Summary

Top 5 papers analyzed

Exercise-associated muscle cramping (EAMC) is a painful condition that causes skeletal muscle to involuntarily contract during or after physical activity. While it is a common issue for marathon runners, the exact cause of EAMC is still not completely understood. Research suggests that the condition could be caused by an abnormality in neuromuscular control at the spinal level in response to fatiguing exercise. This “muscle fatigue” hypothesis is based on epidemiological studies, animal experimental data, and electromyogram recordings during bouts of acute cramping after intense physical activity. The traditional explanation for EAMC was linked to dehydration and electrolyte loss. However, there is evidence to suggest that this is not the case, as serum electrolyte concentrations and hydration status do not appear to be associated with EAMC. This has led to a new theory called altered neuromuscular control, which suggests that EAMC is caused by several factors, including fatigue, inadequate conditioning, and previous muscle injury or damage. These factors increase the excitability of alpha motor neurons, which can cause EAMC. In order to prevent EAMC, athletes should work closely with their trainers to identify any trends in their medical history and note when EAMC occurs. Common EAMC predictors include prior history of EAMC, faster race times, and previous muscle injury or damage. Keeping a “cramp journal” can help athletes identify and address these risk factors before they lead to EAMC. Overall, the cause of EAMC is still uncertain and there is much research yet to be done to develop effective prevention and treatment strategies. However, understanding the potential causes of EAMC can help athletes and sports medicine professionals work together to reduce the risk of this painful condition and improve athletic performance.

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Exercise-associated muscle cramp (EAMC) is a painful involuntary contraction of skeletal muscle that occurs during or after physical activity. EAMC has multiple potential causes, making it difficult to prevent or treat. Risk factors include a history of EAMC, high intensity and long duration of exercise, and underlying chronic disease. EAMC is more commonly associated with endurance-type activities and team sports. Although EAMC is common, it can be a rare occurrence for some athletes, while others may experience it frequently and severely. There is still much uncertainty surrounding the causes and treatment options for EAMC. Further research is needed to develop effective prevention and treatment strategies.

Published By:

RJ Maughan, SM Shirreffs - Sports Medicine, 2019 - Springer

Cited By:

47

Exercise-associated muscle cramping (EAMC) has long been attributed to dehydration and electrolyte loss, however, new evidence suggests that its genesis is due to changes in the nervous system. This theory, known as altered neuromuscular control, suggests that EAMC ensue when several factors (e.g. fatigue, inadequate conditioning, and muscle damage) increase alpha motor neuron excitability. A “cramp journal” is suggested to prevent EAMC by working closely with each athlete to identify trends in their medical history and noting when EAMC occurs. EAMC predictors include: prior history of EAMC, faster race times, and previous muscle injury or damage. This new evidence is important to reevaluate the evidence for each theory on EAMC genesis and could potentially save lives in high-stress athletic events where lives are at risk.

Published By:

KC Miller - Current Sports Medicine Reports, 2015 - journals.lww.com

Cited By:

31

Exercise-associated muscle cramping (EAMC) is a common issue for marathon runners, but the aetiology and management of this condition is not well understood. The most commonly cited hypothesis is the "muscle fatigue" hypothesis, which suggests that EAMC is the result of an abnormality of neuromuscular control at the spinal level in response to fatiguing exercise. This is based on evidence from epidemiological studies, animal experimental data, and electromyogram data recorded during bouts of acute cramping after fatiguing exercise. While early anecdotal reports linked cramps to sweating and changes in serum electrolyte concentrations, more recent research suggests that serum electrolyte concentrations and hydration status are not associated with EAMC. Overall, the cause of EAMC remains unclear, but research suggests that premature muscle fatigue may play a role.

Published By:

MP Schwellnus - Sports Medicine, 2007 - Springer

Cited By:

66

The study aimed to test the hypothesis that nociceptive stimulation of latent myofascial trigger points (MTrPs) increases the occurrence of local muscle cramps. The study carried out an experiment to see if a bolus injection of glutamate into a latent MTrP would increase the occurrence of muscle cramps. The results showed that glutamate and isotonic saline injections into the latent MTrPs induced higher peak pain intensity than into the non-MTrPs. The findings also suggest that nociceptive muscle stimulation of latent MTrPs is more likely to cause muscle cramps. This study highlights the importance of understanding MTrPs and their role in the occurrence of pain and muscular discomfort. It provides valuable information for clinicians when treating patients with myofascial pain syndrome.

Published By:

HY Ge, Y Zhang, S Boudreau, SW Yue… - Experimental brain …, 2008 - Springer

Cited By:

105

A clinical trial has shown that hydroquinine is more effective than a placebo in treating muscle cramps in healthy adults. The study, which was randomised, double-blind and placebo-controlled, involved 68 women and 44 men who reported at least three muscle cramps per week. During the treatment period, participants were randomly given 300mg of hydroquinine or a placebo. Those taking the hydroquinine reported a median of eight fewer cramps and three fewer cramp days. The drug was described as safe to take in the short-term and effective in preventing muscle cramps, with this effect lasting beyond the treatment period.

Published By:

PHP Jansen, KCW Veenhuizen, AIM Wesseling… - The Lancet, 1997 - Elsevier

Cited By:

83