Neuromuscular Function Following Exercise-Heat Stress: Influence of Exercise Modality

Abstract

Background: Exercise-induced hyperthermia is associated with a decrease in force production capacity during brief (<5 seconds) and sustained (>10 seconds) maximal voluntary isometric contractions (MVIC). A reduction in central nervous system drive to exercising muscles is suggested to mediate this decrement to prevent thermal injury. Until recently, the influence of exercise modality on neuromuscular function in the heat remained unclear. Two studies have since elucidated the role of constant load and self-paced exercise on force production capacity and voluntary activation during hyperthermia. Methods: Study one evaluated neuromuscular function after a 40 km cycling time trial in hot (35°C) and cool conditions (20°C). In study two, muscle function was evaluated after passive heating via water immersion to a core temperature of 39.5°C and following constant load exercise to exhaustion at 60% of maximal oxygen uptake (38°C conditions). Prior to (control) and following each intervention, a sustained MVIC (20 s and 45 s, respectively for study 1 and 2) was performed to measure force production. Voluntary activation of the knee extensors was measured via percutaneous electrical stimulation at three intervals during each MVIC. Results: Following self-paced exercise, mean force production decreased similarly in hot (15%) and cool (14%) conditions compared with control, despite a difference in core temperature of 0.8°C (P<0.001). A reduction in mean voluntary activation (P<0.05) accounted for ∼20% of the decrement in force. Interestingly, the extent of decline in voluntary activation was sustained for the duration of MVIC and did not progressively decrease. In the second study, mean force production was reduced following both interventions, but the magnitude of decline was more pronounced after exercise (P<0.05). As with study one, the decline in voluntary activation was similarly maintained (∼93%) following both interventions, with central fatigue accounting for <45% of the loss in force. Conclusion: The loss of force production following exercise-induced hyperthermia appears to stem for both central and peripheral fatigue factors. Modality does not appear to influence neuromuscular function when exercise duration is similar and final core temperature is within ∼1°C. The combination of exercise and heat stress exacerbates the loss of force due to prior contractile activity.