Exercise, vascular wall and cardiovascular diseases

[Guest guest]

The below may be of interest:

Exercise, vascular wall and cardiovascular diseases: an update (part

1).

Leung FP, Yung LM, Laher I, Yao X, Chen ZY, Huang Y.

Sports Med. 2008;38(12):1009-24. doi: 10.2165/00007256-200838120-

00005.

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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Exercise, vascular wall and cardiovascular diseases: an update (part

2).

There is much evidence extolling the virtues of physical activity on

cardiovascular disease (CVD). The evidence derives from different

population groups where leisure time physical activity reduced the

risk of coronary heart disease and cardiovascular mortality in both

men and women. Recent meta-analyses have shown that large risk

reductions for both ischaemic and haemorrhagic stroke can be achieved

by moderate or intense physical activity. There are many data from

human and animal studies confirming a beneficial role for exercise in

the prevention and treatment of CVD.

Physical inactivity and obesity/overweight are not only associated

with a number of health-related risk factors, but are considered to

be independent risk factors for CVD, type 2 diabetes mellitus and

hypertension. Clinical trials confirm that lifestyle interventions

(dietary modification and increased physical activity) reduce the

risk of progressing from impaired glucose tolerance to type 2

diabetes. Moreover, epidemiological studies indicate that the risk of

hypertension increases by being overweight. Modest increases in

exercise intensity and frequency have hypotensive effects in

sedentary hypertensive patients. Long-term training improves

endothelium-dependent dilatation in the aorta and resistance arteries

of the heart, whereas short-term training increases endothelial

function in coronary conduit arteries.

Overall, more scientific evidence will undoubtedly encourage the

widespread advocacy of the clinical benefits of exercise therapy in

the prevention and treatment of CVD.

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Carruthers

Wakefield, UK