It is known that ambulatory exercises such as brisk walking and jogging are potent stimuli for improving aerobic capacity, but it is less understood whether ambulatory exercise can increase leg muscle size and function. The purpose of this brief review is to discuss whether or not ambulatory exercise elicits leg muscle hypertrophy in older adults. Daily ambulatory activity with moderate (>3 metabolic equivalents [METs], which is defined as the ratio of the work metabolic rate to the resting metabolic rate) intensity estimated by accelerometer is positively correlated with lower body muscle size and function in older adults. Although there is conflicting data on the effects of short-term training, it is possible that relatively long periods of walking, jogging, or intermittent running for over half a year can increase leg muscle size among older adults. In addition, slow-walk training with a combination of leg muscle blood flow restriction elicits muscle hypertrophy only in the blood flow restricted leg muscles. Competitive marathon running and regular high intensity distance running in young and middle-aged adults may not produce leg muscle hypertrophy due to insufficient recovery from the damaging running bout, although there have been no studies that have investigated the effects of running on leg muscle morphology in older subjects. It is clear that skeletal muscle hypertrophy can occur independently of exercise mode and load.

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Abstract. Integrins, heterodimeric receptors for the extracellular matrix, are known to modulate transforming growth factor-ß1 (TGF-ß1)-mediated cell behavior. However, the interplay between ß1-integrin and Smad signaling, regulated by TGF-ß1, is not clearly understood. This study focuses on the alterations of the regulatory Smads (R-Smads) by TGF-ß1 in ß1-integrin-transfected HepG2 cells. The phosphorylation at the C-terminal site of R-Smads by TGF-ß1 was impaired in the ß1-integrin-transfected cells. However, the R-Smads were constitutively phosphorylated at the linker region in a MAP kinase-dependent manner. Furthermore, the expression of a mutant Smad3, that lacks the phosphorylation sites in the linker region, restored the TGF-ß1-induced Smad transcriptional activity. These results suggest that ß1-integrin impairs the TGF-ß1-mediated signals through the altered phosphorylation of the R-Smads.