The Effect of Acute Exercise on Heat Stress Response and Autophagy Induction in Humans: Meta‐Analysis

Abstract

Eukaryotes employ heat stress response and autophagy to manage protein homeostasis. Autophagy is responsible for degradation of dysfunctional cellular constituents. On the other hand, heat shock proteins modulate protein folding and repair. Recent studies have shown that inhibition of heat shock factor 1 and upregulation of heat shock protein 70 (HSP70) activates and inhibits autophagy, respectively. In the present studies, we examined how these systems cooperate to maintain protein homeostasis during and after acute exercise in humans. A meta-analysis of studies that investigated the effects of acute exercise on autophagy, HSP70, protein synthesis, and protein breakdown in humans was performed. 53 publications with 566 participants were identified. Linear and nonlinear regression analyses were performed to describe relationships between time since initiation of exercise and expression of HSP70, autophagy activation, protein synthesis and breakdown. Our model shows that LC3 protein expression (a marker of autophagy) activation was increased about 14 h from the start of exercise, whereas HSP70 protein levels were elevated at about 105 h after exercise initiation. After initial increase (first 8 hours), protein synthesis gradually declined. Our model also showed a small increase in protein breakdown at about 24 h after the start of exercise and then steadily decreasing. We conclude that heat stress response and autophagy are linked and cooperate to maintain protein homeostasis during and after one bout of exercise in humans.