Term
| Exercise effects on the CV system |
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Definition
1. Improves endothelial dysfunctions (helps prevents against hypertension, diabetes, and atherosclerosis).
2. Results in net increase in vasodilation.
3. Leads to reduction in BP and systemic vascular resistance=less work at given CO.
4. Increases cardiac output
5. Stimulates angiogenesis for improved O2 supply by increasing numbers of Endothelial Progenitor Cells (EPCs) and Circulating Angiogenic Cells (CACs).
6. Stimulates beta receptors and causes release of leptin which breaks down triglycerides into free fatty acids (beta 2 dominant lipolysis). |
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Term
| How exercise produces vasodilation |
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Definition
1. Increased NO by stimulating endothelial nitric oxide synthase (eNOS).
Nitrite and nitrosothiols (NO equivalents) in blood and myocardium up to a week after exercise ceases
2. Decreased endothelin |
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Term
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Definition
1. Vasodilation
2. Decreased platelet aggregation
3. Stimulates angeogenesis
4. Inhibits inflammation |
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Term
| Peroxisome Proliferator-Activated Receptor Alpha (PPAR-alpha) |
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Definition
| Nuclear transcription factor that stimulates metabolism of free fatty acids. Fibrates may break down PPAR and free fatty acids. |
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Term
| Exercise effects on preload and afterload |
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Definition
1. Exercise induced changes in venous return increase preload and improve cardiac output (through contractility) by Starling’s Law of the Heart
2. Afterload tends to be reduced by chronic exercise training which allows increased cardiac output by reduction in systemic vascular resistance and blood pressure
Selective vasoconstriction of splachnic, kidneys, inactive muscles (unopposed alpha)
Coronary, cerebral, and skeletal muscle vasodilation
Biphasic skin vasoconstriction by SNS then dilation by SNS inhibition to dissipate heat. |
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Term
| Increase of CO in athletes |
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Definition
| Done by increasing SV, not HR. |
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Term
| Exercise effects on heart |
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Definition
Increases: 1. SV (More EDV due to more venous return, less ESV due to increased contractility) 2. Pulse pressure 3. HR (through beta 1 receptors. Bradycardic at rest) 4. CO (through increased HR and SV) 5. venous return (due to increased CO)
Decreases vascular resistance. |
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Term
| Exercise effects on stroke volume |
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Definition
| More EDV due to more venous return, less ESV due to increased contractility=more SV. |
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Term
| Exercise effects of coronory blood flow autoregulation |
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Definition
Coronary blood flow remains constant over a wide range of coronary perfusion pressures (autoregulation) due to vasodilation at low pressure and vasoconstriction at high pressure in order to preserve blood flow
The ability to autoregulate coronary flow is lost at the extremes of perfusion pressure
Exercise alters the ability to autoregulate and increases coronary blood flow to meet myocardial demands |
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Term
| Exercise effects of autonomic nervous system |
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Definition
1. Decreases sympathetic tone.
2. Increases Vagal tone (increased Ach binding to muscarinic receptor).
Net result=vasodilation |
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Term
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Definition
| Nitric Oxide, Vagal simulation and Adenosine inhibit NE release while angiotensin-II potentiates NE release into the synaptic cleft. |
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Term
| Difference between physiologic and pathological hypertrophy |
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Definition
| Physiological hypertrophy also has increased angiogenesis to supply O2 to growing myocytes. Pathological hypertrophy has no angiogenic vessels=ischemia in growing muscle tissue. |
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Term
| Characteristics of the athlete's heart |
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Definition
1. Bradycardia
2. Increased angiogenesis
3. Physiologic hypertrophy
4. Increased CO |
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Term
| Long term effects of physical training |
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Definition
Has both central and peripheral effects
Central
1. Increased CO (mainly from increased SV and reduced peripheral resistance)
2. Increased Blood Volume
Peripheral:
1. Increased capillary density
2. Increased myoglobin
3. Increased oxidative enzymes
4. Increased skeletal muscle mitochondria |
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Term
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Definition
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Term
| Negative effects of exercise |
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Definition
Seen in acute exercise in untrained individual, body cannot supply O2 demands of heart.
Increased heart rate,contractility,afterload,preload may exceed the oxygen demands of the stressed myocardium
Oxygen supply-demand imbalance in subjects with ventricular hypertrophy,coronary artery disease and cardiomyopathies may result in malignant arrhythmias or myocardial infarction |
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