The present study revealed considerable changes in estimated VO2 max in experimental groups over control group. In the experimental groups, the interval group indicated a significant increase in VO2 max above the continuous group. Result of the present study is consistent with the study of Smith and colleagues31; they investigated the effect of aerobic exercise and weight reduction intervention on 133 sedentary hypertensive men and women. Participants were grouped into an aerobic group, an aerobic group with weight reduction, and a control group. Participants engaged in a 6-month treatment period. They reported a significant improvement in aerobic capacity in the treatment groups compared to the control group.
A recent study conducted by Jones and colleagues32 that agrees with the present study exercised 35 participants (22 Caucasians and 13 African Americans) for 6 months. Their report indicated that aerobic exercise significantly increased participants maximal aerobic consumption (from 24±08 to 28±1 mL/kg/min) at P<.001. The present finding is also consistent with the report of Mughal and colleagues,33 who studied the effect of aerobic exercise in patients with essential hypertension. Twenty stage 1 and 2 hypertensives participated in a 12-week endurance ergometer program at 50% VO2 max, 3 to 5 times/week for 30 minutes. They reported significant increase in VO2 max at P<.05. Dengel and associates34 conducted a study on the effect of physical training on maximum aerobic capacity. Thirty-one (63±1 years) hypertensive (153±2/88±1 mm Hg) individuals participated in a 6-month aerobic exercise training program at 75% VO2 max, 3 times weekly for 40 minutes. They reported a significant increase in maximal aerobic capacity (VO2 max: 18.3±3.8 vs output of 20.7±4.2 mL/kg/min, at P<.017). Despite these outstanding results, the limitation of the 2 studies, however, was lack of control groups.
Another related study was conducted by Ferrier and colleagues,35 investigating the effect of aerobic exercise on VO2 max and maximum workload. Twenty (10 men and 10 women) participants with isolated systolic hypertension (ISH) aged (64±7) and 20 age- (64±7) and sex-matched normal (control) control participants were recruited. Participants were involved in a randomized crossover study of moderate-intensity exercise (60% HR max) for 40 minutes, 3 times/week for 8 weeks followed by another 8 weeks of sedentary activity. They reported a significant increase in VO2 max by 13%±5% (P=.04) and workload increase by 8±4 (P=.05) ISH patients in the ISH group. The probable reasons for the significant effect of interval training in the continuous and control groups might be due to the ability of intermittent exercise to intermittently overload the heart for a brief period beyond that which could be achieved during a single continuous bout at the same intensity. Also, the alternate work and rest periods in the interval training are proposed to allow for more cardiovascular work to be accomplished in the training period. Furthermore, the improved anaerobic threshold and work economy increase the participant’s ability to cope with the physical demand of daily activity. Finally, the motivating factor of exercise and rest period (varied procedure followed during each training) could not be ruled out.33–39
Findings from the present study revealed a significant decrease in SBP and DBP in the experimental groups over placebo group. The favorable changes resulting from aerobic training on both SBP and DBP demonstrated in the present study are consistent with the study of Smith and colleagues28 that investigated the effect of aerobic exercise and weight reduction intervention on 133 sedentary hypertensive (SBP: 130–180 mm Hg; DBP: 85–110 mm Hg) men and women. Participants were grouped into aerobic group, aerobic with weight reduction group, and control group. Participants engaged in a 6-month treatment period. They reported a significant reduction in both SBP and DBP in the treatment groups compared to the placebo group. In their study, Westhoff and colleagues40 investigated the effects of aerobic exercise on elderly (≥60 years) hypertensive patients (SBP ≥140 mm Hg and DBP ≥90 mm Hg). Fifty-four patients were randomly assigned to exercise and control groups. The exercise group engaged in a 12-week treadmill exercise program, while the control group did not. They reported a significant decrease in SBP and DBP by 8.5±8.2 mm Hg and 5.1±3.7 mm Hg, respectively, at P<.001.Their results concur with the findings of the present study.
Laterza and colleagues41 conducted a study investigating the effect of aerobic exercise on patients with hypertension. Twenty sedentary hypertensives were randomly assigned to 2 groups; exercise group (n=11; age=46±2 years), nonexercise group (n=12; age=42±2 years), and age-matched normotensive control (n=12; age 42±2). The exercise training consisted of one 60-minute exercise session per week for 4 months. They reported a significant decrease in BP of the hypertensives following exercise at P<.01 compared to the nonexercise hypertensive group.
Jones and colleagues32 investigated the effect of a 6-month aerobic exercise program on the BP of 35 sedentary prehypertensive and hypertensive participants (22 Caucasians; 13 African Americans). They reported nonsignificant changes in the BP of both the Caucasians and African-American participants. Sohn and colleagues42 investigated the effect of walking an extra 30 minutes a day on BP. Nineteen newly diagnosed hypertensive African-American adults were randomly assigned to inter-vention and control groups. The intervention group was advised to walk an extra 30 minutes per day. The control group was not given this advice. All participants used pedometers to record the numbers of daily steps. Also all participants were controlled for age and BMI. They reported a significant reduction in adjusted mean SBP by 9% for those in the intervention group and 2.33% for those in the control group. Similarly, adjusted mean DBP dropped by 7.42% for the intervention group and remained essentially unchanged for the control group at P=.08.
The present study revealed significant reduction in both interval and continuous programs over control group in resting HR. The result of the present study is in agreement with the study of Laterza and colleagues41 that investigated the effect of aerobic exercise training on HR in patients with hypertension. Twenty sedentary hypertensive patients were randomly divided into 2 groups; exercise: exercise trained (n=11; age 46±2 years) and untrained (n=9; age 42±2 years). An age-matched normotensive exercise trained group (n=12; age 42±2 years) was also studied. Participants were involved in an aerobic exercise training program of 3 60-minute exercise sessions per week for 4 months. They reported a significant decrease in HR following exercise in the hypertensive group. Ferrier and colleagues35 investigated the effect of aerobic exercise on resting HR. Twenty (10 men and 10 women) ISH participants and 20 age- and gender-matched normal control participants were recruited. Participants were involved in a randomized crossover study of moderate-intensity excercise (60% HR max) for 40 minutes for 8 weeks followed by another 8 weeks of sedentary activity. They reported no significant effect of exercise on HR in ISH patients.
Himeno and colleagues43 studied the effect of aerobic exercise on HR in mild-to-moderately hypertensive, obese participants. Fourteen mildly hypertensive, obese participants (SBP, 140–160 mm Hg or DBP, 90–100 mm Hg) and 22 normotensive, obese participants, age range from 22 to 51 years (mean ± SD, 35±9 years) (all participants had a BMI of >26 kg/m2. Participants were placed on a hypocaloric diet and exercise program; 33 participants exercised on a cycle ergometer and 3 participants on a treadmill at an HR corresponding to the anaerobic threshold (AT) for 60 minutes, 3 times/week for a total period of 12 weeks. The exercise was maintained for a 1-year follow-up. They reported a nonsignificant effect of exercise on HR in both the hypertensive and normotensive groups following the 12-week training and after 1 year post-training follow-up at P<.05.
RPP, PP and MAP
Results of the present study revealed a significant reduction in both interval and continuous groups’ RPP, PP, and MAP over control. This finding is in agreement with the report of Silver and colleagues,44 who studied the effects of acute and chronic exercise on the arterial baroreflex and chemosensitive cardiopulmonary baroreflex in spontaneously hypertensive rats. Arterial baroreflex and cardiopulmonary baroreflex were evaluated in normotensive rats (n=11) and spontaneously hypertensive rats (SHRs) (n=5) at rest and after 30 minutes of an acute bout of exercise (45 minutes at 50% of VO2 max). In addition, these baroreflexes were evaluated in sedentary (n=5) and exercise-trained (n=9) SHRs. Exercise training was performed on a motor treadmill, 5 days/week, for 60 minutes, at 50% of VO2 max. They reported that exercise training markedly improved baroreflex bradycardia and tachycardia in SHRs (1.9±0.1 vs 0.7±0.1 and 2.9±0.1 vs 1.8±0.2 beats/min/mm Hg, respectively. They also reported that during the recovery period, SHRs showed a significant fall in MAP compared with their respective baseline levels (25 minutes, −11±4 mm Hg; 35 minutes, −11±5 mm Hg; and 45 minutes, −10±5 mm Hg). In normotensive rats, MAP was not changed during the recovery period.
A similar result was reported by Mughal and colleagues,33 who investigated the effects of aerobic exercise in patients with essential hypertension. A 12-week aerobic exercise intervention trial was conducted to examine the influence of brisk walking on resting PP and MAP in patients with essential hypertension. Twenty-seven men with stage 1 or 2 essential hypertension (not on antihypertensive medication) participated in the study. The aerobic exercise training protocol consisted of 30 minutes of brisk walking 3 to 5 times/week, at 50% of VO2 max on an ergometer cycle. They reported a statistically significant decrease in PP, from the baseline value of −3.7 mm Hg (P<.01), and in MAP, of −3.4 mm Hg (P<.01) was noted. They concluded that aerobic exercise caused small reductions in MAP and PP in men with stage 1 or 2 essential hypertension.
Randon and colleagues45 studied 24 elderly hypertensive patients (age 68.9±1.5 years) and 18 age-matched normotensive control participants (age 68.1±1.2 years). Cardiac output (carbon dioxide rebreathing) and BP (auscultatory) were measured at rest and after a 45-minute period of low-intensity bicycle exercise (50% maximal oxygen uptake) and at 15, 30, 60, and 90 minutes after exercise. Left ventricular function (by Doppler echocardiography) was also evaluated. Ambulatory BP monitoring was evaluated after 45 minutes of exercise or 45 minutes of rest, in a randomized order. They reported that in the hypertensive patients, exercise provoked a significant reduction in mean BP during a 22-hour period, at daytime and nighttime. They concluded that the short-term positive effect noted after exercise in elderly hypertensive patients is associated with a decrease in stroke volume and left ventricular end-diastolic volume.
Generally, the factors responsible for the potential antihypertensive effect of long-term aerobic exercises are incompletely understood and unclear.46 However, it is theorized that the biochemical, neural, and hormonal changes in the blood vessel walls induce an acute and long-term blood vessel relaxation. When a person engages in aerobic exercise, the SBP and HR will increase, while the DBP changes little. Immediately following the exercise bout, the SBP of hypertensive individuals will fall below pre-exercise values by 20 to 30 mm Hg and that of normotensive individuals by 8 to 12 mm Hg, an effect that lasts for 12 hours in healthy individuals and beyond 12 hours in hypertensive patients.47,48 This decrease below the baseline following aerobic exercise is called “post-exercise hypotension.”49
There are many potential mechanisms responsible for the “post-exercise hypotensive effects,” including relaxation and vasodilatation of blood vessels in the legs and visceral organ areas.48 The blood vessels may relax after each exercise session because of body warming effects, local production of certain chemicals (such as lactic acid and nitric oxide), decreases in nerve activity, and changes in certain hormones and their receptors.47,48 Over time, as the exercise is repeated, there is growing evidence that a long lasting reduction in resting BP can be measured, which may partly be due to the acute drop in BP that occurs after each bout.47
Another mechanism is that the post-exercise hypotension is accompanied by a decrease in serum catecholamines, norepinephrine, dopamine, cortisol, and sympathetic nervous system and plasma rennin activity.49–52 In addition to a reduction in sympathetic activities, a fall in plasma volume and cardiac index may also be important in the antihypertensive effect of aerobic exercise.46 Exercise has been reported to improve abnormal baroreflex function in patients with hypertension.53,54