Do you want to prevent heart disease? Are you interested in possibly reversing damage to your heart vessels? Well, the research supports these claims. We all know the factors that contribute to heart disease; hypertension, smoking, diabetes, elevated cholesterol, obesity, and poor diet, but did you know that inactivity is also a risk factor. In developed countries heart disease is the number one cause of death.
How much activity or exercise is enough to be beneficial? There are numerous studies and recommendations. The Harvard Alumni Health Study found that the participants with the lowest level of risk for coronary heart disease expended at least 1000 to 2000 calories per week in leisure time activities.² In another study from the Aerobics Center Longevity Study noted that cardiovascular death was decreased by 30-45% between runners and non-runners could be obtained even at low speeds, frequencies and duration.³ There also seems to be a leveling off for those who participate in high levels and durations, meaning excessive activity does not translate into even more cardio protection.
For the physiologically inclined here is the breakdown how the endothelial lining of vessels function and are repaired through physical activity.
Endothelial NO synthase (eNOS) produces NO via conversion of L-arginine (L-Arg.) to L-citrulline in the presence of tetrahydrobiopterin (BH4) and calcium-calmodulin. Shear stress activates eNOS activity by phosphorylation at serine 1177 (S1177). This process is mediated by phosphatidylinositol 3-kinase (PI3K), phosphoinositide-dependent kinase (PDK), and protein kinase B (AKT). NO easily diffuses through plasma membranes. In smooth muscle cells, NO activates guanylate cyclase, which, in turn, converts GTP to cGMP. A reduction of the intracellular calcium concentration (Ca2+) leads to hyperpolarization of the cell membrane and, consequently, smooth muscle relaxation. NO is broken down in the presence of reactive oxygen species (ROS), mainly superoxide, generating peroxynitrite. Peroxynitrite, in turn, oxidates BH4 and promotes eNOS uncoupling, resulting in eNOS-derived superoxide production. Additional sources of superoxide are heme oxygenase (HO1/2), myeloperoxidase, cytochrome P450, the mitochondrial electron transport chain, and nicotinamide- adenine dinucleotide [phosphate], reduced form (NAD[P]H) oxidase, which is activated by tumor necrosis factor a and angiotensin II via the angiotensin II receptor type 1 (AT1-R). Extracellular superoxide dismutase (ecSOD) scavenges superoxide. Vessel growth and arteriolarization of capillaries are mediated by vascular endothelial growth factor (VEGF), transforming growth factor ß (TGF), platelet-derived growth factor (PDGF), fibroblast growth factors 1 and 2 (FGFs 1/2), and insulin-like growth factor (IGF). Circulating progenitor cells (CPCs), mobilized from the bone marrow, contribute to repair of the damaged endothelium and the formation of new vascular structures. Homing of CPCs is mediated by the binding of CXC-chemokine receptor type 4 (CXCR4) to stromal cell–derived factor-1 (SDF-1), which is secreted at the site of injury. The adhesion molecule P-selectin mediates the rolling of blood cells on the surface of the endothelium and initiates the activation of platelets and adhesion of leukocytes at the site of injury, allowing them to transmigrate the endothelial layer and perpetuate an inflammatory atherosclerotic process via the secretion of interleukins and chemokines. Question marks indicate that there are several other endothelial-derived relaxing and constricting factors that affect different ion channels, transporters, and second messengers. Further alterations within the vascular smooth muscle cell and perivascular adipose tissue are involved in the regulation of the vascular tone, but they are not in the focus herein³.
To improve overall cardiovascular health, the American Heart Association recommends at least 150 minutes per week of moderate exercise or 75 minutes per week of vigorous exercise (or a combination of moderate and vigorous activity. Bottom line, physical activity and exercise is good for your heart, get out there and engage in some type of physical activity, and always check with your health care provider prior to starting an exercise program.
- Sesso, H.D., Paffenbarger, R.S. and Lee, I.M., 2000. Physical activity and coronary heart disease in men: The Harvard Alumni Health Study. Circulation, 102(9), pp.975-980.
- Stofan, J.R., DiPietro, L., Davis, D., Kohl 3rd, H.W. and Blair, S.N., 1998. Physical activity patterns associated with cardiorespiratory fitness and reduced mortality: the Aerobics Center Longitudinal Study. American Journal of Public Health, 88(12), pp.1807-1813.
- Winzer, Ephraim Bernhard, Felix Woitek, and Axel Linke. “Physical Activity in the Prevention and Treatment of Coronary Artery Disease.” Journal of the American Heart Association7.4 (2018): e007725.
- http://www.heart.org/HEARTORG/HealthyLiving/PhysicalActivity/FitnessBasics/American-Heart-Association-Recommendations-for-Physical-Activity-in-Adults_UCM_307976_Article.jsp#.WwUSYyOB3dd. Retrieved 23May, 2018.