Impact of aerobic exercise training on age-related changes in insulin sensitivity and muscle oxidative capacity.
By K. Short, J. Vittone, Maureen L. Bigelow, D. Proctor, Robert A. Rizza, Jill M. Coenen-Schimke, K. Nair. Diabetes, 2003
710 citations recorded by the source corpus.
Insulin resistance increases and muscle oxidative capacity decreases during aging, but lifestyle changes-especially physical activity-may reverse these trends. Here we report the effect of a 16-week aerobic exercise program (n = 65) or control activity (n = 37) performed by men and women aged 21-87 years on insulin sensitivity and muscle mitochondria. Insulin sensitivity, measured by intravenous glucose tolerance test, decreased with age (r = -0.32) and was related to abdominal fat content (r = -0.65). Exercise increased peak oxygen uptake (VO(2peak); 10%), activity of muscle mitochondrial enzymes (citrate synthase and cytochrome c oxidase, 45-76%) and mRNA levels of mitochondrial genes (COX4, ND4, both 66%) and genes involved in mitochondrial biogenesis (PGC-1alpha, 55%; NRF-1, 15%; TFAM, 85%). Exercise also increased muscle GLUT4 mRNA and protein (30-52%) and reduced abdominal fat (5%) and plasma triglycerides (25%). None of these changes were affected by age. In contrast, insulin sensitivity improved in younger people but not in middle-aged or older groups. Thus, the muscle mitochondrial response to 4 months of aerobic exercise training was similar in all age-groups, although the older people did not have an improvement in insulin sensitivity.
Subfields: Cell Biology, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/7f538b9ac47753072809008d9b7cc2a5de0d83f8
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Citations in the corpus
- Short‐term sprint interval versus traditional endurance training: similar initial adaptations in human skeletal muscle and exercise performance (2006, background): “Schmitt et al. (2003) observed higher CPTI mRNA content in endurance trained athletes compared with sedentary controls and Short et al. (2003) reported a 66% increase in COX IV mRNA abundance after 16 weeks of endurance exercise training, which suggests longer term training can influence mRNA…”
- Acute exercise remodels promoter methylation in human skeletal muscle. (2012, background): “Exercise increases the messenger RNA (mRNA) expression and protein levels of a plethora of genes regulating mitochondrial function and fuel usage, including PGC-1a, transcription factor A, mitochondrial (TFAM); peroxisome proliferator-activated receptor d (PPAR-d); and pyruvate dehydrogenase kinase,”
- A PGC-1α isoform induced by resistance training regulates skeletal muscle hypertrophy (2012, neutral): “Muscle PGC-1a is induced by exercise in both mice and humans (Short et al., 2003).”
- Pathogenesis of Insulin Resistance in Skeletal Muscle (2010, neutral): “[130] K.”
- Effects of exercise and diet on chronic disease. (2005, background): “Exercise training may ameliorate insulin resistance by direct effects on the muscle, such as enhancing insulin receptor autophosphorylation (417) and increasing GLUT-4 content (72, 79, 167, 351) and glucose transport-phosphorylation (297), by reducing visceral obesity (351), which is associated with”
- Exercise and Physical Activity for Older Adults (2020, positive): “For example, although both moderate- (218) and high-intensity (43) AET are shown to increase glucose transporter content in the muscles of older humans, it is the higher-intensity AET programs that may result in greater improvement in whole-body insulin action (52).”