Endothelial dysfunction and inflammation are characteristics of subclinical atherosclerosis and may increase through progressive menopausal stages. Evaluating endothelial responses to acute exercise can reveal underlying dysfunction not apparent in resting conditions. The purpose of this study was to investigate markers of endothelial function and inflammation before and after acute exercise in healthy low-active perimenopausal (PERI) and late postmenopausal (POST) women. Flow-mediated dilation (FMD), CD31/CD42b and CD62E endothelial microparticles (EMPs), and the circulating inflammatory factors monocyte chemoattractant protein 1 (MCP-1), interleukin 8 (IL-8), and tumor necrosis factor-α (TNF-α) were measured before and 30 min after acute exercise. Before exercise, FMD was not different between groups (PERI: 6.4 ± 0.9% vs. POST: 6.5 ± 0.8%, P = 0.97); however, after acute exercise PERI tended to improve FMD (8.5 ± 0.9%, P = 0.09), whereas POST did not (6.2 ± 0.8%, P = 0.77). Independent of exercise, we observed transient endothelial dysfunction in POST with repeated FMD measures. There was a group × exercise interaction for CD31/CD42b EMPs (P = 0.04), where CD31/CD42b EMPs were similar before exercise (PERI: 57.0 ± 6.7 EMPs/μl vs. POST: 58.5 ± 5.3 EMPs/μl, P = 0.86) but were higher in POST following exercise (PERI: 48.2 ± 6.7 EMPs/μl vs. POST: 69.4 ± 5.3 EMPs/μl, P = 0.023). CD62E EMPs were lower in PERI compared with POST before exercise (P < 0.001) and increased in PERI (P = 0.04) but did not change in POST (P = 0.68) in response to acute exercise. After acute exercise, MCP-1 (P = 0.055), TNF-α (P = 0.02), and IL-8 (P < 0.001) were lower in PERI but only IL-8 decreased in POST (P < 0.001). Overall, these data suggest that perimenopausal and late postmenopausal women display different endothelial and inflammatory responses to acute exercise.

Postmenopause is associated with elevated levels of follicle stimulating hormone (FSH) compared to premenopause. There is evidence to suggest that high levels of FSH may influence lipid levels; however, the association between FSH and lipid levels in postmenopausal women has been largely unexplored.Objective: The purpose of this study was to evaluate the relation between FSH and lipid levels in postmenopausal women from the Kuopio Ischaemic Heart Disease Risk Factor Study.Methods: Postmenopausal women (n=588) aged 53-73 and not using hormone therapy were included. The relation between FSH and total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG) was evaluated using linear regression, adjusting for estradiol, body mass, smoking and other hormonal and lifestyle factors. The relation between FSH, dyslipidemia and abnormal lipid levels were also evaluated.Results: FSH was positively and linearly associated with TC (p=0.001) and LDL-C (p=0.01) in all participants, with stronger relations seen in younger compared to older postmenopausal women. FSH was less strongly associated with HDL-C and TG. FSH was not associated with dyslipidemia; however, higher FSH was associated with increased risk of high TC (p=0.02) and high LDL-C (p=0.03).Conclusions: These data suggest that higher FSH in postmenopausal women is related to higher levels of both TC and LDL-C.

The long-term sequelae of the coronavirus disease 2019 (COVID-19) are multifaceted and, besides the lungs, impact other organs and tissues, even in cases of mild infection. Along with commonly reported symptoms such as fatigue and dyspnea, a significant proportion of those with prior COVID-19 infection also exhibit signs of cardiac damage, muscle weakness, and ultimately, poor exercise tolerance. This review provides an overview of evidence indicating cardiac impairments and persistent endothelial dysfunction in the peripheral vasculature of those previously infected with COVID-19, irrespective of the severity of the acute phase of illness. Additionally, VO2peak appears to be lower in convalescent patients, which may stem, in part, from alterations in O2 transport such as impaired diffusional O2conductance. Together, the persistent multi-organ dysfunction induced by COVID-19 may set previously healthy individuals on a trajectory towards frailty and disease. Given the large proportion of individuals recovering from COVID-19, it is critically important to better understand the physical sequelae of COVID-19, the underlying biological mechanisms contributing to these outcomes, and the long-term effects on future disease risk. This review highlights relevant literature on the pathophysiology post-COVID-19 infection, gaps in the literature, and emphasizes the need for the development of evidence-based rehabilitation guidelines.

Cardiovascular disease is the leading cause of death in women. There is a dramatic rise in risk factors for cardiovascular disease during the menopausal transition that is independent of aging. Endothelial dysfunction is an early hallmark of developing cardiovascular disease and has been shown to increase across the stages of menopause. Exercise is considered one of the most effective lifestyle therapies to maintain and improve endothelial function. However, accumulating evidence suggests that exercise does not have the same benefit on endothelial function in menopausal women as it does in other populations, and factors associated with menopause likely influence the endothelial responsiveness to exercise. This review will detail the current available evidence on endothelial dysfunction, exercise, and menopause, including mechanisms that may mediate the accumulating endothelial dysfunction in women with menopause, the impact of exercise on endothelial function in women, and whether regular exercise is an effective therapeutic and prevention strategy to maintain endothelial function with menopause. We conclude that the effect of exercise on endothelial function differs according to menopausal stage and cardiovascular disease risk burden. Finally, we will address critical gaps in the literature with the goal of identifying future research directions to improve healthy aging in women.