653

Brief Review

Postexercise Hypotension
Key Features, Mechanisms, and Clinical Significance
Michael J. Kenney, Douglas R. Seals

Recent investigations have demonstrated that there is a sustained reduction in arterial blood pressure
after a single bout of exercise, ie, postexercise hypotension (PEH). The purpose of this discussion is to
integrate the available information on this topic and to review studies using sustained stimulation of
somatic afferents in experimental rats as a model to study the role of somatic afferents in PEH. PEH
occurs in response to several types of large-muscle dynamic exercise (ie, walking, running, leg cycling, and
swimming) at submaximal intensities greater than 40% of peak aerobic capacity and exercise durations
generally between 20 and 60 minutes. PEH is observed in both normotensive and hypertensive humans
and in spontaneously hypertensive rats but is generally greater in magnitude in hypertensive subjects. The
maximal exercise-induced reductions in systolic and diastolic arterial blood pressures have been on
average 18 to 20 and 7 to 9 mm Hg, respectively, in hypertensive humans and 8 to 10 and 3 to 5 mm Hg,
respectively, in normotensive humans. PEH has been reported to persist for 2 to 4 hours under laboratory
conditions. Whether PEH is sustained for a prolonged period of time under free-living conditions remains
controversial, although the results of one study indicate that PEH can persist for up to 13 hours. Possible
mechanisms involved in mediating postexercise and poststimulation reductions in arterial blood pressure
include decreased stroke volume and cardiac output; reductions in limb vascular resistance, total
peripheral resistance, and muscle sympathetic nerve discharge; group HI somatic afferent activation;
altered baroreceptor reflex circulatory control; reduced vascular responsiveness to o-adrenergic receptor-
mediated stimulation; and activation of endogenous opioid and serotonergic systems. It appears that the
magnitude of PEH in hypertensive subjects is clinically significant; however, more investigation is
required to determine if the duration is sufficient under real-life conditions to contribute to the reduction
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in blood pressure observed with chronic exercise conditioning. (Hypertension. 1993;22:653-664.)

KEY WORDS • exercise • hypotension • blood pressure • hemodynamics

C linicians have studied exercise in the area of

hypertension for many years. Most of this
interest has focused on two issues: (1) regula-
tion of arterial blood pressure during acute exercise, ie,
whether hypertensive patients have exaggerated arterial
blood pressure responses to exercise, and (2) the use of
chronic exercise as a nonpharmacologic approach to
lowering arterial blood pressure at rest and during daily
physical activity. In recent years, however, clinical sci-
entists and physiologists alike have become interested in
a third component of the exercise response —the sus-
tained reduction of arterial blood pressure after a single
bout of exercise, ie, postexercise hypotension (PEH).
In contrast to the aforementioned aspects of the
exercise response that have received considerable dis-
cussion, 1 " insight into the key features and possible
clinical significance of PEH remains fragmentary.
Therefore, the purpose of this discussion will be to
integrate the available information on this topic, em-
phasizing its fundamental properties, speculating on the
Received February 19, 1993; accepted in revised form June 17,
1993.
From the Department of Anatomy and Physiology, College of
Veterinary Medicine, Kansas State University, Manhattan, and
the Department of Kinesiology, University of Colorado, Boulder.
Correspondence to Michael J. Kenney, PhD, Department of
Anatomy and Physiology, College of Veterinary Medicine, Kansas
State University, Manhattan, KS 66506.
underlying mechanisms, and commenting on its possible
relevance in the treatment of essential hypertension.
Definition and Documentation
For purposes of this review, PEH is defined as a
reduction in systolic and/or diastolic arterial blood
pressure below control levels after a single bout of
exercise (Fig 1). PEH has been documented in anec-
dotal reports,13 clinical accounts,14 and experimental
investigations.12-15-33 Because exercise is associated with
activation of somatic afferents, electrical stimulation of
the sciatic nerve and of hind limb skeletal muscles in the
rat has been used to study the role of somatic afferents
in mediating PEH. In this regard, poststimulation hypo-
tension (PSH) is defined as a reduction in systolic
and/or diastolic arterial blood pressure below control
levels after electrical stimulation of the sciatic nerve or
hind limb skeletal muscles (Fig 2).
Key Features of Postexercise and
Poststimulation Hypotension
The following factors play a role in determining the
occurrence, pattern, and magnitude of the arterial
blood pressure responses after exercise and electrical
stimulation.
Nature of the Exercise Stimulus
Mode. In humans, PEH has been observed in response
to several types of large-muscle dynamic exercise, includ-
 654 Hypertension Vol 22, No 5 November 1993

8
4
—6-«JL Dioitolk
0 FIG 1. Line graph shows diastolic and sys-
tolic arterial blood pressures in older hyper-
-4 tensive humans recorded during 180 min-
-8 utes of recovery after treadmill exercise at
70% of maximal oxygen consumption. Note
-12 that systolic arterial blood pressure was sig-
nificantly reduced from control levels for 2
-16
hours after the cessation of exercise. Also
z- -20 note that the magnitude and duration of the
- u postexercise reduction in diastolic are less
-24
than those observed in systolic arterial blood
-28 pressure. Reprinted with permission from
U a.
Hagberg et al. 12
-32
• 30 60 90 120 150 180
Prt-r
*!(•" MINUTES AFTER CESSATION OF EXERCISE"

ing walking and running,* leg cycling,161921-26-27-30-31 and
swimming.2* Little information is available concerning the
arterial blood pressure responses after resistance exercise
in humans. O'Connor et al35 observed slight elevations in
systolic and diastolic arterial blood pressures immediately
after 30 minutes of upper and lower body resistance
exercise, with a rapid return toward preexercise control
levels during the remainder of the 2-hour postexercise
measurement period. In a second study, Hill and col-
leagues36 reported significant reductions in both systolic
and diastolic arterial blood pressures immediately after 11
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lished after acute resistance exercise in humans. In the rat,
PEH is induced by voluntary running wheel exercise29 and
forced treadmill running,25 whereas PSH is elicited by
electrical stimulation of the gastrocnemius and biceps
femoris skeletal muscles34-37 and of the sciatic nerve. 3842
Intensity. In both humans and rats, PEH has been
observed in response to exercise at submaximal intensities
between 40% and 70% of maximal oxygen consumption,
peak oxygen consumption, age-predicted maximal heart
rate, or resting heart rate reserve.* In addition, arterial
blood pressure in humans is reduced after maximal tread-
mill and leg cycling exercise to exhaustion.19-28-30-31

to 18 minutes of weight training exercise at 70% of

one-repetition maximum. Thereafter, systolic and diastolic
arterial blood pressures abruptly returned toward control
levels but remained slightly (systolic) to moderately (dia-
stolic) depressed throughout a 1-hour postexercise recov-
ery period. Thus, PEH has not been conclusively estab-
The intensity of sciatic nerve stimulation used to
elicit PSH is usually defined as a multiple of the minimal
current required to evoke a muscle twitch.41 PSH occurs
in response to sciatic nerve stimulation at current
intensities between four and 25 times the twitch thresh-

*References 12, 13, 15, 20, 22, 23, 28, 32, 33. •References 12, 13, 15-18, 20, 21-23, 25, 27, 32, 33.

180-

160-
22
: E 140-

FIG 2. Traces and plot of representative data

gUi 180
• +1 from a spontaneously hypertensive rat show
i?« 160- changes in arterial blood pressure, mean arterial
C " I blood pressure, and heart rate during and after
S • I 140- 60 minutes of electrical stimulation of the gas-
2 a. S
trocnemius muscle. Note the poststimulatory
reduction in mean arterial blood pressure, which
f 450- persisted for 15 hours. Reprinted with permis-
sion from Hoffmann and Thoren.34
5 j; 4oo-
• 2 350-

Stlmulatlon

' -2 4 6 8 10 12 14 16
Tim* ( h )

old.38-41 Electrical stimulation of the gastrocnemius and
biceps femoris muscles at current intensities between 3
and 25 mA also elicits PSH.34-37
Duration. Reductions in arterial blood pressure have
been observed after a wide range of exercise durations.
PEH has been reported with exercise durations as short
as 3 to 10 minutes15-24 and as long as 170 minutes,28 but
most studies have used exercise durations between 20
and 60 minutes. 12.13.15-23.25-27,29-33 P S H has been ob-
served with stimulation lasting 3039"41 and 6034-37-38
minutes.
Importance of the Subject Population
PEH has been observed in young and middle-aged
normotensive humans, 1516192 '- 23 - 283132 patients with
borderline essential hypertension,20-26-30 and patients
with established (sustained mild to moderate) essential
hypertension* as well as in older subjects with essential
hypertension.12 In contrast, several studies have re-
ported no significant change in arterial blood pressure
after a single bout of exercise in normotensive hu-
mans.1718-27 Moreover, Hara and Floras22 reported that
diastolic and mean but not systolic arterial blood pres-
sures were reduced after exercise in normotensive hu-
mans, whereas Floras et al20 reported postexercise
reductions in systolic but not diastolic arterial blood
pressure in borderline hypertensive subjects. PEH oc-
curs in both ment and women,12-18-19-26-31 indicating a
lack of gender specificity. PEH is also observed in
spontaneously hypertensive rats (SHR).25-29 PSH occurs
in conscious34-37-38-41 and anesthetized40 SHR, conscious
Wistar-Kyoto normotensive rats,41 and anesthetized
prehypertensive Dahl salt-sensitive rats.39 In contrast,
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PSH is not observed in renal hypertensive38 and Dahl
salt-resistant39 rats. Because Dahl salt-sensitive rats and
SHR exhibit a genetic predisposition for development
of hypertension whereas Dahl salt-resistant and renal
hypertensive rats do not, these results suggest that the
magnitude of PSH may be related to the genetic pre-
disposition of the animal to hypertension.39
Nature of the Arterial Pressure Responses
Peak changes in arterial pressure. In studies to date,
peak exercise-induced reductions in systolic and dia-
stolic arterial blood pressures have been on average 18
to 20 and 7 to 9 mm Hg, respectively, in hypertensive
humans4: and 8 to 10 and 3 to 5 mm Hg, respectively, in
normotensive humans.15-19-21"24-27-28-31-32 Studies in bor-
derline hypertensive humans have reported peak post-
exercise reductions in systolic and mean arterial blood
pressures of approximately 1020-30 and 16 mm Hg,26
respectively. In one study, SHR exhibited a peak exer-
cise-induced reduction in mean arterial blood pressure
of 16 mm Hg.25
In response to muscle and/or sciatic nerve stimula-
tion, the peak reduction in mean arterial blood pressure
is on average 18 to 20 mm Hg in SHR34-37-38-40-41 and 7 to
9 mm Hg in Wistar-Kyoto rats.41 After sciatic nerve
stimulation in prehypertensive Dahl salt-sensitive rats,
the peak reduction in mean arterial blood pressure is 20
mm Hg.39
•References 13, 15, 17, 18, 21, 23, 24, 27, 31-33.
tReferences 12, 13, 15, 16, 18-23, 27, 28, 31-33.
{References 12, 13, 15, 17, 18, 21, 23, 24, 27, 31-33.
Kenney and Seals Hypotension After Exercise 655
Collectively, these observations indicate that (1) in
normotensive humans and rats the peak postexercise
reduction in arterial blood pressure is generally less
than that observed in their hypertensive counterparts
and (2) the magnitude of the peak exercise-induced
decrease in arterial blood pressure in hypertensive rats
is approximately equal to that observed in hypertensive
humans.
Average changes in arterial pressure. Several studies
have reported average decreases in arterial blood pres-
sure during the postexercise measurement period. Be-
tween 30 and 90 minutes after moderate cycling exercise
in humans with mild to moderate essential hyperten-
sion, Cldroux et al18 reported that the hypotensive
response averaged —11 mm Hg for systolic and —4
mm Hg for diastolic arterial blood pressures. Moreover,
the reduction in pressure was maintained during the
period between 2 and 3 hours after exercise, with
systolic arterial blood pressure 9 mm Hg and diastolic
arterial blood pressure 4 mm Hg below control values.
In older humans with essential hypertension, systolic
arterial blood pressure was reduced an average of 13
mm Hg from control values for 3 hours after exercise at
70% maximal oxygen consumption (Fig I). 12 Mean
arterial blood pressure has been reported to be reduced
an average of 8 mm Hg for at least 4 hours after
submaximal cycling exercise in borderline hypertensive
humans,26 whereas Pescatello et al27 reported that sys-
tolic arterial blood pressure was reduced an average of
6 mm Hg over 8.7 hours and diastolic arterial blood
pressure was reduced an average of 9 mm Hg over 12.7
hours after submaximal exercise in mildly hypertensive
men (Fig 3). Mean arterial blood pressure is reduced on
average 14 mm Hg for 50 minutes and 4 mm Hg for 38
minutes after spontaneous wheel running in SHR and
Wistar-Kyoto rats, respectively.29
Time course of the response. Little information is
available concerning the time at which the lowest re-
corded levels of arterial blood pressure occur after a
single bout of exercise. The results of several studies
indicate that the nadir of the postexercise systolic and
diastolic arterial blood pressure responses generally
occurs within the first 60 to 70 minutes of recov-
e r y 12,21,23,26,31 i n these studies the lowest recorded levels
of arterial blood pressure were generally followed by
increases toward control levels before measurements
were stopped. In other studies it is difficult to determine
when the nadir of the PEH response occurred because
the first data point recorded was 30 to 60 minutes after
the cessation of exercise1718-20 or the last recorded data
point was either the lowest or very nearly the lowest
recorded value of arterial blood pressure.15-16-27-30
In general, the nadir for mean arterial blood pressure
after muscle and sciatic nerve stimulation in hyperten-
sive rats ranges between 30 and 180 minutes.34-38-40-41 In
normotensive rats, the peak reduction in mean arterial
blood pressure has been reported to occur within 2
hours after sciatic nerve stimulation.41
Little information is available on the time course for
reattainment of arterial blood pressure to control levels,
because few studies have continued measurements to
this standardized end point. In mildly to moderately
hypertensive humans, diastolic and mean arterial blood
pressures were reduced from control levels when the
measurements were stopped 12.7 hours after the cessa-
 656 Hypertension Vol 22, No 5 November 1993
in
RECOVERY
10 II 12
TIME (hf)
FIG 3. Line graph shows systolic (SBP), mean (MAP),
and diastolic (DBP) arterial blood pressures recorded in
mildly hypertensive men before, during, and for approx-
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imately 13 hours after a single bout of cycling exercise
(EX). Note the sustained postexercise reductions in arte-
rial blood pressures compared with values recorded
before exercise (REST). Reprinted with permission from
Pescatello et al. 27
tion of exercise (Fig 3).27 Other findings have shown
that arterial blood pressure had not yet returned to
control levels when measurements were stopped 2 to 4
hours after exercise in hypertensive humans.1718-2126
Hagberg et al12 reported that systolic arterial blood
pressure remained 12 to 19 mm Hg lower than preexer-
cise values for 2 hours after exercise in older hyperten-
sive humans (Fig 1). In the same subjects, diastolic
arterial blood pressure returned to control values ap-
proximately 75 minutes after cessation of exercise (Fig
1). During the second half hour after graded leg cycling
exercise to exhaustion, Somers et al31 reported signifi-
cant reductions in systolic and diastolic arterial blood
pressures in both hypertensive and normotensive sub-
jects. However, by 2 hours after exercise arterial blood
pressure had returned to control values. Kaufman et al23
reported that diastolic but not systolic arterial blood
pressure returned to control levels by 60 minutes after
exercise in normotensive and hypertensive humans. In
two other studies, PEH in normotensive humans has
been reported to persist for approximately 90 to 100
minutes.21-22
Taken together, these observations indicate that PEH
persists anywhere from approximately 1 to 12 hours or
longer in hypertensive humans. Moreover, it appears
that the length of the PEH response is longer in
hypertensive than normotensive humans. With regard
to PSH, arterial blood pressure remains reduced from
control for 3 to 15 hours after skeletal muscle or sciatic
nerve stimulation in SHR (Fig 2).34-40-41 The length of
PSH is longer in SHR than in normotensive rats.41
Relation between the nature of the stimulus and the
magnitude of the hypotensive response. Little information
is available on the influence of exercise type, duration,
and intensity on the onset, duration, and magnitude of
PEH. In older (mean age, 64 years) humans with
essential hypertension, the magnitude and duration of
PEH are greater after treadmill exercise at 70% versus
50% of maximal aerobic capacity.12 Moreover, in SHR,
the magnitude and duration of PEH are greater after 40
SBP
than 20 minutes of treadmill exercise at the same
intensity.25 In contrast to these observations, Pescatello
et al27 reported that PEH in mildly hypertensive men
(mean age, 44 years) was not different after leg cycling
HAP
exercise at 40% and 70% of peak oxygen uptake. Thus,
although some evidence exists to support a relation
between the magnitude and length of the hypotensive
OBP
response and the intensity and duration of the exercise
stimulus, this has not been demonstrated conclusively.
Influence of familiarization on PEH. Although it is
well established that arterial blood pressure can de-
crease with serial measurements in humans at rest,43-44
little information is available on a possible modulatory
1]
effect of this type of familiarization on the magnitude of
PEH. Kaufman et al23 recorded arterial blood pressure
in two familiarization sessions before completion of an
experimental session involving five 10-minute treadmill
exercise bouts. The absolute levels of systolic and dia-
stolic arterial blood pressure during the resting control
periods decreased from the initial preliminary session to
the experimental session. They noted that the reduction
in arterial blood pressure after exercise during the
experimental session was less than that previously ob-
served by other investigators using a similar exercise
protocol.32 This attenuation of the PEH response may
have resulted in part from the lower level of arterial
blood pressure recorded in the control period before
exercise compared with the values recorded in the initial
preliminary session. These results indicate that in some
instances familiarization with blood pressure measure-
ment can influence the magnitude of PEH measured
under laboratory conditions.
Mechanisms Underlying Postexercise and
Poststimulation Hypotension
In this section, we review potential mechanisms by
which exercise and somatic afferent stimulation may
induce sustained reductions in arterial blood pressure.
Efferent Mechanisms
Systemic and regional hemodynamics. Because arterial
blood pressure is a function of the product of cardiac
output and total peripheral resistance, reductions in
arterial blood pressure observed after exercise and
electrical stimulation of somatic and muscle afferents
must result from decreases in cardiac output, total
peripheral resistance, or both. To date, however, the
experimental findings concerning the regional and sys-
temic hemodynamic adjustments responsible for PEH
have been inconsistent.

Forearm vascular resistance15 and total peripheral
resistance12 have been reported to be significantly in-
creased compared with control values after intermittent
submaximal treadmill exercise in hypertensive humans.
In older subjects with essential hypertension, the in-
crease in total peripheral resistance was associated with
a significant reduction in cardiac output.12 Because
heart rate generally remained either above or un-
changed from control values after exercise, the reduc-
tion in cardiac output was primarily mediated by a
decrease in stroke volume.12 Neither reductions in
cardiac preload nor increases in cardiac afterload could
account for the reduced stroke volume, suggesting that
alterations in myocardial contractility may have contrib-
uted to this hypotensive response. In this regard, de-
creased left ventricular systolic function after prolonged
exercise has been documented in healthy humans.28
After treadmill exercise in SHR, vascular resistance in
the iliac, superior mesenteric, and renal beds was not
markedly changed from control levels, whereas heart
rate was significantly reduced.25 It is not known if this
bradycardic response is associated with a reduction in
cardiac output.
In contrast to these observations, Coats and cowork-
ers19 reported significant increases in heart rate and
cardiac output and decreases in arterial blood pressure
and total peripheral resistance after maximal leg cycle
ergometry in normotensive humans. The increase in
cardiac output was mediated by the sustained tachycar-
dia, as stroke volume remained unchanged from control
levels after exercise. The reduction in total peripheral
resistance involved vasodilation in the nonactive limbs,
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as forearm vascular resistance was significantly reduced
after exercise. Consistent with these observations, Cle-
roux et al18 reported decreases in arterial blood pres-
sure, total peripheral resistance, and forearm vascular
resistance (Fig 4) and increases in cardiac output, heart
rate, and stroke volume after bicycle exercise at 50% of
peak oxygen uptake in humans with mild to moderate
hypertension. Reductions in mean arterial blood pres-
sure and total peripheral resistance also have been
observed for at least 4 hours after submaximal exercise
in borderline hypertensive humans.26 Moreover, Hara
and Floras22 recently reported reductions in diastolic
and mean arterial blood pressures, calf vascular resis-
tance, and total peripheral resistance and tachycardia-
mediated increases in cardiac output after submaximal
treadmill exercise in normotensive humans.
It is not clear what accounts for the inconsistent
hemodynamic changes observed after a single bout of
exercise. It does not appear to be solely an influence of
exercise intensity, as variable changes in both cardiac
output and systemic vascular resistance have been re-
ported after moderate intensities of dynamic exer-
cise.12171822-26 Moreover, there appear to be no consis-
tent relations among the observed hemodynamic
changes and the exercise mode and duration. The
subject population involved could play a role, as older
subjects with essential hypertension demonstrate post-
exercise reductions in cardiac output and increases in
total peripheral resistance.12 Body position also may
contribute to the differences observed in postexercise
systemic hemodynamics; the study that reported de-
creased cardiac output and increased total peripheral
resistance after exercise evaluated subjects during
Kenney and Seals Hypotension After Exercise 657
2
•?
xo-
100-
100-
/ ?
I
JO K » M 10 (0
HYPERTENSIVES NOMiOTCNSVU
OtfnmnwM
FIG 4. Plots show forearm vascular resistance (FVR) and
hand vascular resistance (HVR) recorded in hypertensive
and normotensive subjects at 30, 60, and 90 minutes
after either exercise at 50% of peak oxygen uptake for 30
minutes (AFTER EXERCISE) or a 30-minute rest period
(CONTROL). Note that FVR remained reduced from con-
trol levels for at least 90 minutes after exercise in hyper-
tensive subjects. In contrast, FVR remained at control
levels after exercise in normotensive subjects. Reprinted
with permission from Cleroux et al. 18
seated rest12 rather than supine as in several other
studies that observed the opposite relation.1819-22
Cleroux et al18 believe that the experimental design of
several studies may have influenced postexercise hemo-
dynamic alterations. In the studies by Bennett et al15
and Hagberg and coworkers,12 baseline measurements
were established over a brief period of time immediately
before exercise. C16roux et al18 suggest that the preex-
ercise cardiac output and forearm blood flow values
reported in these studies are relatively high because of
either the anticipation of the impending bout of exercise
or the stress of being in an unfamiliar laboratory setting;
thus, the "artificially" higher preexercise values could
mask postexercise increases in these variables. In their
own study,18 they compared hemodynamics after exer-
cise to those of a nonexercise control period completed
on a separate day. However, differences in experimental
design may not account for all the observed variances
among studies, as Coats et al19 reported no significant
differences in arterial blood pressure, cardiac index,
forearm vascular resistance, or systemic vascular resis-
tance during a control period immediately before exer-
cise compared with a control session completed on a
 658 Hypertension Vol 22, No 5 November 1993
Control
Mean Voltage
Neurognm
ol SNA
EKQ
Blood Praiiure 1W90
(mm Hg)
FIG 5. Original tracing shows muscle sympathetic nerve activity (SNA) and electrocardiogram (EKG) before (Control)
and 60 minutes after treadmill exercise in borderline hypertensive subjects. The level of arterial blood pressure during
control and after exercise is listed below the EKG tracing. Note that SNA and arterial blood pressure were lower 60
minutes after exercise compared with control levels. Reprinted with permission from Floras et al. 20
separate day. It is clear that additional data are needed
to define more completely the nature of the systemic
and regional hemodynamic alterations mediating PEH,
as well as the role of differing methodology in deter-
mining the nature of these responses.
The results of several studies suggest that reductions
in plasma volume are not necessary to observe PEH.
C16roux et al 1718 reported that, in hypertensive humans
after cycling exercise at 50% of maximal oxygen uptake,
arterial blood pressure was reduced, whereas plasma
volume remained unchanged from control values. In
subjects 60 minutes after treadmill exercise at approxi-
mately 70% of maximal heart rate, Kaufman et al23 and
Hara and Floras22 reported reductions in systolic and
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diastolic arterial blood pressures, respectively, without
significant changes in plasma volume. In older humans
with essential hypertension, plasma volume remained
slightly increased from control for 1 hour after exercise
at 50% of maximal aerobic capacity and was reduced on
average 4% for 3 hours after exercise at 70% of maximal
aerobic capacity.12 However, systolic arterial blood
pressure was reduced from control levels after both
intensities of exercise. Moreover, plasma volume was
reduced a similar magnitude in control subjects after 4
hours of sitting, whereas systolic and diastolic arterial
blood pressures remained unchanged from control lev-
els. Taken together, these results suggest that reduc-
tions in plasma volume appear not to play a key role in
PEH.
Sympathetic nerve activity. The results of several stud-
ies indicate that inhibition of basal sympathetic nerve
discharge may contribute to PEH and PSH in hyperten-
sive populations. Floras et al20 reported significant
reductions (10 mm Hg) in systolic arterial blood pres-
sure and muscle sympathetic nerve activity in border-
line hypertensive subjects 60 minutes after treadmill
exercise (Fig 5). Moreover, simultaneous reductions in
arterial blood pressure and sympathetic nerve discharge
(renal and splanchnic) have been observed after pro-
longed sciatic nerve stimulation in SHR4041 and prehy-
pertensive Dahl salt-sensitive rats.39 The results of
studies using plasma levels of norepinephrine as an
indirect measure of sympathetic nerve activity have
been inconsistent, as postexercise plasma levels have
been reported to be slightly increased,26 unchanged,33
and reduced18 from control values in borderline hyper-
60 Mln Alter Exercise
120/88
10 «
tensive, hypertensive, and mildly hypertensive humans,
respectively.
In normotensive humans, Hara and Floras22 reported
that diastolic and mean arterial blood pressures were
reduced, whereas muscle sympathetic nerve activity and
plasma norepinephrine levels remained unchanged
from control levels after submaximal exercise, suggest-
ing that PEH can occur in normotensive humans in the
absence of reductions in sympathetic nerve activity.
Humoral and local factors. Circulating hormones, lo-
cal metabolic factors, or both may play a role in
mediating PEH. Unfortunately, the studies to date have
not provided information that clarifies the influence of
these mechanisms on PEH.
Plasma concentrations of epinephrine have been re-
ported to be unchanged33 and increased18 after exercise
that elicits PEH. PEH is observed after /3-receptor
antagonism with epanolol and atenolol,33 suggesting
that /J-adrenergic receptor-mediated vasodilation does
not play a key role in this response. Mean plasma
vasopressin levels have been reported to be unchanged26
and increased33 after exercise that elicits PEH. Al-
though vasopressin produces vasoconstriction of iso-
lated arterial segments in vitro,45 the increase in arterial
blood pressure after vasopressin administration in intact
animals is less than expected.46 In this regard, vasopres-
sin has been reported to sensitize the arterial barore-
ceptor reflex, increase forearm blood flow, and decrease
forearm vascular resistance.4749 Whether vasopressin
plays a role in PEH has not been determined.
Other humoral factors may also play a role in PEH.
For example, acute exercise increases plasma levels of
immunoreactive atrial natriuretic peptide,50-51 which has
potent local vasodilator effects and can induce de-
creases in arterial blood pressure.52 However, Hara and
Floras22 reported reductions in diastolic and mean
arterial blood pressures after submaximal exercise in
normotensive subjects despite the fact that plasma
levels of atrial natriuretic peptide were reduced com-
pared with control levels.
Endothelium-derived relaxing factor is an endoge-
nous vasodilator released by the vascular endotheli-
u m 53-56 i t j s a powerful vasodilator agent that plays a
role in the vascular relaxation produced by acetylcho-
line and other endothelium-dependent vasodilators
such as bradykinin, histamine, and substance P.53-56 The

chemical mediator of endothelium-derived relaxing fac-
tor is nitric oxide.54 Moncada et al55 have proposed that
there is a nitric oxide-dependent tone in the cardiovas-
cular system that plays a role in the regulation of arterial
blood pressure. Mechanical factors associated with in-
creased arterial blood flow are thought to be one
possible mechanism by which these substances are
released from the endothelium.55 It is possible that the
hyperemia associated with physical exercise stimulates
their release, and this may contribute to the vasodilation
of skeletal muscle during and possibly after exercise.
Reduced vascular responsiveness to adrenergic re-
ceptor activation may also play a role in PEH. Howard
and DiCarlo37 measured changes in rabbit iliac blood
flow velocity induced by bolus injections of the a-adren-
ergic receptor agonist phenylephrine during control
conditions and after a single bout of treadmill exercise.
The reduction in iliac blood flow velocity at the same
dose of phenylephrine was attenuated after exercise
compared with nonexercise control days, suggesting that
the ability of the hind limb vasculature to constrict in
response to activation of a-adrenergic receptors is re-
duced after acute exercise in conscious rabbits. Phenyle-
phrine-induced alterations in iliac blood flow velocity
were obtained without changes in mean arterial pres-
sure or heart rate as the hind limb was functionally
isolated. This allowed for evaluation of the direct effects
of acute exercise on vascular function without eliciting
baroreceptor reflex-mediated changes in arterial pres-
sure. Recent data from the same laboratory indicate
that acute exercise also attenuates phenylephrine-in-
duced contraction of rabbit isolated aortic rings.58 The
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fact that after acute exercise hind limb vascular respon-
siveness to a-adrenergic receptor activation is attenuat-
ed57-58 and muscle sympathetic nerve activity has been
reported to be reduced20 suggests that both local and
neural alterations in skeletal muscle may contribute to
PEH.
Two metabolic factors proposed to be involved in the
local control of skeletal muscle blood flow during exer-
cise are the potassium ion and adenosine,59 both of
which produce vasodilation.60-61 Whether the potassium
ion plays a role in PEH is not clear. Mean plasma levels
of potassium have been reported to be unchanged25 and
increased33 after submaximal exercise that elicits PEH.
Moreover, plasma potassium was unchanged compared
with prestimulation control levels at 15 and 180 minutes
after cessation of electric muscle stimulation in the hind
limb of the SHR that produced PSH.34 A possible
influence of adenosine in mediating PEH has not been
determined.
It is clear that additional studies are needed to define
more completely a role for various humoral and local
factors in mediating PEH.
Peripheral Afferent Mechanisms
Somatic afferent stimulation. Somatic afferents are
involved in mediating PSH because this response is
elicited by electrical stimulation of the cut, central end
of the sciatic nerve in anesthetized rats,39 whereas PSH
is not observed after sham sciatic nerve stimulation.39
Stimulation parameters that activate predominantly
A-delta (or group III) afferent fibers appear to mediate
this effect.41 The hypotension observed in response to
direct electrical stimulation of hind limb skeletal mus-
Kenney and Seals Hypotension After Exercise 659
cles is also of neurogenic origin, as this response is
eliminated if the sciatic nerve has been anesthetized
before the onset of stimulation.34
Sustained stimulation of muscle afferents during ex-
ercise is well established. Contracting skeletal muscle
stimulates both mechanoreceptor and metaboreceptor
(chemosensitive) sensory afferents.6264 Studies in anes-
thetized cats have established that static and rhythmic
contractions of cat hind limb muscles reflexly increase
arterial blood pressure, heart rate, and renal sympa-
thetic nerve activity.6569 Substantial evidence indicates
that these responses are mediated by stimulation of
group HI and IV muscle afferents.677°-72 Whether stim-
ulation of muscle afferents contributes to PEH has not
been established. However, dynamic exercise and elec-
trical stimulation of somatic afferents are known to
produce a number of similar responses, including (1)
sustained increases in arterial pressure and heart
rate, 394164 (2) postcontraction/stimulation reductions in
arterial pressure,* and (3) an increase in pain thresh-
old.7375 Collectively, these observations suggest that
exercise-induced stimulation of muscle afferents may
play a role in PEH. If so, it is not clear whether this
effect is mediated by a sustained activation of these
afferents during the postexercise period or, alterna-
tively, by a decrease in afferent activity on cessation of
exercise.
Baroreceptor afferent stimulation. The rise in arterial
blood pressure above resting levels during short-term
exercise is thought to be mediated by an upward reset-
ting of the baroreceptor reflex operating (set) point.7677
One current hypothesis is that central command causes
this via a direct effect on the medullary areas involved in
baroreceptor reflex control.78 It is unclear whether the
converse of this, ie, a downward resetting of the barore-
ceptor reflex at the cessation of exercise, could be
involved in mediating PEH. The removal of central
command and/or other central inputs at the offset of
exercise should cause the operating point for arterial
pressure to return to resting levels. However, the mech-
anism by which these resting levels could be perceived
as inappropriately high, thus resulting in further lower-
ing of pressure (PEH), is not as obvious. Nevertheless,
a downward resetting of the set point for baroreceptor
reflex control of blood pressure remains a possible
factor in PEH.
Cleroux et al17 reported that the stimulus-response
relation between central venous pressure (stimulus for
cardiopulmonary baroreceptors) and forearm vascular
resistance was shifted downward to lower forearm vas-
cular resistance at a given level of central venous
pressure after exercise compared with control condi-
tions. This apparent alteration in baroreceptor reflex
regulation of forearm vascular resistance was observed
in hypertensive but not normotensive subjects and was
primarily due to changes in the control of skeletal
muscle blood flow. These results raise the possibility
that exercise-induced modulation of the baroreceptor
reflex control of muscle sympathetic nerve activity may
affect skeletal muscle vascular resistance after exercise
in hypertensive subjects.
Several other observations are consistent with the
fact that PEH is associated with altered baroreceptor
'References 12, 15, 17, 18, 20, 23, 29, 31, 32, 39, 41.
 660 Hypertension Vol 22, No 5 November 1993
reflex control of the circulation. For example, barore-
ceptor reflex control of heart rate has been reported to
be enhanced after a short-term bout of maximal exercise
in normotensive79 and borderline hypertensive30 hu-
mans. With regard to regulation of regional blood flow,
Bennett et al15 reported potentiated forearm vascular
resistance responses to lower body negative pressure
(cardiopulmonary baroreceptor unloading) in hyperten-
sive subjects after compared with before a single bout of
exercise. It is unclear, however, exactly how these
changes in baroreceptor reflex control of the circulation
may contribute to PEH.
Thermoreflexes. Exercise increases metabolic heat
production and internal body temperature. In humans,
eccrine sweating and active vasodilation of cutaneous
blood vessels are the two primary effector mechanisms
for dissipating heat under conditions of thermal stress.80
Because activation of these mechanisms increases cuta-
neous vascular conductance, decreases systemic vascu-
lar resistance, and thus can reduce arterial blood pres-
sure, thermally induced physiological adjustments may
contribute to PEH.
As stated previously, several studies have reported
parallel decreases in arterial blood pressure and fore-
arm vascular resistance after exercise,1819 suggesting
that hemodynamic changes in forearm muscle or skin or
both may contribute to PEH. Sustained increases in
blood flow to forearm skin would provide evidence
indicating that thermoregulatory vasodilation plays a
role in PEH. In this regard, hand (primarily skin tissue)
vascular resistance is significantly reduced after submax-
imal exercise in hypertensive and normotensive humans
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(Fig 4).18 However, because forearm skin blood flow is
under different regulatory control than hand blood flow,
changes in the latter may not provide useful information
concerning regulation of blood flow to forearm skin.18
Moreover, as emphasized by Cldroux et al,18 if alter-
ations in hand blood flow were reflected in forearm
hemodynamic changes, it would be expected that fore-
arm vascular resistance should be lower immediately
after exercise compared with time points further re-
moved from the cessation of exercise (ie, when body
temperature has returned to control levels). However,
this was not the case in their hypertensive subjects, as
reductions in forearm vascular resistance were not
significantly different at 30, 60, and 90 minutes after
exercise (Fig 4). In addition, PEH occurs in response to
moderate exercise with durations as short as 3 to 10
minutes.13-24 Taken together, these findings suggest that
PEH is not necessarily associated with thermoregula-
tory vasodilation.
Central Mechanisms
Endogenous opioid pathways. Endogenous opioids are
thought to play an important role in cardiovascular
regulation.81 The opioids are generally classified into
three groups: endorphins, enkephalins, and dynor-
phins.82 Moreover, there are three widely accepted
opioid receptor types referred to as \i-, 5-, and /c-recep-
tors.83 The precise relation among these opioids and
receptors is not well understood; however, there is some
degree of specificity.83 For example, /3-endorphin has
been shown to bind selectively to /x- and 5-receptors,
whereas dynorphin A and [leujenkephalin have affinity
for K- and 5-receptors, respectively.83
MAP
BP
HR
400 ,-
bMtl/Mn
SOC*
5 mm
FIG 6. Tracings show mean arterial pressure (MAP),
pulsatile blood pressure (BP), and heart rate (HR) from a
spontaneously hypertensive rat during control before
sciatic nerve stimulation (A) and 2.5 hours after cessation
of sciatic nerve stimulation (B). Note the marked reduc-
tion in arterial blood pressure after stimulation compared
with control levels. Also note reversal of the stimulation-
induced depressor response by naloxone administered
intravenously (B). Reprinted with permission from Yao et
al. 41
Poststimulation reductions in arterial blood pressure
in SHR are reversed toward control levels after admin-
istration of high doses of naloxone, an opioid receptor
antagonist with a high affinity for /i-receptors (Fig
6),40'41 whereas pretreatment with naloxone prevents
the development of PSH.4042 These findings suggest that
endogenous opioid systems are involved in mediating
PSH. However, because high doses of naloxone can
antagonize 5- and K-receptors as well as ^-receptors,84
these results do not indicate which opioid receptors play
a role in mediating PSH. In this regard, Hoffmann et
al37 reported that selective antagonism of opioid K-re-
ceptors completely reversed PSH in SHR, whereas the
depressor response was partially reversed by antago-
nism of opioid 5-receptors. In contrast, PSH was not
affected by the selective antagonism of opioid ^.-recep-
tors.37 These findings indicate that opioid K- and to
some extent 5-receptors are involved in mediating PSH
in SHR.37
It has been postulated that sustained somatic afferent
stimulation induces activation of central endogenous
opioid systems, which in turn produce sympathoinhibi-
tion.85 This inhibitory influence may be masked during
exercise by the sympathoexcitatory influences of central
command and peripheral chemoreceptor stimulation.85
However, once exercise is completed, the physiological
effects of sustained activation of endogenous opioid
systems may predominate and produce hypotensive and
sympathoinhibitory responses.85 In this regard, plasma
levels of /3-endorphin have been reported to be in-
creased after exercise in humans,86-88 and increased
levels of /3-endorphin in the brain89 and cerebrospinal
fluid90 have been reported after exercise in rats. More-
over, alterations in opioid receptor occupancy have
been demonstrated in specific areas of the brain after
exercise in experimental rats.91 PEH is attenuated in
SHR by the administration of naloxone.29 However, the
involvement of endogenous opioids in mediating reduc-
tions in arterial pressure after submaximal exercise in
normotensive humans is equivocal. Boone et al16 re-
ported that naloxone administration transiently re-
versed reductions in systolic and mean arterial blood
pressures, whereas Hara and Floras22 reported that the
administration of naloxone did not prevent postexercise

reductions in diastolic and mean arterial blood
pressures.
These observations suggest that activation of endog-
enous opioid pathways can contribute to PEH in nor-
motensive humans and hypertensive rats. Because the
magnitude of the PEH response is greater in hyperten-
sive than normotensive humans, it is tempting to spec-
ulate that opioid receptor blockade may produce a
greater effect on PEH in hypertensive humans.
Central serotonin. Central serotonergic mechanisms
have been implicated in mediating PSH. Pretreatment
with /7ara-chlorophenylalanine methyl ester-HCl, a
tryptophan hydroxylase inhibitor, abolishes PSH in
SHR.42 Furthermore, administration of the serotonin
precursor 5-hydroxy-DL-tryptophan before sciatic nerve
stimulation augments the poststimulatory reduction in
arterial blood pressure.42 The mechanism by which
serotonin might contribute to PSH is unknown.
Clinical Significance
An important issue is whether PEH is simply an
interesting short-term physiological phenomenon or
might be an important factor in the blood pressure-
lowering effect of chronic exercise. To contribute to the
sustained lowering of arterial blood pressure observed
with regular exercise, PEH must be sustained at a
sufficient level for a sufficient duration throughout the
day. If this were the case, an acute bout of exercise,
repeated regularly, might be an important nonpharma-
cologic tool in the control of hypertension. To deter-
mine whether PEH has potential clinical implications,
at least three important questions must be answered.
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First, is the PEH response of sufficient magnitude to be
considered clinically significant? Second, is the duration
of the hypotensive response sufficient to lower daily
mean arterial blood pressure? Third, is the hypotension
evoked and sustained under conditions of normal daily
living (ie, outside of the laboratory)?
The peak exercise-induced reductions in systolic and
diastolic arterial blood pressures calculated in this arti-
cle, 18 to 20 and 7 to 9 mm Hg, respectively, would likely
be considered clinically significant for hypertensive hu-
mans. Reductions in arterial blood pressure of approx-
imately the same magnitude are associated with a
reduced risk for stroke and certain other forms of
cardiovascular disease.9293 Thus, one of the criteria for
therapeutic efficacy appears to be satisfied.
On the other hand, although PEH has been consis-
tently documented for 2 to 3 hours, the average duration
of the hypotensive response remains to be determined.
Many studies have not reported data on the time course
for reattainment of control values. One report27 indi-
cates that PEH may be sustained for at least 13 hours,
with diastolic and mean arterial blood pressures still
remaining depressed at the end of this period. However,
this duration of PEH was not confirmed in a recent
investigation31 (see below). For a single session of
exercise, repeated daily, to contribute to a sustained
antihypertensive effect, arterial blood pressure would
have to remain depressed for most of the subsequent 24
hours after exercise.
Finally, it is well established that the absolute levels
and behavior of arterial blood pressure are influenced
significantly by the environment in which the measure-
ments are made.4496"98 In this context, it is important to
Kenney and Seals Hypotension After Exercise 661
emphasize that most human investigations have docu-
mented PEH only under quiet resting conditions in the
laboratory. This is obviously not the case in real life.
The question of whether postexercise reductions in
arterial blood pressure are sustained for a prolonged
period of time under free-living conditions has been
addressed in two recent studies.27-31
Somers and colleagues31 determined the effects of
incremental leg cycling exercise to exhaustion on PEH
in 12 normotensive and 12 borderline or mildly hyper-
tensive men and women. PEH was documented under
resting conditions in the laboratory in both groups. The
subjects then were sent home and recorded their own
blood pressures for a period of 8 to 12 hours. The same
procedure was repeated on a nonexercise control day.
The levels of arterial blood pressure recorded at home
were not different on the exercise and control days in
either the hypertensive or the normotensive subjects,
indicating no sustained effect of the acute exercise
under normal living conditions.
In marked contrast to these results, Pescatello and
colleagues27 documented a prolonged hypotension after
a single bout of submaximal exercise in hypertensive
subjects. Six normotensive men and six mildly hyperten-
sive men cycled for 30 minutes at 40% and 70% of peak
oxygen uptake. Arterial blood pressure was lower at rest
in the laboratory after compared with before exercise in
hypertensive but not normotensive men. Blood pressure
recorded outside the laboratory with an automated
ambulatory monitor for 13 hours remained significantly
below preexercise baseline levels in the hypertensive
subjects (Fig 3). Moreover, the average levels of arterial
blood pressure were significantly lower over this 13-
hour period after exercise compared with the same
period on a nonexercise control day.
The two most obvious differences between the studies
are the methods of outside-the-laboratory blood pres-
sure measurements and the nature of the exercise
stimulus. Concerning the latter, it has been reported
that chronically performed low- to moderate-intensity
exercise has a blood pressure-lowering effect, whereas
higher intensity exercise has a lesser effect, no influ-
ence, or actually produces a "hypertensive" ef-
fect.3-4"100 If true, it is possible that the apparent
discrepancies between the results of the above two
studies27-31 could be explained by this factor.
Thus, the available experimental evidence is equivo-
cal as to whether PEH is sustained for a prolonged
period of time under normal living conditions. Addi-
tional investigations in which ambulatory arterial blood
pressure recordings are performed outside the labora-
tory for 24 to 48 hours after acute exercise will be
needed to answer this question. In these studies, the
nature of the exercise stimulus should be carefully
controlled; low- to moderate- versus high-intensity ex-
ercise should be examined as well as several modes of
exercise commonly performed in daily life (eg, leg
cycling versus walking or jogging). If arterial blood
pressure can be shown to remain depressed for this
period of time, one might reasonably conclude that the
sustained blood pressure-lowering effects of physical
training could, at least in part, be mediated by the
hypotensive effects of single bouts of exercise repeated
on a regular basis.
 662 Hypertension Vol 22, No 5 November 1993
Possible Mechanisms Mediating Postexerclse Hypotension in Human Subjects for Which There Is
Some Experimental Support
Mechanism
Decreased stroke volume and cardiac output
Decreased limb (skin and/or skeletal muscle) vascular resistance
Decreased total peripheral resistance
Reduced sympathetic nerve discharge
Reduced vascular responsiveness to a-adrenergic receptor-mediated stimulation
Group III muscle afferents
Modulation of baroreceptor reflex control of vascular resistance
Endogenous opioid and serotonergic systems
Summary and Conclusions
The experimental findings reviewed here indicate
that PEH is observed in normotensive humans, patients
with borderline essential hypertension, and patients
with established essential hypertension as well as in
SHR. PEH occurs in response to several types of
large-muscle dynamic exercise (eg, walking, running,
cycling, and swimming) at intensities between 40% and
70% of maximal oxygen consumption as well as after
exercise to exhaustion. Moreover, PEH is observed
after a wide range of exercise durations from as short as
3 to 10 minutes to as long as 60 minutes. Because
exercise is associated with activation of somatic affer-
ents, electrical stimulation of the sciatic nerve and of
hind limb skeletal muscles in the rat has been used to
study the role of somatic afferents in mediating PEH.
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PSH has been observed in SHR, Wistar-Kyoto nor-
motensive rats, and prehypertensive Dahl salt-sensitive
rats.
Postexercise reductions in arterial blood pressure are
generally greater in hypertensive compared with nor-
motensive humans and animals. In studies to date,
maximal exercise-induced reductions in systolic and
diastolic arterial blood pressures have been on average
18 to 20 and 7 to 9 mm Hg, respectively, in hypertensive
humans and 8 to 10 and 3 to 5 mm Hg, respectively, in
normotensive humans. Similarly, the maximal stimula-
tion- and exercise-induced reductions in arterial blood
pressure are generally greater in hypertensive compared
with normotensive rats.
Little information is available on the time course for
reattainment of postexercise reductions of arterial
blood pressure to control levels. The results to date
indicate that PEH persists anywhere from 2 to at least
13 hours. The length of the PEH response is generally
longer in hypertensive than normotensive humans. To
date, the two studies27-31 that have addressed the ques-
tion of whether PEH is sustained for a prolonged period
of time under free-living conditions have come to oppo-
site conclusions. No experimentally controlled investi-
gation has determined whether arterial blood pressure
remains reduced from control levels for at least 24 hours
after exercise.
We have also reviewed potential mechanisms by which
exercise and somatic afferent stimulation may induce
sustained reductions in arterial blood pressure. Cardiac
output has been reported to be decreased from control
levels after exercise in older subjects with essential hyper-
Reference
12
18,19,22
18,19,22,26
20,39-41
57,58
34,38-41
17
16,29,37,40-42
tension. The reduction in cardiac output was primarily
mediated by a decrease in stroke volume. Neither reduc-
tions in cardiac preload nor increases in cardiac afterload
could account for the reduced stroke volume, suggesting
that alterations in myocardial contractility may contribute
to PEH. Sustained decreases in limb (forearm and calf)
vascular and total peripheral resistances have been re-
ported more consistently after exercise in normotensive
and hypertensive subjects. These observations suggest that
a sustained vasodilation in skeletal muscle and other
arterial beds may contribute to PEH. Relatedly, reduc-
tions in muscle sympathetic nerve discharge have been
observed after exercise in hypertensive humans, whereas
sympathetic nerve discharge is reduced from control levels
after somatic afferent stimulation in SHR and prehyper-
tensive Dahl salt-sensitive rats. The factors involved in
mediating the exercise-induced changes in forearm vascu-
lar resistance and sympathetic nerve discharge have not
been established; however, baroreceptor reflex control of
forearm vascular resistance is altered after a single bout of
exercise. Moreover, vascular responsiveness to a-adrener-
gic receptor-mediated activation is reduced after exercise.
Somatic afferents are involved in mediating PSH
because this response is elicited by electrical stimulation
of the cut, central end of the sciatic nerve. Whether
muscle afferents contribute to PEH has not been estab-
lished. However, dynamic exercise and electrical stimu-
lation of somatic afferents are known to produce a
number of similar responses, including sustained in-
creases in arterial pressure, heart rate, and sympathetic
nerve activity and postcontraction/stimulation reduc-
tions in arterial pressure. Several observations support a
role for endogenous opioids in mediating PSH. It is
thought that sustained somatic afferent stimulation in-
duces activation of central endogenous opioid systems,
which in turn produce sympathoinhibition and hypoten-
sion. The results of one study have shown that naloxone
administration can transiently reverse PEH in nor-
motensive humans. In general, an important role for
various humoral, local metabolic, and thermal factors in
PEH has not been well established. The Table provides
a list of possible mechanisms involved in mediating PEH
for which there is current experimental support.
In conclusion, it appears that the magnitude of the PEH
response observed in hypertensive subjects is significant
and would likely be considered clinically important. How-
ever, more investigation is required to determine if the
duration of the response is sufficient in real-life conditions

to contribute to the reduction in arterial blood pressure
observed after chronic exercise.
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