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

Nasir Uddin; Jamie Tallent; Stephen D Patterson; Stuart Goodall; Mark Waldron

doi:10.1007/s00421-022-04937-z

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

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

Nasir Uddin, Jamie Tallent, Stephen D Patterson, Stuart Goodall and Mark Waldron

European Journal of Applied Physiology, Vol.122, pp.1797-1810

2022

DOI: https://doi.org/10.1007/s00421-022-04937-z

PMCID: PMC9287254

PMID: 35362800

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Abstract

Fatigue

Electromyography

Transcranial magnetic stimulation

Dehydration

Hyperthermia

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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Title: Corticospinal and peripheral responses to heat-induced hypo-hydration: potential physiological mechanisms and implications for neuromuscular function
Authors: Nasir Uddin (Author) - School of Human Sciences, London Metropolitan University, London, UK
Jamie Tallent (Author) - University of Essex
Stephen D Patterson (Author) - St Mary's University Twickenham London
Stuart Goodall (Author) - Northumbria University
Mark Waldron (Corresponding Author) - University of the Sunshine Coast, Queensland, School of Health and Behavioural Sciences - Legacy
Publication details: European Journal of Applied Physiology, Vol.122, pp.1797-1810
Publisher: Springer
Date published: 2022
DOI: 10.1007/s00421-022-04937-z
ISSN: 1439-6327
PMID: 35362800; PMC9287254
Copyright note: This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
Organisation Unit: University of the Sunshine Coast, Queensland; School of Health and Behavioural Sciences - Legacy
Language: English
Record Identifier: 99629340802621
Output Type: Journal article

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