John Seawright, B.S.
“Do not go gentle into that good night. Rage, Rage against the dying of the light.” Dylan Thomas penned these anguished words as his once strong and youthful father lay aged, blind, and dying; words which paint an agonizing depiction of humanity’s struggle against and defiance of death.
In today’s world, the endless rebellion against suffering and death is continued with a bellicose campaign against cardiovascular disease, the leading cause of death in the United States. The American Heart Association states that 1/3 of Americans suffer from some form of cardiovascular disease and that up to half of these incidences occur in the older population. As we age, the capability of our blood vessels to constrict and dilate to properly regulate the flow of blood diminishes, leading to the development of cardiovascular disease. The inability to constrict and/or dilate is a product of either impaired constriction/dilation signal transduction or structural changes within the blood vessel.
The endothelium, a single layer of cells lining the inside of the blood vessels, is largely responsible for generating and transmitting the dilator or constrictor signal to the surrounding vascular smooth muscle. The endothelium maintains proper function until the ages of approximately 40 and 50 for males and females, respectively, at which point there is a continuous age related, steady decline in endothelial function. The impaired ability to signal dilation or constriction of the vascular smooth muscle is referred to as endothelial dysfunction. In the aged endothelium, the nitric oxide (NO: a vasodilator) signaling pathway is disrupted with age. The NO can be produced in too small a quantity or it can be degraded by free radicals, both of which disrupt the dilating signal, resulting in endothelial dysfunction and leading to an increased risk for cardiovascular disease.
Aging can also induce structural remodeling of the proteins composing the vascular smooth muscle. Focal adhesions, protein groups that attach to the extracellular matrix of the cell, show an age-induced decrease in a number of composing proteins that aid in moving the cell across the extracellular matrix. In addition, with age, there is an increase in the density of the rigid collagen protein and a decrease in elastin, a stretchy protein important for dilation/contraction of the vascular smooth muscle. This age-induced remodeling is responsible for increasing the stiffness of the blood vessel, leading to arteriosclerosis.
It’s not all bad news. One of the cheapest and most effective ways to fight cardiovascular disease is to get your heart beating and your blood flowing. Moderate aerobic exercise, like brisk walking, has been shown to improve vascular function and even restore the endothelial function, eliminating the negative effects of age. See the Suggested Reading #5 for the physical activity guidelines recommended by the American Heart Association.
In today’s world, our resolve to conquer cardiovascular disease and delay death could be punned through the popular edict from the King of Pop with, “Just beat it.”
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- Trott DW, Gunduz F, Laughlin MH, Woodman CR. Exercise training reverses age-related decrements in endothelium-dependent dilation in skeletal muscle feed arteries. J Appl Physiol. 2009;106(6):1925-1934.
- American Heart Association. American Heart Association Recommendations for Physical Activity. 2013; http://www.heart.org/HEARTORG/GettingHealthy/PhysicalActivity/StartWalking/American-Heart-Association-Guidelines_UCM_307976_Article.jsp