Chapter 10.docx

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University of Toronto St. George
Human Biology
Philip Goodman

Chapter 10 – Cardiovascular Adaptions to Aerobic Training Vascular Adaption  Vascular remodeling and enhanced vasodilatory capacity result in reduced vascular resistance  Regular aerobic exercise provides a cardio-protective effect, resulting in improved coronary blood flow, reduced platelet activation and aggregation and increase fibrinolysis Blood Pressure  Aerobic exercise training produces small, yet significant decreases in resting systolic pressure (in normotensive individuals)  Increases are roughly 4 mmHg – reduce risk for future hypertension and cardiovascular disease  Aerobic training also alters exercise blood pressure  At a given absolute workload, SBP, DBP, and mean arterial pressure (MAP) are all lower posttraining  Aerobic training results in a slight increase in SBP and a slight decrease in DBP at maximal exercise, such that MAP is unchanged  Mean arterial pressure is the product of cardiac output and vascular resistance (MAP = Q X TPR [total peripheral resistance]  The lower vascular resistance and unchanged Q (cardiac output) at rest explain the slight decrease in resting arterial pressure following endurance training Muscle Blood Flow  Resting muscle blood flow is unaffected by training status  During moderate exercise muscle blood flow at a given absolute submaximal intensity is either unchanged or reduced following training  Redistribution of flow within exercise skeletal muscle, such that perfusion to high-oxidative fibres is higher and perfusion to low-oxidative fibre is lower following training  The body prioritizes the delivery of oxygen to the muscle fibre types that are most likely to use it in the process of energy production  At higher exercise intensities muscle blood flow is greater after high- intensity aerobic training compared to before Effects of Aerobic Training on Vascular Tone  The primary factor determining vascular resistance is arterial radius  The factor affecting vasomotor tone will ultimately alter blood flow  A smaller metabolic vasodilator signal at the same absolute exercise intensity  Increased mitochondrial oxidative capacity or increase muscle efficiency following training  Heightened blood flow response to high-intensity exercise following a training program could be explained by a reduced sympathetic vasoconstriction, enhanced activity during high-intensity exercise may be reduced by exercise training  Vasodilation is largely a function of endothelium-dependent mechanisms  Two methods are employed for vasodilation: o Flow mediate vasodilation  Period of vascular occlusion to induce a high-flow (hence high-shear-stress) condition upon reintroduction of blow flow  The elevated shear stress induces vasodilation and the dilation of the artery is observed and quantified sing Dopper ultrasound o Receptor-mediated vasodilation  Exercise may improve endothelium-dependent vasodilation via increased production of prostacyclin or endothelial hyperpolarzing factor  Endurance training is associated with increased NO production due to increase amount and activity of endothelial NO synthase, the enzyme responsible for catalyzing NO synthesis  NO increases with aerobic exercise training  Phorsphorylation of eNOS is enhanced with training which increases the enzyme’s activity and the subsequent production of NO  The intensity of training also appears to be an important factor determining improvements in endothelial cell function  Aerobic training of moderate intensity improves endothelium dependent vasodilation
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