Abstract

What is the central question of this review? Is exposure to a hot environment detrimental to neuromuscular performance? What is the main finding and what is its importance? Elevating body temperature improves peak power during short-duration, high-intensity exercise but trades off with an accelerated rate of decay. Higher muscle temperatures and cross-bridge cycling rate resemble a shift in contractile characteristic to a faster phenotype. Prolonged moderate-intensity exercise capacity is impaired in a hot environment. Fatigue appears to combine a reduced drive from the CNS and increased cardiovascular strain to maintain skeletal muscle perfusion and thermoregulation. The effect of thermal stress on human work capacity and neuromuscular function has been of interest to physiologists since the 19th century. The aim of the present review is to examine the impact of exposure to heat stress on neuromuscular performance. Exposure to heat stress during exercise is known to increase strain on the cardiovascular system owing to the competing demands of skeletal muscle perfusion and homeostatic thermoregulation. The effects of exposure to heat stress on the neuromuscular system are more complex, because in some circumstances an elevation in muscle temperature leads to an improvement in function, whereas in other circumstances an increase in temperature leads to a decrement in function that is a consequence of the mode, metabolic demand and duration of the exercise. The ability to sustain isometric tension is impaired with an elevated muscle temperature and so too is locomotor capacity over prolonged periods of time. In contrast, peak power production is enhanced by increasing muscle temperature but is achieved at the expense of maintaining power output, owing to a higher rate of decay in power production. The different effects on neuromuscular function at an elevated muscle temperature are explained, in part, by a higher rate of energy turnover. In addition, the effect of an elevated core temperature also appears to impair neuromuscular performance either owing to a reduced voluntary drive in motor unit recruitment or to a failure in muscle afferent feedback, or a combination of the two.

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