Hyperthermia, but not dehydration, alters the electrical activity of the brain

Heuvel, Anne M. J. van den; Haberley, Benjamin J; Hoyle, David J. R.; Taylor, Nigel A.S.; Croft, Rodney J.

doi:10.1007/s00421-020-04492-5

Cited by 8 publications

(3 citation statements)

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“…Several studies have investigated the effects of hyperthermia with dehydration and exercise (Ftaiti et al 2010 ) and without dehydration (Nielsen et al 2001 ; Nybo and Nielsen 2001 ) on EEG activity, reporting an increased alpha and decreased beta power during prolonged exercise, potentially indicating increased inhibitory activity in pyramidal neurons. This agrees with van den Heuvel et al ( 2020 ), who investigated EEG changes after passive hyperthermia with and without dehydration, and found no independent effect of hypo-hydration on resting EEG, suggesting neural alterations to be related to thermoregulatory factors. In addition, Caputa et al ( 1986 ) reported heightened hypothalamic temperatures (42–43 °C) led to a reduction in exercise capacity in animals; however, trunk temperatures (below 43.5 °C) were unrelated to exercise capacity, indicating a failure of central origin during hyperthermia.…”

Section: Central and Peripheral Responses To Hypo-hydrationsupporting

confidence: 92%

“…Furthermore, studies utilising diuretics (e.g., furosemide) result in hypo-hydration (iso-osmotic hypovolemia) dissimilar to heat-induced hypo-hydration (hyperosmotic hypovolemia), meaning that the mechanisms of performance impairment are unlikely to be the same. Consequently, future studies should differentiate the effects of hypo-hydration from hyperthermia and exercise-induced fatigue, similar to the methods of Periard et al ( 2012 ) and van den Heuvel et al ( 2020 ). Furthermore, future studies should investigate the brain’s intracortical inhibitory and excitatory activity (via paired-pulse TMS) and motor unit activity (via high-density surface EMG) to elucidate the distinct roles of the central and peripheral nervous systems during force output, following heat-induced hypo-hydration.…”

Section: Future Directionsmentioning

confidence: 99%

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Corticospinal and peripheral responses to heat-induced hypo-hydration: potential physiological mechanisms and implications for neuromuscular function

et al. 2022

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Heat-induced hypo-hydration (hyperosmotic hypovolemia) can reduce prolonged skeletal muscle performance; however, the mechanisms are less well understood and the reported effects on all aspects of neuromuscular function and brief maximal contractions are inconsistent. Historically, a 4–6% reduction of body mass has not been considered to impair muscle function in humans, as determined by muscle torque, membrane excitability and peak power production. With the development of magnetic resonance imaging and neurophysiological techniques, such as electromyography, peripheral nerve, and transcranial magnetic stimulation (TMS), the integrity of the brain-to-muscle pathway can be further investigated. The findings of this review demonstrate that heat-induced hypo-hydration impairs neuromuscular function, particularly during repeated and sustained contractions. Additionally, the mechanisms are separate to those of hyperthermia-induced fatigue and are likely a result of modulations to corticospinal inhibition, increased fibre conduction velocity, pain perception and impaired contractile function. This review also sheds light on the view that hypo-hydration has ‘no effect’ on neuromuscular function during brief maximal voluntary contractions. It is hypothesised that irrespective of unchanged force, compensatory reductions in cortical inhibition are likely to occur, in the attempt of achieving adequate force production. Studies using single-pulse TMS have shown that hypo-hydration can reduce maximal isometric and eccentric force, despite a reduction in cortical inhibition, but the cause of this is currently unclear. Future work should investigate the intracortical inhibitory and excitatory pathways within the brain, to elucidate the role of the central nervous system in force output, following heat-induced hypo-hydration.

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