Purpose: Exertional hyperthermia impairs endurance performance. Although the central nervous system mediates premature fatigue, limited understanding of when and how neural perturbations arise during exertional hyperthermia hinders efforts to develop effective strategies to mitigate its impacts. Methods: Fifteen physically active males completed a familiarization trial and three randomized crossover controlled trials involving treadmill walking at 54 ± 4% maximal oxygen consumption (mean ± SD) in a temperate environment (COOL; dry bulb temperature T db : 22.3 ± 0.4°C, relative humidity RH: 68 ± 10%), warm environment with (WARM+FC; T db : 32.0 ± 0.2°C, RH: 71 ± 2%) and without (WARM; T db : 32.1 ± 0.2°C, RH: 70 ± 2%) isolated facial fan cooling, until volitional exhaustion or rectal temperature of 39.5°C. Brachioradialis activation was assessed via electromyography (EMG) through maximal (MVC) and submaximal (sMVC) voluntary isometric handgrip contractions. Primary motor cortex oxygenation was continuously monitored using functional near-infrared spectroscopy (fNIRS). ΔHbdiff (difference between oxyhemoglobin and deoxyhemoglobin changes) indexed cortical activation. ΔHbdiff/EMG quantified cortical activation relative to muscle activation. Results: ΔHbdiff/EMG was higher during MVC in WARM relative to COOL ( P < 0.05) but similar across trials during sMVC. This was observed alongside reduced muscle activation ( P < 0.05). Isolated facial cooling in WARM+FC trials did not mitigate heat-induced neural deficits observed during MVC. Conclusions: Greater cortical activation is required to sustain similar muscle activation during exercise in warm compared with temperate conditions, suggesting a suboptimal neural drive for muscle output with exertional hyperthermia. This may contribute to the onset and development of central fatigue. fNIRS-derived markers may serve as early indicators to mitigate heat-induced deficits and enhance safety during exercise.
Michiko et al. (Mon,) studied this question.