Researchers: Kevin O Murray, Sophia A Mahoney, Ravinandan Venkatasubramanian, Douglas R Seals, Zachary S Clayton
Age-associated cardiovascular (CV) dysfunction, namely arterial dysfunction, is a key antecedent to the development of CV disease (CVD). Arterial dysfunction with aging is characterized by impaired vascular endothelial function and stiffening of the large elastic arteries, each of which is an independent predictor of CVD. These processes are largely mediated by an excess production of reactive oxygen species (ROS) and an increase in chronic, low-grade inflammation that ultimately leads to a reduction in bioavailability of the vasodilatory molecule nitric oxide. Additionally, there are other fundamental aging mechanisms that may contribute to excessive ROS and inflammation termed the “hallmarks of aging”; these additional mechanisms of arterial dysfunction may represent therapeutic targets for improving CV health with aging. Aerobic exercise is the most well-known and effective intervention to prevent and treat the effects of aging on CV dysfunction. However, the majority of mid-life and older (ML/O) adults do not meet recommended exercise guidelines due to traditional barriers to aerobic exercise, such as reduced leisure time, motivation, or access to fitness facilities. Therefore, it is a biomedical research priority to develop and implement time- and resource-efficient alternative strategies to aerobic exercise to reduce the burden of CVD in ML/O adults. Alternative strategies that mimic or are inspired by aerobic exercise, that target pathways specific to the fundamental mechanisms of aging, represent a promising approach to accomplish this goal.
References
- Time-efficient physical training for enhancing cardiovascular function in midlife and older adults: promise and current research gaps.
- Time-efficient, high-resistance inspiratory muscle strength training for cardiovascular aging.
- Cellular and molecular biology of aging endothelial cells.
- Aerobic and resistance exercise training reverses age-dependent decline in NAD+ salvage capacity in human skeletal muscle.
- Maintenance of NAD+ Homeostasis in Skeletal Muscle during Aging and Exercise.
- The hallmarks of aging.