Muscle cramps: A comparison of the two-leading hypothesis. (August 2018)

• Record Type: Journal Article
• Authors: Giuriato, Gaia; Pedrinolla, Anna; Schena, Federico; Venturelli, Massimo
• Is Part Of: Journal of electromyography and kinesiology. Volume 41(2018)
• Page Start: 89
• Page End: 95
• Publication Date: 2018-08
• Subjects: Muscle Cramps -- EAMC -- Neuromuscular hypothesis -- Dehydration hypothesis; Electromyography -- Periodicals; Kinesiology -- Periodicals; Electromyography -- Periodicals; Movement -- physiology -- Periodicals; Muscles -- physiology -- Periodicals; Électromyographie -- Périodiques; Cinésiologie -- Périodiques; Electromyography; Kinesiology; Electronic journals; Periodicals; 616.740757
• DOI: 10.1016/j.jelekin.2018.05.006
• Languages: English
• ISSNs: 1050-6411

Abstract

Abstract: Exercise-Associated Muscle Cramps (EAMC) are a common painful condition of muscle spasms. Despite scientists tried to understand the physiological mechanism that underlies these common phenomena, the etiology is still unclear. From 1900 to nowadays, the scientific world retracted several times the original hypothesis of heat cramps. However, recent literature seems to focus on two potential mechanisms: the dehydration or electrolyte depletion mechanism, and the neuromuscular mechanism. The aim of this review is to examine the recent literature, in terms of physiological mechanisms of EAMC. A comprehensive search was conducted on PubMed and Google Scholar. The following terminology was applied: muscle cramps, neuromuscular hypothesis (or thesis), dehydration hypothesis, Exercise-Associated muscle cramps, nocturnal cramps, muscle spasm, muscle fatigue. From the initial literature of 424 manuscripts, sixty-nine manuscripts were included, analyzed, compared and summarized. Literature analysis indicates that neuromuscular hypothesis may prevails over the initial hypothesis of the dehydration as the trigger event of muscle cramps. New evidence suggests that the action potentials during a muscle cramp are generated in the motoneuron soma, likely accompanied by an imbalance between the rising excitatory drive from the muscle spindles (Ia) and the decreasing inhibitory drive from the Golgi tendon organs. In conclusion, from the latest investigations there seem to be a spinal involvement rather than a peripheral excitation of the motoneurons.