runners. , 1986, Journal of sports sciences.

[10]  Physiotherapy and electromyography in muscle cramp. , 1985, British journal of sports medicine.

[11]  B. Jones,et al.  Medical Complaints After a Marathon Run in Cool Weather. , 1985, The Physician and sportsmedicine.

[12]  G. Vrbóva,et al.  Invited review: Neural control of phenotypic expression in mammalian muscle fibers , 1985, Muscle & nerve.

[13]  R. Hutton,et al.  Dynamic and static stretch responses in muscle spindle receptors in fatigued muscle. , 1985, Medicine and science in sports and exercise.

[14]  S. Ashwal,et al.  Myoadenylate deaminase deficiency in children. , 1985, Pediatric neurology.

[15]  W. Fishbein.  Myoadenylate deaminase deficiency: inherited and acquired forms. , 1985, Biochemical medicine.

[16]  R. Johansson,et al.  Contractile speed and EMG changes during fatigue of sustained maximal voluntary contractions. , 1983, Journal of neurophysiology.

[17]  S. Dimauro,et al.  Familial myoadenylate deaminase deficiency and exertional myalgia , 1982, Neurology.

[18]  F. Cornelio,et al.  Heterogeneity of carnitine-palmitoyltransferase deficiency , 1981, Journal of the Neurological Sciences.

[19]  R. Brumback.  Iodoacetate inhibition of glyceraldehyde-3-phosphate dehydrogenase as a model of human myophosphorylase deficiency (McArdle's disease) and phosphofructokinase deficiency (Tarui's disease) , 1980, Journal of the Neurological Sciences.

[20]  B. Payton.  The Year Book of Cancer 1978 , 1979 .

[21]  A. De Troyer,et al.  Clinical, biological and pathogenic features of the syndrome of inappropriate secretion of antidiuretic hormone. A review of 26 cases with marked hyponatraemia. , 1976, The Quarterly journal of medicine.

[22]  S. Massry,et al.  NEUROLOGICAL MANIFESTATIONS AND MORBIDITY OF HYPONATREMIA: CORRELATION WITH BRAIN WATER AND ELECTROLYTES , 1976, Medicine.

[23]  D. Jones,et al.  Metabolic changes associated with the slowing of relaxation in fatigued mouse muscle. , 1975, The Journal of physiology.

[24]  J. Chaco,et al.  McArdle's syndrome: the reaction to a fat-rich diet , 1975, The American journal of the medical sciences.

[25]  S. Dimauro,et al.  A disorder of muscle lipid metabolism and myoglobinuria. Absence of carnitine palmityl transferase. , 1975, The New England journal of medicine.

[26]  W. Schwartz,et al.  The Syndrome of Inappropriate Secretion of Antidiuretic Hormone , 1967, Journal of the Royal College of Physicians of London.

[27]  B. Brownell,et al.  McArdle's myopathy. A report of a case with observations on the muscle ultrastructure. , 1969, Journal of the neurological sciences.

[28]  R. Layzer,et al.  Muscle phosphofructokinase deficiency. , 1967, Archives of neurology.

[29]  T. Tanaka,et al.  PHOSPHOFRUCTOKINASE DEFICIENCY IN SKELETAL MUSCLE. A NEW TYPE OF GLYCOGENOSIS. , 1965, Biochemical and biophysical research communications.

[30]  F. Norris,et al.  An electromyographic study of induced and spontaneous muscle cramps. , 1957, Electroencephalography and clinical neurophysiology.

[31]  L. G. Bartholomew,et al.  Reversible postoperative neurological symptoms; report of five cases secondary to water intoxication and sodium depletion. , 1956, Journal of the American Medical Association.

[32]  B. McArdle.  MYOPATHY DUE TO A DEFECT IN MUSCLE GLYCOGEN BREAKDOWN , 1951, Clinical science.

[33]  R. Mccance.  Experimental Sodium Chloride Deficiency in Man , 1936 .

[34]  J. Talbott.  HEAT CRAMPS , 1935 .

[35]  E. H. Derrick.  HEAT CRAMPS AND URÆMIC CRAMPS, WITH SPECIAL REFERENCE TO THEIR TREATMENT WITH SODIUM CHLORIDE , 1934 .

[36]  J. Michelsen,et al.  HEAT CRAMPS. A CLINICAL AND CHEMICAL STUDY. , 1933, The Journal of clinical investigation.

[37]  E. Brockbank.  MINERS' CRAMP , 1929, British medical journal.

[38]  R. Oswald.  SALINE DRINK IN INDUSTRIAL FATIGUE. , 1925 .

[39]  D. Edsall.  A DISORDER DUE TO EXPOSURE TO INTENSE HEAT, CHARACTERIZED CLINICALLY CHIEFLY BY VIOLENT MUSCULAR SPASMS AND EXCESSIVE IRRITABILITY OF THE MUSCLES. PRELIMINARY NOTE. , 1908 .