Impacts of sarcopenia and resistance exercise training on mitochondrial quality control proteins.

Background: The progression of sarcopenia with aging may be related to mitochondrial dysfunction due in part to altered mitochondrial dynamics (fusion, fission, mitophagy, and biogenesis). Previous work has identified altered expression of proteins associated with these processes in with aging, but whether further changes occur in sarcopenia remains unclear.

Objectives: The purpose of this study was to assess protein expression of markers of mitochondrial fusion (Mfn2, Opa1), fission (Drp1, Fis1), mitophagy (Parkin), biogenesis (PGC-1α), and content (Complex IV: CIV) in sarcopenic and non-sarcopenic older adults. We also determined whether resistance training affected skeletal muscle mitochondrial content and expression of mitochondrial quality control proteins in sarcopenic older adults.

Design: Longitudinal exercise training study, with cross-sectional baseline comparison.

Setting and participants: Ten older adults with mild-moderate sarcopenia, plus ten non-sarcopenic, matched older adults from Maryland, USA.

Intervention: Twelve-week resistance training.

Measurements: Strength, sarcopenic index (ALM/BMI: appendicular lean mass divided by body mass index), body composition, and mitochondrial morphology and protein expression in vastus lateralis muscle.

Results: No differences in protein expression were observed between sarcopenic and non-sarcopenic participants at baseline; however, ALM/BMI was inversely related to CIV expression (r = -0.55, P = 0.013) across all subjects. Similarly, lean body mass and ALM correlated inversely with expression of the fusion protein Opa1-S (r = -0.55 - -0.51, P ≤ 0.022). Resistance training increased strength in sarcopenic older adults by 13 % (P = 0.02), but this group's expression of mitochondrial quality control proteins was mostly unaltered.

Conclusions: The presence of sarcopenia identified by ALM/BMI was not associated with changes in protein expression that are consistent with impaired mitochondrial dynamics beyond those changes that might occur with aging alone. While short-term resistance training increased strength in older adults with sarcopenia, this was not accompanied by changes in protein expression, with the possible exception of fusion protein Mfn2.