Chapter 7
Physical Activity and Hypertension
“The Pulse is the diastole and systole of the heart
and arteries…”
Rufus of Ephesus, 200 AD
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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 40-69 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 reninangiotensin-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 viceversa.
• 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-152-156
• 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
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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 300-500 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
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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.