Exercise and Sport Sciences Reviews最新文献

Chronic inflammation is associated with a decline in aging skeletal muscle health. Inflammation also seems to interfere with the beneficial skeletal muscle adaptations conferred by exercise training in older individuals. We hypothesize that the cyclooxygenase pathway is partially responsible for this negative inflammatory influence on aging skeletal muscle health and plasticity.

Exaggerated cardiovascular responses to exercise increase the risk of myocardial infarction and stroke in individuals with type 1 diabetes (T1D); however, the underlying mechanisms remain largely elusive. This review provides an overview of the altered exercise pressor reflex in T1D, with an emphasis on the mechanical component of the reflex.

Exercise is advised to improve overall cardiovascular health and endothelial function. However, the role of nutrition on this exercise-induced endothelial adaptation is not clear. Here, we hypothesize that nutrients interact with exercise to influence endothelial function and chronic disease risk.

Twin and family studies show a strong contribution of genetic factors to physical activity (PA) assessed by either self-report or accelerometers. PA heritability is around 43% across the lifespan. Genome-wide association studies have implied biological pathways related to exercise ability and enjoyment. A polygenic score based on genetic variants influencing PA could help improve the success of intervention programs.

Although often short-lived, emotional responsiveness to daily stressors ( i.e. , routine and sometimes unexpected everyday hassles) is associated with increased cardiovascular disease (CVD), morbidity, and mortality. Here, we present the novel hypothesis that a disruption of microvascular homeostasis is a key antecedent. In addition, we postulate that physical activity may mitigate the psychobiological consequences of daily stress, thereby limiting pathophysiological CVD-related sequelae.

As humans age, we lose skeletal muscle mass, even in the absence of disease (sarcopenia), increasing the risk of death. Low mitochondrial mass and activity contributes to sarcopenia. It is our hypothesis that a ketogenic diet improves skeletal muscle mitochondrial mass and function when they have declined because of aging or disease, but not in athletes where mitochondrial quality is high.

Researchers in neuromechanics should upgrade their statistical toolbox. We propose linear mixed-effects models in place of commonly used statistical tests to better capture subject-specific baselines and treatment-associated effects that naturally occur in neuromechanics. Researchers can use this approach to handle sporadic missing data, avoid the assumption of conditional independence in observations, and successfully model complex experimental protocols.

The rate at which an individual can develop force during rapid voluntary contractions can be influenced by both the neural drive to a muscle and its intrinsic musculotendinous properties. We hypothesize that the maximal rate of force development across human individuals is mainly attributable to the rate of motor unit recruitment.

We propose the beneficial effects of exercise are in part mediated through the prevention and elimination of senescent cells. Exercise counters multiple forms of age-related molecular damage that initiate the senescence program and activates immune cells responsible for senescent cell clearance. Preclinical and clinical evidence for exercise as a senescence-targeting therapy and areas needing further investigation are discussed.