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Muscle strength after resistance training correlates to mediators of muscle mass and mitochondrial respiration in middle-aged adults.

Skeletal muscle aging is a multi-dimensional pathology of atrophy, reduced strength, and oxidative damage. While some molecular targets may mediate both hypertrophic and oxidative adaptations in muscle, their responsiveness in humans and relationship with functional outcomes like strength remain unclear. Promising therapeutic targets to combat muscle aging like apelin, vitamin D receptor (VDR), and spermine oxidase (SMOX) have been investigated in preclinical models but the adaptive response in humans is not well defined. In an exploratory investigation, we examined how strength gains with resistance training relate to regulators of both muscle mass and oxidative function in middle-aged adults. Forty-one middle-aged adults (18M, 23F; 50±7y; 27.8±3.7kg/m2; mean±SD) participated in a 10-week resistance training intervention. Muscle biopsies and plasma were sampled at baseline and post-intervention. High-resolution fluo-respirometry was performed on a subset of muscle tissue. Apelin signaling (plasma apelin, P=0.002; Apln mRNA, P<0.001; apelin receptor mRNA Aplnr, P=0.001) increased with resistance training. Muscle Vdr mRNA (P=0.007) and Smox mRNA (P=0.027) were also upregulated after the intervention. Mitochondrial respiratory capacity increased (Vmax, oxidative phosphorylation, and uncoupled electron transport system, P<0.050), yet there were no changes in ADP sensitivity (Km P=0.579), hydrogen peroxide emission (P=0.469), nor transcriptional signals for mitochondrial biogenesis (nuclear respiratory factor 2, Gapba P=0.766) and mitofusion (mitochondrial dynamin like GTPase, Opa1 P=0.072). Muscular strength with resistance training positively correlated to Apln, Aplnr, Vdr, and Smox transcriptional adaptations, as well as mitochondrial respiratory capacity (unadjusted P<0.050, r=0.400-0.781). Further research is required to understand the interrelationships of these targets with aged muscle phenotype.