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Boosting mitochondrial biogenesis or protein synthesis in human skeletal muscle: Novel insights

Over a decade, evidence have reported that endurance exercise (EE) triggers protein kinase activated by AMP (AMPK) to drive mitochondrial biogenesis. AMPK is a sensor of energy status that maintains cellular energy homeostasis. In contrast, strength exercise (SE) induces accretion of skeletal muscle protein synthesis via mammalian target of rapamycin (mTOR) and its downstream proteins (Hardie, 2004; Baar et al., 2006). Now a recent study (Vissing et al., 2011) published in Scandinavian Journal of Medicine and Science in Sports challenges the “AMPK-PKB switch”, a theory termed by Atherton et al. (2005), to demonstrate how exercise specificity influence the molecular responses. Vissing et al. (2011) used a rigorous experimental model that can be applied in future studies. First, untrained individuals were submitted to an exercise training program for 10 weeks prior to acute exercise, to minimize metabolic stress. Second, the authors used sedentary control subjects, to observe the influence of other factors like biopsies sampling, diet control and circadian rhythm. Third, Vissing et al. (2011) monitored the time course for an extense 22 h and found surprising results. AMPK phosphorylation increased in both EE and SE and returned to basal levels, while mTOR was activated only in SE and did not return to basal levels. The new finding in this study is that AMPK may be a “double edged sword” molecule in mediating the widespread muscle adaptations. In another independent study, Wang et al. (2011) investigated the hypothesis if mitochondrial biogenesis stimulated by EE following SE (EE + SE) would be impaired. Contrary to the authors’ hypothesis, SE did not impair mitochondrial biogenesis, but potentiated peroxisome proliferator-activated receptor-g coactivator-1 (PGC-1a), a direct marker of mitochondrial biogenesis in EE + SE group. It is important to highlight that Vissing et al. (2011) did not evaluate PGC-1a and maybe the activation of AMPK observed in SE was not related directly to mitochondrial biogenesis, but maybe other unknown event. A limitation of both studies was that they did not analyze tuberous sclerosis 1/2 and Raptor, proteins involved in the antagonistic AMPK/mTOR mechanism (Mounier et al., 2011). Based on these findings we can launch the following questions: Why proteins involved in protein synthesis were increased in EE + SE (in Wang) or SE (in Vissing), at the same time that mitochondrial biogenesis was induced? May skeletal muscle hypertrophy and resistance, two different phenotypes, share common features? The majority of studies used animal models, while these two studies used humans that could have contributed to the divergence of findings. These pictures add to the rationale that more studies are needed to understand these mechanisms. These can be facilitated by solid experimental delineations like the one used by Vissing et al. (2011). In a practical context AMPK may serve as an important factor to explain why some athletes even with strong muscle mass can achieve striking performance in aerobic events. If this is true, then we can argue if it is possible to set up a training method that can boost both endurance and strength performance. In conclusion, the study of Vissing et al. (2011) adds new important insights of the role of AMPK in mediating skeletal muscle and molecular responses, and calls for a shift in the paradigm in sports and exercise science.