Aging and Cardiovascular Disease: Exercise to the Rescue!
Physical activity can preserve the health of our arteries, potentially adding to our lifespans.
Our species is long-lived compared with other primates. Chimpanzees, for instance, have a life expectancy of about 13 years versus 78.5 years for U.S. babies born in 2009 (Pringle 2013). Why such a big gap? Pringle says vaccines, antibiotics, sanitation, and access to nutritious vegetables and fruits year round give us a huge edge over our great-ape cousins, as does our acquired ability to fight off pathogens and irritants in our environments.
Researchers are finding that exercise's ability to improve cardiovascular health could widen that gap even further. This month's column examines current research on the role of exercise in aging and the cardiovascular system.
Cardiovascular Disease, Oxidative Stress, Inflammation and Aging
Cardiovascular disease (CVD) is the number-one cause of death in the world, accountable for 31% of all deaths (WHO 2016). CVD disorders of the heart and blood vessels cause heart attacks, stroke, elevated blood pressure, peripheral artery disease, rheumatic heart disease, congenital heart disease and heart failure (WHO 2016). Advancing age is a major risk factor for CVD (Seals, Jablonski & Donato 2011).
Gliemann, Nyberg & Hellsten (2016) explain that aging leads to thickening and stiffening in the walls of our large arteries, thus diminishing cardiovascular function via a disorder called endothelial dysfunction. If aging and endothelial dysfunction go hand in hand, it stands to reason that minimizing this dysfunction may improve life expectancy.
What's so important about the endothelium? This thin layer of cells lining the blood vessels (see Figure 1) is central to regulating vascular tone—i.e., maintaining the optimal balance (between constrictor and dilator influences) that blood vessels need to sustain life. Dysfunctions in the endothelium are characterized by declining production of vasodilators, particularly nitric oxide (Seals, Jablonski & Donato 2011). This shortage of vasodilators is a key early step in the development of atherosclerosis (plaque buildup in the arteries).
Gliemann and colleagues note another contributor to atherosclerosis: oxidative stress. The researchers explain that aging and the growth of atherosclerotic plaque accompany rising levels of harmful reactive oxygen species (ROS) in the endothelium. Unfortunately for human longevity, this happens while our aging bodies are losing their ability to make more antioxidants to neutralize the ROS. Essentially, oxidative stress reflects the body's inability to detoxify ROS.
Oxidative stress and endothelium dysfunction produce a chronic, lowgrade, detrimental inflammation (too many inflammatory chemicals and too few anti-inflammatories) in the vascular system. Chronic inflammation is associated with increased risk for disease, poor physical functioning and mortality (Woods et al. 2012).
Exercise: The Best Line of Offense and Defense
Gliemann and colleagues say cardiorespiratory exercise has a major effect on endothelial function because such activity improves vasodilator-to-vasoconstrictor balance, reduces infl ammation and oxidative stress, and encourages growth of new capillaries in skeletal muscle. Exercise has consistently been shown to cause great improvement in vascular structure and function (Gliemann, Nyborg & Hellsten 2016). For example, reductions in nitric oxide in the endothelium are minimized and even reversed with aerobic exercise. Interestingly, scientists are now discovering the specialized molecular mechanisms and signaling pathways that elicit this improvement.
As for chronic inflammation, Woods et al. (2012) conclude that exercise-induced loss of body fat is related to exercise-induced reductions in serum markers of inflammation. The researchers add that visceral fat, in particular, produces proinflammatory proteins that contribute to systemic inflammation. The researchers say cardiorespiratory exercise also increases muscle production of specialized cytokines, molecular messengers that regulate various inflammatory responses to control the body's response to disease and infection.
What's more, cardiorespiratory exercise increases vagal tone, which may reduce systemic inflammation (Woods et al. 2012). Vagal tone is the resting-state regulatory mechanism of the vagus nerve on most of the body's internal organ systems, such as the heart, lungs, eyes, glands and digestive tract.
The Pivotal Role of Activity
Mounting evidence suggests that exercise and higher levels of physical activity play a pivotal role in combating disease, extending the life cycle and enhancing overall quality of life. At the molecular level, aerobic exercise can reduce oxidative stress and inflammatory response while improving vascular function and cardiovascular health. In a population-based cohort study of 661,137 men and women (median age: 62) from the U.S. and Europe, Arem et al. (2015) concluded that meeting the minimum exercise guidelines (i.e., 150–300 minutes of moderate-intensity or 75–150 minutes of vigorous-intensity aerobic activity weekly) provides a substantial benefit for postponing mortality and lowering the risk of adverse cardiac events. Let's keep our clients moving!
Arem, H., et al. 2015. Leisure time physical activity and mortality: A detailed pooled analysis of the dose-response relationship. AMA Internal Medicine, 175 (6), 959–67.
Gliemann, L., Nyberg, M., & Hellsten, Y. 2016. Effects of exercise training and resveratrol on vascular health in aging. Free Radical Biology & Medicine, 98, 165–76.
Lopez-Otin, C., et al. 2016. Metabolic control of longevity. Cell, 166 (4), 802–21.
Pringle, H. 2013. Long live the humans. Scientific American, 309 (4), 48–55.
Seals, D.R., Jablonski, K.L., & Donato, A.J. 2011. Aging and vascular endothelial function in humans. Clinical Science (London, England: 1979), 120 (9), 357–75.
WHO (World Health Organization). 2016. Cardiovascular diseases (CVDs). Accessed Nov. 15, 2016. www.who.int/mediacentre/factsheets/fs317/en/.
Woods, J.A., et al. 2012. Exercise, inflammation and aging. Aging and Disease, 3 (1), 130–40.