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John Seawright, B.S.

Heart disease is a cruel ailment that befalls many Americans. It is a life threatening disease that does not strike only a single individual; the suffering proliferates through the patient’s entire family. Understanding the causes of heart disease can elucidate avenues of treatment, as well as provide pre-emptive strategies to prevent the disease in the first place. 
    Heart disease is a complex malady resulting from a poorly functioning circulatory system. The circulatory system is composed, in part, of arteries and veins that supply oxygen and other nutrients to the body’s tissues. When the smooth muscle around an artery dilates, the diameter of the vessel enlarges and allows a greater amount of blood to flow through the vessel and supply a tissue with oxygen needed nutrients. This process is called vasodilation. The interior of each vessel is lined with a single layer of cells, endothelial cells, which detect the need for blood flow and initiate vasodilation. 
    A major responsibility of endothelial cells is to detect and subsequently alleviate the need for increased blood flow to nutrient-starved tissues. Upon detection, the endothelium produces a molecular signal, such as nitric oxide (NO), which diffuses to the surrounding vascular smooth muscle and promotes vasodilation, allowing increased blood flow. Sindler et al. have shown that the function of endothelial nitric oxide synthase (eNOS), a protein that produces NO, is impaired with age. Any impairment of the endothelium to perceive the need for more blood and/or send NO can reduce the ability of the vessel to vasodilate. This prevents necessary nutrients from reaching nutrient depleted tissues. A poorly functioning endothelium can also lead to atherosclerosis, the development of blood clots that congest arteries, impede nutrient rich blood flow, and eventually, cause a heart attack. 
    To help prevent heart disease, it is essential to improve and/or maintain a healthy endothelium. Using an animal model, Laughlin et al. have shown that aerobic exercise training can increase the amount of eNOS in the vasculature of the heart and provide a means for increasing NO bioavailability and preserving the capacity for vasodilation in these vessels. Furthermore, Seals et al. have demonstrated that moderate aerobic exercise, at an intensity of 70 – 75% maximum heart rate, for 30 minutes, 4-5 days a week, and for 12 weeks can improve blood flow in previously sedentary humans by enhancing their endothelial function. 
    With a little exercise, the capacity of the endothelium to produce NO and regulate blood flow can be improved and maintained, helping to prevent heart disease. Am I destined for a heart attack? NO Way!

Further Readings: 

  1. Widlansky ME, Gokce N, Keaney Jr JF, Vita JA. The clinical implications of endothelial dysfunction. Journal of the American College of Cardiology. 2003;42(7):1149-1160.
  2. Laughlin MH, Pollock JS, Amann JF, Hollis ML, Woodman CR, Price EM. Training induces nonuniform increases in eNOS content along the coronary arterial tree. Journal of Applied Physiology. 2001;90(2):501-510.
  3. Sindler AL, Delp MD, Reyes R, Wu G, Muller-Delp, JM. Effects of ageing and exercise training on eNOS uncoupling in skeletal muscle resistance arterioles. The Journal of Physiology. 2009; 587(15): 3885-3897.
  4. Seals DR, DeSouza CA, Donato AJ, Tanaka H. Habitual exercise and arterial aging. Journal of Applied Physiology. 2008; 105(4):1323-1332.
  • Destined for Heart Disease?-NO Way!

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