Abstract
Mitochondria are critical to skeletal muscle contractile function and metabolic health. Short-term periods of step reduction (SR) are associated with alterations in muscle protein turnover and mass. However, the effects of SR on mitochondrial metabolism/muscle oxidative metabolism and insulin-mediated signaling are unclear. We tested the hypothesis that the total and/or phosphorylated protein content of key skeletal muscle markers of mitochondrial/oxidative metabolism, and insulin-mediated signaling would be altered over 7 days of SR in young healthy males. Eleven, healthy, recreationally active males (means ± SE, age: 22 ± 1 yr, BMI: 23.4 ± 0.7 kg·m2) underwent a 7-day period of SR. Immediately before and following SR, fasted-state muscle biopsy samples were acquired and analyzed for the assessment of total and phosphorylated protein content of key markers of mitochondrial/oxidative metabolism and insulin-mediated signaling. Daily step count was significantly reduced during the SR intervention (13,054 ± 833 to 1,192 ± 99 steps·day-1, P < 0.001). Following SR, there was a significant decline in maximal citrate synthase activity (fold change: 0.94 ± 0.08, P < 0.05) and a significant increase in the protein content of p-glycogen synthase (P-GSS641; fold change: 1.47 ± 0.14, P < 0.05). No significant differences were observed in the total or phosphorylated protein content of other key markers of insulin-mediated signaling, oxidative metabolism, mitochondrial function, or mitochondrial dynamics (all P > 0.05). These results suggest that short-term SR reduces the maximal activity of citrate synthase, a marker of mitochondrial content, without altering the total or phosphorylated protein content of key markers of skeletal muscle mitochondrial metabolism and insulin signaling in young healthy males.NEW & NOTEWORTHY Short-term (7 day) step reduction reduces the activity of citrate synthase without altering the total or phosphorylated protein content of key markers of skeletal muscle mitochondrial metabolism and insulin signaling in young healthy males.
Highlights
Musculoskeletal disuse occurs during illness and injury
We report that in response to 7 days of step reduction (SR) in young, healthy males there was a significant decline in maximal citrate synthase (CS) activity, a marker of mitochondrial content
Due to the purported link between alterations in mitochondrial metabolism and fuel utilization during musculoskeletal disuse, we examined the expression and phosphorylation of proteins involved in skeletal muscle insulin sensitivity
Summary
Musculoskeletal disuse occurs during illness (i.e., bed rest) and injury (i.e., limb immobilization) In addition to these periods of severe disuse, periods of reduced ambulation occur throughout the human life span in times of illness and injury, as well as through gradual reductions in physical activity lifestyle habits with age in the absence of injury/illness. Periods of physical inactivity and reduced physical activity across the lifespan are accompanied by skeletal muscle atrophy [1,2,3], a decline in aerobic capacity [4], and a reduction in whole body insulin sensitivity [5,6,7]. It is plausible that alterations in mitochondrial function during disuse may underpin reductions in aerobic capacity, and contribute to muscle atrophy and impaired insulin sensitivity. In models of more severe musculoskeletal disuse
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