The following are key points to remember from a state-of-the-art review on exercise benefits in cardiovascular diseases (CVDs):

1. Primary prevention. Physical inactivity is an important risk factor for CVD and overall mortality, whereas self-reported leisure-time moderate and vigorous physical activity are independently and inversely associated with CVD and all-cause mortality.
2. ‘Excessive’ exercise/physical activity. Although data suggest that long-term exposure to strenuous endurance exercise might be associated with coronary artery calcification (CAC), atrial fibrillation, and myocardial fibrosis, exposure to very high levels of leisure-time moderate or vigorous physical activity does not appear to increase the risk of CVD or related clinical events.
3. Secondary prevention. An active lifestyle is a cornerstone for secondary CVD prevention. In general, exercise should include 150-300 minutes/week of moderate-intensity or 75-150 minutes/week of vigorous-intensity aerobic exercise or a combination of the two, at least moderate-intensity muscle-strengthening activities involving all major muscle groups at least twice weekly, and limiting sedentary time. Exercise training is contraindicated in some circumstances, including uncontrolled arrhythmia, active myocarditis or pericarditis, severe symptomatic aortic stenosis, decompensated heart failure, acute aortic dissection, acute pulmonary embolism, and in the first 2 days after acute coronary syndrome.
4. Metabolism, inflammation, and cellular integrity. Exercise training is associated with:
• Improved blood lipid profiles, with aerobic exercise followed by resistance training seemingly the most effective intervention to improve high-density lipoprotein (HDL) cholesterol;
• Improved insulin sensitivity;
• Attenuation of low-grade, noninfective systemic chronic inflammation; and
• Promotion of cellular maintenance and repair processes, including attenuation of endoplasmic reticulum stress in atherosclerotic coronary arterioles, promotion of endogenous antioxidant defense capacity, protection against exogenously induced DNA damage, reduction in vascular reactive oxygen species in patients with coronary heart disease (CHD), and attenuation of telomere length attrition in heart tissue.
5. Vascular health.
• Endothelial cell integrity. Regular endurance exercise helps to maintain endothelial cell integrity through mechanisms including a) improved release of circulating angiogenic cells, b) inhibition of neointima formation, c) enhanced angiogenesis, d) activation of antioxidant scavenger mechanisms via mitohormesis, e) a decline in endothelium-derived adhesion molecules, and f) reduced angiotensin II-mediated vasoconstriction in patients with symptomatic CHD.
• Endothelial function. Both aerobic exercise and resistance training improve endothelial function in a dose-response relationship among people with or without CVD, mediated by repetitive increases in shear stress resulting in improved endothelium-dependent coronary vasodilation and nitric oxide (NO) bioavailability.
• Anti-atherogenic adaptions. Regular exercise improves elastin and collagen content resulting in less lipid accumulation and stenosis, stabilizes atherosclerotic plaque, and reduces both the necrotic core area and plaque burden. Although lifetime strenuous endurance exercise has been associated with higher CAC scores and a greater prevalence of atherosclerotic plaques, the plaque composition might be more benign and potentially associated with fewer CVD events.
• Structural adaptations. In conduit arteries, exercise training increases luminal diameter and vasodilation capacity, and decreases wall thickness and vascular stiffness. In coronary arteries, exercise has similar effects in improved vessel size and vasodilation capacity as well as the promotion of collateral blood vessel development.
6. Myocardial regeneration. Exercise prior to myocardial infarction (MI) might reduce infarct size, improve cardiac function after MI, and improve the molecular stress protein response involved in heart repair while downregulating the responses involved with adverse remodeling. Exercise training after MI can induce favorable left ventricular (LV) remodeling with decreased LV diastolic volume and reduce N-terminal pro–B-type natriuretic peptide among patients with moderate LV systolic dysfunction. Potential mechanisms responsible for exercise-mediated improvement in myocardial regenerative capacity include reduced myocardial wall stress, improved autonomic balance (with increased parasympathetic tone), improved vascular endothelial function (above) and myocardial contractility, telemerase activation in damaged myocardial tissue, and stimulation of circulating angiogenic progenitor cells possibly mediated by proangiogenic exerkines.
7. Exerkines. Exercise-derived factors, or exerkines, are a broad variety of signaling molecules released during exercise with cardiovascular health benefits distinct from modification of traditional CHD risk factors. They include hormones, metabolites (including lactate), proteins and peptides (mainly cytokines, such as interleukin-6), nucleic acids, and free radicals (including NO); and exert their effects on multiple organ systems through endocrine, paracrine, and/or autocrine pathways. The cardiovascular effects induced by exerkines include enhancement of vascularization and angiogenesis, decrease in blood pressure, and improvement in endothelial function.
8. Protection against malignant arrhythmia. Regular exercise helps protect against life-threatening arrhythmias, mediated by improvement in the autonomic balance, with higher parasympathetic nervous system tone and a reduction in β2-adrenergic receptor sensitivity and expression.
9. Cardiac preconditioning. Regular exercise also can help prevent fatal arrhythmias by inducing cardiac preconditioning, in which brief periods of myocardial ischemia before prolonged coronary occlusion are protective against subsequent ischemia/reperfusion injury. The mechanisms of exercise-associated preconditioning include heightened defense against oxidative stress, up-regulated expression of sarcolemmal ATP-sensitive potassium channel subunits, mitochondrial adaptations, β3-adrenergic receptor stimulation, and increased cardiac storage of NO metabolites.

Clinical Topics: Acute Coronary Syndromes, Arrhythmias and Clinical EP, Cardiovascular Care Team, Diabetes and Cardiometabolic Disease, Dyslipidemia, Heart Failure and Cardiomyopathies, Invasive Cardiovascular Angiography and Intervention, Pericardial Disease, Prevention, ACS and Cardiac Biomarkers, Implantable Devices, SCD/Ventricular Arrhythmias, Atrial Fibrillation/Supraventricular Arrhythmias, Lipid Metabolism, Acute Heart Failure, Heart Failure and Cardiac Biomarkers, Interventions and ACS, Exercise, Stress

Keywords: Acute Coronary Syndrome, Adrenergic Agents, Angiotensin II, Arrhythmias, Cardiac, Atherosclerosis, Coronary Disease, Cytokines, Embolism, Endothelium, Vascular, Exercise, Heart Failure, Inflammation, Leisure Activities, Life Style, Lipids, Lipoproteins, Myocardial Infarction, Myocarditis, Natriuretic Peptide, Brain, Nitric Oxide, Oxidative Stress, Pericarditis, Plaque, Atherosclerotic, Reperfusion, Primary Prevention, Risk Factors, Secondary Prevention, Sedentary Behavior, Vascular Diseases, Vasoconstriction, Vasodilation, Ventricular Dysfunction, Left, Ventricular Remodeling

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