Relationship between cardiovascular health and endurance exercise

Cardiovascular Effects and Benefits of Exercise

relationship between cardiovascular health and endurance exercise

The therapeutic role of exercise in maintaining good health and treating . These provide an effective method for improving muscular strength and endurance, . Moayyeri A. The association between physical activity and. The American Heart Association explains endurance exercise and how it can reduce the risk of many diseases such as diabetes, heart disease and stroke. The association between blood lipids and cardiovascular health is highly Exercise is good for your blood pressure: effects of endurance.

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relationship between cardiovascular health and endurance exercise

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By comparison, anaerobic exercise is only possible for relatively short bursts because the anaerobic method of energy production rapidly floods the muscles with lactic acid, making it impossible to continue the intense effort for a longer period.

Effects on the Cardiovascular System When you participate in endurance exercise, your cardiovascular system must work harder to deliver oxygen, nutrients and hormones at an accelerated rate.

relationship between cardiovascular health and endurance exercise

Your heart beats faster and pumps a larger volume of blood with each beat. With the heart working harder, your body can get blood to the lungs more quickly, oxygenating it, and then deliver it to your muscles more quickly. In addition, metabolic processes accelerate, requiring a more rapid transport of nutrients. Benefits Regular endurance exercise improves the functional capacity of your cardiovascular system, resulting in a lower resting heart rate and a quicker return to your normal pulse following exercise.

Through regular endurance exercise, your muscles strengthen as you burn fat, leading to an improved muscle-to-fat ratio. These actions would increase cell viability via a reduction in Ca overload during ischemia and early reperfusion.

There is considerable experimental support for the protective role of sarcolemmal KATP channels in myocardial function [ 60 — 64 ]. Activation of these receptors primes the opening of mitochondrial KATP channels [ 68 ].

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However, there is some controversy regarding the role of mitochondrial KATP channels in exercise preconditioning of the heart. For example, Domenech et al. It should be mentioned that the molecular characteristics of mitochondrial KATP channels remains elusive and that additional research is needed to clarify their function in cardiac function. Cyclooxygenase II and Exercise Induced Cardioprotection The phenomenon of ischemic preconditioning whereby brief episodes of sublethal ischemia renders the myocardium resistant to subsequent ischemic stressoccurs in two phases: Vascular Effects of Exercise The etiology of nearly all of the lifestyle-related vascular diseases can be narrowed down to endothelial dysfunction.

The vascular endothelium consists of a monolayer of cells that line all the internal surfaces of cardiovascular system and plays a critical role in regulation of vascular homeostasis [ 75 ].

  • Cardiovascular benefits of exercise
  • Endurance Exercise (Aerobic)
  • The Relationship Between Cardiovascular Health and Endurance Exercise

The endothelium plays a vital role regulating arterial dilation and constriction by manufacturing vasodilator [nitric oxide NOprostacyclin PGI2endothelium-derived hyperpolarizing factor EDHF ] and vasoconstrictor [endothelin-1 ET-1platelet-activation factor PAF ] agents [ 76 ]. A key component of intact endothelial function is NO production by endothelial nitrous oxide synthase eNOSwhich incorporates oxygen into L-arginine.

The anti-inflammatory, vasodilatory and platelet inhibitory effect of NO have important roles in the maintenance of vascular hemostasis [ 77 ]. Hence, endothelial function measurements are considered useful surrogate end points in clinical research [ 78 ], especially since decreased endothelium-derived NO bioavailability has an independent prognostic value for adverse cardiovascular events in the presence of risk factors but without clinically apparent coronary artery disease [ 79 — 81 ] or established coronary atherosclerosis [ 82 — 85 ].

In some studies, the risk of cardiovascular events such as myocardial infarction or ischemic stroke was folds higher in cardiovascular patients with endothelial dysfunction compared to those with a normal endothelial function [ 85 — 87 ]. Exercise and Endothelial Function Physical activity increases vascular expression of eNOS both in animals and human beings [ 88 — 91 ].

The importance of this phenomenon has been confirmed in patients with stable coronary artery disease and chronic heart failure [ 9293 ]. There are several reports suggesting that exercise-induced up-regulation of vascular eNOS expression is closely related to the changes of frequency and the intensity of physical forces within the vasculature, especially shear stress. Exercise-induced increases in heart rate will augment cardiac output and vascular shear stress, leading to increased expression of eNOS [ 88 ].

Increased NO synthesis secondary to amplified shear stress induces extracellular superoxide dismutase SOD expression in a positive feedback manner so as to inhibit the degradation of NO by ROS [ 94 ]. Another parallel mechanism that participates to this harmony is upregulation of eNOS through exercise induced ROS production, since exercise-induced increases in shear stress stimulates vascular production of ROS by an endothelium dependent pathway [ 95 ].

Superoxides are rapidly converted to H2O2 by SOD; hydrogen peroxide then diffuses through the vascular wall and increases the expression and activity of eNOS [ 9798 ]. Thus, increased expression of SOD1 and SOD3 which facilitate the generation of hydrogen peroxide from superoxideaugments the effect of hydrogen peroxide on exercise induced eNOS expression. On the other hand, eNOS expression is not increased in catalase overexpressing transgenic mice [ 8999 ]. Another putative mechanism is exercise-induced increases in arterial compliance which is mediated by reduction of plasma ET-1 concentration as well as the elimination of ET-1 mediated vascular tone.

Twelve weeks of aerobic exercise training results in increased arterial compliance, which was accompanied by decreased plasma ET-1 levels. Moreover, the increase in central arterial compliance observed with ET-receptor blockade before the exercise intervention was eliminated after the exercise training intervention [ ].

Cardiovascular benefits of exercise

These results indicate that endogenous ET-1 participates in the mechanisms underlying the beneficial influence of regular aerobic exercise on central arterial compliance.

Exercise Induced Vascular Remodeling Exercise training has a significant impact on the morphology of various blood vessels. These structural changes are followed by functional changes and lead to improved blood flow. Angiogenesis It has been speculated that endurance exercise stimulates angiogenesis by either a division of preexisting endothelial cells or by bone marrow-derived endothelial progenitor cells and monocyte or macrophage derived angiogenic cells [ ].

Some reports indicate that physical activity improves the mobilization of endothelial progenitor cells in healthy subjects and in patients with cardiovascular risk and coronary artery disease [].

Indeed, angiogenesis is regulated by a net balance between positive angiogenic and negative angiostatic regulators of blood vessel growth. A balance favoring predominantly positive regulators are an angiogenic phenotype whereas a shift favoring negative regulators is an angiostatic phenotype.

relationship between cardiovascular health and endurance exercise

Therefore, an impaired regulation of angiogenesis is often associated with the development of angiogenesis-dependent diseases such as atherosclerosis. Endostatin is an endogenous angiostatic factor identified originally in conditioned media of murine hemangioendothelioma cells []. Several studies show that the proteolytic release of endostatin from collagen XVIII is mediated by proteases of many classes, such as cysteine proteases, matrix metalloproteases, and aspartic proteases [].

The potent antiangiogenic effects of endostatin are mediated via a combination of effects on endothelial cells where endostatin inhibits cellular proliferation and migration and stimulates apoptosis [].