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.
Measuring the DNA telomere length of skeletal muscle in experienced endurance runners may contribute to our understanding of the effects of chronic exposure to endurance exercise on skeletal muscle. This study compared the minimum terminal restriction fragment (TRF) length in the vastus lateralis muscle of 18 experienced endurance runners (mean age: 42 +/- 7 years) to those of 19 sedentary individuals (mean age: 39 +/- 10 years). The runners had covered almost 50,000 km in training and racing over 15 years. Minimum TRF lengths measured in the muscle of both groups were similar (P = 0.805) and within the normal range. Minimum TRF length in the runners, however, was inversely related to their years spent running (r = -0.63, P = 0.007) and hours spent training (r = -0.52, P = 0.035). Therefore, since exposure to endurance running may influence minimum TRF length, and by implication, the proliferative potential of the satellite cells, chronic endurance running may be seen as a stressor to skeletal muscle.
These findings suggest that skeletal muscle from symptomatic athletes with FAMS show extensive regeneration which most probably results from more frequent bouts of satellite cell proliferation in response to recurrent training- and racing-induced muscle injury.
Collision sports, such as Rugby Union (“Rugby”) have a particularly high risk of injury. Of all injuries common to collision sports, concussions have received the most attention due to the potentially negative cognitive effects in the short- and long-term. Despite non-professional Rugby players comprising the majority of the world’s playing population, there is relatively little research in this population. Stellenbosch Rugby Football Club (“Maties”), the official rugby club of Stellenbosch University, represents one of the world’s largest non-professional Rugby clubs, making this an ideal cohort for community-level injury surveillance. The aim of this study was to describe the incidence and events associated with concussion in this cohort. Baseline demographics were obtained on the 807 male student Rugby non-professional players who registered for the 10-week long 2018 season, which comprised 101 matches and 2,915 of exposure hours. All match-related injuries were captured by the medical staff of Stellenbosch Campus Health Service on an electronic form developed from the consensus statement for injury recording in Rugby. The mean age, height and weight of this cohort were 20 ± 2 years, 182 ± 7 cm and 88 ± 14 kg, respectively. Overall, there were 89 time-loss injuries, which equated to an injury rate of 30.6 per 1,000 match hours [95% confidence intervals (CIs): 24.2–36.9], or about one injury per match. The most common injury diagnosis was “concussion” (n = 27 out of 90 injuries, 30%), at a rate of 9.3 per 1,000 match hours (95% CIs: 5.8–12.8). The three most common mechanisms of concussion in the present study were performing a tackle (33%), accidental collision (30%) and being tackled (11%). Concussion was the most common injury in this population, at a rate that was six times higher than the most comparable study from the UK, which had far more exposure time over six seasons and wider range of player ability, from recreational to semi-professional. This might be explained by the training and vigilance of the club’s first aiders observing all matches for concussion. Future studies should try to explain this high rate and subsequently reduce these concussions. The addition of video surveillance data would assist in identifying the etiology of these concussions injuries in order to develop specific targeted interventions.
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