Metabolic Adaptations to Resistance Training in Skeletal Muscle From Young and Older Women

Abstract

Resistance training (RT) is well-characterized for its ability to improve muscle strength and function and is widely recommended to protect against muscle loss that occurs with aging. However, a failure to maintain or increase the cellular factors involved in regulating energy metabolism in response to RT could compromise metabolic health and functional capacity. PURPOSE: To examine the influence of 12 weeks of progressive RT on the expression of skeletal muscle proteins involved in cellular transport of fatty acids (FAT/CD36) and glucose (GLUT4), mitochondrial oxidative phosphorylation (COX1), and transcription factors involved in regulating energy metabolism (peroxisome proliferators activated receptor γ - co activator-1 [PGC-1 α] and myocyte enhancer factor [Mef2]). METHODS: Nineteen women (n=9 older [O], 74±1 yr; n=10 younger [Y], 25±1 yr) underwent 12 wk of progressive RT (3d/week) targeting the knee and hip extensor muscles. Muscle biopsies were obtained from the vastus lateralis muscle before and after RT and protein content of FAT/CD36, GLUT4, COX1, PGC-1Δ, and Mef2 were determined by immunoblot analysis. RESULTS: Before training, COX1 content was ∼2-fold higher (P<0.05) in O compared to Y while no age-related differences were found for PGC-1 Δ, Mef2, FAT/CD36, or GLUT4 before training. In response to RT, COX1 content increased (P<0.05) 37±15% in Y only. Additionally, although RT decreased the abundance of full-length (91 kDa) PGC-1α (P<0.05) in O, the short variant (32 kDa) of PGC-1 α remained unchanged. No change in either PGC-1 Δ variant was found in Y after training. Abundance of Mef2, FAT/CD36, and GLUT4 were maintained after training in both groups. CONCLUSION: These findings indicate that RT does not impact markers for substrate transport and oxidative metabolism in young and older women.