Regulation of macro-autophagy in human skeletal muscle after a single bout of endurance exercise in the fasted state

Details

Supervisors

Francaux, Marc ; Jamart, Cécile

Faculty

Faculté des sciences de la motricité

Degree label

Master [120] en sciences de la motricité, orientation éducation physique

Abstract

Introduction. Autophagy is activated in response to an environmental stress or an energetic deficiency and functions as a control mechanism of cellular quality. Cytoplasmic materials - such as organelles or proteins - are damaged or have to fill a lack of energy under different stress conditions. Macroautophagy, hereafter called autophagy, involves the formation of a double-membrane vesicle named autophagosome, in which macromolecules or entire organelles are non-selectively degraded. Recent studies showed that en durance exercise can regulate the autophagic process. Methods. Sixteen trained cyclists or triathletes were divided randomly in two groups: an exercise group (Cycl, n=8) and a control group (Ctrl, n=8). During one of the two experiments, subjects took a standardized breakfast, during the other visit, they remained fasted. Subjects of the Cycl group had to ride for 2h at 55% of their VO2peak. Four biopsies were taken from the vastus lateralis: (1) before breakfast, (2) one hour after breakfast in the minutes preceding the exercise, (3) immediately after the end of the exercise and (4) one hour after the end of it. Results. LC3b-II protein level decreases after the exercise in the fed state (-83%, P<0.001). As compared to rest, LC3b-II was lower after exercise in the fasted state(-71%, P<0.001). Atg5-Atg12 complex as Beclin-1 protein level did not change after exercise. Akt phosphorylation state at Ser 473 increased after breakfast (+198%, P<0.001). As compared to rest, in the fasted state, Akt phosphorylation was 24% (P=0.047) and 39% (P=0.008) lower immediately and one hour after the end of the exercise, respectively. In the fasted state, FoxO3 phosphorylation at Thr 32 after exercise was 53% lower (P=0.031) as compared to rest. Conclusion. Our results alone are not enough to totally confirm our hypothesis, an increase of autophagic markers and activator pathways. However, we presented a decrease of LC3b-II protein protein expression and activation of autophagy regulatory pathway. Taken together, these results allowed us to think that the autophagic process can be activated after exercise in the fasted state.