https://physoc.onlinelibrary.wiley.com/doi/10.1113/EP093336

Abstract

Exercise and nutritional modulation favourably alter mitochondrial quantity and quality in skeletal muscle. Mitochondrial dynamics, the coordination of fission and fusion events, are poised to mediate key aspects of organelle adaptation that arise from exercise. However, the molecular basis by which exercise affects mitochondrial dynamics remains poorly understood. The objective of this work was to further elucidate the signalling response of mitochondrial dynamics regulators to exercise and explore the synergistic potential to combine exercise and nutritional modulation. In a randomized crossover design, eight healthy, recreationally active men (age 25.8 ± 5.3 years, BMI 24.4 ± 1.2 kg/m^(2), ̇𝑉O2⁢peak 39.2 ± 5.7 ml/kg/min) performed a 1-h bout of workload-matched aerobic exercise on a cycle ergometer at 50–70% of Wmax, either in a fasted or a fed (i.e., following a carbohydrate rich breakfast) state. Gas exchange was measured throughout, and blood samples were collected intermittently. Vastus lateralis muscle biopsies were collected pre-, post- and 3 h post-exercise. Western blotting was performed on cytosolic and mitochondrial fractions. Fasted exercise was accompanied by increased cytosolic acetyl-CoA carboxylase Ser79 phosphorylation (P ≤ 0.001), an effect not observed in the fed group (P > 0.05). The subcellular location of mitochondrial fission effector dynamin-related protein 1 (DRP1) was unchanged (P > 0.05) following exercise. However, group differences (i.e., Fed vs. Fasted) in DRP1 subcellular localization and phosphorylation at residues Ser616 and Ser637 were observed post-exercise. Substrate availability may potentially influence the mitochondrial dynamics signalling response in skeletal muscle to acute aerobic exercise.

Highlights

• What is the central question of this study? This study investigates the mitochondrial dynamics signalling response to acute aerobic exercise in recreationally active males and examines the potential for fasting to enhance this signalling response when synergistically combined with exercise.
• What is the main finding and its importance? Increased cytosolic ACC phosphorylation was observed following fasted exercise, suggesting a distinct subcellular signalling response characterised by increased stress signalling. This was accompanied by post-exercise group differences in the phosphorylation and subcellular localization of DRP1, indicating that substrate availability (i.e., fasting) may influence the mitochondrial dynamics signalling response of skeletal muscle to acute aerobic exercise.

Abstract

It has been hypothesized that age‑related declines in skeletal muscle and vascular function in females may be partly estrogen‑dependent. This study investigated skeletal muscle protein expression of estrogen receptor α (ERα), estrogen receptor β (ERβ), and G protein–coupled estrogen receptor 1 (GPER1), and their association with proteins involved in redox regulation and vascular function, in relation to age, menopausal status, and lifelong physical activity. Skeletal muscle biopsies were obtained from 107 healthy females aged 19–70 years, including 26 postmenopausal females who were lifelong exercise trained. Protein expression of ERα, ERβ, GPER1, and downstream redox‑ and vascular‑related proteins was quantified. Age‑ and menopause‑related differences, associations between protein targets, and effects of lifelong exercise were examined. ERα protein expression was lower in older females with a 48% lower expression in the ≥ 55 years age group compared with the < 30-year group. GPER1 protein expression was 22% lower across all older age groups compared with the < 30-year group. ERβ expression was reduced in mid‑life (45–59 years) but not in the oldest age group. Both ERα and ERβ were positively correlated with endothelial nitric oxide synthase (eNOS) expression, whereas GPER1 showed no association with eNOS. ERβ expression was associated with pro‑oxidative NOX2 expression. Aging in females is associated with a lower ERα and GPER1 protein expression in skeletal muscle. Furthermore, lower ER expression by aging is associated with a lower eNOS expression, indicating associations with proteins involved in nitric oxide-related redox regulation in skeletal muscle in aged females.

Abstract

This review examines physiological limits, longitudinal projections, and best practices for muscle hypertrophy with a focus on bodybuilding and physique sport. Recurring body composition assessments using multicompartment models are recommended for monitoring short-term fat-free mass (FFM) changes and long-term muscular development. Normative data indicate that drug-free male athletes typically gain roughly 1.4 kg of FFM over 12 weeks of resistance training, with an interquartile range of 1–2 kg. A practical upper limit for FFM index in drug-free male athletes is approximately 28.5, although higher values have been observed in the context of elevated adiposity or anabolic androgenic steroid use. Female athletes tend to have roughly 70% less FFM at baseline but make proportionally similar FFM gains in response to resistance training. The present review models plausible short-term and long-term growth trajectories for both male and female lifters. Training practices that optimize hypertrophy include moderate loads (6–12 repetition maximum), training near muscular failure, and sufficient weekly volume (12–30 fractional sets per muscle group). Nutritional factors include maintaining modest caloric surpluses (0.1–0.25% body weight gain weekly), adequate protein intake (1.6–2.2 g/kg/d), sufficient carbohydrate intake (≥3 g/kg/d), and moderate fat intake (0.5–1.5 g/kg/d). Creatine and protein supplementation provide established hypertrophic benefits, while evidence for other supplements remains inconclusive.