Plain language summary
Endurance exercise stimulates mitochondrial biogenesis in skeletal muscles, a crucial adaptive protective mechanism against various metabolic disorders. Mitochondrial biogenesis is a process that involves the expansion of mitochondrial volume and changes in mitochondrial composition. Continuous moderate‐intensity exercise (CM) may lead to mild but prolonged metabolic disturbances, and low‐volume intense intermittent exercise regimes such as repeated‐sprint (RE) and speed endurance (SE) exercises may lead to a distinct degree of metabolic stress. This randomised counter-balanced crossover trial included 12 healthy trained men to investigate the effect of RE and SE exercise and high‐volume CM on metabolic perturbations and its impact on the regulation of molecular response stimulating mitochondrial biogenesis in human skeletal muscle. Compared to CM, PGC‐1α mRNA (Peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (PGC‐1α) mRNA) showed elevation in response to RS and SE exercises in well-trained subjects, and this was associated with high accumulation of muscle lactate, greater decline in muscle pH and elevated plasma adrenaline levels. Elevated metabolic perturbations lead to enhanced mitochondrial biogenesis-related mRNA responses. SE was associated with a greater increase in the PGC‐1α mRNA and severe metabolic stress. SE and CM elevated exercise-induced signalling and mRNA content of genes controlling mtDNA. Further robust research is required to elucidate the role of metabolic stress in initiating mitochondrial biogenesis in skeletal muscles in response to acute exercise, regulating genes modulating mtDNA transcription and mitochondrial remodelling dynamics. However, healthcare professionals can use the results of this study to understand that low-volume high-intensity exercise programmes can promote mitochondrial biogenesis in skeletal muscles in healthy trained men and have a similar effect to that of high-volume moderate-intensity exercise programmes.
Abstract
KEY POINTS Low-volume high-intensity exercise training promotes muscle mitochondrial adaptations that resemble those associated with high-volume moderate-intensity exercise training. These training-induced mitochondrial adaptations stem from the cumulative effects of transient transcriptional responses to each acute exercise bout. However, whether metabolic stress is a key mediator of the acute molecular responses to high-intensity exercise is still incompletely understood. Here we show that, by comparing different work-matched low-volume high-intensity exercise protocols, more marked metabolic perturbations were associated with enhanced mitochondrial biogenesis-related muscle mRNA responses. Furthermore, when compared with high-volume moderate-intensity exercise, only the low-volume high-intensity exercise eliciting severe metabolic stress compensated for reduced exercise volume in the induction of mitochondrial biogenic mRNA responses. The present results, besides improving our understanding of the mechanisms mediating exercise-induced mitochondrial biogenesis, may have implications for applied and clinical research that adopts exercise as a means to increase muscle mitochondrial content and function in healthy or diseased individuals. ABSTRACT The aim of the present study was to examine the impact of exercise-induced metabolic stress on regulation of the molecular responses promoting skeletal muscle mitochondrial biogenesis. Twelve endurance-trained men performed three cycling exercise protocols characterized by different metabolic profiles in a randomized, counter-balanced order. Specifically, two work-matched low-volume supramaximal-intensity intermittent regimes, consisting of repeated-sprint (RS) and speed endurance (SE) exercise, were employed and compared with a high-volume continuous moderate-intensity exercise (CM) protocol. Vastus lateralis muscle samples were obtained before, immediately after, and 3 h after exercise. SE produced the most marked metabolic perturbations as evidenced by the greatest changes in muscle lactate and pH, concomitantly with higher post-exercise plasma adrenaline levels in comparison with RS and CM. Exercise-induced phosphorylation of CaMKII and p38 MAPK was greater in SE than in RS and CM. The exercise-induced PGC-1α mRNA response was higher in SE and CM than in RS, with no difference between SE and CM. Muscle NRF-2, TFAM, MFN2, DRP1 and SOD2 mRNA content was elevated to the same extent by SE and CM, while RS had no effect on these mRNAs. The exercise-induced HSP72 mRNA response was larger in SE than in RS and CM. Thus, the present results suggest that, for a given exercise volume, the initial events associated with mitochondrial biogenesis are modulated by metabolic stress. In addition, high-intensity exercise seems to compensate for reduced exercise volume in the induction of mitochondrial biogenic molecular responses only when the intense exercise elicits marked metabolic perturbations.
Methodological quality
Jadad score
:
3
Allocation concealment
:
No
