Diminished baroreflex control of forearm vascular resistance following training.

The stimulus-response characteristics of cardiopulmonary baroreflex control of forearm vascular resistance (FVR units in mm Hg.min.100 ml.ml-1) were studied in 14 volunteers before and after 10 wk of endurance training. We assessed the relationship between reflex stimulus (changes in central venous pressure, CVP) and response (FVR) during unloading of cardiopulmonary baroreceptors with lower body negative pressure (LBNP, 0 to -20 mm Hg). Changes in CVP during LBNP were estimated from pressure changes in a large peripheral vein in the dependent arm of the subject in the right lateral decubitus position. Maximal oxygen uptake (VO2max) and total blood volume increased with endurance training from 37.8 +/- 1.4 ml.min-1.kg-1 and 63.6 +/- 2.1 ml.kg-1 to 45.3 +/- 1.4 ml.min-1.kg-1 and 69.3 +/- 2.8 ml.kg-1, respectively (P less than 0.05). Reflex forearm vasoconstriction occurred in response to a reduction in estimated CVP, and the absolute change in FVR per unit of CVP was reduced from -5.96 +/- 0.79 to -4.06 +/- 0.52 units.mm Hg-1 (P less than 0.05) following exercise training but was unchanged from -6.10 to 0.57 to -6.22 +/- 0.94 units.mm Hg-1 for the time control group (N = 7). Resting values for FVR were similar before and after exercise training; however, resting estimated CVP was elevated from 9.5 +/- 0.5 mm Hg before training to 11.3 +/- 0.6 mm Hg after training.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiopulmonary baroreflex control of forearm vascular resistance after acute blood volume expansion.

We report the stimulus-response characteristics of cardiopulmonary (CP) baroreflex control of forearm vascular resistance (FVR) in young adult male volunteers before and after: 1) blood volume expansion (8 ml/kg infusion of 5% human serum albumin solution, n = 5) and 2) a redistribution of blood volume toward the heart (6 degrees head-down tilt (HDT), n = 6). We assessed the relationship between reflex stimulus (i.e., changes in central venous pressure (CVP] and response (i.e., FVR) during unloading of CP mechanoreceptors with lower body negative pressure (0 to -20 mm Hg). Changes in CVP were estimated from changes in venous pressure of a large peripheral vein of the dependent arm with the subject in the right lateral decubitus position. In all conditions, reflex forearm vasoconstriction occurred in response to a reduction in estimated CVP. The absolute change in FVR per unit of CVP was reduced from -4.24 +/- 1.68 to -2.15 +/- 1.16 units/mm Hg (p less than 0.05) following blood volume expansion but was similar before (-3.34 +/- 0.89 units/mm Hg) and during 6 degrees HDT (-3.30 +/- 0.92 units/mm Hg). The reduced sensitivity of the CP baroreflex following volume expansion was manifested primarily as a smaller FVR response to LBNP (p less than 0.05). Blood volume expansion and 6 degrees HDT increased resting estimated CVP by 1.5 and 0.9 mm Hg, respectively (p less than 0.05) and resting levels of FVR decreased slightly.(ABSTRACT TRUNCATED AT 250 WORDS)     

Carotid-cardiac baroreflex response and LBNP tolerance following resistance training.

The purpose of this study was to examine the effect of lower body resistance training on cardiovascular control mechanisms and blood pressure maintenance during an orthostatic challenge. Lower body negative pressure (LBNP) tolerance, carotid-cardiac baroreflex function (using neck chamber pressure), and calf compliance were measured in eight healthy males before and after 19 wk of knee extension and leg press training. Resistance training sessions consisted of four or five sets of 6-12 repetitions of each exercise, performed two times per week. Training increased strength 25 +/- 3 (SE)% (P = 0.0003) and 31 +/- 6% (P = 0.0004), respectively, for the leg press and knee extension exercises. Average fiber size in biopsy samples of m. vastus lateralis increased 21 +/- 5% (P = 0.0014). Resistance training had no significant effect on LBNP tolerance. However, calf compliance decreased in five of the seven subjects measured, with the group average changing from 4.4 +/- 0.6 ml.mm Hg-1 to 3.9 +/- 0.3 ml.mm Hg-1 (P = 0.3826). The stimulus-response relationship of the carotid-cardiac baroreflex response shifted to the left on the carotid pressure axis as indicated by a reduction of 6 mm Hg in baseline systolic blood pressure (P = 0.0471). In addition, maximum slope increased from 5.4 +/- 1.3 ms.mm Hg-1 before training to 6.6 +/- 1.6 ms.mm Hg-1 after training (P = 0.0141). Our results suggest the possibility that high resistance, lower extremity exercise training can cause a chronic increase in sensitivity and resetting of the carotid-cardiac baroreflex.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

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.     

Differential baroreflex control of heart rate in sedentary and aerobically fit individuals

PURPOSE: We compared arterial, aortic, and carotid-cardiac baroreflex sensitivity in eight average fit (maximal oxygen uptake, VO2max = 42.2+/-1.9 mL x kg(-1) x min(-1)) and eight high fit (VO2max = 61.9+/-2.2 mL x kg(-1) x min(-1)) healthy young adults. METHODS: Arterial and aortic (ABR) baroreflex functions were assessed utilizing hypo- and hyper-tensive challenges induced by graded bolus injections of sodium nitroprusside (SN) and phenylephrine (PE), respectively. Carotid baroreflex (CBR) sensitivity was determined using ramped 5-s pulses of both pressure and suction delivered to the carotid sinus via a neck chamber collar, independent of drug administration. RESULTS: During vasoactive drug injection, mean arterial pressure (MAP) was similarly altered in average fit (AF) and high fit (HF) groups. However, the heart rate (HR) response range of the arterial baroreflex was significantly attenuated (P < 0.05) in HF (31+/-4 beats x min(-1)) compared with AF individuals (46+/-4 beats x min(-1)). When sustained neck suction and pressure were applied to counteract altered carotid sinus pressure during SN and PE administration, isolating the ABR response, the response range remained diminished (P < 0.05) in the HF population (24+/-3 beats x min(-1)) compared with the AF group (41+/-4 beats x min(-1)). During CBR perturbation, the HF (14+/-1 beats-min(-1)) and AF (16+/-1 beats-min(-1)) response ranges were similar. The arterial baroreflex response range was significantly less than the simple sum of the CBR and ABR (HF, 38+/-3 beats x min(-1) and AF, 57+/-4 beats x min(-1)) in both fitness groups. CONCLUSIONS: These data confirm that reductions in arterial-cardiac reflex sensitivity are mediated by diminished ABR function. More importantly, these data suggest that the integrative relationship between the ABR and CBR contributing to arterial baroreflex control of HR is inhibitory in nature and not altered by exercise training.     

Hypovolemic intolerance to lower body negative pressure in female runners.

PURPOSE: An attenuated baroreflex response and orthostatic intolerance have been reported in endurance-trained male athletes; however, it is still unknown whether this occurs also in females. The purpose of the present study was to examine whether endurance exercise-trained women had a predisposition to orthostatic compromise, and if so, what causative factor(s) may induce orthostatic intolerance. METHODS: We studied cardiovascular and hormonal responses to graded lower body negative pressure (LBNP) (0 to -60 mm Hg) in 26 middle-distance female runners (18.6 +/- 0.1 yr) as the exercise-trained (ET) subjects and 23 age-matched untrained (UT) control subjects. On the basis of the occurrence of syncope episodes during LBNP, ET and UT subjects were further allocated to two groups; ET with presyncope (ET+syncope) and without presyncope (ET-syncope) and UT with presyncope (UT+syncope) and without presyncope (UT-syncope). RESULTS: Occurrence of presyncope episodes during LBNP was higher in ET (65.4%, P < 0.05) than that for UT (34.8%). Leg compliance was higher (P < 0.05) in ET than in UT. LBNP reduced stroke volume (SV) more (P < 0.05), increased heart rate (HR) higher (P < 0.05), and increased forearm vascular resistance (FVR) more in ET+syncope as compared with the other groups. Response of vasoactive hormones to LBNP was higher in ET+syncope (P < 0.05) than that of the other groups except for norepinephrine (NE); high in both ET+syncope and UT+syncope. The relationship between SV and NE, an index of sympathetic neuronal response, had no training-related changes during LBNP. CONCLUSION: We conclude that exercise-trained females have a high incidence of orthostatic intolerance during LBNP, with a greater reduction of SV independent of changes in baroreflex and neurohumoral function. A lower incidence of LBNP intolerance in UT may be accounted for by a lower reduction of SV during LBNP. An increase in leg compliance in the exercise-trained females may play an important role in inducing pronounced reduction of SV and hence the intolerance to LBNP.     

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.     

Leg vascular responsiveness during acute orthostasis following simulated weightlessness

Ten men (35-49 years old) underwent lower body negative pressure (LBNP) exposures before and after 10 d of continuous 6 degrees head-down bedrest in order to predict the effect of weightlessness on the responsiveness of leg vasculature to an orthostatic stress. Heart rate (HR), mean arterial blood pressure (MAP), and impedance rheographic indices of arterial pulse volume (APV) of the legs were measured during rest and at 1 min of -30 mm Hg LBNP. Bedrest-induced deconditioning was manifested by decreases (p less than 0.05) in plasma volume (17%), peak oxygen uptake (16%), and LBNP tolerance (17%). Resting HR was unchanged after bedrest, but HR was higher (p less than 0.05) at 1 min of -30 mm Hg LBNP after, compared with before, bedrest. Responses of MAP to -30 mm Hg LBNP were not altered by bedrest. Resting APV was decreased (p less than 0.05) by simulated weightlessness. However, APV was reduced (p less than 0.05) from rest to 1 min -30 mm Hg LBNP by the same relative magnitude before and after bedrest (-21.4 +/- 3.4% and -20.5 +/- 2.7%, respectively). We conclude that peripheral arterial vasoconstriction, as indicated by reductions in APV during LBNP, was not affected by bedrest. These results suggest that there was no apparent alteration in responsiveness of the leg vasculature following simulated weightlessness. Therefore, it appears unlikely that control mechanisms of peripheral resistance contribute significantly to reduced orthostatic tolerance following spaceflight.     

Hemodynamic responses to seated and supine lower body negative pressure: comparison with +Gz acceleration.

Hemodynamic changes between upright and supine lower body negative pressure (LBNP) to levels of -70 mm Hg were compared in 8 subjects (5 males, 3 females) and correlated with their findings during simulated Shuttle reentry acceleration with a slow onset rate of 0.002 G/s (1,020 s to peak +2 Gz) and during gradual onset exposures (0.03 G/s) to +3 Gz and +4 Gz. Six of the 8 subjects were able to tolerate 2 min at peak +2 Gz, 2-5 min at +3 Gz, and 1-2 min at +4 Gz. Heart rate (HR) at any given level of upright LBNP regularly exceeded supine levels. HR change at -50 mm Hg in upright subjects (+47.7 bpm from 74.1 +/- 1.9 (M +/- S.E.) bpm, control) was 2.6 times greater than in supine subjects (+18.3 bpm from 64.8 +/- 2.8 bpm, control). HR values at -40 mm Hg supine (73.7 +/- 2.6) matched seated upright pre-LBNP control levels (74.1 +/- 1.9 bpm), while values at -70 mm Hg supine (102.5 +/- 4.4 bpm) were not significantly different from those at -40 mm Hg upright (103.1 +/- 4.0 bpm). Peak HR during +3 Gz (145.8 +/- 7.7 bpm) and +4 Gz (152.3 +/- 6.5 bpm) significantly exceeded recorded supine and upright LBNP levels, whereas values at +2 Gz (104.8 +/- 5.5 bpm) closely matched those at -40 mm Hg upright (103.1 +/- 4.0 bpm) and -70 mm Hg supine (102.5 +/- 4.4 bpm). Supine LBNP HR changes in this relatively small group of subjects closely matched those previously reported in the literature.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of repeated Valsalva maneuver straining on cardiac and vasoconstrictive baroreflex responses

INTRODUCTION: We hypothesized that repeated respiratory straining maneuvers (repeated SM) designed to elevate arterial BPs (arterial baroreceptor loading) would acutely increase baroreflex responses. METHODS: We tested this hypothesis by measuring cardiac baroreflex responses to carotid baroreceptor stimulation (neck pressures), and changes in heart rate and diastolic BP after reductions in BP induced by a 15-s Valsalva maneuver in 10 female and 10 male subjects at 1, 3, 6, and 24 h after performing repeated SM. Baroreflex responses were also measured in each subject at 1, 3, 6, and 24 h at the same time on a separate day without repeated SM (control) in a randomized, counter-balanced cross-over experimental design. RESULTS: There was no statistical difference in carotid-cardiac and peripheral vascular baroreflex responses measured across time following repeated SM compared with the control condition. Integrated cardiac baroreflex response (deltaHR/ deltaSBP) measured during performance of a Valsalva maneuver was increased by approximately 50% to 1.1 +/- 0.2 bpm x mm Hg(-1) at 1 h and 1.0 +/- 0.1 bpm x mm Hg(-1) at 3 h following repeated SM compared with the control condition (0.7 +/- 0.1 bpm x mm Hg(-1) at both 1 and 3 h, respectively). However, integrated cardiac baroreflex response after repeated SM returned to control levels at 6 and 24 h after training. These responses did not differ between men and women. CONCLUSIONS: Our results are consistent with the notion that arterial baroreceptor loading induced by repeated SM increased aortic, but not carotid, cardiac baroreflex responses for as long as 3 h after repeated SM. We conclude that repeated SM increases cardiac baroreflex responsiveness which may provide patients, astronauts, and high-performance aircraft pilots with protection from development of orthostatic hypotension.     

Reduction in LBNP tolerance following prolonged endurance exercise training.

Eight young men underwent an 8-month endurance exercise training program. Prior to and following the training program, the subjects' maximal oxygen uptake (VO2max), total blood volume (TBV) and plasma volume (PV), tolerance to lower body negative pressure (LBNP) assessed by the cumulative stress index (CSI) to presyncope, and their hemodynamic responses to 0 to -45 torr LBNP was determined. Hemodynamic measures included rebreathe carbon dioxide cardiac output (Qc), heart rate (HR), directly measured arterial blood pressures (ABP), and strain gauge determination of forearm blood flow (FBF) and leg volume changes (delta LgV). Calculated values of stroke volume (SV), forearm, vascular resistance (FVR), and peripheral vascular resistance (PVR) were made. Following training, each subject had an increased VO2max (mean = +27.4%, P < 0.001), TBV (mean = +15.8%, P < 0.02), and PV (mean = +16.5%, P < 0.02) and each subject had a decreased tolerance to LBNP (mean CSI = -24%, P < 0.001). Stepwise linear regression identified that the major factors to significantly predict the decreased CSI pre- to post-training were a reduced response of PVR to LBNP from -15 to -45 torr (Model R2 = 0.853), the delta TBV (model R2 = 0.981), and the greater post-training reduction in SBP to LBNP of 0 to -45 torr (model R2 = 1.0). These data suggest that physiologic adaptations associated with the increased VO2max and TBV resulting from a prolonged endurance exercise training program can alter the reflex control of vasomotion and cardiac output during LBNP and reduce the LBNP tolerance.     

Reflex venomotor responses to lower body negative pressure following endurance training

The effect of endurance training on reflex venomotor control during an orthostatic challenge was investigated in 11 sedentary male volunteers. An exercise (E) group (n = 6) underwent 12 weeks of endurance exercise training, whereas a control (C) group (n = 5) remained sedentary. Training significantly increased VO2max values in E (pre-training: 37.0 +/- 2.5 ml.kg-1.min-1; post training: 44.6 +/- 2.5 ml.kg-1.min-1), while C showed no significant change. During exposures to two levels of lower body negative pressure (-10 and -40 mm Hg), both C and E groups showed similar graded decreases in forearm venous volume (FVV). The magnitude of the FVV decreases did not differ between groups or when comparing pre-training and post-training values. We conclude that the reflex venoconstrictor response to LBNP was not affected by endurance training.     

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.     

Effects of repeated brain ischemia induced by rapid lower body negative pressure on brain water and Na+,K+-ATPase activity in rats

BACKGROUND: It has been demonstrated that during +Gz exposure cerebral blood flow is significantly reduced resulting in brain ischemia. Animal centrifuge models are commonly used to investigate the mechanisms of +Gz-induced loss of consciousness (G-LOC) and their pathophysiological effects on the brain. These dynamic models are limited because we currently are unable to obtain accurate measures of membrane ion flux or single cell electrophysiological responses from animals under centrifugation. HYPOTHESIS: The aim of the present study was to develop a non-centrifuge animal model of short-term, repeatable and complete brain ischemia using a rodent lower body negative pressure (LBNP), and to investigate the effects of repeated complete brain ischemia induced by LBNP on brain Na+,K+-ATPase activity, Na+, K+ and water contents in rats. METHODS: Eight anesthetized rats were exposed randomly to LBNP of -2.67 kPa, -4.00 kPa, and -5.33 kPa, respectively, at the rate of -0.67 kPa x s(-1). The pressure rapidly returned to control level when EEG became isoelectric (flat). The mean arterial BP (MAP), EEG and ECG were recorded. Twenty-one rats were divided randomly into control, single LBNP exposure, and three LBNP exposures groups (n = 7 in each group). Brain samples were analyzed for Na+,K+-ATPase activity, Na+, K+ and water contents 1 h after single and three 2-min LBNP exposures (-4.00 kPa at a rate of 0.67 kPa x s(-1)), respectively. RESULTS: MAP decreased rapidly during LBNP exposure. The mean time to isoelectric EEG was 41.33 +/- 11.48, 30.67 +/- 3.88 and 25.67 +/- 3.45 s during -2.67, -4.00 and -5.33 kPa LBNP, respectively. Heart rate (HR) significantly decreased when EEG became isoelectric. MAP, HR and EEG rapidly returned after releasing LBNP. The brain Na+,K-ATPase activity decreased significantly after single LBNP exposure and decreased further after three LBNP exposures. The brain K+, Na+ and water contents increased significantly after three LBNP exposures. CONCLUSIONS: A rat model of short-term, repeatable brain ischemia was developed using rapid LBNP. Three -4.00 kPa LBNP exposures (2 min each) cause a significant reduction in brain Na+,K+-ATPase activity and brain edema in rats.     

Peripheral vascular reflexes elicited during lower body negative pressure

To study the interaction between thermal reflexes and baroreflexes on human forearm vasomotor and venomotor control, and to test the hypothesis that peripheral veins are responsive to baroreceptor unloading during gravitational stress, we imposed lower body negative pressure (LBNP) between 10 and 50 mm Hg (Torr) at ambient temperatures (Ta) of 28 and 37 degrees C. We measured arterial and central venous pressures (CVP), heart rate, forearm venous volume, forearm venous pressure, and forearm blood flow in 12 volunteers. Decreases in CVP were relatively large at 10 mm Hg LBNP (p less than 0.01) at both Ta, and less thereafter. Arterial systolic and pulse pressures were not significantly reduced until LBNP exceeded 30 mm Hg (p less than 0.05). With LBNP up to 20 mm Hg, moderate decreases in forearm venous compliance and increases in forearm vascular resistance occurred. Between 30 and 50 mm Hg LBNP, the changes in both compliance and resistance per unit change in CVP were more than tripled. We concluded that unloading of cardiopulmonary mechanoreceptors stimulates increases in both forearm vasomotor and venomotor tone and that addition of arterial baroreceptor unloading adds to these reflex responses.     

eNOS T-786C genotype, physical activity, and peak forearm blood flow in females

BACKGROUND: The purpose of the present study was to determine interactive and main effects of the eNOS T-786C gene polymorphism and habitual physical activity level on forearm vascular resistance (FVR) and forearm blood flow (FBF) at rest and during 3 min of reactive hyperemia. METHODS: We studied healthy, Caucasian (age 25 +/- 1 yr), sedentary (maximal oxygen consumption, [OV0312]O2max: 33.8 +/- 1 mL x kg(-1)x min(-1)), and endurance-trained ([OV0312]O2max: 45.3 +/- 1 mL x kg(-1)x min(-1)) women. FBF was measured using venous occlusion plethysmography before (resting) and after 5 min of arm arterial occlusion at 1 (peak vasodilation), 2, and 3 min of reactive hyperemia. [OV0312]O2max was measured using a standard treadmill protocol, and skinfolds were measured to estimate body composition. RESULTS: There was a significant interaction between eNOS genotype and physical activity level on resting FVR (P = 0.0003). Sedentary subjects with the TT genotype had the lowest resting FVR, but among the endurance-trained group, the TC+CC genotype group had the lowest resting FVR. This interaction was reflected in the resting FBF values (P = 0.03). After accounting for important covariates, there was a main effect of eNOS genotype on peak FBF (TT, 7.0 +/- 0.3 vs TC+CC, 5.9 +/- 0.4 mL x 100 mL(-1) FAV x min(-1), P = 0.03) and the percent decrease in FVR (TT, -62 +/- 2 vs TC+CC, -51 +/- 4%, P = 0.04) at minute 1. CONCLUSIONS: These results of the interactive effects suggest that young females possessing a C allele may reduce their resting FVR by improving their cardiovascular fitness level, but TT homozygotes, who may have normal eNOS gene function, may not improve their resting FVR with improvements in cardiovascular fitness. Furthermore, regardless of physical activity level, the TT genotype showed a favorable hemodynamic response during reactive hyperemia compared with the C allele carriers.     

Baroreflex sensitivity during static exercise in individuals with Down Syndrome

INTRODUCTION: Individuals with Down syndrome (DS) have altered heart rate (HR) and blood pressure (BP) responses to orthostatic challenges and isometric handgrip (IHG) exercise, suggesting possible alteration in baroreflex sensitivity. PURPOSE: This study investigated baroreflex sensitivity (BRS) as a potential mechanism contributing to chronotropic incompetence during IHG in persons with DS. METHODS: Heart rate and BP were continually recorded in 12 individuals with DS and 10 controls, at rest and during 2 min of IHG, at 30% of maximal voluntary contraction (MVC). Spontaneous BRS was derived via the sequence method. RESULTS: No differences were seen in HR at rest between groups. Systolic BP (SBP) was significantly lower in the DS group at rest (106.1+/- 2.9 vs 116.5+/- 3.9 mm Hg, P < 0.05) and during IHG (123.9+/- 4.6 vs 150.1+/- 5.3 mm Hg, P<0.001). A significant group-by-task interaction was found for both change in HR and change in SBP with IHG, because of an attenuated HR and SBP response to IHG in participants with DS (P<0.05). When controlling for resting SBP, the DS group had a lower BRS at rest (16.0+/-1.7 vs 21.2+/-4.2 ms.mm Hg, P< 0.05) and during IHG (7.8 +/-1.0 vs 12.1+/- 2.6 ms.mm Hg, P< 0.05). CONCLUSIONS: Individuals with DS have lower BRS at rest and during IHG than controls and this may be related to their attenuated HR response during perturbation.     

Lower body negative pressure treadmill exercise is more comfortable and produces similar physiological responses as weighted vest exercise

Lower body negative pressure (LBNP) treadmill exercise can generate a hypergravity load on the lower body that may improve athlete performance by mechanical and cardiovascular adaptations. This study compared the cardiovascular responses, subjective exertion and discomfort levels produced by LBNP exercise with those generated by a weighted vest (WV). We hypothesized that LBNP exercise is more comfortable than WV exercise at comparable levels of exercise. Nine subjects exercised on a treadmill at nine conditions, at 5.5 mph for 15 minutes, in which they ran in random order to avoid confounding effects: 100 %, 110 %, 120 %, 130 %, and 140 % body weight (BW), the latter four conditions were achieved by either LBNP chamber or WV. Heart rate (HR) and oxygen consumption (.VO(2)) were monitored continuously using ECG and open circuit spirometry. At the end of each test, subjects were asked to give discomfort and exertion scores using a ten-point visual analog scale (10 = maximal discomfort and exertion). For both HR and .VO(2), no significant differences were observed between LBNP and WV. Subjects reported significantly higher discomfort levels when exercising with the WV than with the LBNP at 120 % BW (5.1 +/- 0.55 vs. 3.1 +/- 0.64; p < 0.05), 130 % BW (6.2 +/- 0.42 vs. 2.3 +/- 0.44; p < 0.01) and 140 % BW (6.9 +/- 0.27 vs. 4.7 +/- 0.60; p < 0.01), while maintaining similar exertions at all conditions. Based on these results, LBNP exercise is more comfortable than standard WV exercise, while maintaining similar exertion, HR and .VO(2) values.     

重力应激正自发性压力感受器—心率反射反应性的评定

为探讨重力应激下自发性压力感受器－心率反射反应性的评定方法，观察了１０人＋６５°头高位倾斜与８人－６．６７ｋＰａ下体负压作用下，以及１５人１６ｄ－６°头低位卧床期间ＢＲＳ的变化。