Obesity with advancing age leads to increased health complications that are involved in various complex physiological processes. For example, inflammation is a critical cardiovascular disease risk factor that plays a role in the stages of atherosclerosis in both aging and obesity. Obesity can also induce profound changes to the neural circuitry that regulates food intake and energy homeostasis with advancing age. Here we discuss how obesity in older adults impacts inflammatory, cardiovascular, and neurobiological functions with an emphasis on how exercise mediates each topic. Although obesity is a reversible disorder through lifestyle changes, it is important to note that early interventions are crucial to prevent pathological changes seen in the aging obese population. Lifestyle modifications such as physical activity (including aerobic and resistance training) should be considered as a main intervention to minimize the synergistic effect of obesity on age-related conditions, such as cerebrovascular disease.

The vascular mechanisms underlying the elevated prevalence of Alzheimer’s disease among females remain unclear. In this study, we found that positive relationships between cerebral pulsatility in the anterior circulation and white matter hyperintensities (WMH) emerged in females in middle age but not until older adulthood in males. In addition, female-specific relationships were present between cerebral pulsatility in the posterior circulation and WMH in older adults.

This narrative review highlights the impact of exercise on vascular health in females over the lifespan with an emphasis on puberty, pregnancy and menopause. These events encompass substantial changes in sex hormone levels, particularly oestrogens and progesterone. They are also accompanied by distinct adaptations of the central, peripheral and cerebral vasculature. Regular exercise is an effective mechanism to reduce vascular risk in females of all ages, especially for those at higher risk for vascular disorders. However, there are large variabilities in the vascular adaptations to exercise in females that may be related to circulating sex hormone levels. In addition, exogenous hormones, such as oral contraceptives taken after puberty or hormonal replacement therapy taken to mitigate symptoms of menopause, may interact with exercise‐induced changes in vascular function. We highlight how more research is needed to understand the optimal exercise interventions to promote vascular health in females across the lifespan, especially during times of hormonal transition.

C1q-TNF-related protein-9 (CTRP9) increases endothelial nitric oxide synthase and reduces vasoconstrictors. There is limited information regarding exercise-mediated CTRP9 in obesity. The purpose of this study was to compare high-intensity interval exercise (HIIE) and continuous moderate-intensity exercise (CME) on the CTRP9 response and an indicator of endothelial function (FMD) in obese participants. Sixteen young male participants (9 obese and 7 normal-weight) participated in a counterbalanced and caloric equated experiment: HIIE (30 min, 4 intervals of 4 min at 80–90% of VO₂ max with 3 min rest between intervals) and CME (38 min at 50–60% VO₂ max). Serum CTRP9 and FMD were measured prior to, immediately following exercise, and 1 h and 2 h into recovery. CTRP9 was significantly increased immediately following acute HIIE and CME in both groups (p = 0.003). There was a greater CME-induced FMD response at 2 h into recovery in obese participants (p = 0.009). A positive correlation between CTRP9 and FMD percent change was observed in response to acute CME when combined with both obese and normal-weight participants (r = 0.589, p = 0.016). The novel results from this study provide a foundation for additional examination of the mechanisms of exercise-mediated CTRP9 on endothelial function in individuals with obesity.