Moreau Kerrie L, Clayton Zachary S, DuBose Lyndsey E, Rosenberry Ryan, Seals Douglas R
Division of Geriatric Medicine, Department of Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States.
Eastern Colorado Health Care System, Geriatric Research Education and Clinical Center, Aurora, Colorado, United States.
Am J Physiol Heart Circ Physiol. 2024 Jan 1;326(1):H123-H137. doi: 10.1152/ajpheart.00392.2023. Epub 2023 Nov 3.
Vascular aging, featuring endothelial dysfunction and large elastic artery stiffening, is a major risk factor for the development of age-associated cardiovascular diseases (CVDs). Vascular aging is largely mediated by an excessive production of reactive oxygen species (ROS) and increased inflammation leading to reduced bioavailability of the vasodilatory molecule nitric oxide and remodeling of the arterial wall. Other cellular mechanisms (i.e., mitochondrial dysfunction, impaired stress response, deregulated nutrient sensing, cellular senescence), termed "hallmarks" or "pillars" of aging, may also contribute to vascular aging. Gonadal aging, which largely impacts women but also impacts some men, modulates the vascular aging process. Regular physical activity, including both aerobic and resistance exercise, is a first-line strategy for reducing CVD risk with aging. Although exercise is an effective intervention to counter vascular aging, there is considerable variation in the vascular response to exercise training with aging. Aerobic exercise improves large elastic artery stiffening in both middle-aged/older men and women and enhances endothelial function in middle-aged/older men by reducing oxidative stress and inflammation and preserving nitric oxide bioavailability; however, similar aerobic exercise training improvements are not consistently observed in estrogen-deficient postmenopausal women. Sex differences in adaptations to exercise may be related to gonadal aging and declines in estrogen in women that influence cellular-molecular mechanisms, disconnecting favorable signaling in the vasculature induced by exercise training. The present review will summarize the current state of knowledge on vascular adaptations to regular aerobic and resistance exercise with aging, the underlying mechanisms involved, and the moderating role of biological sex.
血管老化以血管内皮功能障碍和大动脉僵化为特征，是与年龄相关的心血管疾病（CVD）发生的主要危险因素。血管老化很大程度上是由活性氧（ROS）的过度产生和炎症增加介导的，导致血管舒张分子一氧化氮的生物利用度降低以及动脉壁重塑。其他细胞机制（即线粒体功能障碍、应激反应受损、营养感知失调、细胞衰老），被称为衰老的“标志”或“支柱”，也可能导致血管老化。性腺衰老主要影响女性，但也影响一些男性，它调节血管老化过程。规律的体育活动，包括有氧运动和抗阻运动，是降低衰老过程中CVD风险的一线策略。尽管运动是对抗血管老化的有效干预措施，但随着年龄增长，血管对运动训练的反应存在很大差异。有氧运动可改善中年/老年男性和女性的大动脉僵硬，并通过减少氧化应激和炎症以及维持一氧化氮生物利用度来增强中年/老年男性的内皮功能；然而，在雌激素缺乏的绝经后女性中，并未始终观察到类似的有氧运动训练改善效果。运动适应方面的性别差异可能与性腺衰老以及女性雌激素水平下降有关，这会影响细胞分子机制，破坏运动训练在血管系统中诱导的有利信号传导。本综述将总结目前关于血管对规律有氧运动和抗阻运动的适应性随年龄变化的知识现状、涉及的潜在机制以及生物学性别的调节作用。
