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Exercise, Vascular Wall and Cardiovascular Diseases: An Update (Part 1)
Abstract
Cardiovascular disease (CVD) remains the leading cause of morbidity and premature mortality in both women and men in most industrialized countries, and has for some time also established a prominent role in developing nations. In fact, obesity, diabetes mellitus and hypertension are now commonplace even in children and youths. Regular exercise is rapidly gaining widespread advocacy as a preventative measure in schools, medical circles and in the popular media. There is overwhelming evidence garnered from a number of sources, including epidemiological, prospective cohort and intervention studies, suggesting that CVD is largely a disease associated with physical inactivity. A rapidly advancing body of human and animal data confirms an important beneficial role for exercise in the prevention and treatment of CVD. In Part 1 of this review we discuss the impact of exercise on CVD, and we highlight the effects of exercise on (i) endothelial function by regulation of endothelial genes mediating oxidative metabolism, inflammation, apoptosis, cellular growth and proliferation, increased superoxide dismutase (SOD)-1, down-regulation of p67phox, changes in intracellular calcium level, increased vascular endothelial nitric oxide synthase (eNOS), expression and eNOS Ser-1177 phosphorylation; (ii) vascular smooth muscle function by either an increased affinity of the Ca2+ extrusion mechanism or an augmented Ca2+ buffering system by the superficial sarcoplasmic reticulum to increase Ca2+ sequestration, increase in K+ channel activity and/or expression, and increase in L-type Ca2+ current density; (iii) antioxidant systems by elevation of Mn-SOD, Cu/Zn-SOD and catalase, increases in glutathione peroxidase activity and activation of vascular nicotinamide adenine dinucleotide phosphate [(NAD(P)H] oxidase and p22phox expression; (iv) heat shock protein (HSP) expression by stimulating HSP70 expression in myocardium, skeletal muscle and even in human leucocytes, probably through heat shock transcription factor 1 activity; (v) inflammation by reducing serum inflammatory cytokines such as high-sensitivity C-reactive protein (hCRP), interleukin (IL)-6, IL-18 and tumour necrosis factor-alpha and by regulating Toll-like receptor 4 pathway. Exercise also alters vascular remodelling, which involves two forms of vessel growth including angiogenesis and arteriogenesis. Angiogenesis refers to the formation of new capillary networks. Arteriogenesis refers to the growth of pre-existent collateral arterioles leading to formation of large conductance arteries that are well capable to compensate for the loss of function of occluded arteries. Another aim of this review is to focus on exercise-related cardiovascular protection against CVD and associated risk factors such as aging, coronary heart disease, hypertension, heart failure, diabetes mellitus and peripheral arterial diseases mediated by vascular remodelling. Lastly, this review examines the benefits of exercise in mitigating pre-eclampsia during pregnancy by mechanisms that include improved blood flow, reduced blood pressure, enhanced placental growth and vascularity, increased activity of antioxidant enzymes, reduced oxidative stress and restored vascular endothelial dysfunction.
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“improves cognitive function, learning and memory, and significantly moderates age-related cognitive decline [2, 97, 104, 110, 187, 188, 200], reviewed in [10].”
From The neuropathology of sport (2014) · cites this paper as [110]
In the citing paper
“Exercise training is also associated with improved endothelial function, decreased arterial stiffness, and greater vascular reactivity associated with coronary artery disease, heart failure, and peripheral vascular disease [110].”
From The neuropathology of sport (2014) · cites this paper as [110]
In the citing paper
“Higher levels of physical activity, exercise training, and overall cardiorespiratory fitness reduce the risk for hypertension, obesity, type 2 diabetes mellitus, stroke, and metabolic syndrome, as well as lower cardiovascular mortality [104, 110, 178, 200].”
From The neuropathology of sport (2014) · cites this paper as [110]
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Metadata
- Authors
- Leung, F. P., Yung, L. M., Laher, I., Yao, X., Chen, Z. Y., & Huang, Y.
- Affiliations
- Chinese University of Hong Kong (HK)
- University of British Columbia (CA)
- Venue
- Sports Medicine
- Published
- 2008
- Volume
- 38
- Issue
- 12
- Pages
- 1009-1024
- ISSN
- 0112-1642 (ISSN-L)
- OpenAlex
- W2022629841
- Cited by
- 219
- References
- 277
- Citations by year
- 2026: 3 · 2025: 9 · 2024: 4 · 2023: 6 · 2022: 12 · 2021: 9 · 2020: 10 · 2019: 8 · 2018: 2 · 2017: 11 · 2016: 4 · 2015: 15 · 2014: 27 · 2013: 14 · 2012: 22
- FWCI
- 2.24
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Sports Medicine (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Physiology (medical) › Cardiovascular and exercise physiology
- Health Sciences › Medicine › Physiology (medical) › Exercise and Physiological Responses
- Keywords
- physical activity, cardiovascular disease, endothelial function, vascular smooth muscle, oxidative stress, antioxidant defense, heat shock proteins, inflammation, TLR4, vascular remodeling, angiogenesis, arteriogenesis, endothelial nitric oxide synthase, superoxide dismutase, NADPH oxidase, p22phox, vascular calcification, physical inactivity
- MeSH terms
- Antioxidants, Cardiovascular Diseases, Endothelium, Vascular, Female, Heat-Shock Proteins, Humans, Inflammation, Male, Muscle, Smooth, Vascular, Pre-Eclampsia, Pregnancy, Exercise, Neovascularization, Physiologic
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