Can relaxation lower metaboreflex-mediated blood pressure elevations?

PURPOSE: Relaxation can lower resting blood pressure, and this investigation sought to determine whether relaxation could reduce mean blood pressure (MBP) elevations produced by postexercise circulatory occlusion (PECO). METHODS: Sixteen volunteers trained with relaxation and were able to decrease MBP at rest by at least 5 mm Hg within 2 min. Subjects performed four tests assigned randomly: i). rest with cuff occlusion, ii). rest and cuff occlusion with relaxation, iii). hand-grip exercise followed by PECO rest with cuff occlusion, and iv) hand-grip exercise followed by PECO with relaxation. Data for HR and MBP were collected using a Finapres; ratings of relaxation and discomfort from cuff occlusion were obtained using a 1- to 10-unit scale. Stroke volume (SV) and HR were collected from six subjects to calculate cardiac output and total peripheral conductance (TPC). Dependent variables were compared using an ANOVA. RESULTS: HR (mean +/-SD) was lower during both relaxation conditions as compared with control (-7 +/- 4 bpm vs -2 +/- 3 bpm; P< 0.05). The MBP was reduced during relaxation alone (-6 +/- 3.7 mm Hg; < 0.05) but not during PECO with relaxation. The rating of relaxation was higher during relaxation (6.8 +/- 1.3 units) versus control (3.5 +/- 1.2 units), but ratings were not different between relaxation conditions. Ratings of discomfort were higher during PECO ( P< 0.05). Relaxation did not significantly alter CO or SV (N= 6). During relaxation alone, TPC was increased (0.046 +/- 0.001 vs 0.049 +/- 0.002 L.min.mm Hg; P< 0.05). However, TPC was significantly increased during PECO with relaxation. CONCLUSIONS: These findings suggest that although relaxation can affect cardiovascular regulation and lower HR and MBP at rest, this central signal cannot lower reflex increases in blood pressure originating from a peripheral metabolic stimulus.     

Effect of G-suit protection on carotid-cardiac baroreflex function

INTRODUCTION: To test the hypothesis that G-suit inflation could increase cardiac chronotropic responses to baroreceptor stimulation and enhance baroreflex buffering of BP, the carotid-cardiac baroreflex response of 12 subjects was measured across two levels of lower body negative pressure (LBNP = 0 and 50 mm Hg) and two levels of G-suit inflation (0 and 50 mm Hg) in random order. METHODS: Carotid-cardiac baroreflex stimulation was delivered via a silastic neck pressure cuff and responsiveness quantified by determination of the maximum slope of the stimulus-response function between R-R intervals (ms) and their respective carotid distending pressures (mmHg). RESULTS: Mean +/- SE baseline control baroreflex responsiveness was 3.8+/-0.4 ms x mm Hg(-1). LBNP reduced the baroreflex response to 2.7+/-0.4 ms x mm Hg(-1), but G-suit inflation with LBNP restored the baroreflex response to 4.3+/-0.6 ms x mm Hg(-1). CONCLUSIONS: These results suggest that, in addition to increased venous return and elevated peripheral resistance, G-suit inflation may provide protection against the debilitating effects of blood distribution to the lower extremities during orthostatic challenges such as standing or high +Gz acceleration by increasing cardiovascular responsiveness to carotid baroreceptor stimulation.     

Aerobatic flight effects on baroreflex sensitivity and sympathovagal balance in experienced pilots

BACKGROUND: Aerobatic flights subject pilots to accelerations and, therefore, to heavy physical workloads. OBJECTIVE: Our aim was to document changes in spontaneous baroreflex sensitivity and disturbances of sympathovagal balance after exposure to "push-pull" accelerations. METHODS: During 30-min flights, five aerobatic pilots performed five series of descending spirals: first, 30 s under negative (-3 Gz max), and then 30 s under positive (+4 Gz max) G loading, climbing between each series to regain altitude. A stand-test was performed before (T0), immediately postflight (PF), 1 h (PF1), and 2 h after (PF2) the flight. A Finapres apparatus recorded heart rate (HR) and BP during the stand-tests. RESULTS: Resting HR was higher at PF than T0 in supine (11.2 +/- 5.3%, p < 0.01) and standing (11.0 +/- 4.9%; p < 0.05) positions. Sequence analysis of spontaneous baroflex sensitivity (BRS) and spectral analysis of HR variability showed that: a) supine spontaneous BRS did not differ between preflight and postflight, while parasympathetic modulation of HR variability tended to increase; and b) supine spontaneous BRS was higher at PF1 than PF (PF: 0.011 +/- 0.0014 ms x mmHg(-1), PF1: 0.015 +/- 0.0012 ms x mmHg(-1); p < 0.05) and parasympathetic modulation of HR variability (high frequency component) was higher at PF2 than PF (PF: 0.014 +/- 0.007, PF2: 0.039 +/- 0.009; p < 0.001). CONCLUSIONS: These findings may reflect a change in the sympathovagal balance during the second hour of recovery from repeated push-pull maneuvers.     

Influence of weight training status on hemodynamic adjustments to isometric actions

BACKGROUND: The purpose of this study was to investigate the hemodynamic adjustments to fatiguing isometric handgrip (IHG) performed at 20 and 60% of maximal voluntary contraction (MVC) in 10 weight-trained (WT, 4.8+/-1.6 yrs) and 8 untrained (UT) men. METHODS: Hemodynamic measures were recorded at rest, during sustained IHG to fatigue, and during recovery. Blood pressures and heart rates (HR) were measured by auscultation and electrocardiography, respectively. Stroke volume (SV) was assessed by impedance cardiography. Mean arterial pressure (MAP), cardiac output (CO) and total peripheral resistance (TPR) were calculated. RESULTS: Between group comparisons in peak hemodynamic adjustments (fatigue value-resting value) to IHG were analyzed across intensities by MANOVA and follow-up univariate tests. The peak adjustments in MAP, HR, and SV during IHG at 20 and 60% MVC were dependent on intensity (60%>20% MVC) but were not significantly different (p>0.05) between groups. However, the intensity-dependent, peak adjustments in CO (WT=1.17+/-1.2 L x min-1 vs UT= -0.40+/-1.7 L x min-1, p=0.005) and TPR (WT=4.4+/-6.1 PRU vs UT=10.2+/-8.3 PRU, p=0.02) were significantly different between groups across intensities of IHG. CONCLUSIONS: The results suggest that weight training does not significantly influence the pressor response but may significantly modify the adjustments in total-body circulation and vascular resistance during fatiguing IHG performed at 20 and 60% MVC.     

Cardiovagal baroreflex and aortic hemodynamic responses to isometric exercise and post‐exercise muscle ischemia in resistance trained men

Arterial stiffness is associated with reduced baroreflex sensitivity (BRS) and resistance training; thus a potentially increased cardiovascular risk in resistance‐trained (RT) individuals. The effects of resistance training on arterial stiffness and BRS have been evaluated at rest, but cardiovascular abnormalities that are not shown at rest may be revealed during recovery after exercise. Aortic systolic (aSBP) and diastolic blood pressure (aDBP), stroke volume (SV), augmentation index (AIx), vagal activity, BRS responses to isometric handgrip (IHG), and post‐exercise muscle ischemia (PEMI) were evaluated in 10 RT and 10 untrained (UT) men (21±1 years). Resting aDBP and AIx were lower in RT compared with UT. Heart rate recovery, BRS, and vagal reactivation during PEMI were similar in both groups. Increases in aSBP (13±11 mmHg), AIx (5±10%), and SV (12±12%) during IHG further increased during PEMI (8±14 mmHg, 12±6%, and 10±8%). Increases in aDBP from rest to PEMI were higher in RT (17±9 mmHg) compared with UT (7±8 mmHg). The lower resting aDBP and the enhanced response to PEMI suggest beneficial adaptations in RT men. Wave reflection, aortic SBP, and cardiovagal BRS responses to IHG and PEMI are not affected by resistance training in young healthy men.     

Cardiovascular response to lower body negative pressure (LBNP) following endurance training

Eleven sedentary male volunteers were assigned to either an exercise (E) group (n = 6; endurance exercise for 12 weeks) or a control (C) group (n = 5; no exercise). After training, E significantly increased (p less than 0.01) their VO2max (pretraining: 37.0 +/- 2.3; posttraining: 44.6 +/- 2.5), whereas C showed no significant change. Heart rate (HR), arterial blood pressure (BP) and forearm blood flow (FBF) were measured both pre- and posttraining at rest and during 2 levels of LBNP: -10 mm Hg and -40 mm Hg. Both C and E had similar decreases in systolic BP and similar increases in HR and diastolic BP during LBNP when comparing the pre- and posttraining periods. In both groups, FBF significantly decreased during -40 mm Hg of LBNP in the pretraining period. However, after training, E had a significantly attenuated (p less than 0.05) decrease in FBF at -40 mm Hg (pretraining: -45.0 +/- 3.7%; posttraining: -29.8 +/- 3.1%). In C, there was no difference in the response of FBF to -40 mm Hg of LBNP comparing pretraining and posttraining. These findings indicate that endurance exercise training decreases the forearm vasoconstrictor response to high levels of LBNP.     

Reduced baroreceptor reflex sensitivity and increased blood pressure variability at 2400 m simulated cabin altitude

In a hypobaric chamber nine healthy volunteers were exposed to an atmospheric pressure corresponding to 2400 m above sea level. This is similar to the lowest air pressure encountered inside pressurized commercial airplanes. Heart rate and blood pressure were monitored beat-to-beat in the supine position with a non-invasive device. Blood pressure variability and heart rate variability were measured in the mid-frequency band; subsequently, baroreceptor reflex sensitivity (BRS) was calculated with the transfer-function method. Compared with baseline, there were reduced BRS and increased blood pressure variability at 2400 m (16.5 +/- 3.1 vs. 13.2 +/- 2.0 ms x mm Hg(-1) and 5.4 +/- 1.3 vs. 8.2 +/- 1.1 mm Hg, respectively; p < 0.05). We conclude that autonomic cardiovascular control was disturbed during acute exposure to an air pressure corresponding to 2400 m.     

Endurance training alters arterial baroreflex function in dogs

The present study was designed to determine whether 12 wk of daily exercise alter autonomic neural control of the heart during baroreflex stimulation in healthy dogs. We studied 16 untrained and 12 endurance-trained anesthetized dogs which were instrumented to measure arterial blood pressure (AP), carotid sinus baroreceptor pressure (CBP), electrocardiogram (ECG), heart rate (HR), and R-R interval (RR). The arterial baroreflex was studied during hypertension caused by i.v. bolus infusion of phenylephrine, hypotension caused by i.v. bolus infusion of nitroprusside, and bilateral carotid occlusion (BCO) in which carotid sinus pressure was reduced to 41 +/- 2 mm Hg (mean +/- SEM). Arterial baroreflex sensitivity, which was assessed by determining the change in heart interval (i.e., change in RR) per unit change in systolic AP (delta RR/delta AP), was significantly lower during the hypertensive challenge in the trained dogs compared to the untrained dogs (2.2 +/- 0.3 vs 6.8 +/- 1.5 ms.mm Hg-1, respectively). Similarly, the delta RR/delta AP was substantially lower during the hypotensive challenge in trained dogs vs the untrained dogs (1.2 +/- 0.3 vs 1.8 +/- 0.4 ms.mm Hg-1, respectively). In addition, the HR response to the BCO was significantly less in trained dogs (22 +/- 2 bpm) vs untrained dogs (32 +/- 5 bpm). The open-loop gain (Go), which was used to quantitate the effectiveness of the carotid baroreflex to increase mean systemic AP during BCO, was similar in both untrained and trained dogs (2.9 +/- 0.6 and 2.4 +/- 0.5, respectively). These data indicate that, while endurance training significantly reduces the HR component of the arterial baroreflex, the arterial pressure response apparently is not altered.     

Effects of isometric handgrip protocol on blood pressure and neurocardiac modulation

Isometric handgrip (IHG) remains a well-studied cardiovascular and autonomic stimulus, however the effects of rhythmic IHG protocols remain largely unknown. The purpose of this study was to investigate the acute effects of 4 IHG protocols on blood pressure (BP) and neurocardiac reactivity and recovery responses. 12 healthy older participants (70±5 yrs, ♀=4) each completed 4 bilateral 12-min protocols (sham, IHG1, IHG2, IHG3) on separate visits. IHG1, IHG2, and IHG3 consisted of 4×2-min, 8×1-min, and 16×30-s isometric contractions, respectively, each completed at 30% MVC, while sham consisted of 4×2-min contractions completed at 3% MVC. BP and neurocardiac modulation were assessed during and following each protocol. Systolic BP (SBP) reactivity was increased during IHG1 compared to IHG2 (p<0.05), IHG3 (p<0.05), and sham (p<0.01), although during recovery delta SBP was lower following IHG1 (p<0.01), IHG2 (p<0.01), and IHG3 (p<0.05), compared to sham. Sample entropy, a measure of nonlinear heart rate variability was reduced during IHG1 (p<0.01) and IHG2 (p<0.05), while increased following IHG1 (p<0.05) and IHG3 (p<0.05), compared to sham. In conclusion, recovery responses from rhythmic IHG appear independent of contraction and/or rest period frequency-duration relationships. Investigation of rhythmic IHG protocols warrants further examination.     

Recovery pattern of baroreflex sensitivity after exercise

PURPOSE: To test the association between exercise mode and the recovery pattern of baroreflex sensitivity (BRS) after exercise. METHODS: The study population included healthy male subjects (N = 12, age: 31 +/- 3 yr). Four different interventions were performed in a randomized order: 1) aerobic exercise session on a bicycle ergometer, 2) light resistance exercise session, 3) heavy resistance exercise session, and 4) control intervention with no exercise. All interventions lasted 40 min. R-R intervals and continuous blood pressure were measured before (10 min) and 30-180 min after the interventions. BRSLF was calculated by the transfer function method from the low-frequency band (LF, 0.04-0.15 Hz) of the R-R intervals and systolic blood pressure spectra. RESULTS: BRSLF had blunted until 30 min after aerobic and light resistance exercise (11.1 +/- 4.3 and 10.0 +/- 3.6 vs 17.5 +/- 7.0 ms.mm Hg(-1), P = 0.002 for both, compared with the control intervention, respectively). However, BRSLF was significantly blunted until 60 min after heavy resistance exercise (9.3 +/- 2.3 vs 15.1 +/- 4.7 ms.mm Hg(-1), P = 0.005, compared with the control intervention). The high-frequency power of R-R intervals (0.15-0.4 Hz) was significantly reduced, and the LF power of systolic blood pressure oscillation was significantly augmented 30 min after heavy resistance exercise (P < 0.01 for both), whereas both indices were restored to the control level by 30 min after aerobic and light resistance exercise. CONCLUSION: BRS after acute exercise is associated with exercise intensity, showing relatively rapid recovery after aerobic and light resistance exercise and delayed recovery after heavy resistance exercise. The delayed BRS pattern after heavy resistance exercise is regulated by delicate interplay between the withdrawal of vagal outflow and the probably increased sympathetic vasomotor tone documented by measurements of heart rate and blood pressure variability.     

Regular exercise as an effective approach in antihypertensive therapy

PURPOSE: Exercise has been well documented to exert a beneficial effect on cardiovascular health. The effective control of arterial pressure (BP) is essential from the standpoint of cardiovascular prevention. So far, no study has determined the long-term effect of regular training as a monotherapy on both BP at rest and during exercise. METHODS: Therefore, 10 subjects with hypertension (aged 43 +/- 3 yr) were studied in order to define BP response to long-term aerobic training. BP measurements were obtained at rest and during ergometry (50-100 W). Patients were instructed to exercise weekly (2 x 60 min aerobic exercise). RESULTS: BP during exercise (100 W) did fall already after 6 months of regular training from 184 +/- 10/107 +/- 6 to 170 +/- 10/100 +/- 7, and this was associated with a 14% decrease in the rate-pressure product (at 100 W). After 18 months of training, there were further reductions in BP, at rest from 139 +/- 9/96 +/- 6 to 133 +/- 14/91 +/- 7 (P < 0.05) and during ergometry (100 W) from 184 +/- 10/107 +/- 6 to 172 +/- 8/96 +/- 6 mm Hg (P < 0.001). During a 3-yr follow-up, BP continued to decrease significantly to 130 +/- 13/87 +/- 7 mm Hg at rest and 167 +/- 9/92 +/- 6 mm Hg during exercise. No significant changes in body weight were documented during the training period. CONCLUSION: The data demonstrate that long-term aerobic exercise is associated with a decrease in BP at rest and during exercise, which is comparable to that of drug therapies. This antihypertensive effect of regular training can be maintained as long as 3 yr.     

Effects of acute exercise on attenuated vagal baroreflex function during bed rest.

We measured carotid baroreceptor-cardiac reflex responses in six healthy men, 24 h before and 24 h after a bout of leg exercise during 6 degrees head-down bed rest to determine if depressed vagal baroreflex function associated with exposure to microgravity environments could be reversed by a single exposure to acute intense exercise. Baroreflex responses were measured before bed rest and on day 7 of bed rest. An exercise bout consisting of dynamic and isometric actions of the quadriceps at graded speeds and resistances was performed on day 8 of bed rest and measurements of baroreflex response were repeated 24 h later. Vagally-mediated cardiac responses were provoked with ramped neck pressure-suction sequences comprising pressure elevations to +40 mm Hg, followed by serial, R-wave triggered 15 mm Hg reductions, to -65 mm Hg. Baroreceptor stimulus-cardiac response relationships were derived by plotting each R-R interval as a function of systolic pressure less the neck chamber pressure applied during the interval. Compared with pre-bed rest baseline measurements, 7 d of bed rest decreased the gain (maximum slope) of the baroreflex stimulus-response relationship by 16.8 +/- 3.4% (p < 0.05). On day 9 of bed rest, 24 h after exercise, the maximum slope of the baroreflex stimulus-response relationship was increased (p < 0.05) by 10.7 +/- 3.7% above pre-bed rest levels and 34.3 +/- 7.9% above bed rest day 7. Our data verify that vagally-mediated baroreflex function is depressed by exposure to simulated microgravity and demonstrate that this effect can be acutely reversed by exposure to a single bout of intense exercise.     

Heart rate and blood pressure changes with endurance training: the HERITAGE Family Study

PURPOSE: The purpose of this study was to determine the magnitude of change in resting and exercise heart rate (HR) and blood pressure (BP), by race, sex, and age, after a 20-wk endurance training program in 507 healthy and previously sedentary subjects from the HERITAGE Family Study. METHODS: After baseline measurements, subjects exercised on cycle ergometers 3 d x wk(-1) for a total of 60 exercise sessions starting at 55% of VO2max for 30 min x session(-1) and building to 75% of VO2max for 50 min x session(-1) for the last 6 wk. HR and BP at rest and during exercise (50 W, 60% of VO2max maximal exercise) were each determined in duplicate on two different days both before and after training (resting values at 24-h and 72-h posttraining). RESULTS: After the period of training, there was a small decrease in resting HR (-2.7 to -4.6 beats x min(-1) across groups at 72-h posttraining), and small changes (i.e., < 3 mm Hg) in resting systolic (SBP), diastolic (DBP), and calculated mean BP (MBP), which varied by race, sex, and age. During exercise at the same absolute work rate (50 W), HR, SBP, DBP, and MBP were all significantly reduced, with greater reductions in HR in women compared with men, and greater reductions in BP in blacks and older subjects compared with whites and younger subjects, respectively. At the same relative work rate (60% VO2max), HR, DBP, and MBP were reduced, but SBP remained unchanged. Blacks had a greater reduction in DBP, but whites had a greater reduction in HR. Finally, at maximal exercise, there was a small decrease in HR, with men and whites decreasing more than women and blacks; an 8 mm Hg increase in SBP, with men increasing more than women; a 4 mm Hg decrease in DBP, with blacks decreasing more than whites; and no change in MBP. CONCLUSION: In conclusion, the reductions in resting HR and BP with training were generally small, but the reductions during exercise were substantial and clinically important, with the older and the black populations experiencing greater reductions.     

Resistance exercise,the Valsalva maneuver,and cerebrovascular transmural pressure

PURPOSE: To examine the acute effects of resistance exercise (RE) performed without a Valsalva maneuver (VM) versus a VM performed alone on systolic pressure, intracranial pressure (ICP), and cerebrovascular transmural pressure (CVTMP) (i.e., the important pressure that stresses the cerebral arterial and aneurysmal walls and calculated as systolic pressure minus ICP). METHODS: The subjects for this study consisted of seven (mean +/- SD, Age: 39 +/- 14 yr) fully alert, cooperative, and clinically stable individuals who recently underwent various neurosurgical operations. Heart rate, systolic pressure, ICP, and CVTMP were obtained at rest, during a VM, and during submaximal (8.0 +/- 3.0 kg performed for 18 +/- 10 repetitions) unilateral bicep curl RE. RESULTS: The VM resulted in a significantly greater increase in ICP (VM: 31 +/- 14 mm Hg vs RE: 16 +/- 7 mm Hg, P< 0.05) with a concomitant decrease in CVTMP (VM: 106 +/- 22 mm Hg vs RE: 132 +/- 14 mm Hg, P< 0.05) compared with unilateral bicep curl RE. CONCLUSIONS: Unilateral bicep curl RE results in a greater increase in CVTMP compared to a VM performed alone.     

Cardiovascular responses to head-up tilt after an endurance exercise program

The cardiovascular responses to 10 min of orthostasis were assessed before and after an aerobic exercise program. Five men and five women (18-25 years old) exercised for 7 weeks, four times per week, for 50 min per session at 70% of maximal heart rate (HR). Before and after the exercise program, maximal aerobic power (VO2max) was determined, and HR, systolic (SBP), diastolic (DBP), and pulse (PP) blood pressures were measured each minute during 5 min of supine rest, 10 min of foot-supported 70 degree head-up tilt (HUT), and 5 min of supine rest. Orthostatic tolerance was not determined. Calf compliance was measured in five of the subjects before and after the program as the change in leg volume at occluding pressures of 20, 40, 60, 80, and 100 mm Hg. Following the program, VO2max increased by 8.7% (p = 0.012), while decreases were noted in resting HR (9.4%, p = 0.041), SBP (5.0%, p less than 0.0005), and DBP (14.2%, p less than 0.0005). Despite a greater HR increase during HUT (7.1 beat.min-1, p = 0.034), SBP decreased by 3.4 mm Hg during HUT after the exercise program (p = 0.008). No differences were noted in the changes in DBP, MAP, or PP upon tilting (p greater than 0.05). After the program, the amount of fluid pooled in the calf at high occluding pressures (80 and 100 mm Hg) increased by 0.96 +/- 0.24 and 1.10 +/- 0.33 ml.100 ml tissue-1 (X +/- S.E.M., p = 0.017 and p = 0.028, respectively). We suggest that control of blood pressure during 10 min of orthostasis may be altered by endurance exercise training.     

Interaction of cardiac and muscle mechanical afferents on baroreflex control of the sinus node during dynamic exercise

The effects of cardiopulmonary baroreceptors and muscle mechanoreceptors stimulation on cardiac baroreflex sensitivity (BRS), and heart rate variability (HRV) were evaluated by measuring continuously and non‐invasively systolic blood pressure (SBP) and pulse interval (PI) during upright and supine passive cycling. BRS and HRV were evaluated with the cross‐correlation method (xBRS) and in the frequency domain, respectively. At rest, the shift from upright to supine posture enhanced xBRS from 16.4±12.1 to 23.4±12.9 ms/mmHg, and the high frequency (HF, 0.15–0.4 Hz) power of HRV from 48.9±18.6 to 55.1±14.7 normalized units (NU), while it attenuated the low‐frequency (LF, 0.04–0.15 Hz) power from 51.1±18.6 to 44.9±14.7 NU (P<0.05), respectively. During both upright and supine passive exercise, xBRS and the HF power were attenuated (10.0±8.0 and 12.5±9.0 ms/mmHg; 41.1±21.2 and 41.5±12.7 NU, respectively; P<0.05) and the LF power increased (58.8±21.2 and 58.5±12.7 NU, P<0.05), compared with rest. The effect of mechanoreflex activation overrides that of the cardiopulmonary baroreceptors loading resulting in decreased cardiac vagal outflow and reduced BRS during supine passive exercise.     

Exercise-induced decrease in insular cortex rCBF during postexercise hypotension

The insular cortex (IC), a region of the brain involved in blood pressure (BP) modulation, shows decreases in regional cerebral blood flow (rCBF) during postexercise hypotension (PEH). PURPOSE: To determine whether changes in IC neural activity were caused by prior exercise or by changes in BP, this investigation compared patterns of rCBF during periods of hypotension, which was induced by prior exercise (i.e., PEH) and sodium nitroprusside (SNP) infusion and a cold pressor (CP), to restore BP. METHODS: Ten subjects were studied on three different days with randomly assigned conditions: i) resting baseline; ii) PEH; and iii) SNP-induced hypotension (matched to the PEH BP decrease). Data were collected for heart rate (HR) and mean BP, and rCBF was assessed using single-photon emission computed tomography (SPECT) as an index of brain activation. RESULTS: Using ANOVA across conditions, there were differences (P<0.05; mean +/- SD) from baseline during PEH for HR (+12 +/- 3 bpm) and mean BP (-8 +/- 2 mm Hg) and during SNP-induced hypotension (HR = +15 +/- 4 bpm; MBP = -9 +/- 2 mm Hg), with no differences between PEH and SNP. After exercise, there were decreases (P<0.05) in the leg sensorimotor area, anterior cingulate, and the right and left inferior thalamus, right inferior insula, and left anterior insular regions. During SNP-induced hypotension, there were significant increases in the right and left inferior thalamus and the right and left inferior anterior IC. CP during PEH increased BP and IC activity. CONCLUSIONS: Data show that reductions in IC neural activity are not caused by acute BP decreases. Findings suggest that exercise can lead to a temporary decrease in IC neural activity, which may be a significant neural factor contributing to PEH.     

Baroreflex-mediated heart rate and vascular resistance responses 24 h after maximal exercise

INTRODUCTION: Plasma volume, heart rate (HR) variability, and stimulus-response relationships for baroreflex control of forearm vascular resistance (FVR) and HR were studied in eight healthy men after and without performing a bout of maximal exercise to test the hypotheses that acute expansion of plasma volume is associated with 1) reduction in baroreflex-mediated HR response, and 2) altered operational range for central venous pressure (CVP). METHODS: The relationship between stimulus (DeltaCVP) and vasoconstrictive reflex response (DeltaFVR) during unloading of cardiopulmonary baroreceptors was assessed with lower-body negative pressure (LBNP, 0, -5, -10, -15, -20 mm Hg). The relationship between stimulus (Deltamean arterial pressure (MAP)) and cardiac reflex response (DeltaHR) during loading of arterial baroreceptors was assessed with steady-state infusion of phenylephrine (PE) designed to increase MAP by 15 mm Hg alone and during application of LBNP (PE+LBNP) and neck pressure (PE+LBNP+NP). Measurements of vascular volume and autonomic baroreflex responses were conducted on two different test days, each separated by at least 1 wk. On one day, baroreflex response was tested 24 h after graded cycle exercise to volitional exhaustion. On another day, measurement of baroreflex response was repeated with no exercise (control). The order of exercise and control treatments was counterbalanced. RESULTS: Baseline CVP was elevated (P = 0.04) from a control value of 10.5 +/- 0.4 to 12.3 +/- 0.4 mm Hg 24 h after exercise. Average DeltaFVR/DeltaCVP during LBNP was not different (P = 0.942) between the exercise (-1.35 +/- 0.32 pru x mm Hg-1) and control (-1.32 +/- 0.36 pru x mm Hg-1) conditions. However, maximal exercise caused a shift along the reflex response relationship to a higher CVP and lower FVR. HR baroreflex response (DeltaHR/DeltaMAP) to PE+LBNP+NP was lower (P = 0.015) after maximal exercise (-0.43 +/- 0.15 beats x min-1 x mm Hg-1) compared with the control condition (-0.83 +/- 0.14 beats x min-1 x mm Hg-1). CONCLUSION: Expansion of vascular volume after acute exercise is associated with altered operational range for CVP and reduced HR response to arterial baroreceptor stimulation.     

The chemoreflex: adult versus child comparison

PURPOSE: Compare the influence of the chemoreflex on heart rate (HR) and blood pressure (BP) responses between children and adults. METHODS: Seventy children (35 boys and 35 girls) and 70 adults (35 men and 35 women) performed 30% maximal voluntary contraction static handgrip exercise (SHG) for 3 min, followed by 4 min of muscle ischemia and then 6 min of recovery, while HR and BP were measured. RESULTS: During 3 min of SHG, systolic BP (SBP) increased significantly more in men versus boys (23+/-9 vs 18+/-9%) and women versus girls (21+/-10 vs 15+/-7%), respectively. Diastolic BP (DBP) increased similarly during SHG in adults versus children. During SHG, HR increased similarly in males but significantly more in girls versus women (16+/-10 vs 11+/-9%), respectively. During occlusion, HR fell to baseline and remained through recovery in adults and children. Both SBP and DBP decreased similarly during the first minute of occlusion but remained significantly above baseline in adults and children. During the first minute of recovery, BP decreased to baseline in adults. In children, DBP decreased but remained significantly above baseline through recovery. SBP decreased in children during minute 1 of recovery yet remained significantly above baseline for 1-2 min in children. CONCLUSIONS: The muscle chemoreflex influence on HR and BP is similar in children and adults as evident in the return of HR to baseline, with a similar concomitant maintenance of BP above baseline during occlusion. When occlusion is released, BP returns to baseline in adults, whereas in children DBP remains significantly above baseline through recovery and SBP for 1-2 min. The differing BP response may be explained by a more active arterial chemoreflex in children.     

Accumulation of physical activity reduces blood pressure in pre- and hypertension

PURPOSE: The effectiveness of lifestyle physical activity to reduce BP in prehypertension/hypertension is unclear. The purpose of this study was: 1) to investigate the magnitude and duration of ambulatory BP (AmBP) reduction after the accumulation of one day of lifestyle physical activity (PAaccum) in normotension, prehypertension, and hypertension; and 2) to determine the relationship between energy expenditure (EE) and BP reduction. METHODS: Subjects were eight normotensive (112.3/73.1 +/- 1.6/1.9 mm Hg), 10 prehypertensive (124.3/79.3 +/- 1.2/1.6 mm Hg), and 10 hypertensive (139.7/83.3 +/- 3.7/3.7 mm Hg) adults. EE was analyzed during the PA and corresponding control (C) treatment; AmBP was analyzed for 12 h after the PAaccum and corresponding C. EE of the PA (EEPA) was calculated as the total EE for the duration of the PA. Steps to analyze and compare the BP reduction after PAaccum were: 1) determination of the duration of the BP reduction (95% CI), 2) determination of the magnitude of the BP reduction (paired t-tests of C vs PA), 3) determination of the area of the BP reduction, and 4) comparison of the areas (independent t-test) between prehypertension and hypertension. Correlation between EE(PA-C) and BP reduction was examined RESULTS: No BP differences were found for normotension or for DBP in any group. Significant difference in SBP after the PAaccum were found for prehypertensives (magnitude; area = 6.6 +/- 2.3 mm Hg; 21.7 +/- 15.2 mm Hg x h(-1)) for 6 h and for hypertensives (12.9 +/- 4.3 mm Hg; 123.4 + 42.8 mm Hg x h(-1)) for 8 h; area was significantly different between groups. No correlation was found between EE(PA-C) and BP reduction. CONCLUSION: The PAaccum reduces SBP in hypertension and prehypertension but does not appear to be related to the EE(PA-C). PAaccum can be utilized as an approach to treat prehypertension and hypertension.