Short‐term muscle disuse atrophy is not associated with increased skeletal muscle lipid accumulation or impaired oxidative enzyme activity in young or old men (863.1)

Abstract

Aging is accompanied by a loss of skeletal muscle mass (sarcopenia) and metabolic function. A period of disuse (e.g. injury/illness) also causes muscle atrophy. The accumulation of periods of disuse throughout the lifespan has been proposed as a key factor in the development of sarcopenia. However, it is unknown whether brief periods of disuse also impair muscle metabolic function. We investigated the effects of 5 days of limb immobilization in healthy young (n=12; 23±1 y) and old (n=70±1 y) men on intramyocellular triacylglycerol (IMTG) content, the maximal activity and activation status of selected mitochondrial enzymes and the mRNA expression of genes associated with mitochondrial biogenesis, in muscle biopsies taken before and after disuse. At baseline, IMTG content was greater in old compared with young men (56.3±6.8 and 34.8±7.3 µmol.g‐1, respectively; P<0.05) but no changes were observed following immobilization. Disuse did not reduce muscle citrate synthase, β‐HAD or cytochrome C oxidase activity. However, muscle pyruvate dehydrogenase complex activation status increased following immobilization in the elderly men. The muscle mRNA expression of PGC1α and citrate synthase declined following immobilization in both groups. We conclude that 5 days of muscle disuse is not accompanied by a net increase in muscle lipid deposition or a decline in muscle oxidative capacity in young or elderly men.