The Effects of Acute Aerobic and Resistance Exercise on mTOR Signaling and Autophagy in Human Skeletal Muscle

Exercise serves as a powerful stimulus to induce skeletal muscle adaptation. For instance, it is well understood that aerobic exercise (AE) elicits an adaptive response ultimately leading to increased fatigue resistance and capillarization, whereas resistance exercise (RE) is known to elicit an adaptive response leading to increased muscle strength and size. However, the precise molecular mechanisms mediating these unique adaptations to different forms of exercise remain to be completely resolved. The purpose of this study was to investigate the adaptive cellular response of skeletal muscle following acute AE and RE. Specifically, this study focused on two molecular processes: 1) mammalian/mechanistic target of rapamycin (mTOR) signaling pathway, a regulator of muscle protein synthesis, and 2) autophagy, a process through which proteins and organelles are broken down in the muscle fiber. In a counterbalanced, crossover design, six healthy, recreationally active young men (27±3 yr) completed acute AE (40 min of cycling ~70% maximal HR) and acute RE [8 sets, 10 reps, ~65% 1-repetition maximum (1RM)] separated by ~1wk. Muscle biopsies (vastus lateralis) were obtained before, at 1 and 4h post exercise and western blot analyses were used to examine the phosphorylation of mTOR signaling proteins and various markers of autophagy. Phosphorylation of mTORSer2448 increased only following RE at 4h (P < 0.05). However, phosphorylation of p70S6K1Thr389, a downstream marker of mTOR, increased following both AE and RE at 4h (P < 0.05). However, p70S6K1Thr389 was phosphorylated to a greater extent at 1h following RE compared to AE (P < 0.05). LC3BII was decreased at 1h and 4h postexercise in response to both AE and RE (P < 0.05). These data indicate that both acute AE and RE stimulate, to some degree, mTOR signaling in skeletal muscle, a pathway associated with increased muscle protein synthesis. Further, based on markers examined in the current study, both acute AE and RE similarly stimulate autophagy, which is associated with muscle protein breakdown. These data indicate that, at least in the immediate hours post exercise, the unique adaptations to AE and RE exercise may be mediated through cellular pathways other than mTOR and autophagy.