Exercise intensity and postexercise hypotension

Lifestyle modifications are advocated for the prevention, treatment and control of hypertension, with exercise being an integral component. Higher levels of physical activity and greater fitness are associated with a reduced incidence of hypertension 1. Furthermore, a number of studies with well-controlled randomized experimental designs, examining the effects of aerobic endurance training programmes in hypertension, generally demonstrate training to exert a significant antihypertensive effect 2,3. Recent guidelines therefore recommend that everybody who is able should engage in regular aerobic physical activity, such as brisk walking, for at least 30 min per day most days of the week, as a means to lower blood pressure 1,4. Kraul et al. 5 were the first to observe an immediate reduction in blood pressure after exercise. These blood pressure reductions below control levels following acute exercise have been termed postexercise hypotension (PEH) 6. Currently, there is a growing body of evidence in the literature that a single bout of aerobic exercise significantly reduces blood pressure during the postexercise period in young, middle-aged and older subjects 7. Although PEH can be detected in normotensive individuals 8, it was found to be much less consistent and of lesser magnitude than in hypertensive individuals 9–11. In the present issue of the journal, Pescatello et al. 12 also reported baseline blood pressure as a predictor of PEH, such that the men with the highest baseline blood pressure experience the largest postexercise reduction in blood pressure. The immediacy by which this PEH occurs might suggest that the hypotensive influence of dynamic exercise, ascribed to endurance training programmes, may partly reflect an acute phenomenon, with the blood pressure reductions accumulating as the training progresses 13. However, to contribute to the sustained lowering of blood pressure observed with regular exercise, PEH must initially be sustained at a sufficient level, but also for a sufficient duration throughout the day 6. If this is the case, an acute bout of exercise, which is repeated regularly, might become an important non-pharmacological tool in the management of hypertension. In studies that have observed a transient decline in blood pressure following acute exercise, the average decrement in blood pressure was approximately 8/9 mmHg in the normotensive population, 14/9 mmHg in the borderline hypertensive population and 10/7 mmHg in the hypertensive population 7. The introduction of ambulatory blood pressure (ABP) monitoring devices has allowed observation of the hypotensive effect of short-term sessions over longer periods of time (e.g. during 24 h after exercise). In this respect, Rondon et al. 14 recently showed that one 45-min period of relatively low-intensity bicycle exercise, at 50% of VO2max, induced a postexercise blood pressure reduction in elderly hypertensive patients, which lasted for 22 h. Nevertheless, to be used as a non-pharmacological tool in the management of hypertension, more needs to be known about the different characteristics of the exercise required to evoke PEH, including exercise intensity. Most of the studies investigating the influence of exercise intensity on PEH have used submaximal cycle ergometer or treadmill exercise protocols at intensities ranging between 40 and 100% of VO2max, heart rate reserve or predicted maximal heart rate, and the majority of them only measured blood pressure for a short period of time 8–11,14–20. However, studies comparing the influence of different exercise intensities on PEH are scarce. Previous research involving acute exercise in hypertensive populations suggested that exercise intensity had little impact on the manifestation of PEH, neither on the quantity nor on the duration of any blood pressure reduction 1. However, most of these studies only measured blood pressure for a short time period in the range 1–4 h. In the present issue of the journal, the main aim of the investigation by Pescatello et al. 12 was to examine the influence of one bout of light (LITE) and of moderate (MOD) endurance exercise on PEH in hypertensive subjects. Therefore, 49 middle-aged men with high normal to stage 1 hypertension randomly completed three blinded experiments: a control session and two cycle exercise bouts, one at 40% (LITE) and the other at 60% (MOD) of VO2max. Each experiment lasted for 40 min and was followed by a 45-min recovery period in the seated position, after which subjects were attached to the ABP monitor. The subsequent 9 h were available for statistical analysis (i.e. the time period when all men were awake and out-of-bed). The authors concluded that, over the course of these 9 h, LITE was as effective as MOD in eliciting PEH in this middle-aged male hypertensive population. These results support the previous results obtained by the same group 10 showing that blood pressure was significantly lower compared to a control session for 12.7 h after a single 30-min bout of cycle ergometry at 40 and 70% of VO2max in hypertensive patients, independent of exercise intensity. By contrast, Quinn 20 submitted 16 men and women with documented stage 1–2 hypertension to two 30-min exercise bouts conducted at 50 and 75% of VO2max, as well as a sitting control session, in random order, and on separate days. Following each of these sessions, subjects sat quietly for 30 min and were fitted with the ABP system for the next 24-h period. The results obtained suggest that 75% of VO2max appears to offer a more sustained and substantial reduction in both systolic blood pressure and diastolic blood pressure compared to a 50% work bout in these hypertensive patients. The 75% exercise intensity significantly reduced systolic blood pressure for 10.5 h (15.4 h) versus 5.8 h (2.7 h) for the 50% intensity exercise in the hypertensive men (women), and diastolic blood pressure for an average of 11.9 h (9.8 h) versus 5.5 h (2.9 h), respectively. These data suggest that, by contrast to the aforementioned studies 10,12, a slightly higher exercise intensity elicits a greater effect on blood pressure than a lower intensity. One possible explanation for this observation was proposed by Marceau et al. 21. They found that a higher intensity exercise training (70% of VO2max) produced greater benefits, especially during the evening and sleeping hours, compared to a lower intensity exercise training (50% of VO2max) in 11 sedentary subjects with mild to moderate hypertension. This might explain why there is no difference attributable to exercise intensity when only daytime blood pressure is measured. Finally, Pescatello et al. 12 also reported that exercise intensity differentially modulated PEH depending on the duration of the observation. Indeed, for the first 5 h after exercise, PEH was greater after MOD exercise but, for the remainder of the day, LITE appeared to be as effective as MOD in evoking PEH. One possible explanation, as suggested by Pescatello et al. 12, would be an exercise-induced alteration in baroreceptor function (i.e. either a shift to a lower blood pressure operating point or an increased responsiveness to changes in blood pressure during the postexercise period). However, MacDonald 7 reported that it is unlikely that a downward set point established by the baroreceptors following exercise is responsible for the difference in PEH because resistance exercise is accompanied by much higher increases in blood pressure than endurance exercise, such that PEH should be greater following resistance exercise. However, this does not appear to be the case. Both Brown et al. 22 and MacDonald et al. 23 found similar decrements in blood pressure following resistance and endurance type of exercises. Another possible explanation, as proposed by Pescatello et al. 12, would be sympathetic inhibition or functional sympatholysis, defined as an intensity-dependent blunting of responsiveness to α- and β-adrenergic receptor stimulation and/or reduced noradrenaline releases, which are more pronounced after MOD than LITE exercise over this time period. However, until now, there is considerable disagreement as to whether changes in sympathetic activity might be responsible for PEH 7. To explain these different responses of blood pressure to different intensities, more research is needed, also examining possible mechanisms at the same time. Although more research is warranted to accurately describe the characteristics of exercise eliciting PEH and the mechanisms explaining PEH, it appears reasonable to conclude that a single bout of exercise may help in the non-pharmacological control of hypertension and may be an additional component in the treatment of hypertensive individuals. To date, it appears that an exercise intensity of approximately 40% of VO2max, which corresponds to leisurely brisk walking, would suffice to lower blood pressure.