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Ambulatory blood pressure after acute exercise in older men with essential hypertension
AJH
2000;13:44 –51
Ambulatory Blood Pressure After Acute Exercise in Older Men With Essential Hypertension Nadine S. Taylor-Tolbert, Donald R. Dengel, Michael D. Brown, Steve D. McCole, Richard E. Pratley, Robert E. Ferrell, and James M. Hagberg We sought to determine whether reductions in blood pressure in hypertensives after acute exercise persist for more than the 2 to 3 h found in controlled laboratory settings. Subjects (n ⴝ 11) were obese (32 ⴞ 4% body fat), sedentary (VO2max 27 ⴞ 4 mL/kg/min) 60 ⴞ 6-year-old men with stage 1 or 2 essential hypertension. Ambulatory blood pressure was recorded on 1 day preceded by 45 min of 70% VO2max treadmill exercise and on another day not preceded by exercise. Systolic blood pressure was lower by 6 to 13 mm Hg for the first 16 h after exercise (P < .05) compared to the day without prior exercise. Twenty-four-hour, day, and night average systolic blood pressures were significantly lower on the day after exercise. There was a trend for peak systolic blood pressure to be lower during the entire 24 h and the day portion of the recording; peak systolic blood pressure was significantly lower during the night portion of the recording after exercise. Systolic blood pressure load (percent of systolic blood pressure readings >140 mm Hg) was reduced during the entire 24 h and the day portion of the recording after exercise. Diastolic blood pressure was lower for 12 of the first 16 h after acute
exercise (hours 0 to 4, 5 to 8, 13 to 16) (P < .05) compared to the day without prior exercise. Twenty-four-hour, day, and night average diastolic blood pressure was also significantly lower on the recording after exercise. Peak diastolic blood pressure was lower over the entire 24-h period. Diastolic blood pressure load (percent of diastolic blood pressure readings >90 mm Hg) was lower during the entire 24 h and the day portion of the day after exercise. Preliminary data also suggest that common genetic polymorphisms at the angiotensinogen, lipoprotein lipase, and angiotensin converting enzyme loci may affect the blood pressure-lowering response after acute exercise. Thus, in sedentary, obese hypertensive men a single aerobic exercise session reduced blood pressure enough to result in significantly lower 24-h average systolic, diastolic, and mean arterial blood pressure. This could result in a reduced cardiovascular load during the 24 h after acute exercise in older hypertensive men. Am J Hypertens 2000;13:44 –51 © 2000 American Journal of Hypertension, Ltd.
Received July 14, 1998. Accepted May 5, 1999. From the Center on Aging and Department of Kinesiology, University of Maryland, College Park (NST-T, MDB, SDM, JMH); GRECC and Division of Geriatrics, Baltimore VA Medical Center, Baltimore, Maryland (DRD, REP); and Department of Human Genetics, University of Pittsburgh Graduate School of Public Health, Pittsburgh, Pennsylvania (REF). This research was supported by a grant to JMH from the Maryland Affiliate of the American Heart Association. DRD was sup-
ported by NIA NRSA F32 AG05555, MDB was a Predoctoral Fellow supported by NIA grant R03 AG12781, and REP was supported by NIA Grant AG00494. This work was also supported by research funds provided by the University of Maryland-College Park DRIF fund. REF was supported by NIH grants HL39107 and HL45778. Address correspondence and reprint requests to Dr. James Hagberg, Department of Kinesiology, University of Maryland, College Park, MD 20742-2611; e-mail: [email protected]
© 2000 by the American Journal of Hypertension, Ltd. Published by Elsevier Science, Inc.
KEY WORDS:
blood pressure load, genetic markers
0895-7061/00/$20.00 PII S0895-7061(99)00141-7
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E
levated blood pressure (BP) is a risk factor for cardiovascular (CV) disease and has deleterious effects on such target organs as the heart and kidney.1 The overwhelming majority of hypertensives have stage 1 or 2 hypertension (blood pressure, 140 to 179/90 to 109 mm Hg) and pharmacologic therapy in these individuals has generally not resulted in substantial reductions in CV disease mortality and morbidity. Furthermore, aggressive pharmacologic therapy in these individuals is often associated with negative side effects. These facts led the Joint National Committee on the Detection, Evaluation, and Treatment of High Blood Pressure Report V to recommend exercise training as one initial nonpharmacologic means of controlling BP in persons with stage 1 or 2 hypertension. Long-term exercise training lowers BP in a majority of individuals with essential hypertension.2 We and other investigators have also reported that in sedentary hypertensive individuals acute aerobic exercise transiently reduces BP for up to 3 h in controlled laboratory settings.3– 6 This response could be of even greater clinical significance if such BP reductions persisted longer than the 3 h observed in laboratory studies. However, the studies that have assessed the effect of acute exercise on the ambulatory BP of hypertensive persons have reported inconsistent results, with Pescatello et al5 reporting BP reductions for up to 12 h after exercise and Rueckert et al6 and Somers et al7 reporting no BP reductions after acute exercise. Thus, we sought to determine whether BP reductions after acute exercise persist for more than the 3 h observed in controlled laboratory settings. Each subject underwent two 24-h ambulatory BP recordings, one preceded and a second not preceded by aerobic exercise, so that the effect of aerobic exercise could be ascertained independent of diurnal variations in BP. We hypothesized that BP reductions would be evident for a number of hours, for the daytime and nighttime hours, and for the entire 24-h period after a single bout of submaximal endurance exercise. METHODS Subjects were initially screened by telephone to exclude smokers and those who were physically active or had overt CV diseases that would inhibit their ability to exercise. They then underwent a physical and CV examination and a screening blood chemistry to ensure they had essential hypertension. Subjects with diabetes were excluded using fasting blood glucose levels and oral glucose tolerance tests. Those taking antihypertensive medications suspended their use with the approval of their private physician and were medication free for ⱖ1 week before testing and ⱖ6 weeks before ambulatory BP monitoring sessions. Subjects provided their written consent to participate
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after the study and its risks had been described to them. The study was approved by the Institutional Review Boards of the University of Maryland-College Park and the University of Maryland at Baltimore. Subjects completed a maximal treadmill exercise test8 to exclude those with evidence of CV disease. Subjects also underwent 4 consecutive weeks of weekly casual BP measurements to ensure they had stage 1 or 2 hypertension.9 After 20 min of quiet seated rest, three BP measurements were taken by auscultation using a Hawksley random-zero sphygmomanometer and an appropriate size cuff according to American Heart Association (AHA) guidelines.10 Casual BP was the average of these 12 measurements. Body composition was measured by underwater weighing using a stainless steel tank, an electronic load cell, and customized computer software.8 To be included in the study, subjects had to have casual BP averaging 140 to 179/90 to 109 mm Hg, percent body fat ⬎25%, and a maximal treadmill exercise test terminated by subjective exhaustion with no CV signs, symptoms, or decompensation,11 and ⬍0.2 mV ST-segment depression. This population is especially appropriate for this study because of the high prevalence of hypertension in middle-aged and older obese sedentary men.1 Qualified subjects then underwent a second maximal treadmill exercise test to assess their maximal oxygen consumption (VO2max) using a standardized protocol.8 Exercise was terminated when the subject was unable to continue. VO2 was measured continuously during this test. Standard criteria were used to ensure that a true VO2max was achieved.12 After this test, subjects underwent 6 to 8 weeks of instruction in the principles of the American Heart Association Step I diet, which they then maintained for the remainder of the study to eliminate any dietary effects on BP. Adherence to this diet was assessed by frequent dietary records. Ambulatory BP was recorded on two separate days with a SpaceLabs model 90207 Ambulatory BP Monitor (Redmond, WA). The two recordings were separated by ⱖ5 days but were made within a 2-week time span. One recording was immediately preceded by acute exercise (exercise day), whereas the second recording was not preceded by exercise (control day). The two trials were administered in random order. All recordings were started on a weekday other than Friday. The control day recording started at the same time as the recording on the experimental day and all recordings began between 8 and 9 am. The BP data from the monitor were reviewed before each recording to ensure they read within ⫾3 mm Hg of simultaneously measured sphygmomanometer values and to ensure they were within the range of the subject’s casual BP values during the 4 weeks of screening. BP measurements during the ambulatory recordings
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were made every 15 min for the first 4 h, every 20 min from hour 4 until the hour of sleep, every 30 min during the subject’s normal sleeping hours, and every 20 min from the time of awakening to the end of the recording. Subjects were instructed to pause momentarily at the time of each measurement and relax their arm while maintaining their body position. They also recorded their activity at the time of each BP measurement and were given a copy of this log and asked to repeat their activities on the second recording day. Subjects were instructed not to exercise outside of the laboratory before or during the ambulatory BP recordings. Data from the ambulatory monitors were transferred to a laboratory computer and analyzed using the SpaceLabs analysis software package. The analysis software automatically edited values outside of normal physiologic ranges (systolic BP ⬎260, ⬍70 mm Hg; diastolic BP ⬎150, ⬍40 mm Hg; pulse pressure ⬎150, ⬍20 mm Hg; heart rate ⬎200, ⬍20 beats/min). Spurious readings due to factors such as movement artifact were also automatically edited by the software. In addition, BP readings that were different by ⬎15 mm Hg from any other BP within 1 h and that could not be explained by changes in physical activity noted in the log were manually edited. On the control day 62 ⫾ 2 BP values (mean ⫾ SE), or 85 ⫾ 4% of the total possible, were included in the final analyses. On experimental day 61 ⫾ 2 BP values, or 83 ⫾ 4% of the total possible, met the inclusion criteria and were included in the final analysis. The software system calculated hourly averages based on the edited data set, and subsequently averaged them to determine 24 h, day (6 am to 6 pm) and night (6 pm to 6 am) average values. These hourly BP values were also averaged for six 4-h periods across the 24-h recording. Systolic and diastolic BP load were calculated as the percentage of readings that were ⬎140 and ⬎90 mm Hg, respectively.13,14 Peak systolic and diastolic BP, defined as the highest value for that BP, were determined for the entire 24 h and for the day and night portions of the two recordings. Acute Exercise Session The acute exercise session consisted of three 15-min bouts of treadmill exercise at a speed and grade that elicited ⬃70% VO2max. These bouts of exercise were separated by 4 min of seated recovery. This exercise protocol was selected as it is representative of what might be prescribed to older obese hypertensive individuals enrolling in a supervised exercise program. Each subject’s VO2 was measured during the last 3 min of each exercise bout with the system used during the VO2max test. One subject was excluded from final data analyses because his intensity was 88% VO2max during the acute exercise session, whereas the intensity for the remaining sub-
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TABLE 1. SUBJECT CHARACTERISTICS Variable
Mean ⴞ SE
Range
60 ⫾ 2 153 ⫾ 2 96 ⫾ 2 92.9 ⫾ 4.4 174 ⫾ 2 32 ⫾ 1 27 ⫾ 1
49–67 142–165 90–109 75–115 164–182 26–40 22–34
Age (yr) Casual systolic BP (mm Hg) Casual diastolic BP (mm Hg) Body weight (kg) Height (cm) Body fat (%) VO2max (mL/kg/min)
Casual BP values are the average of 4 weeks of weekly screening values.
jects averaged 71% VO2max. Heart rate, BP, and rating of perceived exertion (RPE)15 were also determined at the end of each exercise bout. The ambulatory BP recording after this session started within 30 min of the end of the exercise. In an attempt to obtain preliminary data addressing whether common genetic polymorphisms affect the 24-h ambulatory BP responses after acute exercise, subjects had their DNA isolated and typed for genetic variations at the angiotensinogen (AGT),16 lipoprotein lipase (LPL),17 and angiotensin converting enzyme (ACE)18 loci. Statistics All data are expressed as mean ⫾ SE. The primary statistical comparisons were performed using planned comparisons within a repeated measures ANOVA framework of the six 4-h average periods between the exercise and control day. Secondary analyses were performed using paired t tests for the remaining BP outcome variables (24-h, day, and night average BP values; percent BP load; 24-h day, and night peak BP values) on the exercise and control day BP recordings. P ⬍ .05 was accepted as statistically significant. RESULTS The 11 subjects in this study were middle-aged to older men with stage 1 or 2 essential hypertension9 (Table 1). They were obese as evidenced by their body weight and percent body fat, and were sedentary as evidenced by their VO2max values. Their VO2 during the acute bout of exercise was 19 ⫾ 1 mL/kg/min (range, 15 to 23 mL/kg/min), which was equivalent to 71 ⫾ 1% of their VO2max (range, 67 to 77% VO2max). Their heart rate during exercise was 129 ⫾ 7 beats/ min (range, 111 to 157 beats/min) and they rated their perceived exertion during the exercise between fairly light and somewhat hard on the RPE scale (12 ⫾ 1 units; range, 10 to 14 units). Their systolic and diastolic BP during exercise averaged 173 ⫾ 4 mm Hg (range, 147 to 186 mm Hg) and 92 ⫾ 2 mm Hg (range, 82 to 103 mm Hg), respectively. The initial sphygmomanometer BP did not differ between the control and
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FIGURE 1. Systolic BP for the 24-h ambulatory BP recording preceded by and not preceded by 45 min of acute aerobic exercise at 70% VO2max. Values are expressed as mean ⫾ SE. *P ⬍ .05 for the difference between the two recordings.
FIGURE 2. Diastolic BP for the 24-h ambulatory BP recording preceded by and not preceded by 45 min of acute aerobic exercise at 70% VO2max. Values are expressed as mean ⫾ SE. *P ⬍ .05 for the difference between the two recordings.
exercise days and neither the control nor the exercise day values differed significantly from the 4-week average screening casual BP values. Systolic BP was significantly lower for the first four of the 4-h periods on the exercise compared to the control day (Figure 1) with the differences ranging from 6 to 13 mm Hg. As a result of these systolic BP differences, 24-h average systolic BP was significantly lower on the exercise day (Table 2). Average systolic BP was also significantly lower during both the day and night portions of the BP recording on the exercise day (Table 2). There was a trend for peak systolic BP to be lower during the entire 24 h (⫺6 ⫾ 4 mm Hg, P ⬍ .08) and the day portion (⫺6 ⫾ 4 mm Hg, P ⬍ .08) of the exercise day recording; peak systolic BP was significantly lower during the night after exercise (⫺9 ⫾ 3 mm Hg, P ⬍ .01). The systolic BP load (percent of systolic BP readings ⬎140 mm Hg) was reduced substantially during the entire 24 h and the day portion of the exercise day (⫺17 ⫾ 5% and ⫺26 ⫾ 6%, respectively; both P ⬍ .01). Systolic BP load during the night also tended to lower on the exercise day (⫺8 ⫾ 5%, P ⬍ .08).
Diastolic BP was significantly lower for three of the first 4-h periods on the exercise compared to the control day (hours 0 to 4, 5 to 8, and 13 to 16; Figure 2) with the differences amounting to ⬃5 mm Hg. Average diastolic BP for the entire 24-h recording, and for the day and night portions of the recording were also significantly lower on the exercise than on the control day (Table 2). Peak diastolic BP was lower over the entire 24-h recording period (⫺6 ⫾ 3 mm Hg, P ⬍ .05) and tended to be lower during the day portion of the exercise day (⫺5 ⫾ 3 mm Hg, P ⬍ .08). Diastolic BP load (percent of diastolic BP readings ⬎90 mm Hg) was lower during the entire 24-h (⫺11 ⫾ 4%, P ⬍ .05) and the day portion (⫺15 ⫾ 6%, P ⬍ .05) of the exercise compared to the control day. Mean arterial BP was also significantly lower for the first four of the 4-h periods on the exercise compared to the control day (Figure 3), with the reductions ranging from 4 to 8 mm Hg. Average mean arterial BP for the entire 24-h recording and for the day and night portions of the recordings were significantly lower on the exercise compared to the control day (Table 2). AGT TT genotype individuals (n ⫽ 3) decreased
TABLE 2. AVERAGE BP DIFFERENCES BETWEEN THE CONTROL AND EXERCISE DAY AMBULATORY BP RECORDINGS FOR THE ENTIRE 24 H AND FOR THE DAY AND NIGHT PORTIONS
Systolic BP (mm Hg) Diastolic BP (mm Hg) Mean arterial BP (mm Hg) Heart rate (beats/min)
24 h
Day
Night
⫺7.4 ⫾ 1.8* ⫺3.6 ⫾ 1.3* ⫺4.8 ⫾ 1.4* 4.8 ⫾ 0.8*
⫺9.0 ⫾ 2.6* ⫺3.9 ⫾ 1.8† ⫺5.6 ⫾ 2.0* 6.1 ⫾ 1.8*
⫺6.4 ⫾ 1.9* ⫺3.5 ⫾ 1.4† ⫺4.6 ⫾ 1.3* 0.2 ⫾ 1.7
* P ⬍ .01, † P ⬍ .05 for the difference between the control and exercise days. A negative value indicates a value lower and a positive value indicates a higher value on the recording after exercise. The day values are the averages from 6 am to 6 pm; the night values are the averages from 6 pm to 6 am.
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FIGURE 3. Mean arterial BP for the 24-h ambulatory BP recording preceded by and not preceded by 45 min of acute aerobic exercise at 70% VO2max. Values are expressed as mean ⫾ SE. *P ⬍ .05 for the difference between the two recordings.
24-h systolic (⫺16 ⫾ 3 v ⫺5 ⫾ 2 mm Hg, P ⫽ .02), diastolic (⫺9 ⫾ 1 v ⫺3 ⫾ 2 mm Hg, P ⫽ .04), and mean BP (⫺11 ⫾ 1 v ⫺4 ⫾ 2 mm Hg, P ⫽ .02) more
FIGURE 4. Individual changes in 24-h systolic, diastolic, and mean BP in the subjects as a function of angiotensinogen (AGT) and lipoprotein lipase (LPL) PvuII genotype. Values are expressed as changes from the control day to the day after exercise. Thus, a negative value indicates a lower BP on the experimental compared to the control day.
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FIGURE 5. Heart rate for the 24-h ambulatory BP recording preceded by and not preceded by 45 min of acute aerobic exercise at 70% VO2max. Values are expressed as mean ⫾ SE. *P ⬍ .05 for the difference between the two recordings.
than AGT MT genotype individuals (n ⫽ 4) (Figure 4). These differences were also evident during the day and night. LPL HindIII ⫹/⫺ genotype individuals (n ⫽ 2) tended to reduce 24-h systolic, diastolic, and mean BP more than ⫹/⫹ genotype carriers (n ⫽ 6) (P ⫽ NS). However, LPL HindIII ⫹/⫺ carriers reduced night systolic (⫺16 ⫾ 5 v ⫺6 ⫾ 2 mm Hg, P ⫽ .04), diastolic (⫺8 ⫾ 2 v ⫺4 ⫾ 1 mm Hg, P ⫽ .06), and mean BP (⫺11 ⫾ 2 v ⫺4 ⫾ 2 mm Hg, P ⫽ .04) more than LPL HindIII ⫹/⫹ carriers. The day BP responses of these genotype groups were only minimally different. LPL PvuII ⫺/⫺ or ⫹/⫺ genotype individuals (n ⫽ 6) tended to decrease 24-h systolic, diastolic, and mean BP more than LPL PvuII ⫹/⫹ genotype carriers (n ⫽ 2) (P ⫽ .10 to .19) (Figure 4). These genotype groups were only slightly different during the day. However, LPL PvuII ⫺/⫺ and ⫹/⫺ individuals tended to reduce night systolic, diastolic, and mean BP more than LPL PvuII ⫹/⫹ and carriers (all P ⫽ .07 to .15). ACE homozygotes (II and DD, n ⫽ 6) tended to reduce day systolic, diastolic, and mean BP more than ACE heterozygotes (n ⫽ 2) (all P ⫽ .07 to .19). However, ACE homozygotes had somewhat higher values during the night and the 24-h BP values were similar in the different ACE genotype groups. Heart rate on the exercise day was significantly higher, by 6 to 14 beats/min, for the first two of the 4-h periods compared to the control day (Figure 5). Heart rate during the remaining 16 h was similar on the exercise and control days. DISCUSSION The primary finding of this study is that a single acute bout of aerobic exercise, similar to what might be prescribed in the cardiac rehabilitation program,11,19
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reduced systolic, diastolic, and mean arterial BP in sedentary, obese middle-aged to older hypertensive men for a substantial portion of the subsequent 24 h compared to a control day when no previous exercise was performed. Systolic BP remained lower for 16 h after exercise and diastolic BP was lower for 12 of the first 16 h after exercise, although the reductions were smaller than those for systolic BP. These differences resulted in 24-h, day, and night average systolic and diastolic BP being lower on the day after exercise. In addition, the BP load (ie, the percentage of systolic and diastolic BP readings that were ⬎140 and ⬎90 mm Hg, respectively) and the peak systolic and diastolic BP values were also lower during the 24 h after the exercise session compared to the recording not preceded by exercise. The changes in all of these indices indicate a decreased CV load during substantial portions of the 24 h after a single bout of exercise in these men. Most previous studies that assessed the effect of acute exercise on the BP of hypertensives after exercise were conducted in well-controlled laboratory settings. These studies initially showed 30 to 40 mm Hg reductions in systolic and 15 to 20 mm Hg reductions in diastolic BP after 30 to 45 min of submaximal exercise in hypertensive individuals.20 –22 However, later studies designed to account for habituation effects on BP found that although systolic BP remained lower after acute exercise, the reductions in diastolic BP were less substantial and less consistent.3,4,23–26 Previously, we found that 45 min of exercise at 50% VO2max reduced systolic BP by 8 to 12 mm Hg for the 1-h recovery period during which subjects were studied.3 In our previous study, 45 min of exercise at 70% VO2max resulted in 12 to 20 mm Hg reductions in systolic BP for 2 h with less substantial reductions evident during the third hour of recovery.3 Diastolic BP was inconsistently and only minimally reduced after both of these exercise bouts. Kaufman et al4 and Cleroux et al23 reported generally similar findings after exercise at ⬃50% VO2max in hypertensives. Hannum and Kasch24 also reported similar findings in hypertensives after exercise at 60% VO2max. Three previous studies have assessed BP for prolonged periods after a single bout of exercise.5–7 Pescatello and co-workers5 monitored the BP of 6 individuals with high-normal BP for 13 h after exercise. They reported that systolic BP was reduced by 5 mm Hg for 8.7 h and that diastolic and mean arterial BP were reduced by 8 and 7 mm Hg, respectively, for 12.7 h after exercise. However, it is unclear whether these comparisons were made to BP values measured immediately before exercise or to ambulatory BP values on a day not preceded by exercise. They also reported that exercise at 40% and 70% VO2max did not affect recovery BP responses and data from both exercise intensities were combined in their final data
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analyses. The present data, where BP values after exercise were compared to a recording made on a day not preceded by exercise, are generally consistent with the findings of Pescatello and co-workers. However, the present results extend these findings to individuals with stage 1 and 2 hypertension. The results also indicate that the effect for systolic, diastolic, and mean arterial BP is substantial enough to result in statistically and clinically significant reductions in the 24-h average BP values. In another study that monitored BP after exercise, Somers and co-workers7 reported that BP reductions were not sustained in hypertensives who measured their own BP at home for 8 to 12 h after a bout of maximal exercise. A key issue relative to their results may be the intensity of the exercise as maximal exercise clearly results in markedly different hemodynamic, hormonal, and neural responses than submaximal exercise. Thus, it is not particularly surprising that the BP responses of hypertensives may differ after submaximal and maximal exercise. In fact, one subject in our study who exercised at a substantially higher intensity than the 11 other individuals (88% v 71% VO2max), and was excluded from final data analyses, experienced no reductions in BP during his ambulatory recording on the day after exercise compared to the control day. Thus, it is possible that the lack of a sustained reduction in BP in the study by Somers and co-workers7 may be a function of the exercise intensity and the data cannot be used as evidence of a lack of sustained reduction in BP after acute submaximal exercise in hypertensive individuals. Rueckert et al6 also found no sustained reductions in ambulatory BP after acute exercise in hypertensive men and women. They used an acute exercise session that was virtually identical to that in the present study (ie, 45 min of exercise at ⬃70% of heart rate reserve). It is unclear why the present results differ from those of Rueckert et al6 except for the fact that their subjects were kept in a semirecumbent position for 70 min of the first 2 h after exercise. Perhaps the resultant altered orthostatic forces may have affected the hemodynamics in such a way that the sustained BP reductions were not evident. These reductions in BP for 24 h after a single bout of exercise compare favorably to the ⬃10 mm Hg average reductions in both systolic and diastolic BP that have been reported to occur with endurance exercise training programs.2 The BP-lowering effect of acute aerobic exercise is not present in the final 8 h of the 24-h ambulatory recording, which is the time when most casual BP determinations have been made in previous exercise training studies in hypertensives with respect to their last previous bout of exercise. Thus, unless the BP-lowering effect after acute exercise is prolonged substantially as a result of endurance
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exercise training, which is not known, it is unlikely that this response contributes substantially to the reductions in casual BP observed with prolonged exercise training. In the present study, we did not measure casual BP on the morning after exercise to determine whether casual BP was still reduced at this time. On the other hand, if this response is evident in trained persons that remain hypertensive, the BP-lowering effect of acute exercise would be superimposed on their casual BP reduction elicited with their training program. The potential additive effect of these two responses would lower their CV disease risk to an even greater extent than that resulting from their reduced casual BP observed the next morning. On a practical level, another important effect of these results is that they can provide immediate positive feedback for hypertensive patients concerning the potential benefits of exercise. Although such information may be important for optimizing patient adherence, it is not known whether the BP-lowering response after acute aerobic exercise is in any way predictive of the BP-lowering response associated with long-term endurance exercise training. The duration of exercise that results in the BP-lowering response after exercise is also unknown. If the same responses found in this study were evident after only 10 min of exercise, a hypertensive person could go for a vigorous 10-min walk at breakfast, lunch, and dinner and they would experience significant reductions in BP for nearly every hour of the day. We also sought to derive some very preliminary data as to whether common genetic polymorphisms might identify hypertensives who had the greatest reductions in BP after acute exercise. Although these results must be viewed with some caution because of the small sample size, they provide evidence consistent with the possibility that common genetic polymorphisms at critical loci involved in systems that affect BP, including the renin-angiotensin system and the insulin resistance syndrome, may identify hypertensives most likely to reduce their 24-h ambulatory BP after an acute bout of submaximal exercise. In conclusion, these results indicate that systolic, diastolic, and mean arterial BP are reduced for up to 12 to 16 h after a single submaximal exercise session in hypertensive patients. These reductions in BP were consistent and substantial enough to result in significant reductions in 24 h average systolic, diastolic, and mean arterial BP values after this acute bout of aerobic exercise. These BP changes result in a reduced CV load for a prolonged period after acute exercise in older, obese, sedentary, hypertensive men. Furthermore, it appears that some common polymorphic genetic variations may affect these responses.
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Somers VK, Conway J, Johnston J, Sleight P: Effects of endurance exercise training on baroreflex sensitivity and blood pressure in borderline hypertension. Lancet 1991;337:1363–1368.
26.
Somers VK, Conway J, LeWinter M, Sleight P: Role of baroreflex sensitivity in post-exercise hypotension. J Hypertension 1985;3(suppl 3):S129 –S130.
American College of Sports Medicine Position Stand: The recommended quantity and quality of exercise for developing and maintaining cardiorespiratory and muscular fitness in healthy adults. Med Sci Sports Exercise 1990;22:265–274.
Wilcox RG, Bennett T, Brown AM, MacDonald IA: Is
2000;13:44 –51
Ambulatory Blood Pressure After Acute Exercise in Older Men With Essential Hypertension Nadine S. Taylor-Tolbert, Donald R. Dengel, Michael D. Brown, Steve D. McCole, Richard E. Pratley, Robert E. Ferrell, and James M. Hagberg We sought to determine whether reductions in blood pressure in hypertensives after acute exercise persist for more than the 2 to 3 h found in controlled laboratory settings. Subjects (n ⴝ 11) were obese (32 ⴞ 4% body fat), sedentary (VO2max 27 ⴞ 4 mL/kg/min) 60 ⴞ 6-year-old men with stage 1 or 2 essential hypertension. Ambulatory blood pressure was recorded on 1 day preceded by 45 min of 70% VO2max treadmill exercise and on another day not preceded by exercise. Systolic blood pressure was lower by 6 to 13 mm Hg for the first 16 h after exercise (P < .05) compared to the day without prior exercise. Twenty-four-hour, day, and night average systolic blood pressures were significantly lower on the day after exercise. There was a trend for peak systolic blood pressure to be lower during the entire 24 h and the day portion of the recording; peak systolic blood pressure was significantly lower during the night portion of the recording after exercise. Systolic blood pressure load (percent of systolic blood pressure readings >140 mm Hg) was reduced during the entire 24 h and the day portion of the recording after exercise. Diastolic blood pressure was lower for 12 of the first 16 h after acute
exercise (hours 0 to 4, 5 to 8, 13 to 16) (P < .05) compared to the day without prior exercise. Twenty-four-hour, day, and night average diastolic blood pressure was also significantly lower on the recording after exercise. Peak diastolic blood pressure was lower over the entire 24-h period. Diastolic blood pressure load (percent of diastolic blood pressure readings >90 mm Hg) was lower during the entire 24 h and the day portion of the day after exercise. Preliminary data also suggest that common genetic polymorphisms at the angiotensinogen, lipoprotein lipase, and angiotensin converting enzyme loci may affect the blood pressure-lowering response after acute exercise. Thus, in sedentary, obese hypertensive men a single aerobic exercise session reduced blood pressure enough to result in significantly lower 24-h average systolic, diastolic, and mean arterial blood pressure. This could result in a reduced cardiovascular load during the 24 h after acute exercise in older hypertensive men. Am J Hypertens 2000;13:44 –51 © 2000 American Journal of Hypertension, Ltd.
Received July 14, 1998. Accepted May 5, 1999. From the Center on Aging and Department of Kinesiology, University of Maryland, College Park (NST-T, MDB, SDM, JMH); GRECC and Division of Geriatrics, Baltimore VA Medical Center, Baltimore, Maryland (DRD, REP); and Department of Human Genetics, University of Pittsburgh Graduate School of Public Health, Pittsburgh, Pennsylvania (REF). This research was supported by a grant to JMH from the Maryland Affiliate of the American Heart Association. DRD was sup-
ported by NIA NRSA F32 AG05555, MDB was a Predoctoral Fellow supported by NIA grant R03 AG12781, and REP was supported by NIA Grant AG00494. This work was also supported by research funds provided by the University of Maryland-College Park DRIF fund. REF was supported by NIH grants HL39107 and HL45778. Address correspondence and reprint requests to Dr. James Hagberg, Department of Kinesiology, University of Maryland, College Park, MD 20742-2611; e-mail: [email protected]
© 2000 by the American Journal of Hypertension, Ltd. Published by Elsevier Science, Inc.
KEY WORDS:
blood pressure load, genetic markers
0895-7061/00/$20.00 PII S0895-7061(99)00141-7
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E
levated blood pressure (BP) is a risk factor for cardiovascular (CV) disease and has deleterious effects on such target organs as the heart and kidney.1 The overwhelming majority of hypertensives have stage 1 or 2 hypertension (blood pressure, 140 to 179/90 to 109 mm Hg) and pharmacologic therapy in these individuals has generally not resulted in substantial reductions in CV disease mortality and morbidity. Furthermore, aggressive pharmacologic therapy in these individuals is often associated with negative side effects. These facts led the Joint National Committee on the Detection, Evaluation, and Treatment of High Blood Pressure Report V to recommend exercise training as one initial nonpharmacologic means of controlling BP in persons with stage 1 or 2 hypertension. Long-term exercise training lowers BP in a majority of individuals with essential hypertension.2 We and other investigators have also reported that in sedentary hypertensive individuals acute aerobic exercise transiently reduces BP for up to 3 h in controlled laboratory settings.3– 6 This response could be of even greater clinical significance if such BP reductions persisted longer than the 3 h observed in laboratory studies. However, the studies that have assessed the effect of acute exercise on the ambulatory BP of hypertensive persons have reported inconsistent results, with Pescatello et al5 reporting BP reductions for up to 12 h after exercise and Rueckert et al6 and Somers et al7 reporting no BP reductions after acute exercise. Thus, we sought to determine whether BP reductions after acute exercise persist for more than the 3 h observed in controlled laboratory settings. Each subject underwent two 24-h ambulatory BP recordings, one preceded and a second not preceded by aerobic exercise, so that the effect of aerobic exercise could be ascertained independent of diurnal variations in BP. We hypothesized that BP reductions would be evident for a number of hours, for the daytime and nighttime hours, and for the entire 24-h period after a single bout of submaximal endurance exercise. METHODS Subjects were initially screened by telephone to exclude smokers and those who were physically active or had overt CV diseases that would inhibit their ability to exercise. They then underwent a physical and CV examination and a screening blood chemistry to ensure they had essential hypertension. Subjects with diabetes were excluded using fasting blood glucose levels and oral glucose tolerance tests. Those taking antihypertensive medications suspended their use with the approval of their private physician and were medication free for ⱖ1 week before testing and ⱖ6 weeks before ambulatory BP monitoring sessions. Subjects provided their written consent to participate
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after the study and its risks had been described to them. The study was approved by the Institutional Review Boards of the University of Maryland-College Park and the University of Maryland at Baltimore. Subjects completed a maximal treadmill exercise test8 to exclude those with evidence of CV disease. Subjects also underwent 4 consecutive weeks of weekly casual BP measurements to ensure they had stage 1 or 2 hypertension.9 After 20 min of quiet seated rest, three BP measurements were taken by auscultation using a Hawksley random-zero sphygmomanometer and an appropriate size cuff according to American Heart Association (AHA) guidelines.10 Casual BP was the average of these 12 measurements. Body composition was measured by underwater weighing using a stainless steel tank, an electronic load cell, and customized computer software.8 To be included in the study, subjects had to have casual BP averaging 140 to 179/90 to 109 mm Hg, percent body fat ⬎25%, and a maximal treadmill exercise test terminated by subjective exhaustion with no CV signs, symptoms, or decompensation,11 and ⬍0.2 mV ST-segment depression. This population is especially appropriate for this study because of the high prevalence of hypertension in middle-aged and older obese sedentary men.1 Qualified subjects then underwent a second maximal treadmill exercise test to assess their maximal oxygen consumption (VO2max) using a standardized protocol.8 Exercise was terminated when the subject was unable to continue. VO2 was measured continuously during this test. Standard criteria were used to ensure that a true VO2max was achieved.12 After this test, subjects underwent 6 to 8 weeks of instruction in the principles of the American Heart Association Step I diet, which they then maintained for the remainder of the study to eliminate any dietary effects on BP. Adherence to this diet was assessed by frequent dietary records. Ambulatory BP was recorded on two separate days with a SpaceLabs model 90207 Ambulatory BP Monitor (Redmond, WA). The two recordings were separated by ⱖ5 days but were made within a 2-week time span. One recording was immediately preceded by acute exercise (exercise day), whereas the second recording was not preceded by exercise (control day). The two trials were administered in random order. All recordings were started on a weekday other than Friday. The control day recording started at the same time as the recording on the experimental day and all recordings began between 8 and 9 am. The BP data from the monitor were reviewed before each recording to ensure they read within ⫾3 mm Hg of simultaneously measured sphygmomanometer values and to ensure they were within the range of the subject’s casual BP values during the 4 weeks of screening. BP measurements during the ambulatory recordings
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were made every 15 min for the first 4 h, every 20 min from hour 4 until the hour of sleep, every 30 min during the subject’s normal sleeping hours, and every 20 min from the time of awakening to the end of the recording. Subjects were instructed to pause momentarily at the time of each measurement and relax their arm while maintaining their body position. They also recorded their activity at the time of each BP measurement and were given a copy of this log and asked to repeat their activities on the second recording day. Subjects were instructed not to exercise outside of the laboratory before or during the ambulatory BP recordings. Data from the ambulatory monitors were transferred to a laboratory computer and analyzed using the SpaceLabs analysis software package. The analysis software automatically edited values outside of normal physiologic ranges (systolic BP ⬎260, ⬍70 mm Hg; diastolic BP ⬎150, ⬍40 mm Hg; pulse pressure ⬎150, ⬍20 mm Hg; heart rate ⬎200, ⬍20 beats/min). Spurious readings due to factors such as movement artifact were also automatically edited by the software. In addition, BP readings that were different by ⬎15 mm Hg from any other BP within 1 h and that could not be explained by changes in physical activity noted in the log were manually edited. On the control day 62 ⫾ 2 BP values (mean ⫾ SE), or 85 ⫾ 4% of the total possible, were included in the final analyses. On experimental day 61 ⫾ 2 BP values, or 83 ⫾ 4% of the total possible, met the inclusion criteria and were included in the final analysis. The software system calculated hourly averages based on the edited data set, and subsequently averaged them to determine 24 h, day (6 am to 6 pm) and night (6 pm to 6 am) average values. These hourly BP values were also averaged for six 4-h periods across the 24-h recording. Systolic and diastolic BP load were calculated as the percentage of readings that were ⬎140 and ⬎90 mm Hg, respectively.13,14 Peak systolic and diastolic BP, defined as the highest value for that BP, were determined for the entire 24 h and for the day and night portions of the two recordings. Acute Exercise Session The acute exercise session consisted of three 15-min bouts of treadmill exercise at a speed and grade that elicited ⬃70% VO2max. These bouts of exercise were separated by 4 min of seated recovery. This exercise protocol was selected as it is representative of what might be prescribed to older obese hypertensive individuals enrolling in a supervised exercise program. Each subject’s VO2 was measured during the last 3 min of each exercise bout with the system used during the VO2max test. One subject was excluded from final data analyses because his intensity was 88% VO2max during the acute exercise session, whereas the intensity for the remaining sub-
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TABLE 1. SUBJECT CHARACTERISTICS Variable
Mean ⴞ SE
Range
60 ⫾ 2 153 ⫾ 2 96 ⫾ 2 92.9 ⫾ 4.4 174 ⫾ 2 32 ⫾ 1 27 ⫾ 1
49–67 142–165 90–109 75–115 164–182 26–40 22–34
Age (yr) Casual systolic BP (mm Hg) Casual diastolic BP (mm Hg) Body weight (kg) Height (cm) Body fat (%) VO2max (mL/kg/min)
Casual BP values are the average of 4 weeks of weekly screening values.
jects averaged 71% VO2max. Heart rate, BP, and rating of perceived exertion (RPE)15 were also determined at the end of each exercise bout. The ambulatory BP recording after this session started within 30 min of the end of the exercise. In an attempt to obtain preliminary data addressing whether common genetic polymorphisms affect the 24-h ambulatory BP responses after acute exercise, subjects had their DNA isolated and typed for genetic variations at the angiotensinogen (AGT),16 lipoprotein lipase (LPL),17 and angiotensin converting enzyme (ACE)18 loci. Statistics All data are expressed as mean ⫾ SE. The primary statistical comparisons were performed using planned comparisons within a repeated measures ANOVA framework of the six 4-h average periods between the exercise and control day. Secondary analyses were performed using paired t tests for the remaining BP outcome variables (24-h, day, and night average BP values; percent BP load; 24-h day, and night peak BP values) on the exercise and control day BP recordings. P ⬍ .05 was accepted as statistically significant. RESULTS The 11 subjects in this study were middle-aged to older men with stage 1 or 2 essential hypertension9 (Table 1). They were obese as evidenced by their body weight and percent body fat, and were sedentary as evidenced by their VO2max values. Their VO2 during the acute bout of exercise was 19 ⫾ 1 mL/kg/min (range, 15 to 23 mL/kg/min), which was equivalent to 71 ⫾ 1% of their VO2max (range, 67 to 77% VO2max). Their heart rate during exercise was 129 ⫾ 7 beats/ min (range, 111 to 157 beats/min) and they rated their perceived exertion during the exercise between fairly light and somewhat hard on the RPE scale (12 ⫾ 1 units; range, 10 to 14 units). Their systolic and diastolic BP during exercise averaged 173 ⫾ 4 mm Hg (range, 147 to 186 mm Hg) and 92 ⫾ 2 mm Hg (range, 82 to 103 mm Hg), respectively. The initial sphygmomanometer BP did not differ between the control and
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FIGURE 1. Systolic BP for the 24-h ambulatory BP recording preceded by and not preceded by 45 min of acute aerobic exercise at 70% VO2max. Values are expressed as mean ⫾ SE. *P ⬍ .05 for the difference between the two recordings.
FIGURE 2. Diastolic BP for the 24-h ambulatory BP recording preceded by and not preceded by 45 min of acute aerobic exercise at 70% VO2max. Values are expressed as mean ⫾ SE. *P ⬍ .05 for the difference between the two recordings.
exercise days and neither the control nor the exercise day values differed significantly from the 4-week average screening casual BP values. Systolic BP was significantly lower for the first four of the 4-h periods on the exercise compared to the control day (Figure 1) with the differences ranging from 6 to 13 mm Hg. As a result of these systolic BP differences, 24-h average systolic BP was significantly lower on the exercise day (Table 2). Average systolic BP was also significantly lower during both the day and night portions of the BP recording on the exercise day (Table 2). There was a trend for peak systolic BP to be lower during the entire 24 h (⫺6 ⫾ 4 mm Hg, P ⬍ .08) and the day portion (⫺6 ⫾ 4 mm Hg, P ⬍ .08) of the exercise day recording; peak systolic BP was significantly lower during the night after exercise (⫺9 ⫾ 3 mm Hg, P ⬍ .01). The systolic BP load (percent of systolic BP readings ⬎140 mm Hg) was reduced substantially during the entire 24 h and the day portion of the exercise day (⫺17 ⫾ 5% and ⫺26 ⫾ 6%, respectively; both P ⬍ .01). Systolic BP load during the night also tended to lower on the exercise day (⫺8 ⫾ 5%, P ⬍ .08).
Diastolic BP was significantly lower for three of the first 4-h periods on the exercise compared to the control day (hours 0 to 4, 5 to 8, and 13 to 16; Figure 2) with the differences amounting to ⬃5 mm Hg. Average diastolic BP for the entire 24-h recording, and for the day and night portions of the recording were also significantly lower on the exercise than on the control day (Table 2). Peak diastolic BP was lower over the entire 24-h recording period (⫺6 ⫾ 3 mm Hg, P ⬍ .05) and tended to be lower during the day portion of the exercise day (⫺5 ⫾ 3 mm Hg, P ⬍ .08). Diastolic BP load (percent of diastolic BP readings ⬎90 mm Hg) was lower during the entire 24-h (⫺11 ⫾ 4%, P ⬍ .05) and the day portion (⫺15 ⫾ 6%, P ⬍ .05) of the exercise compared to the control day. Mean arterial BP was also significantly lower for the first four of the 4-h periods on the exercise compared to the control day (Figure 3), with the reductions ranging from 4 to 8 mm Hg. Average mean arterial BP for the entire 24-h recording and for the day and night portions of the recordings were significantly lower on the exercise compared to the control day (Table 2). AGT TT genotype individuals (n ⫽ 3) decreased
TABLE 2. AVERAGE BP DIFFERENCES BETWEEN THE CONTROL AND EXERCISE DAY AMBULATORY BP RECORDINGS FOR THE ENTIRE 24 H AND FOR THE DAY AND NIGHT PORTIONS
Systolic BP (mm Hg) Diastolic BP (mm Hg) Mean arterial BP (mm Hg) Heart rate (beats/min)
24 h
Day
Night
⫺7.4 ⫾ 1.8* ⫺3.6 ⫾ 1.3* ⫺4.8 ⫾ 1.4* 4.8 ⫾ 0.8*
⫺9.0 ⫾ 2.6* ⫺3.9 ⫾ 1.8† ⫺5.6 ⫾ 2.0* 6.1 ⫾ 1.8*
⫺6.4 ⫾ 1.9* ⫺3.5 ⫾ 1.4† ⫺4.6 ⫾ 1.3* 0.2 ⫾ 1.7
* P ⬍ .01, † P ⬍ .05 for the difference between the control and exercise days. A negative value indicates a value lower and a positive value indicates a higher value on the recording after exercise. The day values are the averages from 6 am to 6 pm; the night values are the averages from 6 pm to 6 am.
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FIGURE 3. Mean arterial BP for the 24-h ambulatory BP recording preceded by and not preceded by 45 min of acute aerobic exercise at 70% VO2max. Values are expressed as mean ⫾ SE. *P ⬍ .05 for the difference between the two recordings.
24-h systolic (⫺16 ⫾ 3 v ⫺5 ⫾ 2 mm Hg, P ⫽ .02), diastolic (⫺9 ⫾ 1 v ⫺3 ⫾ 2 mm Hg, P ⫽ .04), and mean BP (⫺11 ⫾ 1 v ⫺4 ⫾ 2 mm Hg, P ⫽ .02) more
FIGURE 4. Individual changes in 24-h systolic, diastolic, and mean BP in the subjects as a function of angiotensinogen (AGT) and lipoprotein lipase (LPL) PvuII genotype. Values are expressed as changes from the control day to the day after exercise. Thus, a negative value indicates a lower BP on the experimental compared to the control day.
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FIGURE 5. Heart rate for the 24-h ambulatory BP recording preceded by and not preceded by 45 min of acute aerobic exercise at 70% VO2max. Values are expressed as mean ⫾ SE. *P ⬍ .05 for the difference between the two recordings.
than AGT MT genotype individuals (n ⫽ 4) (Figure 4). These differences were also evident during the day and night. LPL HindIII ⫹/⫺ genotype individuals (n ⫽ 2) tended to reduce 24-h systolic, diastolic, and mean BP more than ⫹/⫹ genotype carriers (n ⫽ 6) (P ⫽ NS). However, LPL HindIII ⫹/⫺ carriers reduced night systolic (⫺16 ⫾ 5 v ⫺6 ⫾ 2 mm Hg, P ⫽ .04), diastolic (⫺8 ⫾ 2 v ⫺4 ⫾ 1 mm Hg, P ⫽ .06), and mean BP (⫺11 ⫾ 2 v ⫺4 ⫾ 2 mm Hg, P ⫽ .04) more than LPL HindIII ⫹/⫹ carriers. The day BP responses of these genotype groups were only minimally different. LPL PvuII ⫺/⫺ or ⫹/⫺ genotype individuals (n ⫽ 6) tended to decrease 24-h systolic, diastolic, and mean BP more than LPL PvuII ⫹/⫹ genotype carriers (n ⫽ 2) (P ⫽ .10 to .19) (Figure 4). These genotype groups were only slightly different during the day. However, LPL PvuII ⫺/⫺ and ⫹/⫺ individuals tended to reduce night systolic, diastolic, and mean BP more than LPL PvuII ⫹/⫹ and carriers (all P ⫽ .07 to .15). ACE homozygotes (II and DD, n ⫽ 6) tended to reduce day systolic, diastolic, and mean BP more than ACE heterozygotes (n ⫽ 2) (all P ⫽ .07 to .19). However, ACE homozygotes had somewhat higher values during the night and the 24-h BP values were similar in the different ACE genotype groups. Heart rate on the exercise day was significantly higher, by 6 to 14 beats/min, for the first two of the 4-h periods compared to the control day (Figure 5). Heart rate during the remaining 16 h was similar on the exercise and control days. DISCUSSION The primary finding of this study is that a single acute bout of aerobic exercise, similar to what might be prescribed in the cardiac rehabilitation program,11,19
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reduced systolic, diastolic, and mean arterial BP in sedentary, obese middle-aged to older hypertensive men for a substantial portion of the subsequent 24 h compared to a control day when no previous exercise was performed. Systolic BP remained lower for 16 h after exercise and diastolic BP was lower for 12 of the first 16 h after exercise, although the reductions were smaller than those for systolic BP. These differences resulted in 24-h, day, and night average systolic and diastolic BP being lower on the day after exercise. In addition, the BP load (ie, the percentage of systolic and diastolic BP readings that were ⬎140 and ⬎90 mm Hg, respectively) and the peak systolic and diastolic BP values were also lower during the 24 h after the exercise session compared to the recording not preceded by exercise. The changes in all of these indices indicate a decreased CV load during substantial portions of the 24 h after a single bout of exercise in these men. Most previous studies that assessed the effect of acute exercise on the BP of hypertensives after exercise were conducted in well-controlled laboratory settings. These studies initially showed 30 to 40 mm Hg reductions in systolic and 15 to 20 mm Hg reductions in diastolic BP after 30 to 45 min of submaximal exercise in hypertensive individuals.20 –22 However, later studies designed to account for habituation effects on BP found that although systolic BP remained lower after acute exercise, the reductions in diastolic BP were less substantial and less consistent.3,4,23–26 Previously, we found that 45 min of exercise at 50% VO2max reduced systolic BP by 8 to 12 mm Hg for the 1-h recovery period during which subjects were studied.3 In our previous study, 45 min of exercise at 70% VO2max resulted in 12 to 20 mm Hg reductions in systolic BP for 2 h with less substantial reductions evident during the third hour of recovery.3 Diastolic BP was inconsistently and only minimally reduced after both of these exercise bouts. Kaufman et al4 and Cleroux et al23 reported generally similar findings after exercise at ⬃50% VO2max in hypertensives. Hannum and Kasch24 also reported similar findings in hypertensives after exercise at 60% VO2max. Three previous studies have assessed BP for prolonged periods after a single bout of exercise.5–7 Pescatello and co-workers5 monitored the BP of 6 individuals with high-normal BP for 13 h after exercise. They reported that systolic BP was reduced by 5 mm Hg for 8.7 h and that diastolic and mean arterial BP were reduced by 8 and 7 mm Hg, respectively, for 12.7 h after exercise. However, it is unclear whether these comparisons were made to BP values measured immediately before exercise or to ambulatory BP values on a day not preceded by exercise. They also reported that exercise at 40% and 70% VO2max did not affect recovery BP responses and data from both exercise intensities were combined in their final data
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analyses. The present data, where BP values after exercise were compared to a recording made on a day not preceded by exercise, are generally consistent with the findings of Pescatello and co-workers. However, the present results extend these findings to individuals with stage 1 and 2 hypertension. The results also indicate that the effect for systolic, diastolic, and mean arterial BP is substantial enough to result in statistically and clinically significant reductions in the 24-h average BP values. In another study that monitored BP after exercise, Somers and co-workers7 reported that BP reductions were not sustained in hypertensives who measured their own BP at home for 8 to 12 h after a bout of maximal exercise. A key issue relative to their results may be the intensity of the exercise as maximal exercise clearly results in markedly different hemodynamic, hormonal, and neural responses than submaximal exercise. Thus, it is not particularly surprising that the BP responses of hypertensives may differ after submaximal and maximal exercise. In fact, one subject in our study who exercised at a substantially higher intensity than the 11 other individuals (88% v 71% VO2max), and was excluded from final data analyses, experienced no reductions in BP during his ambulatory recording on the day after exercise compared to the control day. Thus, it is possible that the lack of a sustained reduction in BP in the study by Somers and co-workers7 may be a function of the exercise intensity and the data cannot be used as evidence of a lack of sustained reduction in BP after acute submaximal exercise in hypertensive individuals. Rueckert et al6 also found no sustained reductions in ambulatory BP after acute exercise in hypertensive men and women. They used an acute exercise session that was virtually identical to that in the present study (ie, 45 min of exercise at ⬃70% of heart rate reserve). It is unclear why the present results differ from those of Rueckert et al6 except for the fact that their subjects were kept in a semirecumbent position for 70 min of the first 2 h after exercise. Perhaps the resultant altered orthostatic forces may have affected the hemodynamics in such a way that the sustained BP reductions were not evident. These reductions in BP for 24 h after a single bout of exercise compare favorably to the ⬃10 mm Hg average reductions in both systolic and diastolic BP that have been reported to occur with endurance exercise training programs.2 The BP-lowering effect of acute aerobic exercise is not present in the final 8 h of the 24-h ambulatory recording, which is the time when most casual BP determinations have been made in previous exercise training studies in hypertensives with respect to their last previous bout of exercise. Thus, unless the BP-lowering effect after acute exercise is prolonged substantially as a result of endurance
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exercise training, which is not known, it is unlikely that this response contributes substantially to the reductions in casual BP observed with prolonged exercise training. In the present study, we did not measure casual BP on the morning after exercise to determine whether casual BP was still reduced at this time. On the other hand, if this response is evident in trained persons that remain hypertensive, the BP-lowering effect of acute exercise would be superimposed on their casual BP reduction elicited with their training program. The potential additive effect of these two responses would lower their CV disease risk to an even greater extent than that resulting from their reduced casual BP observed the next morning. On a practical level, another important effect of these results is that they can provide immediate positive feedback for hypertensive patients concerning the potential benefits of exercise. Although such information may be important for optimizing patient adherence, it is not known whether the BP-lowering response after acute aerobic exercise is in any way predictive of the BP-lowering response associated with long-term endurance exercise training. The duration of exercise that results in the BP-lowering response after exercise is also unknown. If the same responses found in this study were evident after only 10 min of exercise, a hypertensive person could go for a vigorous 10-min walk at breakfast, lunch, and dinner and they would experience significant reductions in BP for nearly every hour of the day. We also sought to derive some very preliminary data as to whether common genetic polymorphisms might identify hypertensives who had the greatest reductions in BP after acute exercise. Although these results must be viewed with some caution because of the small sample size, they provide evidence consistent with the possibility that common genetic polymorphisms at critical loci involved in systems that affect BP, including the renin-angiotensin system and the insulin resistance syndrome, may identify hypertensives most likely to reduce their 24-h ambulatory BP after an acute bout of submaximal exercise. In conclusion, these results indicate that systolic, diastolic, and mean arterial BP are reduced for up to 12 to 16 h after a single submaximal exercise session in hypertensive patients. These reductions in BP were consistent and substantial enough to result in significant reductions in 24 h average systolic, diastolic, and mean arterial BP values after this acute bout of aerobic exercise. These BP changes result in a reduced CV load for a prolonged period after acute exercise in older, obese, sedentary, hypertensive men. Furthermore, it appears that some common polymorphic genetic variations may affect these responses.
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Wilcox RG, Bennett T, Brown AM, MacDonald IA: Is