Passive hyperthermia reduces maximal but not explosive torque production

Abstract

Introduction: hyperthermia can reduce maximal voluntary force/torque (MVT) of skeletal muscle due to reduced neural activation (Todd et al., 2005). Rate of force/torque development (RTD) may be a more functionally relevant measure of neuromuscular performance than MVT; however, the effect of hyperthermia on RTD has received little attention. Primary determinants of RTD include neural activation and electrically evoked involuntary RTD (Maffiuletti et al., 2016), and whilst neural activation may decrease with hyperthermia, increased muscle temperature improves involuntary RTD, so it is unclear how voluntary RTD will be affected by hyperthermia. This study aimed to investigate the effects of progressive passive whole-body hyperthermia on MVT and voluntary RTD, as well as the neural and contractile factors contributing to any effects.

Methods: nine male participants completed two trials; one involving passive heating to a rectal temperature (Tre) of 39.5˚C (HOT) and the other (CON) where Tre was maintained at ~37˚C. The same neuromuscular measurements of the knee extensors were completed when participants first entered the chamber (Tre ~37˚C; Base), and at Tre=38.5˚C (ModHyp) and Tre=39.5˚C (SevHyp), in the HOT trial, and at equivalent time points into the CON trial. MVT, voluntary activation (VA) determined via interpolated twitch, and EMG at MVT normalised to maximal M-wave (EMGMVT) were measured during MVCs. Explosive voluntary RTD and normalised EMG were measured over 0-50 (RTD50; EMG50) and 0-100 (RTD100; EMG100) from torque/EMG onsets during explosive contractions. Involuntary RTD50 was measured during evoked octets at 300Hz.

Results: in the HOT trial, MVT declined throughout and was 15% lower at SevHyp than Base (P=0.016), which coincided with declines in EMGMVT (-44%; P<0.005) and VA (-16%; P<0.005) from Base to SevHyp. In contrast, voluntary RTD50 and RTD100 remained unaffected in the HOT trial (P>0.05), despite 23-31% decreases in EMG50 and EMG100 from Base to SevHyp (P<0.001). Involuntary RTD50 however, increased from Base to ModHyp (10%; P<0.001) and from ModHyp to SevHyp (4%; P<0.001). There were no changes in any dependent variables throughout the CON trial.

Conclusion: as expected MVT declined as a result of passive hyperthermia which was largely due to reduced neural activation (i.e., EMGMVT and VA). In contrast, this study provides novel evidence that voluntary RTD was largely unaffected by passive hyperthermia, despite considerable reductions in explosive neural activation, which likely occurred due to the increased involuntary RTD, and thus cancelling out of neural and contractile effects.

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Identifiers

ORCID for Ralph Gordon: orcid.org/0000-0002-8441-9292

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