Journal of Sports Sciences ISSN: 0264-0414 (Print) 1466-447X (Online) Journal homepage: http://www.tandfonline.com/loi/rjsp20 Aetiology of skeletal muscle ‘cramps’ during exercise: A novel hypothesis M. P. Schwellnus , E. W. Derman & T. D. Noakes To cite this article: M. P. Schwellnus , E. W. Derman & T. D. Noakes (1997) Aetiology of skeletal muscle ‘cramps’ during exercise: A novel hypothesis, Journal of Sports Sciences, 15:3, 277-285, DOI: 10.1080/026404197367281 To link to this article: http://dx.doi.org/10.1080/026404197367281 Published online: 01 Dec 2010. Submit your article to this journal Article views: 942 View related articles Citing articles: 68 View citing articles Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=rjsp20 Download by: [Australian Catholic University] Date: 24 September 2017, At: 18:51 Journal of Sports Sciences, 1997, 15, 277-285 Aetiology of skeletal muscle `cramps’ during exercise: A novel hypothesis M .P. SCH WELLN US,* E.W. D ERM AN and T.D. N OAKES M RC/UCT B ioenergetics of Exercise Research Unit, University of Cape Town M edical School, Sports Science Institute of South Africa, PO B ox 115, Newlands 7725, South Africa Accepted 3 September 1996 The aetiology of exercise-associated muscle cramps (EAMC), de® ned 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 ¯ uid 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 scienti® c literature including data from recent studies do not support these hypotheses 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 re¯ ex. In two animal studies, abnormal re¯ ex 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 re¯ ex 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 re¯ ex 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. Keywords: Exercise, fatigue, muscle cramps. Downloaded by [Australian Catholic University] at 18:51 24 September 2017 Introduction gnosis and management of this condition is, however, not well understood. Skeletal muscle cramps are one of the most common Muscle cramps can occur in a variety of medical con- clinical problems encountered by medical staff attend- ditions (Table 1). The majority of these conditions are ing to athletes at endurance events including marathons rare and, in our experience, most athletes with exercise- (Robertson, 1988) and triathlons (Hiller et al., 1987). associated muscle cramping (EAMC) do not suffer The lifetime prevalence of skeletal muscle cramping in from the congenital or acquired medical conditions marathon runners and triathletes has been reported to listed in Table 1. In this review, we will de® ne and clas- be as high as 30-50% and 67% respectively (Manjra, sify skeletal muscle cramping, and then discuss the 1991; Kantarowski et al., 1990). The aetiology, dia- pathophysiology of EAMC. Historical perspectives on the aetiology of EAMC will be reviewed, and a sum- mary of recent research data pointing to the aetiology * Author to whom all correspondence should be addressed. of EAMC will be presented. Based on these recent 0264-0414/97 © 1997 E. & F.N. Spon 278 Schwellnus et al. Table 1 Classi® cation of the causes of skeletal muscle ® ndings, a novel hypothesis for EAMC will be pro- cramps posed. Congenital abnorm alities 1. Metabolic abnormalities De® nitions and terminology (a) Carbohydrate metabolism (glycogen storage diseases) c Type I: glucose-6-phosphatase de® ciency It is dif® cult to de® ne muscle `cramping’ , but it has c Type II: lyposomal alpha-glucosidase de® ciency been suggested that a cramp is a `spasmodic painful c Type III: debrancher enzyme de® ciency (muscle involuntary contraction of a muscle’ (Layzer and Row- and liver) land, 1971). For the purposes of this review, the defini- c Type IV: myophosphorylase de® ciency tion can be modi® ed to exclude cramps occurring in c Type V: phosphorylase kinase de® ciency smooth muscle as well as skeletal muscle cramping that (b) Fat metabolism may occur at rest. Exercise-associated muscle cramping c Carnitine palmityl transferase de® ciency is therefore de® ned as a `painful spasmodic involuntary (c) Purine neucloetide de® ciency c Myodenalate deaminase de® ciency contraction of skeletal muscle that occurs during or 2. Other congenital abnormalities immediately after muscular exercise’ . (a) Myotonia congenita (b) Autosomal dominant cramping disease Acquired medical diseases Classi® cation of skeletal muscle cramps 1. Neuromuscular diseases Skeletal muscle cramps can occur as part of the general (a) Lower motor neuron disease symptom complex of a variety of congenital and (b) Myotonic dystrophy (c) Nerve root compression acquired abnormalities (Table 1). There are also spe- (d) Peripheral neuropathy ci® c clinical syndromes where skeletal muscle cramping 2. Endocrine diseases is the principal symptom. These syndromes are EAMC, (a) Thyroid disease occupational cramps, nocturnal calf muscle cramps (b) Diabetes mellitus and pregnancy-associated cramps. A detailed discus- 3. Fluid and electrolyte abnormalities sion on the aetiological factors, clinical presentation (a) Hypocalcaemia and management of these conditions, with the excep- (b) Hypomagnasaemia tion of EAMC, is beyond the scope of this paper. (c) Hypokalaemia Aspects of these conditions have recently been reviewed (d) Hyperkalaemia (e) Hyponatraemia (Layzer and Rowland, 1971; McGee, 1990; Riley and 4. Pharmaceutical agents Suresh, 1995). (a) Nifedipine (b) Beta-agonists: terbutaline, salbutamol (c) Ethanol Physiology of skeletal muscle relaxation (d) Clo® brate (e) Pencillamine Skeletal muscle cramping is an abnormality of skeletal (f) Nicotinic acid muscle relaxation (Layzer and Rowland, 1971). An (g) Diuretics understanding of the physiological requirements for Downloaded by [Australian Catholic University] at 18:51 24 September 2017 (h) Phenothiazines 5. Toxins skeletal muscle relaxation should therefore form the (a) Strychnine poisoning basis of any hypothesis which could explain the aeti- (b) Lead toxicity ology of EAMC. The physiological requirements for (c) Tetanus skeletal muscle relaxation can be categorized as fol- (d) Black widow spider bite lows: 6. Other acquired medical conditions (a) Cirrhosis of the liver (b) Neoplastic disease Adenosine tri-phosphate (c) Diarrhoea (d) Sarcoidosis Adenosine tri-phosphate (ATP) is required for two pro- cesses that are essential for skeletal muscle relaxation. Speci® c acquired skeletal m uscle cramp syndromes First, ATP is required for the detachment of the myosin 1. Exercise-associated muscle cramps (EAMC) head from the actin molecule and, secondly, for the 2. Occupational cramps pumping of Ca2+ from the cytoplasm into the longitu- 3. Nocturnal calf muscle cramps dinal portion of the sarcoplasmic reticulum (Ganong, 4. Pregnancy-associated cramps 1993). Adenosine tri-phosphate depletion has been Aetiology of skeletal muscle `cramps’ during exercise 279 postulated as the mechanism for persistent skeletal Normal motor neuron activity muscle contraction in the following conditions (Layzer Persistent spontaneous motor neuron depolarization and Rowland, 1971): rigor mortis, experimental use of will result in a sustained muscle contraction. This ATP blockers (iodoacetate, dinitro¯ uorobenzene), mechanism for abnormal sustained muscle contraction myophosphorylase de® ciency, phosphofructokinase is observed in the rare hereditary syndrome of hyper- de® ciency (Layzer et al., 1967), carnitine palmityl excitable motor neuron (also known as myokymia, neu- transferase de® ciency (Bank et al., 1975) and myoade- romyotonia, pseudomyotonia, continuous muscle ® bre nylate deaminase de® ciency (Ashwal and Peckham, activity, armadillo syndrome) (Layzer and Rowland, 1985; Fishbein, 1985). Intracellular ATP depletion will 1971). Disturbances of serum electrolyte