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(Hypertension. 1995;25:391-398.)
© 1995 American Heart Association, Inc.
Articles |
Effects of Different Training Intensities on the Cardiopulmonary Baroreflex Control of Forearm Vascular Resistance in Hypertensive Subjects
From the Hypertension Research Unit, Centre Hospitalier de l'Université Laval Research Center, Laval University, Québec, Canada.
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Abstract |
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Abstract We recently reported that ambulatory blood pressure decreased during the awake period after training at low intensity but not after training at moderate intensity in subjects with mild to moderate hypertension. The reasons for the failure of moderate-intensity training to reduce blood pressure are not clear. In the present article, we report the effects of different training intensities on cardiopulmonary baroreflex control of forearm vascular resistance, left ventricular function, vascular reactivity, and resistive vessel structure. After moderate-intensity training, the cardiopulmonary baroreflex control of forearm vascular resistance was significantly attenuated, left ventricular performance was enhanced, and vascular reactivity and resistive vessel wall thickness in the calf were reduced compared with values after the control sedentary period. No significant changes in these indexes were found after low-intensity training compared with sedentary values. These results indicate that attenuation of the cardiopulmonary baroreflex control of skeletal muscle vascular resistance after training at moderate intensity may contribute to the lack of antihypertensive effects, as seen from unchanged ambulatory blood pressure levels during the awake period, after training at this intensity. A decreased vascular smooth muscle response to sympathetic nervous stimulation appears to be partly involved in the alteration in the baroreflex control of forearm vascular resistance after moderate-intensity training. Although these findings should be confirmed in a greater number of subjects, the present results point to a key mechanism that might explain why moderate endurance exercise training fails to lower arterial blood pressure in hypertensive subjects.
Key Words: exercise • muscles • vascular resistance • ventricular function, left • norepinephrine • vasodilation
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Introduction |
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It is generally recognized that physical training reduces blood pressure (BP) in subjects with essential hypertension.1 2 3 Although the mechanisms underlying this effect are not well understood, it is becoming clear that the amplitude of the BP reduction is not proportional to the intensity of the training program. In fact, a meta-analysis of earlier studies revealed that the fall in BP tended to be inversely correlated to training intensity.1 More recently, we reported that ambulatory BP during the awake period decreased significantly after training at a low intensity (50% of maximal oxygen uptake) but not after training at a moderate intensity (70% of maximal oxygen uptake).4 However, the reasons for the failure of moderate-intensity training to reduce BP are not clear.
The baroreflex control of skeletal muscle vascular resistance, mainly the cardiopulmonary reflex, contributes importantly to the reflex control of circulation (see Mark and Mancia5 ). It was previously suggested that an attenuated cardiopulmonary baroreflex control of circulation could contribute to the maintenance of high BP in essential hypertension and might be involved in the evolution of this condition.6 Indeed, the cardiopulmonary baroreflex control of forearm vascular resistance (FVR) becomes progressively attenuated as essential hypertension progresses in severity.6
Earlier studies on the effects of training on the cardiopulmonary baroreflex control of FVR have produced inconsistent results.7 8 9 10 11 12 It was suggested that these inconsistencies may be related to the BP status of the subjects examined (ie, hypertensive versus normotensive), to the training intensity of the programs used, or both.13 Indeed, one study that included hypertensive subjects and used a low-intensity training program found an enhanced baroreflex after training,8 whereas some but not all9 other studies that examined normotensive subjects and used a moderate-intensity training program reported an attenuated baroreflex after training.10 11 12 To our knowledge, no study has yet specifically examined the effects of different training intensities on the cardiopulmonary baroreflex control of FVR in hypertensive subjects.
Because this baroreflex mechanism is involved in rapid adjustments of the circulation and is frequently elicited during the day, we hypothesized that an attenuation of the baroreflex control of skeletal muscle vascular resistance might contribute to the failure of moderate-intensity training to reduce awake ambulatory BP in hypertensive subjects. Furthermore, we speculated that an augmentation of the baroreflex control of skeletal muscle vascular resistance might contribute to the reduction in awake ambulatory BP after low-intensity training. We used reflex vascular responses in the forearm during changes in central blood volume to evaluate the cardiopulmonary baroreflex control of skeletal muscle vascular resistance.5 6 7 8 12 14 15 The results presented here were obtained during the course of a study of which the ambulatory BP results were previously published in detail.4
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Methods |
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Subjects
Eleven subjects with established mild to moderate hypertension gave informed consent to participate in this study, which was approved by our institutional ethics committee on human research. Patients with a smoking habit; a history of myocardial infarction, heart failure, angina pectoris, or exercise-induced angina pectoris; or any medically significant deviation from normal laboratory values were excluded. None of the subjects was receiving antihypertensive therapy or any other medication during the study. Medication was gradually withdrawn in those subjects previously on antihypertensive therapy, and they remained without treatment during an additional 6-week period before entering the study. As previously described,4 hypertensive subjects qualified for the study if the mean of three measurements of their seated diastolic pressure was between 90 and 114 mm Hg on the last two visits.
Study Outline
The study protocol was previously described in detail
elsewhere.4 Briefly, we used a 3x3 Latin square crossover
design to compare the effects of training at two different intensities
with those of a control sedentary period on the reflex control of FVR.
The subjects were evaluated at four study end points. The first
evaluation occurred after a 4-week baseline period and subsequent
evaluations after each of three 10-week periods, during which the
subjects remained sedentary, trained at 50% of maximal oxygen uptake,
or trained at 70% of maximal oxygen uptake according to the Latin
square sequences.4
Each evaluation required 3 separate days at 2- to 3-day intervals. Additional exercise sessions were performed during these intervals so that each measurement was performed 40 to 64 hours after the previous exercise session. Ambulatory BP, 24-hour urinary electrolyte excretion, and blood volume were measured first.4 Reflex control of FVR and maximal oxygen uptake were then measured on days 2 and 3, respectively.
Training Program
The subjects exercised three sessions per week at 1-day
intervals on cycle ergometers (model 819, Monark). Each session
included a 5-minute warm-up, a 45-minute period of exercise at the
predetermined workload, and a 10-minute cool-down period. The workload
required to induce an increase in oxygen uptake up to 50% or 70% of
maximal values was adjusted along the course of the 10-week periods by
taking heart rate into account.4 BP and heart rate were
monitored every 15 minutes during exercise.
Measurements
The measurement methods briefly presented below were
previously validated in our laboratory and described in detail
elsewhere.4 14 16
Maximal oxygen uptake was determined by analysis of expired gases (Energy Expenditure Unit 2900, Sensormedics) during an increased work test schedule on a cycle ergometer (Ergomedic 829E, Monark).4 BP was measured by a standard mercury sphygmomanometer, with the first and the fifth Korotkoff sounds taken as the systolic and diastolic values, respectively. Mean arterial pressure was calculated as diastolic plus one-third pulse pressure. Heart rate was measured with a tachograph triggered by the R wave of the electrocardiogram recorded in lead III (7P4, Grass Instrument Co), and both traces were recorded on polygraph paper.
Forearm and calf blood flows were measured by venous occlusion plethysmography (EC-4, DE Hokanson Inc) using mercury-in-Silastic strain gauges.17 Measurements were derived from the average of three consecutive flow curves. Blood flow variability (standard deviation) calculated on two sequential averages was 5.1%, with a correlation coefficient of .85 (P<.01), in agreement with previous reports.6 14 15 FVR and calf vascular resistance were calculated by dividing mean arterial pressure by the respective blood flow. Blood samples for plasma norepinephrine assay were withdrawn via an antecubital vein catheter.16 Plasma norepinephrine was measured in duplicate with a specific and sensitive radioenzymatic assay.18 In our hands, this method allows detection of norepinephrine levels as low as 60 pmol/L.
Indexes of Central Blood Volume
Echocardiographic measurements of left ventricular dimensions
(Mark III Ultrasonograph, Advanced Technology Laboratories) were
performed in a left lateral decubitus position. Left ventricular
internal diameter in diastole (LVIDD) was determined in M-mode after
the parasternal long axis was located in two-dimensional
mode.14 16 Central venous pressure (CVP) was estimated by
measuring venous pressure from the antecubital vein catheter connected
via a saline-filled line to a pressure transducer (P 23 ID, Gould Inc).
The transducer was positioned at the midsternal level while the arm
hung down on the side of the bed in a left lateral decubitus position
to allow simultaneous determination of LVIDD. Although the dependent
arm method is usually performed with the right arm in a right lateral
decubitus position,15 19 we found that venous recordings
were similar in both arms.14
Indexes of Left Ventricular Function
Measurements of LVIDD and left ventricular internal diameter in
systole (LVIDS) as well as interventricular septal thickness (IVST) and
posterior wall thickness (PWT) were made according to the Penn
convention.20 The intrasubject variability (standard
deviation) of LVIDD, LVIDS, IVST, and PWT measurements 1 week apart in
a control group of subjects ranged from 2.0% to 2.3%. Stroke volume
was calculated as the difference between end-diastolic and
end-systolic volumes using the formula of Teichholz et
al.21 Cardiac output was obtained from the product of
stroke volume and heart rate recorded at the time of echocardiographic
measurements.16 The intrasubject variabilities for stroke
volume and cardiac output were 5.0% and 8.0%, respectively, with
correlation coefficients of .85 and .76 (both P<.01).
Left ventricular shortening fraction (calculated as {[LVIDD- LVIDS]/LVIDD}x100%) and ejection fraction (stroke volume divided by end systolic volumex100%) were taken as indexes of left ventricular contractility. End-systolic wall stress was calculated with the equation of Wilson and coworkers.22 The intrasubject variability of these indexes ranged from 3.0% to 7.4% and correlation coefficients from .76 to .83. Finally, left ventricular mass was calculated according to Devereux and Reichek20 and expressed per unit of body surface area.
Maneuvers
Baroreflex control of FVR was examined during passive leg
raising (LR), which activates cardiopulmonary receptors and induces
reflex vasodilation in the forearm,23 and during lower
body negative pressure (LBNP), which deactivates cardiopulmonary
receptors and induces reflex vasoconstriction in the
forearm24 as described previously in
detail.14 The pressure within the LBNP device was reduced
by 15 (LBNP15) and 40 (LBNP40) mm Hg below atmospheric pressure.
During LBNP40, arterial baroreceptors and cardiopulmonary receptors are
deactivated,6 14 25 and the FVR response therefore
involves both arterial and cardiopulmonary baroreflexes.
Baroreflex control of FVR was examined from the slope of the relation between FVR and LVIDD as well as between FVR and estimated CVP for each subject at each study end point. Slopes were calculated taking into account the FVR response during LR and LBNP15 maneuvers only and also considering the results during LBNP40. In a control group of subjects, intrasubject variability of FVR/CVP and FVR/LVIDD relations calculated with three and four data points ranged from 10.4% to 15.2% and correlation coefficients from .63 to .98.
Cold Pressor Test
A 60-second cold pressor test during which one hand was immersed
in ice water was performed to examine the FVR response to a stimulus
different from that originating from the cardiopulmonary
region.26 During the cold pressor test, measurements were
performed before and during the last 30 seconds of
immersion.14
Maximal Vasodilation Tests
Maximal blood flows were induced by occluding arterial inflow to
the forearm or calf for 13 minutes by inflating a cuff positioned
around the upper arm or the thigh at 40 mm Hg above systolic pressure.
During the last 2 minutes, exercise consisting of flexing and extending
the fingers or the foot at the ankle was added. This method induces
maximal postischemic hyperemia, and calculated vascular resistance at
this time provides an index of the structure of resistance vessels in
the limb under study.27 28 29 30 The intrasubject variability of
minimal vascular resistance in a control group of subjects was 3.4%
for forearm and 3.7% for calf, with correlation coefficients of .94
and .88, respectively.
Protocol
On study days, all subjects were instructed to have a light
breakfast and abstain from caffeine. Baroreflex control of FVR was
evaluated over a 2-hour period (from 8 to 10 AM) with the
subjects in a supine position, as previously described in
detail.14 Briefly, reflex FVR responses were evaluated
over 1 hour and central blood volume responses over the other hour in
random order. Alternate 10-minute periods of rest and stimulus
application (ie, LR, LBNP15, and LBNP40) were used, and measurements
were made during the last 5 minutes. The small catheter used for blood
sampling for plasma norepinephrine determination and for estimation of
CVP was inserted in an antecubital vein 20 minutes before the
evaluation was begun. Blood samples were withdrawn during the last
minute of each situation. The cold pressor test was performed after the
maneuvers, followed by forearm and calf maximal vasodilation tests. All
measurements were made after each of the four study end points except
the maximal vasodilation tests, which were not performed at
baseline.
Statistical Analysis
Results are expressed as mean±SEM. The effects of training on
the variables at rest and during the various maneuvers were examined
with an ANOVA for repeated measurements.31 The FVR/LVIDD
and FVR/CVP slopes calculated individually for each subject with and
without the data during LBNP40 by the method of least-squares
regression were also compared with ANOVA for repeated measurements.
When a significant (P<.05) F ratio was observed, Fisher's
protected least significant difference test was used to locate
significant differences.
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Results |
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Of the 11 mild to moderate hypertensive subjects enrolled in the study, 9 (1 woman, 8 men; age, 43±2 years; weight, 76±3 kg; height, 175±2 cm) completed all the stages and were included in the analysis. Two subjects withdrew for reasons unrelated to the study. Compliance was 98±2% during training at 50% of maximal oxygen uptake and 96±3% during training at 70% of maximal aerobic capacity. Good-quality echocardiographic measurements could not be obtained in 1 man. The FVR/LVIDD relations and left ventricular function data therefore pertain to 8 subjects.
Compared with the control sedentary period, training at 50% of maximal oxygen uptake did not significantly affect maximal aerobic capacity, whereas training at 70% of maximal oxygen uptake induced a 14% increase (P<.01) (Table 1). Maximal oxygen uptake was higher after the sedentary period than at baseline (P<.05). Training at 50% and 70% of maximal oxygen uptake induced small, similar decreases in body weight, although only the difference after training at 70% was statistically significant compared with that found after the sedentary period (Table 1).
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The effects of these interventions on 24-hour ambulatory BP were
previously reported in detail elsewhere.4 During the awake
period (ie, between 7 AM and 10 PM),
superimposable BP values were found at the baseline evaluation
(152±3/97±2 mm Hg) and after the sedentary period (151±3/96±2
mm Hg). After training at 50% of maximal oxygen uptake, systolic
(-6±2 mm Hg, P<.01) and diastolic pressures (-5±2
mm Hg, P<.05) were significantly reduced, whereas no
significant changes (-4±2/-2±2 mm Hg, both P
.05) were
seen after training at 70% of maximal oxygen uptake compared with
values measured after the control sedentary period.4
Pertinent to the present report is the fact that even more marked
differences in ambulatory BP were found after training at 50%
(-6±4/-5±3 mm Hg) compared with 70% (-1±4/-2±4 mm Hg) of
maximal aerobic capacity between 8 and 10 AM,
corresponding to the period of baroreflex assessment.
Results at Rest
The main cardiovascular and biochemical variables measured during
supine rest at each study end point are presented in Table 1. Heart
rate did not differ at any study end point. Except for diastolic
pressure, which increased after training at 50% of maximal oxygen
uptake, BP was not different after any training regimen compared with
that taken after the control sedentary period. Somewhat higher BP
values were found during the baseline evaluation compared with the
sedentary evaluation.
Similar forearm blood flow and FVR values were found during baseline and sedentary evaluations as well as after training at 70% of maximal oxygen uptake. After training at 50% of maximal oxygen uptake, forearm blood flow was higher and FVR was lower (both P<.05) than during the sedentary evaluation. Concerning baseline hemodynamics in the calf, similar blood flow (1.8±0.1 and 1.9±0.2 mL · 100 mL-1 · min-1, respectively) and vascular resistance levels (61.4±6.2 and 54.8±6.7 U) were also found during the sedentary evaluation and after training at 70% of maximal oxygen uptake. Calf blood flow (2.5±0.3 mL · 100 mL-1 · min-1, P<.05) was higher, but the decrease in calf vascular resistance did not reach significance (51.7±7.1 U, P=.26) after training at 50% of maximal oxygen uptake compared with the sedentary evaluation. Resting values of estimated CVP and plasma norepinephrine did not change during the course of the study.
Left ventricular structure and function indexes are presented in Table 2 and Fig 1. Left ventricular mass index, LVIDD, end-diastolic volume, and cardiac output were similar at each study end point. Stroke volume and left ventricuar shortening fraction and ejection fraction were increased, and end-systolic wall stress decreased after training at 70% of maximal oxygen uptake compared with the sedentary evaluation.
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Responses to Maneuvers
LR and LBNP15 did not induce any significant change in BP or heart
rate (data not shown). In contrast, LBNP40 induced a significant
decrease in systolic pressure (approximately -5 mm Hg) compared with
resting levels during all evaluations; this decrease was associated
with reflex tachycardia (approximately +10 beats per minute). Changes
in systolic pressure and heart rate in response to LBNP40 were similar
at all four study end points.
The slopes of the linear relations between FVR and LVIDD and between FVR and CVP at rest and during the maneuvers are presented in Table 3. Statistical comparison of these relations yielded identical conclusions, whether or not the data from LBNP40 were included in the analysis. Fig 2 illustrates mean FVR and LVIDD during the maneuvers (including LBNP40), with the slopes reflecting the mean values of individual regression lines from Table 3. For clarity, the relations at baseline and after training at 50% and 70% of maximal oxygen uptake are compared in turn to the relation observed after the control sedentary period. The relation was unchanged after the sedentary period compared with the baseline evaluation (Fig 2, top).
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After training at 50% of maximal oxygen uptake, the slope of the FVR/LVIDD relation was also unchanged (Fig 2, middle). Although resting FVR was significantly decreased (Table 1) compared with the sedentary evaluation, all FVR values were shifted downward and to the right after training at 50% of maximal oxygen uptake. Thus, resting FVR levels were not significantly different (P=.36) after training at 50% of maximal oxygen uptake (60.3±7.1 U) compared with those after the sedentary period (63.0±3.3 U) when the small, nonsignificant difference in resting LVIDD during these two evaluations was taken into account (Table 2) (this was done by substituting resting LVIDD values in the individual regression equations after training at 50% of maximal oxygen uptake with those after the sedentary period).
After training at 70% of maximal oxygen uptake, the FVR/LVIDD slope was significantly decreased compared with sedentary values (Fig 2, bottom). Furthermore, the slope of the baroreflex after training at 70% of maximal oxygen uptake was significantly lower compared with the value after training at 50% of maximal oxygen uptake (Table 3). The lower slope of the FVR/LVIDD relation after training at 70% of maximal oxygen uptake was related to smaller reflex changes in FVR, although greater changes in LVIDD were observed during the maneuvers. For example, during LBNP40, FVR increased by 25.3±3.6 U after the sedentary period but by only 15.5±1.5 U after training (P<.05), whereas LVIDD decreased by -5.1±0.8 and -6.4±0.6 mm (P<.05), respectively.
Similar findings were made by comparing the FVR/CVP relations after the baseline period and after training at 50% and 70% of maximal oxygen uptake with the relation after the sedentary period (Table 3). As for LVIDD, greater changes in CVP during the maneuvers contributed to lowering the slope of the FVR/CVP relation after training at 70% of maximal oxygen uptake (eg, during LBNP40, CVP decreased by -3.83±0.56 and -4.29±0.42 mm Hg [P<.05] after the sedentary period and after training, respectively). The attenuation of the FVR/CVP relation after training at 70% compared with 50% of maximal oxygen uptake tended to be positively associated with the loss of ambulatory diastolic pressure control between 8 and 10 AM (r=.66, P=.05).
With regard to plasma norepinephrine concentrations, no significant changes were found during LR or LBNP15 maneuvers compared with resting values (data not shown). Significant increases from resting levels were found in response to LBNP40 (baseline, +714±162; sedentary, +564±250; training at 50%, +832±250; and training at 70%, +640±246 pmol/L), but these were not significantly different at any of the study end points.
Cold Pressor Test
Immersion of one hand in ice water for 60 seconds induced large,
significant increases in FVR. This response was significantly
attenuated after training at 70% of maximal oxygen uptake compared
with the sedentary evaluation whether the increase in FVR was expressed
in absolute units (Fig 3) or as a percentage of change
from baseline (data not shown).
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Maximal Vasodilation Tests
Minimal postischemic FVR was similar after training at 50%
(2.47±0.19 U, P=.23) and 70% (2.43±0.20 U,
P=.17) of maximal oxygen uptake compared with that found
after the control sedentary period (2.73±0.23 U). Calf minimal
vascular resistance was unchanged after training at 50% of maximal
oxygen uptake (3.25±0.72 U, P=.81) but significantly
reduced after training at 70% of maximal oxygen uptake (2.18±0.17 U,
P=.03) compared with sedentary values (3.08±0.39 U).
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Discussion |
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The results of the present study indicate that 10 weeks of physical training at 70% of maximal oxygen uptake significantly attenuated the baroreflex control of FVR in hypertensive subjects, as seen in the lower slopes of the relations between FVR and physiological indexes of central blood volume (ie, LVIDD or CVP) during LR and LBNP maneuvers. This alteration tended to be associated with the loss of ambulatory BP control at the same time of day, ie, between 8 and 10 AM, after training at this intensity compared with findings after training at 50% of maximal oxygen uptake.
Based on skeletal muscle blood flow at rest,32 it can be estimated that skeletal muscle vascular resistance contributes approximately 20% to resting total peripheral resistance. BP maintenance during orthostatic challenges relies to a large extent on vasoconstriction in skeletal muscles.5 Thus, reflex control of circulation in skeletal muscles is important both quantitatively and qualitatively in ensuring appropriate BP maintenance during orthostatic challenges. Therefore, an important implication of the present findings is that attenuation of the cardiopulmonary baroreflex control of skeletal muscle vascular resistance after training at 70% of maximal oxygen uptake may contribute to the lack of antihypertensive effect, as seen from unchanged ambulatory BP levels, during the awake period after training at this intensity.4 Although these findings must await further confirmation in a larger sample, the present results point to a key mechanism that may explain why moderate endurance exercise training fails to lower arterial BP in hypertensive subjects (for review, see Marceau et al4 ). This alteration may be all the more important in preventing a BP reduction in light of the finding that vascular remodeling, as seen from a decrease in minimal postischemic calf vascular resistance, occurred in the leg after training at this intensity.
We had anticipated that the cardiopulmonary baroreflex control of FVR would be augmented after training at 50% of maximal oxygen uptake. We reasoned that an enhanced baroreflex control of circulation could participate in lowering BP with low-intensity training. However, modification of the cardiopulmonary baroreflex control of skeletal muscle vascular resistance is not likely to have contributed to the decreased ambulatory BP during the awake period after training at 50% of maximal oxygen uptake,4 as reflex control of FVR was unchanged after training at this intensity.
Potential Mechanisms
An interesting question concerns the mechanism or mechanisms
underlying the attenuation of the cardiopulmonary baroreflex control of
FVR after training at 70% of maximal oxygen uptake. In a recent study
of normotensive subjects, the reduction in baroreflex control of FVR
was related to an increase in blood volume.12 In the
present study, blood volume was not modified after training
compared with volume after the sedentary period.4 Although
blood volume was significantly higher at baseline than after the
sedentary period,4 the present results indicate that
the slopes of the FVR/LVIDD and FVR/CVP relations were not different
during these evaluations. The decreased responsiveness of
cardiopulmonary baroreflex control of FVR after training at 70% of
maximal oxygen uptake is therefore not likely to be related to an
altered stimulus to cardiopulmonary receptors via a change in blood
volume.
Alterations may occur at the afferent level, at the central integration level, and at the efferent level of the baroreflex. Modifications of the central integration of the baroreflex control of FVR could not be ascertained in our study. Nevertheless, several results underline the possibility that alterations may have occurred along the afferent or efferent portion of the cardiopulmonary baroreflex.
Along the afferent portion, a change in the discharge characteristics of the cardiopulmonary receptors could have been involved in part in the attenuation of the baroreflex. Reflex changes in FVR were smaller after training at 70% of maximal oxygen uptake, although changes in LVIDD and CVP were greater. Greater changes in these indexes of venous return should have triggered greater reflex FVR responses. Changes in left ventricular performance can markedly influence vagal cardiac afferent activity.33 In the present study, several indexes of cardiac function suggest that left ventricular performance increased after training at 70% of maximal oxygen uptake, which should have induced a reduction in resting FVR. It has been shown that the amplitude of the reflex response in vascular resistance depends on the baseline vascular resistance level.34 However, resting FVR was unchanged after training at 70% of maximal oxygen uptake. Therefore, the attenuation of the baroreflex control of FVR after training at 70% of maximal oxygen uptake was independent of a shift in resting FVR after training at this intensity.
Along the efferent portion of the cardiopulmonary baroreflex, a nonspecific change in the neural release of norepinephrine could have been involved in the reduced FVR responses after training at 70% of maximal oxygen uptake. However, similar plasma norepinephrine increases in response to LBNP40 were found after training at 70% of maximal oxygen uptake and during the other situations. Antecubital venous plasma norepinephrine has been shown to be derived mainly from local release in the forearm.35 We interpret our plasma norepinephrine results as suggesting that LBNP40 induced a similar increase in efferent sympathetic nervous activity after training at 70% of maximal oxygen uptake and during the other evaluations. Thus, the reduced FVR response to LBNP40 is not likely to be related to a reduced release of norepinephrine.
The reduced FVR responses may also be related to an alteration at the
effector organ level, that is, the vascular smooth muscle, of the
baroreflex. The smaller reflex increase in FVR during the cold pressor
test after training at 70% of maximal oxygen uptake suggests a
reduction in the ability to increase vasomotor tone in response to an
increase in neural drive. Our results showing an unchanged minimal
vascular resistance in the forearm after training at this intensity
suggest that the structure of resistive vessels was unaffected. Thus,
alteration in norepinephrine/smooth muscle cell signal transduction
might have occurred. This interpretation agrees with the report of a
decreased vasoconstrictor responsiveness to 
-adrenergic receptor
stimulation after training.36 These considerations should
be taken with caution, however, because venous plasma norepinephrine
and maximal vasodilation are indirect indexes of sympathetic nervous
activity and vascular structure, respectively. Furthermore,
unchanged37 or increased38 vasomotor
responses to -adrenergic stimulation have also been reported after
training.
Study Limitations
In the present study, responses after training were compared
with those found after a control sedentary period of equal duration
occurring at random before, between, or after the two training periods
according to the Latin square sequence. A potential study limitation
with this experimental design is that a carryover effect from a
previous 10-week training period may have altered the results during
the sedentary period. However, the baroreflex control of FVR was
unaltered after the sedentary period compared with baseline as
indicated by similar resting FVR levels and reflex changes after the
sedentary period and during the baseline evaluation. Furthermore,
conclusions about the effects of training at 70% of maximal oxygen
uptake on the baroreflex control of FVR are identical whether
posttraining results are compared with sedentary or with baseline
results. We conclude that alterations in baroreflex regulation of FVR
can occur and become reversed within a 10-week period of training and
detraining.
The LR and LBNP maneuvers are likely to produce a stress continuum that affects all baroreceptive populations simultaneously, but to different degrees, depending on stimulus level. However, the observation that BP and heart rate did not change during LR and LBNP15 during the different evaluations suggests that arterial baroreceptors were not activated or deactivated, respectively, during these maneuvers, a contention amply supported in the literature.5 24 In our study, identical conclusions were reached whether the slopes of the relations between FVR and indexes of venous return were calculated using data during rest, LR, and LBNP15 only or together with the data during LBNP40. In addition, several lines of evidence suggest that arterial baroreceptors exert a minimal influence on limb vascular resistance in humans (see Mancia and Mark39 ). Therefore, the cardiopulmonary reflex control of FVR is likely to have been involved more importantly than the arterial baroreflex in the alterations found after training at 70% of maximal oxygen uptake.
Comparison With Previous Studies
The results of the present study indicating that the
cardiopulmonary baroreflex control of FVR is reduced in hypertensive
subjects after 10 weeks of training at 70% of maximal oxygen uptake
agree with most but not all9 40 earlier studies in
normotensive subjects trained at a similar intensity.10 11 12
Although one study that reported an unchanged baroreflex control of FVR
used shorter training periods (approximately 10 weeks)9
than those that reported an attenuation of this reflex (approximately
30 weeks),10 11 at least one study that used a 10-week
training period also reported an attenuated baroreflex.12
Furthermore, one of the short-duration studies that reported unchanged
FVR responses during LBNP at -10 mm Hg found reduced FVR responses
during LBNP at -40 mm Hg.40
The importance of relating FVR reflex responses to the physiological stimulus to the cardiopulmonary receptors rather than to the level of LBNP has been emphasized recently.12 Although most previous studies did not take into account central blood volume, at least one,12 in addition to a preliminary report,41 related FVR responses to CVP and found an attenuated baroreflex control of FVR after training at moderate intensity. It should be noted that these previous studies examined the baroreflex control of FVR only during deactivation of the cardiopulmonary receptors. In the present study, we examined the reflex FVR/LVIDD and FVR/CVP relations during LBNP and LR, thereby providing information on the reflex during both deactivation and activation, respectively, of the receptors.
Jingu et al8 reported that the baroreflex control of FVR was augmented after training at 50% of maximal oxygen uptake based on the observation that reflex FVR responses during LBNP at -10 and -40 mm Hg were increased, whereas CVP levels at baseline and during LBNP were similar. Therefore, our results after training at 50% of maximal oxygen uptake do not agree with those of Jingu et al. The reasons for this discrepancy are not clear. It should be noted that the subjects in the study of Jingu et al and in the present study displayed similar mean arterial pressure levels (106±8 and 108±3 mm Hg, respectively). However, in agreement with our finding of an unaltered baroreflex control of FVR in hypertensive subjects after low-intensity training, McDonald and colleagues42 reported an unchanged reflex increase in FVR on leg lowering in normotensive subjects after 10 weeks of training at 60% of maximal oxygen uptake.
In conclusion, the results of the present study indicate that attenuation of the cardiopulmonary baroreflex control of skeletal muscle vascular resistance after training at 70% of maximal oxygen uptake might prevent the reduction of BP in subjects with essential hypertension. However, the baroreflex control of FVR is unaffected after training at 50% of maximal oxygen uptake, which significantly reduced awake ambulatory BP. A decreased effector organ response, that is, vascular smooth muscle, to sympathetic nervous stimulation appears to be involved, at least in part, in the alteration in baroreflex control of FVR after training at 70% of maximal oxygen uptake.
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Acknowledgments |
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This work was supported by grants from the Fonds de la Recherche en Santé du Québec (FRSQ) and from the Fondation des Maladies du Coeur du Québec. Jean Cléroux is the recipient of a scholarship from the FRSQ. The authors acknowledge the excellent work of Réal Dion for echocardiographic measurements and Jacques Renaud for the plasma norepinephrine assays.
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Footnotes |
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Reprint requests to Jean Cléroux, PhD, Hypertension Research Unit, CHUL Research Center, 2705 boul Laurier, Québec, Québec, Canada G1V 4G2.
Received June 28, 1994; first decision July 27, 1994; accepted October 31, 1994.
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