Īerobic exercise has also been shown to initiate cellular and molecular changes to improve oxidative capacity. A decrease in angiotensin levels results in more vasodilation and less vascular dysfunction leading to lower blood pressure. Lastly, blood pressure may also be impacted by decreased angiotensin levels found in exercise-trained individuals. However, evidence supporting this is limited at the moment. Some studies have also shown exercise increases levels of prostacyclins, which may have an additional vasodilator effect. Ĭonsequently, greater amounts of nitric oxide induce more vasodilation and decrease blood pressure. Additionally, aerobic exercise increases the availability of NO by preventing its removal by reactive oxygen species. Collectively, this related activation/inactivation response results in decreased blood pressure. Immediately following exercise, the parasympathetic system (which was previously inactive before commencing exercise) reactivates, and the previously active sympathetic system inactivates. The mechanism for this is likely due to aerobic exercise's effect on parasympathetic and sympathetic nervous activity, nitric oxide (NO), the prostanoid system, the renin-angiotensin system, and vascular remodeling. demonstrated an average reduction of systolic blood pressure (sBP) by -4.8 mmHg and diastolic blood pressure (dBP) by -3.2 mmHg following one exercise session and continued reductions of sBP by -3.2 mmHg and dBP by -1.8 mmHg up to 24 hours after exercise. It has been well documented that consistent aerobic training reduces blood pressure in both the long and short term - in some cases as quickly as a few hours following one bout of exercise. In efforts to optimize oxygen-carrying capacity and meet metabolic needs, changes in blood volume and mass are important and quick ways the body may adapt to aerobic training. Androgens cause an increase in catecholamine and cortisol levels, leading to further erythropoietin (EPO) release and reticulocyte production. ĭuring blood volume expansion, it is hypothesized that exercise augments erythropoiesis by way of androgen production. This is thought to improve the ability to buffer lactate and improve the body’s ability to produce energy through anaerobic metabolism. Expansion in RBC volume is often accompanied by an increase in RBC mass as well. Additionally, over a 30 day period of exercise, both plasma and red blood cell volume may increase an additional 8 to 10% relative to pre-training levels. Studies have noted a single episode of exercise may augment blood volume 10% to 12% within a 24 hour period and may reach peak volumes between 10 and 14 days of training. Activation of this hormonal pathway causes water retention by the kidneys and increases plasma albumin, causing hypervolemia. One way exercise may lead to increased blood volume is through activation of the renin-angiotensin-aldosterone cascade. Mechanisms inherent to blood volume and blood mass also allow the body to adapt following aerobic exercise. Alterations to any of these variables may result in additional alterations in stroke volume and, subsequently, cardiac output. During exercise, an increase in primarily left ventricular (LV) end-diastolic volume augment stroke volume however, a reduction in left ventricular end-systolic volume may also play a small role. Various factors have been shown to affect LV end-diastolic volume, including heart rate, intrinsic myocardial relaxation, ventricular compliance, ventricular filling pressures, atrial contraction, and pericardial and pulmonary constraints. In the acute setting, adjustments in stroke volume are reflected by changes within the left ventricle. Additionally, changes in stroke volume also influence cardiac output. As aerobic exercise occurs, β-adrenergic stimulation by catecholamine release and vagal withdrawal leads to increased heart rate and oxygen delivery to tissues. During acute exercise, the main driver for augmentation is an increase in heart rate. In order to change cardiac output, there may be a change in either heart rate or stroke volume. The ultimate goal of the cardiovascular response to acute aerobic exercise is to maximize cardiac output and match the metabolic demands of the musculoskeletal system.
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