Harber MP, Konopka AR, Douglass MD, Minchev K, Kaminsky LA, Trappe TA, Trappe S. Aerobic exercise training improves whole muscle and single myofiber size and function in older women. Am J Physiol Regul Integr Comp Physiol 297: R1452-R1459, 2009. First published August 19, 2009 doi:10.1152/ajpregu.00354.2009.-To comprehensively assess the influence of aerobic training on muscle size and function, we examined seven older women (71 Ϯ 2 yr) before and after 12 wk of cycle ergometer training. The training program increased (P Ͻ 0.05) aerobic capacity by 30 Ϯ 6%. Quadriceps muscle volume, determined by magnetic resonance imaging (MRI), was 12 Ϯ 2% greater (P Ͻ 0.05) after training and knee extensor power increased 55 Ϯ 7% (P Ͻ 0.05). Muscle biopsies were obtained from the vastus lateralis to determine size and contractile properties of individual slow (MHC I) and fast (MHC IIa) myofibers, myosin light chain (MLC) composition, and muscle protein concentration. Aerobic training increased (P Ͻ 0.05) MHC I fiber size 16 Ϯ 5%, while MHC IIa fiber size was unchanged. MHC I peak power was elevated 21 Ϯ 8% (P Ͻ 0.05) after training, while MHC IIa peak power was unaltered. Peak force (Po) was unchanged in both fiber types, while normalized force (Po/cross-sectional area) was 10% lower (P Ͻ 0.05) for both MHC I and MHC IIa fibers after training. The decrease in normalized force was likely related to a reduction (P Ͻ 0.05) in myofibrillar protein concentration after training. In the absence of an increase in Po, the increase in MHC I peak power was mediated through an increased (P Ͻ 0.05) maximum contraction velocity (Vo) of MHC I fibers only. The relative proportion of MLC1s (Pre: 0.62 Ϯ 0.01; Post: 0.58 Ϯ 0.01) was lower (P Ͻ 0.05) in MHC I myofibers after training, while no differences were present for MLC 2s and MLC 3f isoforms. These data indicate that aerobic exercise training improves muscle function through remodeling the contractile properties at the myofiber level, in addition to pronounced muscle hypertrophy. Progressive aerobic exercise training should be considered a viable exercise modality to combat sarcopenia in the elderly population.

These data suggest that reductions in FOXO3A and myostatin messenger RNA are potentially associated with exercise-induced muscle hypertrophy. Additionally, it appears that mitochondrial biogenesis can occur with aerobic training in older women independent of increased PGC-1α protein. Aerobic exercise training alters molecular factors related to the regulation of skeletal muscle, which supports the beneficial role of aerobic training for improving muscle health in older women.

The purpose of this investigation was to examine the influence of an acute bout of resistance exercise (RE) on intramuscular triglyceride (IMTG) and muscle glycogen concentrations and intracellular signaling in women with high body fat content. Six overweight women with a high percent body fat (age 29+/-3 yr; BMI 28+/-3 kg/m(2), body fat 38+/-4%) performed 6 sets of 10 repetitions of knee extension exercise at 70% 1RM. Muscle biopsies were obtained from the vastus lateralis before, 1 min after (POST1), and 2 h after (POST2) exercise. Acute RE reduced (p<0.05) IMTG content approximately 40% at POST1 and POST2 (75+/-5; 45+/-6; 50+/-10 mmol/kg/dry wt). Muscle glycogen was also reduced (p<0.05) approximately 25% at POST1 and remained lower at POST2 (317+/-14; 241+/-30; 235+/-26 mmol/kg/dry wt). ERK1/2, SAPK/JNK, and p38 phosphorylation were increased (p<0.05) approximately 2-3-fold at POST1 and ERK1/2 remained elevated and POST2 whereas SAPK/JNK and p38 returned to basal levels. AMPKalpha phosphorylation was unchanged in response to RE. These results show that both IMTG and muscle glycogen stores serve as an important energy source during RE in overweight women and the MAP kinase signaling response to RE is not compromised by high levels of body fat.

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