Exercise and Sport Sciences Reviews最新文献

Physical inactivity is a global health problem. Childhood is an opportune time to establish healthy physical activity behaviors, including the participation in organized physical activity, such as sports. We hypothesize that financial incentives can improve young people's participation in physical activity and sports. The design of the incentive and the context in which it operates are crucial to its success.

Aerobic exercise is established to increase cardiorespiratory fitness (CRF), which is linked to reduced morbidity and mortality. However, people with metabolic diseases such as type 1 and type 2 diabetes may be more likely to display blunted improvements in CRF with training. Here, we present evidence supporting the hypothesis that altered skeletal muscle signaling and remodeling may contribute to low CRF with metabolic disease.

Of the "Yamanaka factors" Oct3/4 , Sox2 , Klf4 , and c-Myc (OSKM), the transcription factor c-Myc ( Myc ) is the most responsive to exercise in skeletal muscle and is enriched within the muscle fiber. We hypothesize that the pulsatile induction of MYC protein after bouts of exercise can serve to epigenetically reprogram skeletal muscle toward a more resilient and functional state.

Males and females experience different trajectories of neuromuscular function across the lifespan, with females demonstrating accelerated deconditioning in later life. We hypothesize that the menopause is a critical period in the female lifespan, during which the dramatic reduction in sex hormone concentrations negatively impacts synaptic input to the motoneuron pool, as well as motor unit discharge properties.

Acute inflammation impairs vascular function in an age-dependent manner and affects cardiovascular event risk. Regular aerobic exercise preserves vascular function with aging and potentially modifies how acute inflammation affects the vasculature. We hypothesize high cardiorespiratory fitness may accompany greater arterial responsiveness post-acute inflammation in older adults.

Human "heat tolerance" has no accepted definition or physiological underpinnings; rather, it is almost always discussed in relative or comparative terms. We propose to use environmental limits to heat balance accounting for metabolic rate and clothing, that is, the environments for which heat stress becomes uncompensable for a specified metabolic rate and clothing, as a novel metric for quantifying heat tolerance.

Human skeletal muscle cell (HSkMC) models provide the opportunity to examine in vivo training-induced muscle-specific mitochondrial adaptations, additionally allowing for deeper interrogation into the effect of in vitro exercise models on myocellular mitochondrial quality and quantity. As such, this review will compare and contrast the effects of in vivo and in vitro models of exercise on mitochondrial adaptations in HSkMCs.

Duchenne muscular dystrophy (DMD), caused by deficiency of functional dystrophin protein, is a fatal, progressive muscle disease that frequently includes metabolic dysregulation. Herein, we explore the physiologic consequences of dystrophin deficiency within the context of obesity and insulin resistance. We hypothesized that dystrophin deficiency increases the frequency of insulin resistance, and insulin resistance potentiates muscle pathology caused by dystrophin deficiency.