Animal studies of effect of chronic exercise on the heart and atherosclerosis: A review

Froelicher, Victor F.

doi:10.1016/0002-8703(72)90473-5

Cited by 32 publications

(11 citation statements)

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“…Early reports [7,91] showed a direct relationship between increased capillarization and the total distance and/or speed of running. However, it appears that excessive exer cise can lead to a decrease in capillary supply, which has been observed in rats [92], pigs [93] and dogs [94], In contrast to the evident overall lack of effect of exer cise on capillary' growth in adult animals, training by run ning did increase the density of arterioles in pigs [93] and rats [95] and enlarged the diameters of large coronary arteries in man [96], dog and rat [97], An overall increase in the size of the whole coronary vascular bed after train ing has also been shown using vascular casts [98,99], Increases in arteriolar vessels should also be reflected in a higher maximal coronary conductance and/or coronary vascular reserve and this has been described in several species [79,100], although it is not a consistent finding [101. 102] possibly because of methodological inadequa cies in estimating 'maximal' flow [79].…”

Section: Vesselsmentioning

confidence: 95%

Postnatal Growth of the Heart and Its Blood Vessels

Hudlická

Brown²

1996

J Vasc Res

100

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Although rapid growth of the heart during early postnatal development ceases with maturation of the organism, the potential for cardiomyocyte growth is not lost and may be observed even in senescent hearts. Rapid developmental heart growth is accompanied by a proportional growth of capillaries but not always of larger vessels, and thus coronary vascular resistance gradually increases. Growth of adult hearts can be enhanced by thyroid hormones, catecholamines and the renin-angiotensin system hormones, but these do not always stimulate growth of coronary vessels. Likewise, chronic exposure to hypoxia leads to growth, mainly of the right ventricle and its vessels but without vascular growth elsewhere in the heart. On the other hand, ischaemia is a potent stimulus for the release of various growth factors involved in the development of collateral circulation. Heart hypertrophy develops in response to training, pressure or volume overload. Training usually leads to growth of larger coronary vessels but little growth of capillaries, except in young animals. However, growth of the capillary bed, but not the resistance vasculature capacity, can be induced by either increased coronary blood flow, bradycardia (electrically or pharmacologically induced) or increased inotropism, all of which are involved in the training stimulus. Thus, what actually promotes growth of larger vessels as opposed to capillaries in training is unclear. Pressure overload hypertrophy is mediated by both the renin-angiotensin system and the response of cardiomyocytes to stretch; both lead to activation of early oncogenes (c-fos, c-jun, c-myc) and angiotensin II activates several protein kinases involved in cell growth. In this condition, growth of larger vessels is inadequate, although some capillary growth may occur. Volume overload leads to cardiomyocyte hypertrophy and hyperplasia and some increase in vascular supply. Deficits in capillary supply in pressure or volume overload hypertrophy can be reversed by chronic administration of ACE inhibitors, dipyridamole, the bradycardic drug alinidine or pacing-induced bradycardia respectively, but in neither case is training effective. Mechanical and humoral factors are involved in growth of cardiomyocytes and vessels. For cardiomyocytes, stretch is most important, activating oncogenes, protein kinases and possibly the inositol phosphate pathway, but not ion channels, with regulation by the balance of angiotensin II, TGF-β1 and IGF-1, but not FGFs. For vessels, growth is stimulated by stretch and shear stress, possibly with involvement of VEGF. Increased shear stress disrupts the glycocalyx on the luminal side of vessels and releases plasminogen activator and metalloproteinases which disrupt the basement membrane and enable endothelial cell migration and proliferation. It also causes rearrangement of the endothelial cytoskeleton and transmission of mechanical signals to the abluminal side disturbing extracellular matrix and causing distortion of capillary basement membrane. Stretch acting from the ablum...

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Section: Vesselsmentioning

confidence: 95%

Postnatal Growth of the Heart and Its Blood Vessels

Hudlická

Brown²

1996

J Vasc Res

100

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“…1,2 Exercise can also positively influence risk factors that are associated with cardiovascular disease: hypertension, diabetes mellitus, obesity, increased plasma lipids, and endothelial dysfunction. 3 However, the mechanism(s) by which exercise might benefit cardiovascular disease is not known.…”

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confidence: 99%

Role of Arterial Wall Antioxidant Defense in Beneficial Effects of Exercise on Atherosclerosis in Mice

Meilhac

Ramachandran

Chiang

et al. 2001

ATVB

107

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Abstract-The mechanism(s) by which exercise reduces atherogenic risk remains unknown. This study tested the hypothesis that sustained exercise-induced oxidative stress may increase antioxidant defense in the arterial wall. Acute exercise induced an increase in antibodies to oxidatively modified proteins and catalase in the aortic walls of normal mice compared with sedentary control mice. In male atherogenic diet-fed low density lipoprotein (LDL) receptordeficient mice, exercise lowered plasma cholesterol (15%) and decreased atherosclerotic lesions by 40% compared with values in sedentary control mice, with a concomitant increase in arterial catalase and endothelial NO synthase. Because these mice lack the LDL receptor, the results indicate that the LDL receptor might not be responsible for the exercise-induced lowering of plasma cholesterol. Vitamin E supplementation to exercising LDL receptor-deficient mice did not reduce atherosclerotic lesion formation significantly as opposed to lesion formation in untreated exercised mice. Moreover, vitamin E counteracted the beneficial effects of exercise by preventing the induction of aortic catalase activity and endothelial NO synthase expression. These results might indicate that although vitamin E might have prevented the exercise-induced oxidative stress, its availability in the artery was insufficient to prevent the atherosclerotic process.These results indicate that exercise-induced plasma oxidative stress could be responsible for the prevention of atherosclerosis by stimulating arterial antioxidant response. Furthermore, vitamin E supplementation could be deleterious in exercisers by inhibiting antioxidant enzyme buildup in the arterial wall. (Arterioscler Thromb Vasc Biol.

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“…Based on other experimental protocols and their effects on cardiac size and metabolism, the 1 hour/ day exercise protocol used here probably can be classified as mild exertion (Froelicher, 1972). Although we cannot state with certainty how swimming activity is perceived by rats, they showed no aversion to the water after a period of training of several days and did not appear to be exhausted by the swimming.…”

Section: Discussionmentioning

confidence: 88%

“…Coronary artery luminal areas are increased in trained man (Scheuer and Tipton, 1977) and rat (Bloor and Leon, 1970;Froelicher, 1972), and structural adaptation of systemic resistance vessels takes place in the exercised rat (Weiss, 1978). Many but not all studies of the effect of exercise on experimental atherosclerosis show some reduction in disease (Froelicher, 1972).…”

Section: Discussionmentioning

confidence: 99%

Hydrolase activities in the rat aorta. III. Effects of regular swimming activity and its cessation.

Wolinsky

Goldfischer

Katz

et al. 1979

Circulation Research

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SUMMARY It is possible that one of the consequences of regular physical activity could be a change in vascular metabolism. We studied the effects of regular swimming activity on specific activities of aortic hydrolases of male rats. Enzymes included: neutral a-glucosidase and lysosomal /3-galactosidase, JV-acetyl-/}-glucosaminidase, cathepsin C, acid a-glucosidase, and acid cholesteryl esterase. After 8 or 16 weeks of a 1-hour/day swimming protocol, specific activities of four of the six aortic enzymes studied were increased over control levels, increases ranging from 7 to more than 42%. Acid cholesteryl esterase was one of the enzymes most affected by the exercise, increasing 25-30% above control levels. An 8-week sedentary period, after 8 weeks of a swimming regimen, resulted in return of the activity of acid cholesteryl esterase, but not those of the other hydrolases, to control levels. Decreases in body weight, blood pressure, and serum lipid levels also occurred in the swimming rats. Weight reduction per se was excluded as an explanation for the increases in aortic enzymes or decrease in serum cholesterol found with swimming. These findings show that regular physical activity is yet another factor with discrete and significant effects on the catabolic activity of vascular tissue. Ore Res 45: 548-553, 1979VIGOROUS exercise appears to be associated with a reduced prevalence of death from coronary heart disease in man (Paffenberger and Hale, 1975); less extreme exercise has not been so clearly related. Apart from the question of degree of exercise, it remains uncertain whether exercise itself is protective or whether it results in a favorable clustering of other factors associated with reduced risk. Among the latter are a decreased total serum cholesterol level (including decreased low density lipoproteins and increased high density lipoproteins), a decreased serum triglyceride level (Lopez-S et al., 1974;Fletcher and Cantwell, 1974;Wood et al., 1976;Cantwell, 1978), reduced systolic and diastolic blood pressure levels (Scheuer and Tipton, 1977), and increased vital capacity (Kannel, 1967). Similar decreases in serum lipids and blood pressure with swimming or running activity have been described for the rat (Papadopolou° et al., 1969;Tipton et al., 1977).We recently (Wolinsky and Fowler, 1978) have emphasized the importance of understanding the direct effects of putative risk factors for vascular disease on cellular metabolism of the blood vessel wall in addition to noting the levels of certain circulating lipoprotein classes, the blood pressure

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Animal studies of effect of chronic exercise on the heart and atherosclerosis: A review

Cited by 32 publications

References 50 publications

Postnatal Growth of the Heart and Its Blood Vessels

Postnatal Growth of the Heart and Its Blood Vessels

Role of Arterial Wall Antioxidant Defense in Beneficial Effects of Exercise on Atherosclerosis in Mice

Hydrolase activities in the rat aorta. III. Effects of regular swimming activity and its cessation.

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