Post exercise hypotension (PEH) is a phenomenon of a prolonged decrease in resting blood pressure in the minutes and hours following acute exercise. Knowledge of PEH is potentially useful in designing first line strategies against hypertension as well as allowing a further understanding of blood pressure regulation in both health and disease. Following a brief review of blood pressure responses to exercise, this paper will provide a current and comprehensive summary of PEH and integrate the current state of knowledge surrounding it.
Blood pressure responses during exercise
During dynamic exercise, cardiac output increases dramatically to ensure adequate perfusion to the working musculature. This increase is achieved by a withdrawal of parasympathetic tone (causing an increased heart rate and contractility), an increase in sympathetic activity (directly and indirectly increasing heart rate and contractility) and pronounced vasoconstriction of the venous vasculature (causing a greater venous return and therefore stroke volume). In parallel, the need for increased blood flow and oxygen delivery to the exercising muscle is achieved through regional vasodilation of those arterioles supplying blood to the exercising tissue in combination with a vasoconstriction of arterioles, which perfuse non-essential tissues. Although the mechanism of vasodilation at the onset of exercise is not fully understood, many compounds (eg, potassium, adenosine, nitric oxide, etc) have been implicated in the exercise induced changes. Contraction of the active muscle mass also assists in returning blood towards the heart. This ‘muscle pump’ effect further increases venous return and stroke volume.
Increased cardiac output and vasoconstriction in non-exercising vascular beds increases systolic blood pressure (SBP), but the significant vasodilation at the exercising muscle beds helps to buffer this increase and results in a minimal rise in diastolic blood pressure (DBP). As exercise continues at the same intensity, blood pressure is often found to diminish from the peak values achieved early in exercise. This may be attributed to a redistribution of blood to the periphery for heat dissipation, and a resultant reduction in cardiac filling.1 Interestingly, endurance and resistance exercise elicit unique cardiovascular responses. These responses differences are discussed below and summarised in Figure 1.
During endurance exercise (ie cycling, running), SBP is tightly coupled to the exercise intensity and can often reach values of over 200 mm Hg.2 Although it is usually reported that DBP changes little throughout changes in the exercise intensity, Palatini3 has suggested that changes in DBP are more variable and can range from a slight decrease, due to the vasodilation of the muscle vasculature, to an increase of 10 to 20 mm Hg, presumably from the occlusion of blood flow caused by the forceful contractions of the exercising muscle. Following exercise, blood pressure rapidly returns to normal. As shown in Figure 1, there is often a transient pressure ‘undershoot’ caused by a pooling of blood in the dilated, previously exercised muscle beds. This pressure decrement is more pronounced following intense exercise. The baroreceptors work to counter the circulating vasodilatory substances to initially return homeostasis within 10 min following exercise.
Resistance exercise (ie weight lifting) elicits more pronounced increments in both systolic and diastolic blood pressure. MacDougall et al4 demonstrated average peak blood pressure values of 320/250 mm Hg during the double leg press in resistance trained volunteers, with some individuals reaching values of 480/350 mm Hg. This immense change in blood pressure is due to sympathetic vasoconstriction in non-exercising vascular beds, mechanical compression of the blood vessels in the exercising muscle beds, and the Valsalva manoeuvre (a forced expiration against a closed glottis used to stabilise the trunk muscles during heavy weight lifting which greatly increases intrathoracic pressure).2 The changes in blood pressure during resistance exercise are oscillatory and related to the phase of the lift. Blood pressure increases to maximal values as determined by the resistance encountered during the lifting phase. Pressure then declines, often to below resting values at the completion of the lift, and then increases again during the lowering phase of the exercise.5 The restoration of baseline blood pressure is similar to that of endurance exercise, although the transient pressure ‘undershoot’ is often more pronounced following heavy resistance exercise (Figure 1).
Blood pressure following exercise
A number of investigators have examined the effects of chronic exercise training on resting blood pressure in hypertensive populations (ie see review by Seals and Hagberg).6 It is generally accepted that the mechanisms underlying the sustained decrease in blood pressure of hypertensive individuals after training are a decrease in the resting heart rate and a decrease in circulating catecholamines.7 This decrease in circulating catecholamines is directly related to a decrease in sympathetic nerve activity.
Studies examining the acute effects of exercise on blood pressure have noted the transient pressure undershoot, described above, but have normally been terminated when blood pressure has re-attained normal values. However, more recent studies examining blood pressure responses in the prolonged post exercise period have documented that an acute bout of exercise may transiently decrease resting blood pressure in the minutes or hours following exercise. Although there are no defined criteria for the magnitude of the pressure decrement or duration of the response, this transient reduction in blood pressure has been termed post exercise hypotension (PEH). Post stimulatory hypotension (PSH) refers to the same phenomenon when it is elicited by simulating exercise by electrically stimulating muscles in certain animal models.
Post exercise hypotension
Does PEH occur in all individuals?
PEH has been well documented in humans with both borderline hypertension10,11,12 and hypertension.13,14,15 However, its occurrence in normotensive humans is inconsistent. Although we have found that PEH can be detected in normotensive individuals,16 it was found to be much less consistent and of lesser magnitude than in hypertensive individuals. This may be due to other compensatory mechanisms, such as the baroreflex, that are activated in normotensive subjects, and prevent the degree of PEH from affecting orthostatic tolerance.
Although there are reports of gender differences in blood pressure17 and sympathetic nerve activity,18 PEH appears to be unaffected by gender, since gender specific19,20 and mixed gender studies15,21,22,23 have found similar degrees of hypotension. It also occurs independent of age, having been observed in young24,25 middle aged25 and older adults.13 PEH/PSH has been documented in normotensive26 and spontaneously hypertensive rats27,28 as well as Dahl salt-sensitive rats.29 Limited work suggests that PSH does not occur in Dahl salt-resistant29 or renal hypertensive rats.30 Given the inconsistency of the PEH response in normotensive humans, the lack of hypotension found in these animal studies is not unexpected. It has been suggested that the degree of PSH may be related to the genetic pre-disposition of the animal to hypertension.29 Further research is needed to examine the effects of genetic predisposition on PEH in the normotensive human population.
Magnitude of the blood pressure decline
In those studies that have observed a decline in blood pressure following exercise, the average decrement in pressure was approximately 8/9 (SBP/DBP) mm Hg in the normotensive population,16,20,21,22,23,25,31,32,33,34,35 14/9 mm Hg in the borderline hypertensive population10,11,12,34,36,37,38,39 and 10/7 mm Hg in the hypertensive population.13,15,25,40,41,42,43,44,45 Rodents generally experience a decline of greater magnitude than humans. Absolute decrements in mean arterial pressure between the two species are approximately 50% greater in hypertensive rodents than in hypertensive or borderline hypertensive humans.12,15,19,26,27,28,30,36,37,38,39,44,46,47,48,49,50,51,52,53,54
The effect of variations in exercise on PEH
Type of exercise
PEH has been noted after a variety of aerobic type exercise, including walking,14,20,25,40,55,56 running,9,15,34,57,58 leg ergometry10,11,12,16,19,22,24,31,32,33,35,36,37,38,39,41,43,44,45,59,60,61,62,63 and arm ergometry.37 We recently examined the effects of the exercising muscle mass by comparing the PEH response to both leg and arm ergometry at the same relative intensity.37 No differences in the magnitude of PEH were evident and lead us to conclude that the amount of exercising muscle mass does not appear to influence the magnitude of the PEH observed.
Limited data suggest that PEH may occur after resistance exercise.16,23,64,65 It should be noted that reductions in blood pressure in the seconds or minutes following resistance exercise can be attributed to the sudden perfusion of the previously occluded muscle mass and a transient pressure undershoot.4 These decrements should not be confused with PEH, which is found in the prolonged minutes or hours after exercise. Although O'Connor et al66 found elevations in both systolic and diastolic blood pressure after resistance exercise, others have found significant reductions. These reductions were found after whole body circuit training23,65 and prolonged unilateral leg press exercise.16 Studies directly comparing the haemodynamic responses to aerobic and resistance exercise indicate that there is no difference in the magnitude or duration of the observed hypotension between exercise modalities.16,23
In rodents, PEH has been found after spontaneous67 and forced49,68 running. Stimulation of the sciatic nerve,26,29,30,46,69,70 the biceps femoris or the gastrocnemius muscles52,53,54 have also been demonstrated to evoke PSH.
Intensity of the exercise
In examining the effects of exercise intensity on PEH, the majority of studies have utilised submaximal cycle ergometry protocols at 40–100% of maximal exercise capacity, as indicated by measurements of V̇O2, heart rate reserve, or predicted maximal heart rate.10,11,19,22,24,31,32,33,35,41,43,44,45,59,60,61,63,71,72 Treadmill exercise at similar intensities has also been documented to elicit PEH.14,15,20,25,34,40,55,56,57,58 Direct comparisons of the effect of exercise intensity have, for the most part, found that PEH occurs independent of exercise intensity. We have found no difference in the magnitude of hypotension following 30 min of cycle ergometry at power outputs eliciting 50% and 75% V̇O2 Peak in normotensive volunteers.36 Pescatello et al44 were unable to document PEH in a normotensive population, but found no difference in the magnitude of PEH observed following 30-min bouts of cycle ergometry at 40 and 70% of V̇O2 Peak in a hypertensive population. Using an even broader exercise spectrum, Forjaz et al62 found similar PEH following 45 min of exercise at intensities of 30, 50 and 80% of V̇O2 Max. Using a resistance exercise model, Brown et al,23 compared three sets of five exercises at 40 and 70% of one repetition maximum (RM) and demonstrated significant PEH in a normotensive population with similar pressure decrements between trials. The decrease in blood pressure was comparable to the drop found after 25 min of cycle ergometry at 70% of V̇O2 Peak. Only one study has reported a difference in the hypotensive response to different exercise intensities. In that study, Piepoli et al72 found a decrement only after maximal cycle exercise (5 min stages of 25 Watt increments) when compared with moderate (5-min stages of 12.5 Watt increments) and minimal (constant 50 Watt) intensity exercise in normotensive sedentary volunteers. However, in sedentary individuals, maximal exercise could more adversely affect the haemodynamic response to exercise than in the other studies. Significant thermoregulatory or prostaglandin effects may occur after maximal exercise in such a population, which may differ from other forms of PEH.
In rats, PEH has been documented following treadmill exercise at 30 m/min and 10% grade,68,72 70% V̇O2 Max, and spontaneous, self selected running.67 Stimulation of the biceps femoris and gastrocnemius muscles at current intensities of 3 to 25 mA in the awake rat has been found to induce PSH.30,52,54 Additionally, sciatic nerve stimulation at intensities ranging from 4 to 25 times twitch intensity has also been documented to cause PSH in awake26,29,30,46,70 and anaesthetised69 rats.
Duration of the exercise
PEH has been observed after as little as 10 min12,73 and as long as 170 min74 of exercise, although the majority of studies have used endurance exercise lasting between 20 and 60 min.9,10,15,16,19,24,32,34,35,36,37,38,39,41,42,43,45,47,57,58,59,60,63,75,76,77 Inter-experimental comparisons are difficult across studies, since a variety of exercise intensities and blood pressure measurement techniques have been used.
In hypertensive subjects, Bennett et al73 suggested that the magnitude of the pressure decrement increases with a longer duration of exercise, although this could not be substantiated in a normotensive population. However, in that study, blood pressure was measured during 3 min rest periods following successive 10 min exercise bouts. A brief period of hypotension immediately following exercise is often attributed to a pooling of blood in the vasodilated muscle beds. The mechanism for such decrements immediately following exercise may be considerably different from those involved in PEH. Forjaz et al78 have found a greater decrement in both SBP and DBP and a longer duration of PEH in SBP following 45 min of exercise as compared with 25 min of exercise. Conversely, we have recently found a similar magnitude of PEH following 10, 15, 30 and 45 min of exercise at 70% V̇O2 Peak12 in a normotensive and borderline hypertensive population. Although inconclusive, the results of our study suggest that the duration of the hypotension may be influenced by the exercise duration.
We have found that as little as 15 min of resistance exercise (unilateral seated leg press at 65% 1 RM) can evoke PEH.16 Blood pressure reductions in that study were similar to those found after a short duration (∼13 min) of bilateral cycle ergometry at 65% of V̇O2 Peak.
PSH has been demonstrated in rodents following 30 to 60 min of sciatic nerve stimulation or direct stimulation of the gactrocnemius or biceps femoris muscles.52,53,54 In spontaneously hypertensive rats, Overton et al49 directly compared the effects of 20 and 40 min of treadmill running at 60–70% V̇O2 Peak. In this population, the animals that completed 40 min of exercise exhibited significantly greater decrements in blood pressure than those who ran for 20 min.
Duration of the response
The onset of hypotension following exercise has been found to occur within the initial minutes after exercise33,72,79 or at some time point between 30 min and 1 h following exercise.9,16,31,44,49,57,61 Most studies have measured blood pressure for only 1–2 h following exercise12,13,16,20,22,23,25,34,36,37,38,39,55,58,75 and the majority of these have found a nadir in blood pressure during that time with a return or trend towards baseline pressure at the cessation of measurement.
PEH will have clinical utility only if the relative hypotension is sustained for a significant duration and during activities of daily living. There have been a handful of studies that have examined the time course of PEH using ambulatory monitoring.15,34,38,41,44,56,61 We are aware of seven that have truly attempted to examine whether the hypotension is preserved during subsequent mild exercise or routine daily activities. Results from these studies are contradictory and may be confounded by the fact that post exercise activity was not controlled in all but one study, and that most investigators used intermittent auscultatory methods to determine blood pressure. Given the great differences in blood pressure between rest and activity and the influences of the breathing cycle and other cyclic waves on blood pressure, these auscultatory methods are prone to sampling error and may provide inaccurate or inconsistent results. Furthermore, some studies failed to address the influences of diurnal variations in blood pressure by only comparing post-exercise blood pressure to a pre-exercise control value.15,34,61 These studies failed to detect any long term reduction in blood pressure, while those comparing post exercise blood pressure to blood pressure following a control period of rest, in a free-living environment, have found significant decrements in blood pressure for up to 12.7 h in hypertensive individuals.40,41,44 Again, no differences were found in normotensives. However, these studies may be misleading as a bout of exercise may induce a more sedentary period post exercise under free living conditions. In the rodent model, it has been reported that exercise induces an opioid mediated drop in activity level, including reflexive activity.52 Whether or not this occurs in humans is unknown. However, for those not involved in regular activity, a single session of moderate intensity often induces a decrease in physical activity and exercise energy expenditure in the hours post exercise.80
We have recently completed a study in a controlled setting using continuous, indwelling blood pressure monitoring and tracked the blood pressure changes during a standardised protocol of mild exercise and activities of daily living following both rest and a bout of cycle ergometry. We showed a significant decrease in SBP, DBP, and mean arterial pressure (MAP) to the end of the 70-min monitoring period, with no trend towards returning to baseline values when preceded by prior exercise.38 In our study, the decrement in SBP averaged 16 mm Hg, and was as much as 23 mm Hg below control levels when preceded by a bout of exercise. It may be that activities of daily living following exercise potentiate the reductions in blood pressure. Studies in our laboratory using a similar borderline hypertensive population have found blood pressure returning to normal within the first hour after exercise when subjects remained sedentary.12,36 A long duration, controlled study needs to be completed to truly assess the time course of PEH.
Hoffman and Thoren54 have found that blood pressure can remain significantly attenuated for 15 h in the hypertensive rat following electrical stimulation of the biceps femoris muscle, with the nadir not occurring until 6 h post stimulation. Others have found decrements in blood pressure persisting at the cessation of measurement between 20 min and 6 h post exercise.26,27,28,46,48,50,53
The question remaining, in both the human and rodent models, is why do some studies report a rapid return to control levels, while others report long duration hypotension? The possibility exists that pronounced, long duration blood pressure oscillations occur post exercise. This is supported by Pescatello et al44 who took measurements every 30 min for over 12 h post exercise that would suggest an oscillatory pattern of SBP. Those studies that have observed blood pressure returning toward control levels, or terminated measurements within the first 2 h following exercise, may not truly represent the longer term changes in blood pressure.
Mean arterial blood pressure is a functional product of cardiac output and total peripheral resistance. With reference to these two basic components, the following is known:
Cardiac output (Qc)
Although no studies have attempted to directly measure cardiac output during the hypotensive period after exercise, indirect measures have yielded contradictory results. Qc has been found to be increased through increased heart rate20,22,33,35,58,63,77 stroke volume,50 or both.10,42 Conversely, others have reported Qc to be decreased.13,15,57 In all such instances the decrements were found to be due to reductions in stroke volume.
In humans, it is common to observe an increased heart rate during some or all of the hypotensive period,20,22,33,35,58,63,77 whereas rodents often display decreased or unchanged heart rates.30,48,49,50,54 Of interest is that, with the exception of one study,43 changes in human cardiac output post exercise appear dependent on the initial state of hypertension. Those studies reporting indices of Qc in normotensives found increases in Qc during the post exercise hypotensive period, whereas hypertensives showed a decreased Qc.13,15,20,22,57,58,63 These changes in Qc cannot be attributed to the exercise modality, duration or intensity since these studies have used a wide variety of protocols. In separate studies, using identical exercise protocols, Floras and colleagues demonstrated an increased Qc in normotensive and decreased Qc in hypertensive individuals.57,58
In the vast majority of cases, indices of systemic and regional resistance are decreased below pre exercise values during the hypotensive period. A number of studies have found decreased peripheral resistance at sites other than those of the exercising muscle, suggesting that the reduction is a whole body phenomenon.22,35,43 However, Hagberg et al13 found increases in total peripheral resistance in older hypertensives, suggesting that the mechanism(s) for PEH may differ between subject populations.
Mechanisms affecting cardiac output and peripheral resistance
Cutaneous vasodilation is the primary mechanism for heat loss in humans. Given that exercise increases body temperature, it is possible that a re-distribution of blood to the periphery may be responsible for PEH. Franklin et al31 investigated this possibility by having normotensive subjects rest in a cool, neutral or warm environment after exercise. Hypotension was only evident in the group exposed to the warm environment. Although this may appear to support the hypothesis that cutaneous vasodilation mediates PEH, it is likely that this is a different phenomenon. Given the variability in PEH responses of normotensive individuals and the persistence of PEH for at least 1 h following mild exercise as brief as 13 min,16 in which whole body heat dissipation would presumably have returned to normal, it is unlikely that cutaneous vasodilation is the primary mechanism responsible for PEH.
During intense exercise, it is known that the increased blood pressure may drive plasma into the interstitial space, reducing blood volume. A reduction in blood volume would, in turn, cause decreased venous return to the heart. This would translate into a decreased stroke volume and therefore cardiac output. Although Hagberg et al13 found slight post-exercise reductions in plasma volume in one group of hypertensives, the magnitude of the reduction was similar to that after a control period of rest. Other studies using measures of haematocrit and/or haemoglobin have found plasma volume to be unchanged after exercise and during periods of hypotension.12,16,25,36,37,42 No studies have measured plasma volume during long duration PEH. However, it is generally accepted that, due to the increased osmolarity following exercise, plasma volume can expand to a greater extent than before exercise. Hypotension has been found to persist for greater than the one hour after moderate to intense exercise in which this increased plasma volume can occur.20,43 Thus, it would appear unlikely that reductions in plasma volume are responsible for PEH.
Efferent sympathetic nerve activity
A number of studies have examined the influence of sympathetic nerve activity on PEH. The use of microneurography has allowed researches to directly measure sympathetic nerve activity. Measures of muscle sympathetic nerve activity (MSNA) as an indication of vascular tone have yielded contradictory results. Halliwell et al59 has documented decrements in MSNA in a normotensive population, whereas others have found no changes.58,76 Floras and co-workers reported a reduced muscle sympathetic nerve activity following exercise in borderline hypertensives.10 It has been suggested that borderline hypertensive subjects (and presumably hypertensive subjects) exhibit higher than normal MSNA in the resting condition, and thus the observed hypotension was due to a transient suppression of augmented sympathetic outflow. Rodent data are no more conclusive. Following exercise, blood pressure and lumbar sympathetic nerve activity have been found to be reduced in spontaneously hypertensive rats50 and measures of splanchnic sympathetic nerve activity have also been found to be decreased in this population.26 On the other hand, in separate studies, Kenney et al reported both unchanged renal and elevated lumbar sympathetic nerve activity81 and decreased renal sympathetic nerve activity29 after prolonged stimulation of the sciatic nerve in Dahl salt-sensitive rats.
Heart rate variability has also been used as an indication of the autonomic nervous system control. In both normotensive33,63 and borderline hypertensive38,39 individuals, these indirect indices suggest that sympathetic outflow is increased over the same interval in which PEH is observed. This may be a reflexive response to partially offset the exercise induced hypotension.
Measures of plasma noradrenaline levels as an indirect measure of ‘spill over’ from sympathetic activity are inconsistent during PEH. Levels have been reported to be increased in normotensives,60 increased19 and unchanged39 in borderline hypertensives, and decreased in hypertensive individuals.43 Brownley et al41 reported no change in urinary catecholamines after exercise in both normo and hypertensive individuals, with PEH only occurring in those with high blood pressure. Therefore, there is considerable disagreement as to whether changes in sympathetic activity might be responsible for PEH.
Afferent nerve activity
There is some indication that afferent nerve activity to cardiovascular control centres may be involved in PEH/PSH. During exercise, unmyelintated group III afferents, termed ‘ergoreceptors’, are activated.82 It is likely that any role in afferent induced hypotension would be in response to activation of these ergoreceptors. There are three such places that afferent activity that may influence PEH might originate:
Direct muscle stimulation of the biceps femoris or gastrocnemius muscle of the rat has been found to elicit PEH.52,53,54 However, PEH is abolished following stimulation of sciatic nerve anaesthetised animals. Kenney et al29 have observed PSH following stimulation of the medial end of the severed sciatic nerve. Although this evidence strongly supports skeletal muscle afferent involvement in PEH/PSH in rats, the potential mechanism of action is unknown.
Similar to skeletal muscle, cardiac afferents can be activated during exercise via increased heart rate, contractility and tension. In assessing their influence on PEH, Collins and DiCarlo51 examined the hypotensive response of rats to exercise during either cardiac efferent blockade or combined efferent and afferent blockade. The combined efferent and afferent blockade resulted in a significant attenuation of PEH as compared to both control and cardiac efferent blockade, suggesting an influence of cardiac afferents on PEH.
During exercise, blood pressure rises with a withdrawal of baroreceptor mediated control. Baroreceptors are believed to ‘re-set’ the cardiovascular control centre to a higher operating set-point during exercise.83 It is unlikely that a downward set point established by the baroreceptors following exercise is responsible for PEH. Resistance exercise is accompanied by mechanical compression of blood vessels and the Valsalva manoeuvre; as such, blood pressure is increased to a much greater extent than during endurance exercise.2 If baroreceptor re-setting were responsible for PEH, it would be expected that PEH would be greater following resistance exercise. However, this is not the case. Both Brown et al23 and MacDonald et al16 found similar decrements in blood pressure following resistance and endurance type exercise, whereas O'Connor et al66 found decrements only after endurance exercise. However, the possibility exists that the sensitivity of the baroreceptors is decreased with exercise, as the reduced blood pressure may no longer be an adequate stimulus to elicit the cardiovascular control centre excitation necessary to raise blood pressure. The most compelling evidence for baroreceptor mediated PEH comes from sinoaortic denervated rats. Chandler and DiCarlo27 found hypotension only after exercise in intact rats. No PEH was evident in sinoaortic denervated animals. Although with this method it is not possible to deduce whether the ‘set-point’ or the sensitivity of the baroreceptors is responsible for mediating PEH, these data would suggest that the sensitivity is altered. Additionally, using the phenylephrine11 and nitroprusside59 methods, baroreceptor sensitivity has been found to be depressed during at least some, but not all, periods of hypotension. However, using the lower body negative pressure method of baroreceptor sensitivity assessment, Bennett et al73 found an increased baroreceptor sensitivity following exercise that elicited PEH. Similar increases in sensitivity have been observed using neck suction, indicating a baroreceptor mediated restraint of PEH.63
Noradrenaline and adrenaline
Sympathetic stimulation during exercise causes the adrenal medullae to release adrenaline and noradrenaline in proportion to the exercise intensity. Noradrenaline acts predominantly on peripheral alpha-receptors, causing vasoconstriction. The degree of vasoconstriction is dependent on the location within the body. The kidneys, spleen and skin are known to be highly sensitive to alpha-receptor stimulation, whereas skeletal and cardiac muscle are not. Both noradrenaline and adrenaline also increase heart rate and contractility, and therefore cardiac output. The end product of the increases in peripheral resistance and cardiac output is an elevated arterial pressure. It has recently been shown that hypertensive individuals have increased basal sympathetic nerve activity.84 Conversely, a decrease in circulating catecholamines after exercise could lead to PEH. However, as previously discussed, noradrenaline does not appear to contribute to PEH.
The circulating adrenaline released from the adrenal medullae binds to muscle β-receptors and has a moderate vasodilatory effect. Measures of circulating adrenaline indicate that levels are elevated60 or unchanged14,39 during the hypotensive period. Our finding that PEH is largely independent of exercise intensity combined with the fact that it also persists during adrenaline infusion60 and β-receptor blockade14 suggests that any role of adrenaline in PEH is minimal.
Renin angiotensin system
Renin is released from the kidneys during periods of low perfusion pressure. This enzyme causes the conversion of angiotesinogen to angiotensin I. In turn, angiotensin I is acted on by a converting enzyme to form angiotensin II which has powerful vasoconstriction and water and salt retention properties. However, during PEH, unchanged55 and increased19,33 concentrations of circulating renin and increased angiotensin II concentrations have been found,55 and therefore do not appear to play a significant role in PEH.
Anti diuretic hormone (vasopressin)
In addition to its primary role in controlling body water content, anti diuretic hormone can act as a vasoconstrictor of arterial smooth muscle. It is released from the pituitary gland during periods of low pressure or increased osmolality. Although long duration, exhaustive exercise can increase plasma osmolality, hypotension has been found during exercise in which insignificant changes in osmolality19,55 and increased55 or unchanged19 levels of vasopressin are present. Wilcox et al55 found no significant correlations between levels of anti-diuretic hormone and the magnitude of PEH.
Atrial natriuretic peptide (ANP)
Endurance exercise results in increased right atrial filling. This increased volume and an increased heart rate can result in ANP release.85 ANP has potent vasodilatory and sodium retention effects. The circulating half life of ANP is only 2–3 min, but it may still exert residual effects after it is cleared from the circulation.86 The mechanism for this persistence is unknown. It would, however, appear that ANP is not responsible for PEH. Although Hara and Floras58 do not report ANP values during exercise, concentrations were significantly decreased from baseline values at one hour post exercise. We have recently examined the effects of resistance and endurance exercise on post exercise blood pressure and ANP release.16 Although blood pressure was significantly reduced after exercise in both cases, no significant increases in circulating ANP concentrations were observed during or post exercise.
Potassium exerts a dilatory effect on vascular smooth muscle. It is released by tissue in response to low oxygen concentrations, and then is believed to diffuse back to the pre-capillary sphincters, the metarterioles and arterioles to have vasodilatory effects.87 This increase is proportional to the exercise intensity and directly reflects the activity of the muscle sodium-potassium pump.88 However, the increase is short lived and often found to undershoot basal levels within minutes of recovery.88,89 Because plasma K+ concentration is proportional to exercise intensity, yet PEH does not appear to be intensity dependent36,44,62 and persists for hours after exercise, it is unlikely that K+ is involved in the PEH.
Adenosine is released by active tissues during exercise and also causes substantial vasodilation. Although no studies have measured adenosine concentrations during PEH, Sparks90 suggested that during flow restricted exercise adenosine is responsible for an initial vasodilation during the minutes following exercise in dogs. Although the re-uptake of adenosine is also very rapid following exercise, further work examining potential links between adenosine and the onset of PEH in humans is warranted.
Prostaglandins (PGs) are known to be liberated during exercise and cause vasodilation of arteries and veins.91 The lungs efficiently metabolise PGEs, PGFs and, to a lesser extent, PGAs; therefore, continued production of these prostaglandins would be necessary for the sustained regulation of blood pressure. Although most studies examining the role of prostaglandins have used an occluded blood flow model, Wilson and Kapoor92 measured increased PGF1α and PGE2 during wrist flexion exercise. Indomethacin, an inhibitor of prostaglandin synthesis, diminished the prostaglandin release and decreased blood flow suggesting that the released prostaglandins were responsible for vasodilation and hyperaemia. In a flow restricted model, Morganroth et al93 concluded that prostaglandins mediate a decrease in peripheral resistance for 35–40 min post exercise. No study has directly assessed the contribution of prostaglandins on PEH.
Reduced vascular sensitivity/nitric oxide
There is some evidence to suggest that an exercise induced decrease in vascular sensitivity may be responsible for PEH. Although Landry et al60 was the first to suggest that variations in vascular sensitivity after exercise may be responsible for the observed drop in blood pressure in humans, much of the evidence was derived from other species. In excised rabbit aortic rings, reduced α-adrenergic mediated isometric tension was observed following exercise.94 In a separate study using rats, increased iliac blood flow was demonstrated to be mediated by decreased adrenergic receptor sensitivity.95 Although no PEH was observed in that study and the reduced sensitivity could be related to numerous factors, inhibition of nitric oxide attenuated the decreased sensitivity after exercise, suggesting that nitric oxide may be partly responsible for the decreased sensitivity post exercise. Using ganglionic blocked, intact, Dahl salt-sensitive rats, Van Ness et al48 found an exercise induced attenuation in blood pressure responsiveness to the α-adrenergic agonist phenylephrine that persisted until the cessation of measurement at 30 min post infusion. Reduced vascular responsiveness in humans requires further study, but remains an interesting possibility.
Opioids and/or serotonin
It has been hypothesised that exercise-induced alterations in the opioid system may be a mechanism that centrally affects blood pressure.32,54 Although little is known about the mechanics of this system, it is speculated that opioids cause a decrease in sympathetic activity.32 The β-endorphins are known to increase during exercise, and it has been found that infusion of β-endorphins resulted in a prolonged drop in blood pressure.96 In the rodent model, Hoffmann et al52 showed that binding of β-endorphin to the κ-, and to a lesser extent the δ-receptors, was responsible for PEH. Human studies examining the contribution of the β-endorphins to PEH have elicited contradictory results when blocking the opioid system with naloxone, an opioid receptor antagonist.32,58
There has been some suggestion that a chemical link exists between the serotonergic system and the endorphins. Preliminary animal studies have found a significant drop in blood pressure following infusion of β-endorphins. However, no hypotension was found when β-endorphins were infused into animals pre-treated with pCPA, a specific depletor of serotonin. Additionally, the hypotensive effect of the β-endorphins was potentiated by fluoxetine, a specific serotonin re-uptake inhibitor.97 These results infer that β-endorphins may be a stimulus for serotonin release which, in turn, or in conjunction with the β-endorphins cause decreases in sympathetic outflow. The mechanism for this inhibition of sympathetic outflow is unknown. Interestingly, serotonin has been found to increase during exercise in brain tissue of rats98 and in blood samples of humans99 and may be involved in PEH.
Studies examining the role of serotonin on PSH have been quite convincing in the rodent model. Blood pressure depression following stimulation has been found to be abolished with the infusion of pCPA46,53 and augmented following treatment with the serotonin precursor 5-HTP or the serotonin re-uptake inhibitor zimelidine.46 A recent study augmenting central serotonin levels in humans using a similar serotonin reuptake inhibitor found no difference in the magnitude of the hypotension following exercise.39 This would suggest significant differences between the mechanism of PEH across species, or between PEH and PSH.
An understanding of the factors that cause and effect PEH may lead to a better understanding of the causes of hypertension, a condition that affects more than one in 10 individuals. In addition, it is possible that the phenomenon may be exploited to provide a practical intervention in the management of this disease. Should the long duration of PEH, as shown in some studies to persist for up to 12 h, be elicited by short duration exercise, the possibility exists that modest bouts of exercise, spaced throughout the waking hours may assist in the control of hypertension.
PEH has been well documented to occur in the laboratory. Although some studies suggest that the hypotensive effect occurs during periods of free living, a well controlled study has yet to determine the extent to which lowered blood pressure persists beyond 70 min post exercise. Further work needs to examine the time course of PEH under normal living conditions. It is encouraging for those with hypertension that it is generally accepted that borderline and hypertensive individuals will experience a greater drop in blood pressure post exercise than those without high blood pressure.
It is evident that, although PEH occurs in both humans and rodents, the mechanism(s) of action may not be consistent between species. In general, the magnitude of PEH does not appear to be correlated with the exercise intensity, duration or the amount of exercising muscle mass. PEH has been found after a variety of exercise stimuli including both endurance and resistance exercise. However, the possibility exists that the duration of the PEH may be influenced by any of these factors and warrants further study.
A review of the available literature has failed to elucidate any definitive mechanism(s) underlying PEH. Although the decreased blood pressure following exercise has mainly been found to be due to a decreased vascular resistance, the underlying cause for this decreased resistance has not yet been determined. It is unlikely that PEH is the result of thermoregulation or changes in blood volume. Although some data has suggested decreases in efferent nerve activity following exercise, contradictory reports across both humans and rodents are inconclusive. Reports of afferent nerve activity may have a role in contributing to PEH; however, the site of action (baroreceptors, hormones or efferent nerve activity) needs to be further investigated. Significant evidence in the rodent model has suggested that central serotonin levels may influence PEH, but our recent study in humans indicates that central serotonin is not responsible for PEH in our borderline hypertensive population. It also appears unlikely that circulating hormones or other local factors are responsible for PEH per se. Measured concentrations of potential vasodilators such as adrenaline, adenosine, potassium and atrial natriuretic peptide have been reported to be increased or unchanged during PEH. Vasoconstricting agents such as renin, angiotensin II and anti-diuretic hormone have been found to be increased, decreased or unchanged after exercise that elicits PEH. There are reports of PEH persisting for up to 17 h after exercise. At this time, each of these substances could be presumed to have returned to normal levels. The possibility does exist that any of these substances may be responsible for alterations in vascular sensitivity and therefore, indirectly mediate PEH. The role of nitric oxide in this possible change in vascular responsiveness has yet to be determined, but does appear encouraging from animal work. The contradictory results found between mechanisms such as muscle sympathetic nerve activity, the opioid system as well as the large variations observed between the existence, magnitude and response of PEH, suggest that it is a phenomenon which is not controlled by a single factor.
For PEH to be used as a non-pharmacological treatment for hypertension, an accurate time course must be established for this effect. As indicated above, PEH has been shown to persist for some time, but it needs to be confirmed whether the phenomenon is maintained for long periods during activities of daily living, using precise measurement techniques and controlling the activity following exercise.
If PEH is to be used in the management of hypertension, there is a need to establish the interaction between exercise and various antihypertensive medications on PEH. Although mildly hypertensive individuals may be able to control their condition with exercise alone, more severely inflicted individuals may need to remain on medication. An early study by Wilcox et al14 documented the additive effect of exercise and β-adrenergic antagonist drugs on PEH. However, the constraints of β-adrenergic blockade on exercise capacity may make this an unsuitable combination. The increasing popularity of other antihypertensive drugs such as calcium channel blocking agents and inhibitors of angiotensin-converting enzyme, which are more conducive to exercise, require investigation.
To gain a better understanding of blood pressure regulation, and the condition of hypertension, further insight is needed as to the mechanism(s) of PEH. As outlined in the text above, alterations in vascular sensitivity may play a dominant role in PEH and requires further investigation. It is unknown whether a potential change in vascular sensitivity would be mediated by local factors such as nitric oxide, or by central command, but research in this area should progress rapidly as the measurement techniques for vascular sensitivity and nitric oxide improve.
It is likely that a complex matrix of blood pressure regulating factors including both central and peripheral mechanisms are responsible for PEH. Given the many factors regulating blood pressure, the interaction between such factors and the redundancies built in to the blood pressure control system, it may prove difficult to identify a single causal mechanism for PEH. However, future research in this area will advance our understanding of blood pressure regulation, and certainly warrants further investigation.
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MacDonald, J. Potential causes, mechanisms, and implications of post exercise hypotension. J Hum Hypertens 16, 225–236 (2002). https://doi.org/10.1038/sj.jhh.1001377
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