Skeletal muscle metabolism, morphology and function in master athletes

Skeletal muscle mass and function deteriorates with advancing age (sarcopenia). Physical inactivity and obesity are associated with advancing age and exacerbate inherent age-related decrements in physiological function, skeletal muscle mass and morphology. The study of older individuals that have chronically undertaken structured exercise training (Master Athletes; MA) provide an opportunity to elucidate the contribution of inherent ageing and biological ageing factors to age-related physiological deterioration. Chapter 2 describes the first systematic review to quantitatively and qualitatively summarise the literature surrounding MA. We established that, at present, there are few high-quality studies, utilising sophisticated measurement tools to comprehensively assess whether, and to what extent, physiological function and muscle morphology are enhanced/preserved in MA compared with trained and untrained older and younger individuals. Accordingly, in Chapter 3, we conducted a detailed mechanistic study to compare physical function, cardiorespiratory fitness, body composition, muscle strength, architecture and fibre-type morphology in MA, with healthy untrained younger and agematched older individuals. We shed light on the morphological mechanisms through which chronic exercise training enhances skeletal muscle function and body composition, with implications for sarcopenia diagnosis. Based on the superior phenotype observed in MA, the final experimental in this thesis, Chapter 4, describes an investigation of in vivo skeletal muscle remodelling responsiveness in MA. This work demonstrates that basal and exercise-induced rates of muscle protein synthesis are equivalent between older untrained individuals and MA. As such, untrained older individuals retain a capacity to adapt to exercise and that it may never be too late to benefit from exercise training

Winter wheat, 1994

"July 1994.""Publication costs paid by Missouri Seed Improvement Association."The objective of the Missouri Winter Wheat Performance Tests is to provide wheat growers in Missouri with a reliable, unbiased, up-to-date source of information that will permit valid comparisons among improved wheat varieties. This information should help Missouri wheat growers select varieties best suited to their particular area and growing conditions. This report summarizes soft and hard winter wheat variety trials conducted throughout Missouri during the 1993-94 cropping season

Acute resistance exercise training does not augment mitochondrial remodelling in master athletes or untrained older adults

Background: Ageing is associated with alterations to skeletal muscle oxidative metabolism that may be influenced by physical activity status, although the mechanisms underlying these changes have not been unraveled. Similarly, the effect of resistance exercise training (RET) on skeletal muscle mitochondrial regulation is unclear. Methods: Seven endurance-trained masters athletes ([MA], 74 ± 3 years) and seven untrained older adults ([OC]. 69 ± 6 years) completed a single session of knee extension RET (6 x 12 repetitions, 75% 1-RM, 120-s intra-set recovery). Vastus lateralis muscle biopsies were collected pre-RET, 1 h post-RET, and 48h post-RET. Skeletal muscle biopsies were analyzed for citrate synthase (CS) enzyme activity, mitochondrial content, and markers of mitochondrial quality control via immunoblotting. Results: Pre-RET CS activity and protein content were ∼45% (p < .001) and ∼74% greater in MA compared with OC (p = .006). There was a significant reduction (∼18%) in CS activity 48 h post-RET (p < .05) in OC, but not MA. Pre-RET abundance of individual and combined mitochondrial electron transport chain (ETC) complexes I-V were significantly greater in MA compared with OC, as were markers of mitochondrial fission and fusion dynamics (p-DRP-1(Ser616), p-MFF(Ser146), OPA-1 & FIS-1, p < .05 for all). Moreover, MA displayed greater expression of p-AMPK(Thr172), PGC1α, TFAM, and SIRT-3 (p < .05 for all). Notably, RET did not alter the expression of any marker of mitochondrial content, biogenesis, or quality control in both OC and MA. Conclusion: The present data suggest that long-term aerobic exercise training supports superior skeletal muscle mitochondrial density and protein content into later life, which may be regulated by greater mitochondrial quality control mechanisms and supported via superior fission-fusion dynamics. However, a single session of RET is unable to induce mitochondrial remodelling in the acute (1h post-RET) and delayed (48 h post-RET) recovery period in OC and MA

Recent advances in understanding resistance exercise training-induced skeletal muscle hypertrophy in humans

Skeletal muscle plays a pivotal role in the maintenance of physical and metabolic health and, critically, mobility. Accordingly, strategies focused on increasing the quality and quantity of skeletal muscle are relevant, and resistance exercise is foundational to the process of functional hypertrophy. Much of our current understanding of skeletal muscle hypertrophy can be attributed to the development and utilization of stable isotopically labeled tracers. We know that resistance exercise and sufficient protein intake act synergistically and provide the most effective stimuli to enhance skeletal muscle mass; however, the molecular intricacies that underpin the tremendous response variability to resistance exercise-induced hypertrophy are complex. The purpose of this review is to discuss recent studies with the aim of shedding light on key regulatory mechanisms that dictate hypertrophic gains in skeletal muscle mass. We also aim to provide a brief up-to-date summary of the recent advances in our understanding of skeletal muscle hypertrophy in response to resistance training in humans