Preliminary Evidence of Differential Expression of Myogenic and Stress Factors in Skeletal Muscle of Older Adults With Low Muscle Strength.

Abstract

The age-related loss of muscle strength and mass, or sarcopenia, is a growing concern in the aging population. Yet, it is not fully understood which molecular mechanisms underlie sarcopenia. Therefore, the present study compared the protein expression profile, such as catabolic, oxidative, stress-related, and myogenic pathways, between older adults with preserved (8 ♀ and 5 ♂; 71.5 ± 2.6 years) and low muscle strength (6 ♀ and 5 ♂; 78.0 ± 5.0 years). Low muscle strength was defined as chair stand test time more than 15 seconds and/or handgrip strength less than 16 kg (women) or less than 27 kg (men) according to the EWGSOP2 criteria. Catabolic signaling (ie, FOXO1/3a, MuRF1, MAFbx, LC3b, Atg5, p62) was not differentially expressed between both groups, whereas the mitochondrial marker COX-IV, but not PGC1α and citrate synthase, was lower in the low muscle strength group. Stress factors CHOP and p-ERK1/2 were higher (~1.5-fold) in older adults with low muscle strength. Surprisingly, the inflammatory marker p-p65NF-κB was ~7-fold higher in older adults with preserved muscle strength. Finally, expression of myogenic factors (ie, Pax7, MyoD, desmin; ~2-fold) was higher in adults with low muscle strength. To conclude, whereas the increased stress factors might reflect the age-related deterioration of tissue homeostasis, for example, due to misfolded proteins (CHOP), upregulation of myogenic markers in the low strength group might be an attempt to compensate for the gradual loss in muscle quantity and quality. These data might provide valuable insights into the processes that underlie sarcopenia.