Exercise, sport, & movement最新文献

Context: Postural orthostatic tachycardia syndrome (POTS) is characterized by increased heart rate (HR) with standing and is associated with dizziness, palpitations, and exercise intolerance, with poorly understood mechanisms.

Objective: To review the literature on cardiorespiratory fitness in POTS, and explore possible determinants of exercise intolerance.

Design: Systematic review of studies assessing exercise capacity in POTS.

Eligibility criteria: Eligible studies were original prospective and retrospective cohort studies and randomized controlled trials investigating formal exercise assessments (maximal exercise duration with or without gas exchange oxygen consumption (VO₂) measures) in patients with established POTS using standard criteria.

Study selection: A literature search revealed 199 unique studies, of which we identified 17 cohorts with 1321 subjects with POTS and 502 age- and sex-matched controls. Peak VO₂ was measured in 15 studies and exercise hemodynamics (stroke volume (SV), cardiac output) was measured in 10 studies.

Main outcome measures: Outcome measures were peak VO₂, gas exchange parameters, and hemodynamics (i.e., HR, SV, cardiac output).

Results: All studies described higher HR at standing and submaximal exercise, with earlier peak HR in POTS. Peak VO₂ was reduced in 80% of studies, but only in 30% when matched for deconditioning. Seven of 10 studies (70%) reported reduced SV with standing/exercise versus controls, but only 10% showed reduced cardiac output. Intravenous fluids did not affect hemodynamics or peak VO₂. Exercise training, as well as propranolol, improved peak VO₂.

Conclusion: Patients with POTS reach peak HR faster. Increased HR accompanies reduced SV, but cardiac output is generally maintained or increased, making it unlikely to cause symptoms. Reducing HR may improve exercise capacity in POTS by delaying peak HR and reducing symptoms.

Endothelial function is critical to cardiovascular health, regulating blood vessel function through the release of vasodilators and constrictors-namely, nitric oxide-controlling redox balance, platelet activation and aggregation, leukocyte adhesion, and proliferation of vascular smooth muscle. Vascular dysfunction, characterized by impaired endothelial function, significantly increases cardiovascular disease (CVD) risk. CVD is the leading cause of death in the United States and most of the world. Advancing age is a primary risk factor; however, several health behaviors influence vascular aging. Risk factors such as poor diet, a sedentary lifestyle, and poor sleep can reduce endothelial function, even early in life. Exercise has emerged as a protective factor that can potentially confer vascular protection in the context of negative health behaviors. In this review, we seek to address the importance of endothelial function for cardiovascular health, identify key risk factors and mechanisms that contribute to endothelial dysfunction, summarize the protective effects of exercise against endothelial dysfunction (including mechanisms), and highlight key knowledge gaps and future directions.

Purpose: This study aimed to assess the incidence of adverse events (AE) in older adults participating in a year-long exercise intervention, investigating potential dose-response relationships between exercise duration and AE frequency, and identifying demographic factors associated with AE risk.

Methods: A total of 648 older adults were randomized into one of three exercise groups: low-intensity stretching and toning (S&T), 150 minutes of aerobic exercise per week (150Ex), or 225 minutes of aerobic exercise per week (225Ex). Adverse events were tracked during the intervention, with event rates calculated based on participant adherence and time in the study. Generalized linear models were employed to compare AE incidence across groups. Post hoc comparisons were used to calculate incidence rate ratios (IRRs) for AE between groups, adjusting for multiple comparisons.

Results: Overall, 306 AE were reported, with 44% related to the intervention. No significant dose-response relationship was observed for all-cause AE between groups. However, intervention-related AE were more frequent in the aerobic exercise groups. Participants in the 150Ex group had a 77% higher rate of intervention-related AE compared to the S&T group, and the 225Ex group had an 88% higher rate. Higher adherence was associated with fewer all-cause AE, and greater comorbid burden was associated with more AE.

Conclusions: While aerobic exercise increased the risk of intervention-related AE, the overall risk of all-cause AEs was not found to be different across exercise intensities. Higher adherence to the exercise regimen was associated with fewer AE. These findings suggest aerobic exercise is generally safe in older adults, with the benefits outweighing the risks.

Although improvements in prevention and screening have curbed the incidence of some cancers, the global burden of cancer is substantial and continues to grow. The sustained high prevalence of many cancers reveals the need for additional strategies to reduce occurrence. Observational studies have linked physical inactivity to the risk of 13 different cancers. Indeed, physical activity can reduce the occurrence of several cancers by more than 20%, whereas sedentary behavior can increase cancer risk. Thus, physical activity presents a viable lifestyle intervention to reduce the global burden of cancer, and current research efforts are focused on establishing the effective physical activity mode and intensity for cancer prevention. Preclinical cancer studies have provided insight into the mechanisms mediating these effects. There is growing evidence that physical activity can 1) reduce the risk of obesity and, by extension, metabolic dysregulation; 2) improve immune surveillance and reduce inflammation; 3) enrich the colonic environment by favoring beneficial microbes and reducing transit time; and 4) regulate sex hormones. This graphical review describes the current state of knowledge on the benefits of physical activity for cancer prevention and associated plausible mechanisms.

In contrast with other leading causes of mortality, the cancer death rate in the United States continues to decline, reflecting improvements in prevention, screening, and treatment. Despite these advances, there has been limited development of strategies to counter the unwanted and debilitating effects associated with cancer and its treatments. Indeed, syndromes including cachexia, cardiotoxicity, fatigue, and mucositis among others plague cancer survivors, leading to poor life quality and premature mortality. The systemic nature of these impairments creates a strong rationale for treatment strategies to mitigate syndromes affecting cancer survivors. Currently, however, there are limited treatments approved by the US Food and Drug Administration to counter the debilitating side effects of cancer and cancer treatments. In noncancer clinical populations, physical activity is a well-established strategy to increase muscle mass, improve cardiovascular health, enhance energy levels, and promote gut health. Although physical activity programs are widely encouraged for cancer survivors, researchers are just beginning to understand the physiological basis of their positive effects and how they can be maximized for different cancer populations and treatments. This graphical review describes the benefits of physical activity and associated mechanisms for ameliorating select side effects of cancer and its therapeutics.