Abstract
This study aimed to investigate whether acute passive heat stress 1) decreases muscle Maximal Voluntary Contraction (MVC); 2) increases peripheral muscle fatigue; 3) increases spinal cord excitability, and 4) increases key skeletal muscle gene signaling pathways in skeletal muscle. Examining the biological and physiological markers underlying passive heat stress will assist us in understanding the potential therapeutic benefits. MVCs, muscle fatigue, spinal cord excitability, and gene signaling were examined after control or whole body heat stress in an environmental chamber (heat; 82 °C, 10% humidity for 30 min). Heart Rate (HR), an indicator of stress response, was correlated to muscle fatigue in the heat group (R = 0.59; p < 0.05) but was not correlated to MVC, twitch potentiation, and H reflex suppression. Sixty-one genes were differentially expressed after heat (41 genes >1.5-fold induced; 20 < 0.667 fold repressed). A strong correlation emerged between the session type (control or heat) and principal components (PC1) (R = 0.82; p < 0.005). Cell Signal Transduction, Metabolism, Gene Expression and Transcription, Immune System, DNA Repair, and Metabolism of Proteins were pathway domains with the largest number of genes regulated after acute whole body heat stress. Acute whole-body heat stress may offer a physiological stimulus for people with a limited capacity to exercise.
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