Abstract
Exercise training and physical activity are known to be associated with high mitochondrial content and oxidative capacity in skeletal muscle. Metabolic diseases including obesity and insulin resistance are associated with low mitochondrial capacity in skeletal muscle. Certain transcriptional factors such as PGC‐1α are known to mediate the exercise response; however, the precise molecular mechanisms involved in the adaptation to exercise are not completely understood. We performed multiple measurements of mitochondrial capacity both in vivo and ex vivo in lean or overweight individuals before and after an 18‐day aerobic exercise training regimen. These results were compared to lean, active individuals. Aerobic training in these individuals resulted in a marked increase in mitochondrial oxidative respiratory capacity without an appreciable increase in mitochondrial content. These adaptations were associated with robust transcriptome changes. This work also identifies the Tribbles pseudokinase 1, TRIB1, as a potential mediator of the exercise response in human skeletal muscle.
Highlights
Impairments in skeletal muscle mitochondrial capacity adversely impact muscle function and whole-body metabolic health
Sedentary and/or overweight individuals are characterized by impaired skeletal muscle mitochondrial oxidative metabolism when compared to more active people (Bajpeyi et al, 2011; Phielix et al, 2012; Sparks et al, 2005, 2013)
This difference in muscle mitochondrial capacity is influenced by underlying molecular mechanisms
Summary
Impairments in skeletal muscle (muscle) mitochondrial capacity adversely impact muscle function and whole-body metabolic health. Associations between impaired muscle mitochondrial capacity and the development and presence of obesity and insulin resistance have been frequently described (Bajpeyi et al, 2011; Phielix et al, 2012; Sparks et al, 2005, 2013). In comparison to healthy active individuals, those with sedentary behavior, obesity, and insulin resistance manifest lower skeletal muscle mitochondrial capacity (Bajpeyi et al, 2011; Meex et al, 2010; Phielix et al, 2008; Sparks et al, 2013). Some studies have found exercise training-induced improvements in muscle mitochondrial capacity before PGC-1α gene expression was elevated (Wright et al, 2007). We performed unbiased transcriptomic analyses in skeletal muscle to identify putative regulators of skeletal muscle mitochondrial capacity
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