Chapter 7 Physical Activity and Hypertension “The Pulse is the diastole and systole of the heart and arteries…” Rufus of Ephesus, 200 AD

P-146 Hypertension is a major risk factor for CHD and stroke. During middle and old age elevations from 115 mmHg systolic or 75 mmHg diastolic are directly related to increased risk of death from all causes. At ages each difference of 20 mmHg systolic or 10 mmHg diastolic is associated with a doubling of deaths from CAD and more than a doubling of deaths from stroke. Hypertension is defined as 140/90 or greater. Primary (essential) hypertension—the cause is unknown/unpredictable is about 90-95% of cases. Secondary hypertension (cause is known) results from renal nephritis, hypersecretion of corticosteroids from adrenal gland, including hyperaldosteronism, pheochromocytoma (tumor in the adrenal medulla)— which leads to hypersecretrion of catecholamines, or malfunction of the renin- angiotensin-aldosterone system. Table 7.1, p-147.

Magnitude of the Problem Mortality from CHD & stroke have dropped but from hypertension remain high. Many adults have prehypertension (about 25%). Hypertension is disproportionately high among African Americans. Like stroke—it is highest in the southeast. Hypertension coast $76.6 billion in health care services, meds and missed days of work (2010). Some of the decline in hypertension can be explained by the fact that more people today have their hypertension normalized by antihypertensive medications. Demographics of hypertension—p-148.

Treating Hypertension P-149 Antihypertensive meds: calcium channel blockers; ACE inhibitors or SNS blockers; Diuretics; SNS receptor blockers,; Combined (ACE + SNS + Diuretic) Low sodium diet Potassium For mild to med Hypertension: weight-loss, low salt, increased physical activity. Lifestyle modifications: Maintain normal bodyweight; reduce sodium; regular aerobic exercise; limit ETOH; Potassium; Diet rich in fruits, veggies, and low-fat dairy with lower sat and unsat fat. Chart—p-150. Primary Prevention: Focuses on lifestyle changes. Decrease sodium, increase potassium, lose weight, reduce stress, increase PA.

Hypertension Etiology BP is the algebraic product of blood flow (Q) and total peripheral resistance to flow: The volume of blood, its rate of flow and especially the diameter of the blood vessels. Hypertension develops from an abnormal elevation in one or all of the factors that influence blood flow or resistance to flow: and the specific mechanisms that alter blood flow or resistance vary with race, age, and body comp. BP increases during activity of the sympathetic nervous system. The parasympathetic nervous system releases the neurotransmitter acetylcholine from the vagus nerve to slow the heart and relax muscle cells thus lowering BP and on the kidneys. Systolic and diastolic BP depend on the changing of the balance of the symp and paras nervous system. Greater symp and BP increases and vice- versa.

Primary Prevention: Exercise, diet, immunizations, etc. Secondary Prevention: Treatment. Tertiary Prevention: Helping people manage and control a health problem.

Physical Activity and Reduced Hypertension Risk: The Evidence P-152 Epidemiologic studies provide evidence that mod-intensity physical activity is associated with primary prevention and treatment (secondary prevention) of mild hypertension. Studies: P Physical Activity & Treatment of Hypertension: The Evidence: Aerobic exercise reduced SBP/DBP of about 7/5 mmHg among people with hypertension and about 3/2 mmHg among normotensive. There is also evidence to support the effectiveness of resistance exercise for reducing BP. P-157. BP reductions after aerobic or resistance exercise are similar for men and women regardless of age.

Postexercise Hypotension Postexercise hypotension (PEH) is a prolonged decrease in RBP in the minutes and hours following acute exercise. P-160. Why? Reduced Q (Particularly stroke volume in people with hypertension) and decreased resistance to blood flow in small arterioles in the muscles that were exercised. PEH varies widely in people with normal BP. Exercise cause SBP to increase (200 mmHg +). –Increased Q and constriction of vessels supplying organs not involved in exercise. At the same time—dilation of vessels supplying the contracting muscles dilate— causing no change in DBP from resting or a small decrease. During resistance exercise SBP can rise mmHg because of additional mechanical compression on vessels to the contracting muscles and also due to increased chest pressure during breath holding.. Unlike with cardio---increases in BP with weight lifting rise and fall with the rhythm of the resistance.. Stress Reactivity: P-161.

Strength of Evidence P-158 When judged by criteria of Mill’s canons, the evidence is moderately strong that leisure-time physical activity is independently associated with reduced risk of developing hypertension and is effective in reducing BP among adults who have mild hypertension. Exercise and Hypertension: Plausible Mechanisms: Decreased Q;-- decreased SNS activity; increased vagal tone; decreased catecholamine levels; decreased B-recptors; increased alpha receptors; renal effects—increased sodium excretion. Decreased total peripheral resistance:-- decreased SNS nerve activity; decreased resting catecholamine levles; increased alpha receptors; decreased alpha receptors; decreased insulin; endothelial relaxers. Insulin: Insulin resistance and hyperinsulinemia have been reported in the development of hypertension. People with hypertension are commonly insulin resistant, hyperinsulinemic, and hyperglycemic. There seems to be a direct relationship between plasma insulin concentration and BP. One way of preventing hypertension is preventing obesity—as obesity is related to insulin resistance and has been shown to be an independent direct risk factor for CVD and primary hypertension.