Exercise and Sport Sciences Reviews

Based on recent studies from our group and others, we hypothesize that mitochondrial dysfunction during aging may be the root cause of mobility decline through deficits in the musculoskeletal and central nervous systems. Mitochondrial dysfunction could be a therapeutic target to prevent mobility decline in aging.

Sex hormone concentrations, particularly testosterone, are primary determinants of sex-based differences in athletic and sports performance, and this relationship may inform fair competition and participation for athletes. This article describes the sex-based dichotomy in testosterone and the implications for sex-based differences in individual sports performance, including factors that relate to athletic performance for transgender individuals, and areas of future investigation.

Exercise transiently impacts the expression, regulation, and activity of TERT/telomerase to maintain telomeres and protect the genome from insults. By protecting the telomeres (chromosome ends) and the genome, telomerase promotes cellular survival and prevents cellular senescence. By increasing cellular resiliency, via the actions of telomerase and TERT, exercise promotes healthy aging.

A prominent toxicity of androgen suppression in prostate cancer patients is loss of skeletal muscle. Exercise may induce tumor-suppression through the endocrinal function of skeletal muscle, however, this is currently unknown. In this review we summarise our work demonstrating the acute and chronic myokine response to exercise and the tumor-suppressive effect of circulatory milieu alteration in prostate cancer patients.

Some people experience pleasure during physical activity whereas it can be unpleasant for others. Modifying affective responses during physical activity in real-world situations may be an intervention strategy for increasing physical activity. This paper follows an experimental medicine framework to summarize evidence identifying, assessing, and influencing affective response during real-world physical activity to inform interventions targeting this mediating mechanism.

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.

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.

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.

Yoga, a physical and contemplative practice, offers the practitioner a unique mind-body exercise experience demonstrating preliminary efficacy in improving cognitive health. We examine the evidence for underlying mechanisms that explain the yoga-cognition relationship in healthy older adults. The cognitive benefits of yoga may be the result of improved stress regulation and neurocognitive resource efficiency that facilitate bidirectional brain-body communication.

No abstract text is available yet for this article.

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.

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.

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.

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.

No abstract text is available yet for this article.

No abstract text is available yet for this article.

Approximately 6 million individuals have heart failure in the United States alone and 15 million in Europe. Left ventricular assist devices (LVAD) improve survival in these patients, but functional capacity may not fully improve. This article examines the hypothesis that patients supported by LVAD experience persistent reductions in functional capacity and explores mechanisms accounting for abnormalities in exercise tolerance.

No abstract text is available yet for this article.

In this review, we highlight recent studies from our group and others that have characterized the cardiovascular adjustments that occur after acute heat exposure. Special emphasis will be placed on underlying mechanisms and clinical implications. Finally, we postulate that these acute cardiovascular adjustments may predict the long-term adaptive response to chronic heat therapy.