Exercise training promotes skeletal muscle mitochondrial biogenesis and an increase in maximal oxygen consumption. Primary myotubes retain some metabolic properties observed in vivo but it is unknown whether this includes exercise-induced mitochondrial adaptations. The goal of this study was to test if primary myotubes from exercise-trained women have higher mitochondrial content and maximal oxygen consumption compared with untrained women.
Six trained and nine untrained white women participated in this study. Muscle biopsies from the vastus lateralis muscle of the right leg were obtained and primary muscle cells were isolated. Maximal respiration rates, mitochondrial mRNA and protein content, and succinate dehydrogenase activity were measured in skeletal muscle and primary myotubes from trained and untrained women.
Trained women, compared with untrained women, had higher maximal whole-body oxygen consumption (+18%, P = 0.03), in vivo maximal skeletal muscle oxidative capacity measured with near infrared spectroscopy (+48%, P < 0.01), and maximal oxygen consumption in permeabilized muscle fibers (+38%, P = 0.02), which coincided with higher protein levels of muscle mitochondrial enzymes. Primary myotubes from trained women had higher maximal oxygen consumption (+38%, P = 0.03), suggesting that some elements of exercise-induced metabolic programming persists ex vivo. Consistent with this idea, myotubes from trained women had higher mRNA levels of transcriptional regulators of mitochondrial biogenesis in addition to higher protein levels of mitochondrial enzymes.
These data suggest the existence of an “exercise metabolic program,” where primary myotubes isolated from exercise-trained individuals exhibit greater mitochondrial content and oxidative capacity compared with untrained individuals. These myotubes may be a useful model to study molecular mechanisms relevant to exercise adaptations in human skeletal muscle.
1East Carolina Diabetes and Obesity Institute, East Carolina University, Greenville, NC; 2Department of Kinesiology, East Carolina University, Greenville, NC; 3Human Performance Laboratory, East Carolina University, Greenville, NC; and 4Department of Physiology, East Carolina University, Greenville, NC
Address for correspondence: Katsuhiko Funai, Ph.D., East Carolina University, 115 Heart Drive, ECHI 4107, Greenville, NC 27834; E-mail: email@example.com.
Submitted for publication April 2017.
Accepted for publication June 2017.