• Introduction
• Assessment of Blood Pressure
• Control of Blood Pressure
• Etiology
• Pathophysiology
• Exercise Effectiveness
  • Prevention
  • Treatment
  • Who benefits?
  • Mechanisms
• Clinical Managment
  • Screeing
    • Clinical Blood Pressures
    • Ambulatory Blood Pressure
  • Pharmacology
  • Exercise Prescription
  • Case Studies

INTRODUCTION

Blood pressure is the lateral pressure exerted on the wall of the artery as the blood flows through the vessel. Systolic blood pressure is the pressure on the vessel walls during systole whereas diastolic blood pressure is the pressure on the vessel walls during diastole.

In 2003, the Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC7) redefined high blood pressure. The new classification of pre-hypertension was added. This adds 45,000,000 more people in need of treatment for high blood pressure. Prehypertension was added as a classification because prehypertension is at high risk of progressing to hypertension pressures of 130/80-139/89 mm Hg are twice the risk of lower pressures starting at pressures of 115/75 mm Hg, each 20 mm Hg increment doubles the risk of end organ damage

The only treatment for prehypertension is diet and exercise.

High blood pressure is prehypertension (>120/>80 mm Hg); whereas hypertension is blood pressure >140/>90 mm Hg.

• Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC7)

ASSESSMENT OF BLOOD PRESSURE

Blood pressure is the most variable variable in physiology. It can vary 70 mm Hg throughout the day.

We can measure blood pressure with

Auscultation

The most common assessment of blood pressure is auscultation (i.e. listening to sounds). These sounds are the sounds of Korotkow:

Click here to hear the sounds of Korotkow

More often the blood pressure is recorded as

sound I/sound IV
systolic/clinical diastolic

however, a more accurate indication of blood pressure is

sound I/sound IV-sound V
systolic/true diastolic - clinical diastolic

In the clinical setting systolic blood pressure represents cardiac output and diastolic blood pressure represents peripheral vascular resistance.

Clinical pressures can has been found to underestimate resting arterial pressures

-30 to + 2 mm Hg for Systolic

-11 to + 11 mm Hg for Diastolic

and during exercise:

-16 to 0 mm Hg for Systolic

-20 to + 4 mm Hg for Diastolic

• Griffin, et al, Med Sci Exerc Sport 29:149, 1997

Ambulatory Monitoring

Ambulatory monitoring is an assessment of blood pressure in a more real-life setting. It can be programmed to take blood pressures every 2 to 120 minutes for up to 48 hours. Typically, we take blood pressures every 15 +/- 5 min during daytime hours and every 30+/-5 min during nighttime hours.

The ambulatory monitor control box is attached to a belt or shoulder strap. ECG electrodes monitor the heart beat which activates the microphone to listen for sounds.

The best technology used an electrocardiogram to signal the control box to listen to the blood pressure sounds.

The advantages of ambulatory monitoring:

• Mann et al, Clin Science 59:497, 1980
• White et al, Am J Cardiol 65:60, 1990
• James et al, Hypertension 11:545, 1988

Ambulatory monitoring has been utilized in:

Inappropriate populations include

• Ventricular dysrhythmia
• Sleep Apnea
• Transplant Patients

Normal ambulatory blood pressure is illustrated to the left.

Normal nighttime pressure is considered <120/<80 mm Hg during 10:00 pm to 6:00 am (22:00 to 0600 hrs)

Whereas normal daytime pressure is considered <140/<90 mm Hg during 6:00 am to 10:00 pm (0600 to 2200 hrs).

This is a recording of a hypertensive adult. In this pattern the daytime blood pressures are elevated.

This type of pattern is considered a dipping pattern because the blood pressure is normal during the sleeping hours.

In this pattern the nighttime blood pressures are also elevated. This pattern is termed, non-dipping and is considered more severe than nocturnal dipping hypertension.

These control systems are not exclusive. They interact to maintain blood pressure in reactive and long term situations. The green arrows indicates the system primarily increases blood pressure, whereas the red arrow indicates the system primarily decreases blood pressure. This is not to say the opposite cannot occur. Less stimulation to these control mechanisms can result in the opposite response.

Baroreceptors are reflexive whereas Renin-Angiotensin is long term.

The central nervous system can be both reflex and long term.

NATURAL HISTORY OF HYPERTENSION

Environmental influences then determine the course of hypertension:

Stress is implicated in the etiology of hypertension by either over reactive catecholamine response or periods of increased catecholamine response. The classic catecholamine response is an increase in heart rate, stroke volume, cardiac output and vasoconstriction.

Sodium (Na+) has a role in the etiology of hypertension because of its relationship to fluid shifts. Increases in Na+ are associated with increases in fluid, increases in blood volume, and increases in cardiac output. Na+ can be increased by diet and/or insulin resistance. Insulin resistance increases Na+.

The exact mechanism for low potassium and calcium intake in the etiology of hypertension is uncertain. Increases in potassium and calcium intake, however, lowers high blood pressure.

Obesity is associated with hypertension because of the excess work the body has to do to transport a larger body mass and insulin resistance.

EXERCISE EFFECTIVENESS

The predominant type of exercise used in most exercise and blood pressure studies is cardiovascular exercise.

Prevention

Different prevention studies have reported:

• 1.52 greater risk for the development of hypertension in the low fit groups when compared with the highly fit persons
• The relative risk of hypertension, after adjustment for age, initial blood pressure, body fat, and other confounders was 1.9 times higher in the least fit compared with the fittest group
• 25% greater risk of hypertension among inactives than among actives

• Fagard, Physical activity in the prevention and treatment of hypertension in the obese. Medicine and Science in Sports and Exercise 31: (Supplement 1):S624, 1999.

Treatment

In the exercise treatment of high blood pressure, both acute and training studies have been reported. The acute studies observe the blood pressure response to a single session of exercise. These acute studies may provide information on the long-term training effects of exercise.

Using ambulatory blood pressure technology we found that systolic blood pressure can be reduced (red section of the graph on the right) 5-8 mm Hg for 11 to 12 hours following exercise.

Diastolic blood pressure, not pictured, can be reduced 6-8 mm Hg for 6-8 hours following exercise.

This phenomenon is called Post Exercise Hypotension.

In training studies, the range of blood pressure reduction is 5-25 for systolic and 3-25 for diastolic.

However, patients with hypertension reduce, on the average, 11 for systolic and 8 for diastolic.

Normotensives adults do not reduce blood pressure significantly with training.

In addition to lowering blood pressure a significant number of patients can stop taking their blood pressure medications.

The primary mode of exercise in blood pressure studies has been cardiovascular exercise. What about resistance exercise?

The figure to the left summarizes only three studies that utilized resistance training for hypertensive patients. These three studies had a total of 52 patients in the exercise groups and 54 in the control groups.

They all presented dynamic circuit training for 9-26 weeks; 2-3/week at 40-79% of 1RM for 10 separate exercises. 10-25 reps were done for 1-3 sets.

No study reported significant reductions in blood pressure using resistance exercise.

These results may not be surprising considering the cardiovascular response to dynamic and static work. The figure to the right illustrates the blood pressure and heart rate response to dynamic (cycle ergometer at 600 kpm/min) vs. static (sustained handgrip at 40% MVC). These two examples are the extremes of aerobic and resistance work.

Systolic blood pressure increases more in dynamic work because the cardiac output demand is larger. Similar conditions for heart rate. Diastolic blood pressure decreases in dynamic work because the peripheral resistance is reduced, yet increased in static work because the muscle contraction increases resistance to blood flow.

Resistance work can be made more dynamic and may result in different blood pressure responses for muscle endurance vs. strength training.

In 2004, the traditional exercise prescription which was based on 1284 hypertensive patients in 74 exercise training studies, was modified to include physical activity and the accumulation of physical activity. The primary differences between the two prescriptions are found in mode and duration. Mode was modified to include more general endurance physical activities beyond the specific dynamic cardiovascular endurance exercise; and resistance was recommended as a supplement to physical activity. The duration was reduced; and allowed for accumulating the duration over the course of the day. These new recommendations were based on eight studies, of which only one study observed subjects with high blood pressure; and was limited only to women. We developed a series of studies to confirm whether the new guideline were appropriate:

Our next study took us into the laboratory to control the accumulation of activity and to compare the blood pressure reductions to continuous work. Here, 20 people with prehypertension walked twice on a treadmill for 40 minutes. One day they would walk for the entire 40 minutes continuously (long); and the other day they split the 40 minutes into four 10 minute sessions (accumulation). The order they walked was randomized. We timed the workouts so that both would end around noon.

The systolic blood pressure dropped 6 mm Hg for both types of workouts. But, this figure illustrates the duration of the blood pressure reduction for the accumulation of walking was four hours longer than for continuous walking. Thus, the accumulation of short sessions of physical activity appeared better than one single continuous session.

WHO BENEFITS?

Only 75% of the patients with hypertension benefit from exercise treatment. There are characteristics of individuals who benefit more than others listed below. However, because high blood pressure has a genetic component, perhaps the effectiveness of treatment also has a genetic component.

• Hagberg, J.M., R.E. Frerell, R.D. Dengel, and KR. Wilund. Exercise training-induced blood pressure and plasma lipid improvements in hypertensives may be genotype dependent. Hypertension 34:18-23, 1999.
• Wilmore, J.H., P.R. Stanforth, J. Gagnon, T. Rice, S. Mandel, A.S. Leon, D,C. Rao, J.S. Skinner, and C. Bouchard. Heart rate and blood pressure changes with endurance training: The HERITAGE Family Study, Medicine and Science in Sports and Exercise 33:107-116, 2001.
• Rankinen, R., T. Rice, L. Perusse, Y.C. Chagnon, J. Gagnon, A.L. Leon, J.S. Skinner, J.H. Wilmore, D.C. Rao, and C. Bouchard. NOS3 Glu298Asp genotype and blood pressure response to endurance training: The HERITAGE Family Study Hypertension 36:885-889, 2000.
• Rankinen, T., J. Gagnon, L. Perusse, Y.C. Chagnon, T. Rice, A.S. Leon, J. S. Skinner, J.H. Wilmore, D.C. Rao, and C. Bouchard. AGM M235T and ACE ID polymorphisms and exercise blood pressure in the HERITAGE Family Study American Journal of Physiology, Heart and Circulatory Physiology 279:H368-H374, 2000.
• Rivera, M.A., M. Echegaray, T. Rankinen, L. Perusse, T Rice, J Gagnon, A.S. Leon, J.S. Skinner, J.H. Wilmore, D.C. Rao, and C. Bouchard. TGF-beta1 gene-race interactions for resting and exercise blood pressure in the HERITAGE Family Study Journal of Applied Physiology 91:1808-1813, 2001.

HERITAGE Family Study was a four center genetic study observing the link between exercise effectiveness and genetics. The centers were Texas A & M, Laval University, University of Minnesota, and Indiana University. Families totaled 239 caucasian men and 253 caucasian women from 99 nuclear families and 91 African American men and 179 African American women from 105 nuclear families. Familes were concidered the natural mother and father with three offspring >17 years old for the caucasian (C) families and at least two first degree relatives for the African Amercian (AA) families. Training was 20 weeks of computer controlled cycle ergometry, 3 days a week for 60 minutes each session. The cycle ergometers were programed to start at 55% of VO2max and progress to 75% VO2max by the sixth week of training. Of the 744 subjects, 507 (166 African Americans) completed the blood pressure aspects of the study.

The blood pressure results are summarized to the left. These subjects were normotensive. The blood pressure reductions were small, but signficant considering the number of subjects. There were also racial differences; with African Americans having higher blood pressures and larger reductions in blood pressures.

One mechanism of blood pressure has been considered an increase in Nitric Oxide, specifically, eNOS. Thus, the polymorphism of Glu298Asp (eNOS) was observed in blood pressure reduction in 471 caucasian subjects from 99 family units. No significant changes in blood pressure were detected based on the variations of the eNOS genes.

The angiotensinogen (AGT) and angiotensin converting enzyme (ACE) genetics were also observed in the HERITAGE study during submaximal exercise. Systolic blood pressure response to 50 Watts of cycle ergometry is illustrated to the left before and after training.

Transforming growth factor (TGF) phenotypes were observed of TGF role in target-organ damage from hypertension. TGF was higher in both African Americans and Caucasians with hypertension. The HERITAGE study, however, focused on the normotensive adults and found no sigficant interactions between the races.

Hagberg and colleagues divided 18 hypertensive subjects into their genotypes for high blood pressure. These primary genotypes, ACE, LPL, and Apo had sub genotypes.

After 9 months of exercise (40 minutes of exercise per session at 75% to 85% of VO2 max) he observed their reduction in systolic blood pressure. (see figure to left).

It appears that the change in blood pressure with exercise has a genetic component.

• Women are more successful than men in reducing both systolic and diastolic blood pressure with exercise. Comparing studies for men and women, 100% of the studies observing women reported a decrease in systolic blood pressure whereas only 72% of the studies observing men reported reductions. The average reduction in systolic blood pressure reported for women was 14.7 mm Hg whereas the average reduction reported for men was 8.7 mm Hg.
• Asian and Pacific Islanders are more effective in reducing blood pressure with exercise than Caucasians. Over 90% of the studies targeting Asians and Pacific Islander reported blood pressure reductions; whereas only 65% of those targeting Caucasians reported reductions. The average systolic/diastolic blood pressure reduction in Asians and Pacific Islanders was 11.7/6.7 mm Hg vs. 8/6.8 mm Hg in Caucasians. The information for African-Americans is limited despite the fact that African-Americans have the highest rate of hypertension.
• The higher Na+:K+ ratio, the greater the blood pressure reduction with exercise. When it comes to the sodium (Na+) to potassium (K+) ratio, it’s found in the blood; serum to be exact. However, these are data an exercise leader will rarely have.
• People in the early stages of high blood pressure, where the peripheral vascular resistance is normal, are more effective in reducing blood pressure with exercise than people in the later stages.
• The people with higher blood pressures exhibit the larger reductions in blood pressure, whereas people with more normal blood pressures hardly show any reduction in blood pressure with exercise.
  • What does this mean when comparing people at the different stages of high blood pressure? People in the borderline stages have lower blood pressures than people in the more advanced stages. Yet, those people who are borderline are more effective than those in the later stages at reducing blood pressure with exercise. These are two separate things. The classification of high blood pressure can help you determine who will benefit more whereas the actual blood pressure value can help you determine how much of a reduction in blood pressure your client might accomplish.
• Beta Blockers are a common medication given to patients with high blood pressure. Selective beta blockers target the heart directly whereas non-selective beta blockers have more total body effects. In any case, the primary action of both types of beta blockers is to blunt heart rate, contractility and consequently cardiac output. When cardiac output is reduced in adults without heart disease, physical work capacity is lowered. The inability to exercise may compromise the potential to reduce blood pressure through physical activity. In other words, your client who is taking beta blockers may not be able to exercise hard enough to reduce blood pressure. Some studies show no reduction in blood pressure for people who exercise and take non-selective beta blockers whereas others do not. In any case, the beta blocker is not the best medication for people who want to do physical activity to help control blood pressure.
• Intensity of Exercise is an important aspect of the exercise prescription to determine the outcome.

This figure summarizes the blood pressure reduction found for studies that utilized intensities above 75% of VO2max vs. those that utilized lower intensities. The lower intensities resulted in greater reductions in blood pressure.

MECHANISMS OF BLOOD PRESSURE REDUCTION

In the hemodynamic determinants of blood pressure, exercise reduces the elevated component. That is, if cardiac output is the elevated determinant, cardiac output will decrease with exercise treatment. Similarly, if peripheral vascular resistance is elevated, peripheral vascular resistance will decrease with exercise treatment. The reduction in cardiac output is more responsive than elevated peripheral vascular resistance.

To consider what reduces the hemodynamic determinants of blood pressure, the next level of blood pressure control should be considered.

But, what can exercise do for these blood pressure control systems?

Exercise training has no effect on

• Renin Angiotensin System
• Atrial Naturetic Factor
• Anti-Diuretic Hormone

Exercise training has a more dramatic effect on the sympathetic nervous system

• Krieger, EM, GJJ da Silva, and CE Negrao. Effects of exercise training on baroreflex control of the cardiovascular system. Annals of the New York Academy of Sciences 940:338-347, 2001.

The contribution of the sympathetic (SE) and parasympathetic (VE) nervous systems are illustrated before and after training in hypertensive and normotensive rats.

It obvious that the amount of sympathetic activity is reduced with training and the amount of parasympathetic activity is increased in both normotensive and hypertensive groups.

The sensitivity of the baroreflex can be increased with training as summarized in the figure to the left. Sensitivity of the reflex increases as the curve moves to the left. Normotensive rats move from the NS (sedentary) curve to the NT curve (trained) whereas hypertensive rats move from the HS (sedentary) curve to the HT curve (trained) with training.

However, the influence of this control on resting blood pressure is unclear. Does the change in baroreceptor activity result in lower pressures or does the change in sympathetic activity result in more sensitive baroreceptor activity?

Sympathetic vascular regulation can be divided into

• neural component
• vascular component

Exercise training of the neural component accounts for a 30% decrease in sympathetic outflow to the skeletal muscle vascular beds.

Exercise training of the vascular component is an attenuation of the vascular response to sympathetic vasoconstriction and perhaps a local circulating vasodilator substance.

Muscle sympathetic nerve activity is under the control of arterial baroreflexes. There is evidence that the baroreceptors are "re-set" to a lower regulatory blood pressure with exercise training.

The "re-setting" of the baroreceptors is considered the focal point for exercise training. When the baroreceptors are regulated around a lower pressure, there is less sympathetic activity. The lower sympathetic activity can not only affect peripheral vascular resistance, but cardiac output as well.

CLINICAL MANAGEMENT

• Evaluation of Blood Pressure
• Treatment of Blood Pressure

The Joint Committee on the Detection, Evaluation and Treatment of High Blood Pressure has recommendations for taking blood pressures(5).   These are:

1. Patients should be seated with their arm bared, supported, and at the heart level.   The right and left arms should have similar pressures in apparently health adults.
2. Patients should not have smoked or ingested caffeine within 30 minutes before the measurement.
3. Measurement should begin after 5 minutes of rest.
4. The approximate cuff size must be used to ensure an accurate measurement.   A cuff that is too small will measure blood pressure too high.
5. The bladder should nearly (at least 80%) or completely encircle the arm.
6. The width of the cuff should be 20% of the diameter of the arm.
7. Measurements should be taken with a mercury sphygmomanometer, a recently calibrated aneriod manometer, or a calibrated electrical device.
8. Inflate the cuff rapidly.   Deflate the cuff slowly (2-3 mmHg per second) until systolic pressure is found, then deflate the cuff faster for diastolic pressure.
9. Both systolic and diastolic blood pressures should be recorded.   The disappearance of sound (fifth phase) should be used for the diastolic reading.
10. Two or more readings separated by 2 minutes should be averaged.   If the first two readings differ by more than 5 mmHg, additional reading should be obtained.

The treatment of high blood pressure includes

• Life-Style Modification
• Medications

The treatment goal for hypertension is to lower the blood pressure <140/90 mm Hg. The treatment goal for hypertensive diabetic patients is to lower the blood pressure <130/80 mm Hg.

Targeting the systolic blood pressure is the focus of the therapy because systolic blood pressure is more related to the end organ diseases than the diastolic blood pressure.

The table below summarizes the treatment for the different stages of hypertension.

* Compelling indications refers to conditions such as congestive heart failure, diabetes, CHD, stroke or kidney diseases

In the past, mono-drug therapy was the initial step in medications. Combination therapy can now be considered especially if the presenting blood pressure is greater than 20/10 mm Hg above the target blood pressure.

The lifestyle recommendations of the JNC7th Report are summarized in the table

ANTIHYPERTENSIVE PHARMACOLOGY

The goal of antihypertensive pharmacology is to reduce blood pressure through one or more of the blood pressure control mechanisms.

The primary classes (with subclasses) of antihypertensive medications are summarized in the chart below.

See the 7th Report for a summary of drug and trade names, dosage and daily frequency of these meds.

Diuretics act to decrease plasma volume at the level of the kidney. The three types of diuretics act at different locations of the glomerulus. Normally Na+ is reabsorbed in the ascending loop of the glomerulus. Water is reabsorbed with the Na+; thus maintaining a fluid balance. Loop Diuretics inhibit the Na+/K+/Cl- co transporter in the asscending loop. Thus, Na+ is increased in the distal tubule, pulling water with it through. The result is a diuresis and naturesis (loss of Na+).

Thiazide Diuretics inhibit the Na+/Cl- transporter in the distal tubule. There is less sodium loss with thiazides, but more potassium loss. The Potassium-Sparing Diuretics, on the other hand, act like aldosterone receptor antagonists at the distal tubule to block aldosterone-sensitive Na+ reabsorption. The water loss is not affected, and the potential for hypokalemia is prevented. Aldosterone Receptor Antagonists are considered potassium sparing diuretics even though it is considered a separate class of antihypertensive medications. Aldosterone in the hormone responsible for sodium and water reabsorption as well as potassium secretion in the kidneys. Aldosterone is synthesized and released from the adrenal cortex. Angiotensin II, plasma concentration of potassium, and adrenocorticotropic hormone (ACTH) stimulate aldosterone production and release. Thus, blocking the action of aldosterone fluid volume is reduce dl; thus, reducing blood pressure.

Beta Blockers and Ca⁺⁺ channel blockers were discussed as anti-anginal meds. The dihydropyradines are used more in hypertension than angina. Beta-blockers act to reduce cardiac output whereas the Ca⁺⁺ channel blockers act to reduce peripheral vascular resistance.

The vascular smooth muscle activates vasocontraction through alpha receptors. Norepinepherine is the neurotransmitter activating both the apha₁ and alpha₂ receptors that stimulate smooth muscle contraction.

The apha-blockers block the Nor-epi at the apha₁- receptor; resulting in vasodilation.

ACE Inhibitors and ARBs work through the Renin Angiotensin system. ACE inhibitors inhibit the formation of Angiotensin II whereas ARBs block the angiotensin II receptors on the vasculature and myocardium. ACE Inhibitors also result in a naturesis and diuresis (via decreasing aldosterone) which is prevented with the use of ARBs.

Vasodilators obviously act to decrease peripheral vascular resistance in the control of blood pressure. Hydralazine is a direct vasodilator.

To summarize, the antihypertensive medications target either cardiac output (blue arrows) or peripheral vascular resistance (black arrows).

The algorithm for meds is summarized to the right. The first line of treatment is physical activity and diet. Diet focuses on less alcohol and sodium.

The algorithm for medical treatment of hypertension is trial and error. If the source of the hypertension as diagnosed in medical practice, medications that target the source of the hypertension could be targeted. However, different meds are given until the blood pressure is controlled. For example, African Americans do not respond to ACE inhibitors or ABEs. This may be due to the source of their hypertension may not be renal in nature.

EXERCISE PRESCRIPTION IN HYPERTENSION

There are two exercise presriptions for hypertension; both from the American College of Sports Medicine. the first is the traditional exercise from 1993 and the second is the physical activity prescription from 2004. The 1993 recommendations are based on 72 studies with 1284 patients; whereas the 2004 recommendations are based on 8 physical activity studies, of which only one was for hypertension.

Precautions:

This figure summarizes the blood pressure reduction found for studies that utilized intensities above 75% of VO2max vs. those that utilized lower intensities. The lower intensities resulted in greater reductions in blood pressure.

Check the blood pressure response to resistance exercise to gaurantee a safe blood pressure response. The medical director may provide the criterion blood pressures; if not, the American College of Sports Medicine guidelines states that exercise should be terminated when diastolic blood pressure exceeds 115 mm Hg.

Medications become a precaution with exercise: Beta-Blockers reduce cardiac output (in non-cardiac patients) to the extent that the individual cannot reach their target intensity. If their ability to exercise is compromised, the ability to use exercise to improve blood pressure may be compromised too. Diuretics often deplete potassium stores. Fatal arrhythmias are more probable in hypokalemia. Always check the electrolytes in patients taking diuretics to make sure their potassium is within normal range. If not, send them home to check with their doctor to increase potassium. Vasodilators obviously vasodilate to reduce blood pressure. It is possible for too much dilation to occur with exericse causing a post-exercise hypotension. Make sure patients taking vasodilators have a long slow cool down.

To investigate the interaction between medications and exericse, Kelerman et al provided an exericse program for 51 hypertensive patients for 10 weeks. Mode was circuit training and aerobics. The 51 patients were randomized into three groups

• placebo
• Beta Blocker
• Diuretic

Medications and exercise did not appear to be additive.

In another study, we investigated the time of day to exercise and it's affect on dipping and non-dipping hypertension. Subjects were 5 dipping and 9 non-dipping hypertensive patients. The ambulatory blood pressure from one morning exercise session was compared to a comparible control day; and the ambulatory blood pressure from one evening exercise session was compared to a comparible control day.

• Park, S., C.A. Jastremski, and J.P. Wallace, Time of day for exercise on blood pressure reduction in dipping and nondipping hypertension, Journal of Human Hypertension 19:597-605, 2005.

The figure to the left is the 24 hour ambulatory blood pressure following morning execise for the dippers (blue) and non-dippers (red).

The reduction in blood pressure for the dippers (blue) was primarily in the first 12 hours; wehreas the largest reduction for the non-dippers was in the night-time hours.

The figure to the right is the 24 hour ambulatory blood pressure following the evening exercise in the dippers (blue) and non-dippers (red).

The reduction in blood pressure for the dippers was limited to 4 hours following exercise (until they went to bed); whereas the reduction for the non-dippers extended through the 24 hours.