Skeletal muscle hypertrophy after aerobic exercise training

Abstract

Current dogma suggests that aerobic exercise training has minimal effects on skeletal muscle size. We and others have demonstrated that aerobic exercise acutely and chronically alters protein metabolism and induces skeletal muscle hypertrophy. These findings promote an antithesis to the status quo by providing novel perspective on skeletal muscle mass regulation and insight into exercise countermeasures for populations prone to muscle loss.

Figure 1

Anabolic responses to acute and chronic aerobic exercise in young and old subjects. A. The increase in muscle protein synthesis (MPS) was similar between young and old participants after acute aerobic exercise with amino acid infusion (10). Data reported as the difference between means before and after exercise. B. The increase in basal MPS (~22%) after 16 weeks of aerobic exercise training in young and old subjects were not different (34). Data reported as mean ± standard deviation. C. Similar increase in quadriceps femoris cross sectional area (~4 cm²) after 12 weeks of aerobic exercise training in young and old men (22). Data reported as mean ± standard error.

Figure 2

Comparison of skeletal muscle hypertrophy in relation to mechanical work completed during a 12-week aerobic exercise training program (18). A. Aerobic exercise training induced similar hypertrophy of the quadriceps femoris in weight stable young (n=7; 20±1y) and older men (n=6; 74±3y). B. Young men completed nearly twice the mechanical work during the aerobic training program. C. When skeletal muscle hypertrophy is expressed relative to the anabolic stimulus (i.e. work performed (MJ)), it appears that old men were more sensitive at converting mechanical work into skeletal muscle mass accretion (i.e. anabolic sensitivity). MJ = Mega joules. * = difference between groups, ^† = training effect, P<0.05.

Figure 3

In a condensed model, aerobic exercise training alters key intracellular signaling pathways and mRNA expression related to both skeletal muscle protein metabolism (e.g., FOXO3a, myostatin) (21) and mitochondrial dynamics and proliferation (22) that may be associated with skeletal muscle hypertrophy. Reduced myostatin, a negative regulator of growth, appears to promote a positive protein balance through the AKT-mTOR pathway and increased muscle protein synthesis (MPS). When phosphorylated, FOXO3a is excluded from the nucleus, which inhibits the transcription of ubiquitin E3 ligases, MuRF-1 and Atrogin-1. Reduction of MuRF-1 and Atrogin-1 may assist in lowering muscle protein breakdown (MPB) and promote a positive net protein balance. Emerging evidence (2) proposes that PGC-1α inhibits FOXO3a expression therefore lowering muscle catabolism and increasing mitochondrial biogenesis as observed after aerobic exercise training. Collectively, increased mitochondrial dynamics and abundance may lead to improved mitochondrial energetics (i.e., reduced ROS, increased ATP), which have been hypothesized to modulate MPB and MPS. Aerobic exercise appears to alter MPB and MPS to create a positive muscle protein balance and skeletal muscle growth; however, further research is needed to fully elucidate the mechanisms associated with these hypotheses. ROS = reactive oxygen species, ATP = adenosine triphosphate, P = phosphorylation.

Figure 4

Aerobic exercise training (AET) has an effect on many mechanisms that may collectively promote skeletal muscle hypertrophy.