Acute effects of heat intervention and hybrid exercise on protein synthesis, ribosome biogenesis and autophagy

The use of kaumatherapy (i.e. heat exposure like sauna-bathing) as passive intervention has become of growing interest to promote skeletal muscle adaptations such as strength gains and preservation of muscle mass. Importantly, the effects of a single exposure to heat (HE) in combination with hybrid exercises, designed to induce both aerobic and resistance adaptations (EX), on protein turnover remains unclear. The objective of this investigation was to evaluate the responses to HE, EX and their combination (EX + HE) on the expression of mRNA and protein related to proteosynthesis, ribosome biogenesis and content, as well as autophagy and cellular stress pathways. Eight-week-old male mice C57BL/6 J mice (n = 8 per condition) underwent acute HE (45min, 40 °C), EX (high-intensity inclined treadmill running) or EX + HE immediately after exercise. Mice were euthanized 240 min post-interventions and quadriceps muscles were harvested for analysis. Acute HE increased the mRNA expression of markers of ribosome biogenesis (POL1RA, UBF), but did not enhance ribosomal content (rRNA 18 S and 28 S) nor ribosomal transcription (pre-rRNA 45 S). Concerning the modulation of protein synthesis, EX induced an increase of MTORC1 downstream targets (P-S6K1, P-RPS6) and protein synthesis flux (assessed by puromycin incorporation) while HE alone did not and post-exercise HE had no additional effects. EX + HE also led to enhanced protein synthesis rates, but did not confer any additional benefit compared to EX alone. Finally, only EX + HE increased the autophagy flux marker LC3-B II/I, the microautophagy marker LAMP2A and phosphorylation level of P-NFκB Ser536. However, no changes in protein carbonylation were detected at this time point. These results suggest that acute post-exercise HE has no additional effects on protein synthesis at 4 h post-exercise but, when combined with EX, increases autophagy and P-NFκB Ser536, suggesting a heightened cellular stress response.