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Biomedical subjects

P B Raven

Publications and source records attributed to P B Raven.

At least 37 records · Page 2Linked to original sources
PubMed1999

Ventilatory responses to dynamic exercise elicited by intramuscular sensors.

PURPOSE: Eight subjects, aged 27.0+/-1.6 yr, performed incremental workload cycling to investigate the contribution of skeletal muscle mechano- and metaboreceptors to ventilatory control during dynamic exercise. METHODS: Each subject performed four bouts of exercise: exercise with no intervention (CON); exercise with bilateral thigh cuffs inflated to 90 mm Hg (CUFF); exercise with application of lower-body positive pressure (LBPP) to 45 torr (PP); and exercise with 90 mm Hg thigh cuff inflation and 45 torr LBPP (CUFF+PP). Ventilatory responses and pulmonary gas exchange variables were collected breath-by-breath with concomitant measurement of leg intramuscular pressure. RESULTS: Ventilation (VE) was significantly elevated from CON during PP and CUFF+PP at workloads corresponding to > or = 60% CON peak oxygen uptake (VO2peak) and during CUFF at workloads > or = 80% CON VO2peak, P < 0.05. The VO2 at which ventilatory threshold occurred was significantly reduced from CON (2.17+/-0.28 L x min(-1)) to 1.60+/-0.19 L x min(-1), 1.45+/-0.15 L x min(-1), and 1.15+/-0.11 L x min(-1) during CUFF, PP, and CUFF+PP, respectively. The slope of the linear regression describing the VE/CO2 output relationship was increased from CON by approximately 22% during CUFF, 40% during PP, and 41% during CUFF+PP. CONCLUSIONS: As intramuscular pressure was significantly elevated immediately upon application of LBPP during PP and CUFF+PP without a concomitant increase in VE, it seems unlikely that LBPP-induced increases in VE can be attributed to activation of the mechanoreflex. These findings suggest that LBPP-induced reductions in perfusion pressure and decreases in venous outflow resulting from inflation of bilateral thigh cuffs may generate a metabolite sensitive intramuscular ventilatory stimulus.

Adult↗
PubMed1999

Resetting of the carotid arterial baroreflex during dynamic exercise in humans.

Recent investigations have demonstrated that at the onset of low-to-moderate-intensity leg cycling exercise (L) the carotid baroreflex (CBR) was classically reset in direct relation to the intensity of exercise. On the basis of these data, we proposed that the CBR would also be classically reset at the onset of moderate- to maximal-intensity L exercise. Therefore, CBR stimulus-response relationships were compared in seven male volunteers by using the neck pressure-neck suction technique during dynamic exercise that ranged in intensity from 50 to 100% of maximal oxygen uptake (VO(2 max)). L exercise alone was performed at 50 and 75% VO(2 max), and L exercise combined with arm (A) exercise (L + A) was performed at 75 and 100% VO(2 max). O(2) consumption and heart rate (HR) increased in direct relation with the increases in exercise intensity. The threshold and saturation pressures of the carotid-cardiac reflex at 100% VO(2 max) were >75% VO(2 max), which were in turn >50% VO(2 max) (P < 0.05), without a change in the maximal reflex gain (G(max)). In addition, the HR response value at threshold and saturation at 75% VO(2 max) was >50% VO(2 max) (P < 0.05) and 100% VO(2 max) was >75% VO(2 max) (P < 0.07). Similar changes were observed for the carotid-vasomotor reflex. In addition, as exercise intensity increased, the operating point (the prestimulus blood pressure) of the CBR was significantly relocated further from the centering point (G(max)) of the stimulus-response curve and was at threshold during 100% VO(2 max). These findings identify the continuous classic rightward and upward resetting of the CBR, without a change in G(max), during increases in dynamic exercise intensity to maximal effort.

Adult↗
PubMed1999

Carotid baroreflex function during prolonged exercise.

The present investigation was designed to uncouple the hemodynamic physiological effects of thermoregulation from the effects of a progressively increasing central command activation during prolonged exercise. Subjects performed two 1-h bouts of leg cycling exercise with 1) no intervention and 2) continuous infusion of a dextran solution to maintain central venous pressure constant at the 10-min pressure. Volume infusion resulted in a significant reduction in the decrement in mean arterial pressure seen in the control exercise bout (6.7 +/- 1.8 vs. 11.6+/- 1.3 mmHg, respectively). However, indexes of central command such as heart rate and ratings of perceived exertion rose to a similar extent during both exercise conditions. In addition, the carotid-cardiac baroreflex stimulus-response relationship, as measured by using the neck pressure-neck suction technique, was reset from rest to 10 min of exercise and was further reset from 10 to 50 min of exercise in both exercise conditions, with the operating point being shifted toward the reflex threshold. We conclude that the progressive resetting of the carotid baroreflex and the shift of the reflex operating point render the carotid-cardiac reflex ineffectual in counteracting the continued decrement in mean arterial pressure that occurs during the prolonged exercise.

Adult↗
PubMed1998

Cardiovascular function following reduced aerobic activity.

PURPOSE: The aim of this study was to test the hypothesis that a sustained reduction of physical activity (deconditioning) would alter the cardiovascular regulatory function. METHODS: Nineteen young, healthy volunteers participated in physical deconditioning for a period of 8 wk. Before (pre) and following (post) physical deconditioning, the responses of heart rate (HR), mean arterial pressure (MAP, measured by Finapres), central venous pressure (CVP), stroke volume (SV, Doppler), and forearm blood flow (FBF, plethysmography) were determined during lower body negative pressure (LBNP). The carotid baroreflex (CBR) function was assessed using a train of pulsatile neck pressure (NP) and suction, and the aortic baroreflex control of HR was assessed during steady-state phenylephrine (PE) infusion superimposed by LBNP and NP to counteract the PE increased CVP and carotid sinus pressure, respectively. RESULTS: Active physical deconditioning significantly decreased maximal oxygen uptake (-7%) and LBNP tolerance (-13%) without a change in baseline hemodynamics. Plasma volume (-3% at P = 0.135), determined by Evans Blue dilution, and blood volume (-4% at P = 0.107) were not significantly altered. During LBNP -20 to -50 torr, there was a significantly greater drop of SV per unit decrease in CVP in the post- (14.7 +/- 1.6%/mm Hg) than predeconditioning (11.2 +/- 0.7%/mm Hg) test accompanied by a greater tachycardia. Deconditioning increased the aortic baroreflex sensitivity (pre vs post: -0.61 +/- 0.12 vs -0.84 +/- 0.14 bpm.mm-1 Hg, P = 0.009) and the slope of forearm vascular resistance (calculated from [MAP-CVP]/FBF) to CVP (-2.75 +/- 0.26 vs -4.94 +/- 0.97 PRU/mm Hg, P = 0.086). However, neither the CBR-HR (-0.28 +/- 0.03 VS -0.39 +/- 0.10 bpm.mm-1 Hg) nor the CBR-MAP (-0.37 +/- 0.16 vs -0.25 +/- 0.07 mm Hg/mm Hg) gains were statistically different between pre- and postdeconditioning. CONCLUSIONS: We concluded that the functional modification of the cardiac pressure-volume relationship resulted in the reduced LBNP tolerance, despite the accentuated aortic and cardiopulmonary baroreflex function following deconditioning.

Adult↗
PubMed1997

Interaction of central venous pressure, intramuscular pressure, and carotid baroreflex function.

Seven healthy volunteer men participated in an experiment involving lower body positive pressure (LBPP) of 30 Torr and acute volume expansions of 5-6% (VE-I) and 9-10% (VE-II) of their total blood volume (TBV) to differentiate the effect of increased intramuscular pressure and central venous pressure (CVP) on the maximal gain (Gmax) of the carotid baroreflex. During each experimental condition, the heart rate (HR), mean arterial pressure (MAP; intraradial artery or Finapres), and CVP (at the 3rd-4th intercostal space) were monitored continuously. Gmax was derived from the logistic modeling of the HR and MAP responses to ramped changes in carotid sinus transmural pressure using a protocol of pulsatile changes in neck chamber pressure from +40 to -65 Torr. The increase in CVP during +30-Torr LBPP was 1.5 mmHg (P < 0.05) and was similar to that observed during VE-I (1.7 mmHg, P > 0.05). The Gmax of the carotid baroreflex of HR and MAP was significantly decreased during LBPP by -0.145 +/- 0.039 beats x min(-1) x mmHg(-1) (38%) and -0.071 +/- 0.013 mmHg/mmHg (25%), respectively; however, VE-I did not affect Gmax. During VE-II, CVP was significantly greater than that elicited by LBPP, and the Gmax of the carotid baroreflex of the HR and MAP responses was significantly reduced. We conclude that carotid baroreflex responsiveness was selectively inhibited by increasing intramuscular pressure, possibly resulting in an activation of the intramuscular mechanoreceptors during LBPP. Furthermore, it would appear that the inhibition of the carotid baroreflex, via cardiopulmonary baroreceptor loading (increased CVP), occurred when a threshold pressure (CVP) was achieved.

Adult↗
PubMed1997

Baroreflex regulation of blood pressure during dynamic exercise.

From the work of Potts et al. Papelier et al. and Shi et al. it is readily apparent that the arterial (aortic and carotid) baroreflexes are reset to function at the prevailing ABP of exercise. The blood pressure of exercise is the result of the hemodynamic (cardiac output and TPR) responses, which appear to be regulated by two redundant neural control systems, "Central Command" and the "exercise pressor reflex". Central Command is a feed-forward neural control system that operates in parallel with the neural regulation of the locomotor system and appears to establish the hemodynamic response to exercise. Within the central nervous system it appears that the HLR may be the operational site for Central Command. Specific neural sites within the HLR have been demonstrated in animals to be active during exercise. With the advent of positron emission tomography (PET) and single-photon emission computed tomography (SPECT), the anatomical areas of the human brain related to Central Command are being mapped. It also appears that the Nucleus Tractus Solitarius and the ventrolateral medulla may serve as an integrating site as they receive neural information from the working muscles via the group III/IV muscle afferents as well as from higher brain centers. This anatomical site within the CNS is now the focus of many investigations in which arterial baroreflex function, Central Command and the "exercise pressor reflex" appear to demonstrate inhibitory or facilitatory interaction. The concept of whether Central Command is the prime mover in the resetting of the arterial baroreceptors to function at the exercising ABP or whether the resetting is an integration of the "exercise pressor reflex" information with that of Central Command is now under intense investigation. However, it would be justified to conclude, from the data of Bevegard and Shepherd, Dicarlo and Bishop, Potts et al., and Papelier et al. that the act of exercise results in the resetting of the arterial baroreflex. In addition, if, as we have proposed, the cardiopulmonary baroreceptors primarily monitors and reflexly regulates cardiac filling volume, it would seem from the data of Mack et al. and Potts et al. that the cardiopulmonary baroreceptor is also reset at the beginning of exercise. Therefore, investigations of the neural mechanisms of regulation involving Central Command and cardiopulmonary afferents, similar to those being undertaken for the arterial baroreflex, need to be established.

Animals↗
PubMed1996

Diminished forearm vasomotor response to central hypervolemic loading in aerobically fit individuals.

The aim of this study was to test the hypothesis that cardiopulmonary baroreflex control of forearm vascular resistance (FVR) during central hypervolemic loading was less sensitive in exercise trained high fit individuals (HF) compared to untrained average fit individuals (AF). Eight AF (age: 24 +/- 1 yr and weight: 78.9 +/- 1.7 kg) and eight HF (22 +/- 1 yr 79.5 +/- 2.4 kg) voluntarily participated in the investigation. Maximal aerobic power (determined on a treadmill), plasma volume and blood volume (Evans blue dilution method) were significantly greater in the HF than AF (60.8 +/- 0.7 vs. 41.2 +/- 1.9 ml.kg-1.min-1, 3.96 +/- 0.17 vs 3.36 +/- 0.08 1, and 6.33 +/- 0.23 vs 5.28 +/- 0.13 1). Baseline heart rate (HR), central venous pressure (CVP), mean arterial pressure (MAP, measured by an intraradial catheter or a Finapres finger cuff), forearm blood flow (FBF, plethysmography), and FVR, calculated from the ratio (MAP-CVP)/FBF, were not different between the HF and the AF. Lower body negative pressure (LBNP, -5, -10, -15, and -20 torr) and passive leg elevation (LE, 50 cm) combined with lower body positive pressure (LBPP, +5, +10, and +20 torr) were utilized to elicit central hypovolemia and hypervolemia, respectively. Range of CVP (from LBNP to LE+LBPP) was similar in the AF (from -3.9 to +1.9 mm Hg) and HF (from -4.0 to +2.2 mm Hg). However, FVR/CVP was significantly less in the HF (-1.8 +/- 0.1 unit.mm Hg-1) than AF (-34 +/- 0.1 unit.mm Hg-1). The FVR decrease in response to increase in CVP was significantly diminished in the HF (-1.46 +/- 0.45 unit.mm Hg-1) compared to the AF (-4.40 +/- 0.97 unit.mm Hg-1), and during LBNP induced unloading the FVR/CVP of the HF (-2.01 +/- 0.49 unit.mm Hg-1) was less (P < 0.08) than the AF (-3.28 +/- 0.69 unit.mm Hg-1). We concluded that the cardiopulmonary baroreceptor mediated FVR reflex response was significantly less sensitive to changes in CVP in individuals who practice exercise training.

Adult↗
PubMed1996

Unaltered oxygen uptake kinetics at exercise onset with lower-body positive pressure in humans.

The purpose of this study was to determine the influence of a reduced skeletal muscle blood flow on oxygen uptake (VO2) kinetics at the onset of cycle ergometer exercise. Seven healthy subjects performed rest-to-exercise transitions with a lower-body positive pressure (LBPP) of 45 Torr. Two work rates were selected for each subject: a moderate intensity (VO2, approximately 1.9 l min-1; delta[lactate], approximately 1 mequiv l-1) below the estimated lactate threshold and a heavy intensity (VO2, approximately 2.6 l min-1; delta[lactate], approximately 3 mequiv l-1) above this threshold. Pulmonary gas exchange variables and ventilatory (VE) responses were computed breath-by-breath from mass spectrometer and turbine volume meter signals, respectively, and mean response times (MRT) calculated. Samples of 'arterialized' venous blood were used for the determination of [lactate], pH and [K+]. While the application of 45 Torr LBPP had no effects on VO2 kinetics during moderate exercise (MRT: 33.5 +/- 1.2 s at 45 Torr vs. 32.8 +/- 1.3 s at 0 Torr; P > 0.05) or on [lactate], pH or [K+], breathing frequency (f) was increased (P < 0.05) and tidal volume (VT) reduced (P < 0.05). The addition of LBPP during heavy exercise did not alter VO2 kinetics (MRT: 35.2 +/- 1.5 s at 45 Torr vs. 34.8 +/- 1.5 s at 0 Torr; P > 0.05), or [lactate], pH or [K+]. Although both the VE (via an increased f) and CO2 output (VCO2) were significantly greater with LBPP by approximately 30 l min-1 and approximately 500 ml min-1, respectively, end-tidal CO2 partial pressure was decreasing, suggesting an additional ventilatory stimulus. These data can be interpreted to suggest that oxygen delivery is not critically dependent upon blood flow to the working muscle at exercise onset, while LBPP-induced increases in VE during suprathreshold exercise may be related to an accumulation of metabolites at the working muscle or the effects of pressure per se.

Adult↗
PubMed1995

Effect of dynamic exercise on human carotid-cardiac baroreflex latency.

We compared the beat-to-beat responses of heart rate (HR) after brief activation of carotid baroreceptors in resting humans with the responses obtained during mild-to-moderate levels of dynamic exercise [25 and 50% of peak O2 uptake (VO2peak)] to investigate the effect of exercise on baroreflex latency. Carotid baroreceptors were activated by a pressure pulse (5 s) of neck suction (NS, -80 Torr) and neck pressure (NP, +40 Torr) during held expiration. At rest the peak change in HR to NS/NP occurred during the first several heartbeats (1st-3rd beat), whereas during mild and moderate exercise peak HR responses occurred near the end of the NS/NP pulse (6th-8th beat). In contrast, time (s) to the peak change in HR was not different between rest and exercise (P > 0.05). Reflex tachycadia to NP progressively decreased during exercise (17 +/- 3, 10 +/- 1, and 4 +/- 1% of control, rest vs. 25% VO2peak, vs. 50% VO2peak, respectively, P < 0.05), and a strong positive correlation was found between the magnitude of the reflex tachycardia and a measure of HR variability (cardiac vagal tone index, r = 0.74, P < 0.0001). Reflex bradycardia to NS gradually increased during exercise (13 +/- 2, 17 +/- 2, and 18 +/- 2% of control, rest vs. 25% VO2peak, vs. 50% VO2peak, respectively, P = 0.10) and was negatively correlated with cardiac vagal tone (r = 0.42, P < 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Cardiopulmonary baroreceptors modulate carotid baroreflex control of heart rate during dynamic exercise in humans.

Numerous studies have reported that, at rest, maximal carotid baroreflex gain is modulated by cardiopulmonary baroreceptors. The purpose of this study was to measure the maximal gain for carotid baroreflex control of heart rate (HR) and blood pressure [mean arterial pressure (MAP)] during dynamic exercise alone and when exercise was accompanied by two levels of cardiopulmonary baroreceptor unloading. Lower body negative pressure (LBNP) produced similar reductions in central venous pressure (CVP) at rest and during exercise. Baroreflex gain for HR at rest was not affected by low-level LBNP but was significantly increased by high-level LBNP [-0.31 +/- 0.05 to -0.57 +/- 0.23 beats.min-1.mmHg-1 carotid sinus pressure (CSP), no LBNP vs. high-level LBNP, P < 0.05]. Exercise combined with low- and high-level LBNP resulted in reflex HR gains (-0.83 +/- 0.44 and -0.83 +/- 0.17 beats.min-1.mmHg-1 CSP, low- vs. high-level LBNP, P < 0.05) that were significantly greater than the algebraic sum of the HR gain measured during exercise and LBNP alone. Neither exercise nor the two levels of LBNP significantly altered baroreflex gain for MAP. The slope relating HR gain to CVP at rest was significant (0.07 +/- 0.02 beats.min-1.mmHg CSP-1.mmHg CVP-1, P < 0.01) and increased 114% during exercise (P < 0.05). A similar analysis of MAP gain found no difference in slope between rest and exercise (P > 0.05). Together these data indicate 1) a tonic inhibitory interaction between cardiopulmonary baroreceptors and carotid baroreflex control of HR during exercise, and 2) a nonlinear relationship between deactivation of cardiopulmonary baroreceptors and changes in carotid baroreflex gain. This interaction may improve overall cardiovascular regulation when central blood volume and/or CVP is reduced, as has been reported during prolonged exercise in the heat.

Adult↗
PubMed1995

Aortic-cardiac reflex during dynamic exercise.

We investigated the aortic-cardiac reflex during low-intensity cycling in 10 healthy volunteers. Baroreflex function was assessed by the ratio of change in heart rate to mean arterial pressure (delta HR/delta MAP) during phenylephrine (PE) infusion. The ratio obtained during PE combined with low-level lower body negative pressure (LBNP) and calculated neck pressure (NP) was assessed as the gain of the aortic-cardiac reflex. Exercise (approximately 25% maximal O2 uptake or 25 +/- 2 W) significantly increased HR from 64 +/- 2 to 98 +/- 2 beats/min, MAP from 90 +/- 3 to 98 +/- 3 mmHg, cardiac output from 6.6 +/- 0.5 to 12.0 +/- 1.4 l/min, and O2 uptake from 3.8 +/- 0.2 to 10.4 +/- 0.6 ml.min-1.kg-1. However, delta MAP (+11.8 +/- 0.4 vs. + 11.3 +/- 0.8 mmHg), delta HR (-12.7 +/- 2 vs. -12.9 +/- 2 beats/min), and delta HR/delta MAP (1.10 +/- 0.19 vs. 1.15 +/- 0.15 beats.min-1.mmHg-1) were not statistically different between rest and exercise during PE. Although PE significantly increased central venous pressure in both supine rest (from 6.7 +/- 0.7 to 10.4 +/- 0.7 mmHg) and exercise (5.8 +/- 0.8 to 8.6 +/- 0.9 mmHg) conditions, when LBNP (-15 +/- 2 vs. -16 +/- 1 Torr for rest vs. exercise) was applied, both rest and exercise central venous pressures were returned to the preinfusion baseline values, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Cardiovascular adaptations following detraining.

We have recently summarized our data concerning endurance exercise training and its effect on blood pressure regulation during lower body negative pressure (LBNP). We found that endurance trained (ET) subjects were less tolerant to LBNP than their untrained (UT) counterparts. This decreased tolerance to LBNP was linked to a fitness related adaptation in cardiac compliance, an attenuated cardiopulmonary reflex regulation of peripheral vasoconstriction and an attenuated aortic-cardiac reflex. More recently we have found that 15 days of bed rest deconditioning (a severe form of detraining) in UT subjects resulted in a more responsive aortic-cardiac reflex. In severe detraining investigations, spaceflight and bed rest deconditioning a reduction in total blood and plasma volume were the manifest physiological changes. Therefore, we postulate that the increased aortic-reflex responsiveness was a compensation for the blood and plasma volume losses associated with detraining. Subsequently, we hypothesized that a generalized reduction of the normal daily aerobic activities of a healthy, young adult population would produce a moderate reduction in total blood and plasma volume and an up-regulation of the reflex blood pressure regulatory mechanisms.

Adaptation, Physiological↗
PubMed1995

Autonomic nervous system control of the heart: endurance exercise training.

The purpose of this study was to assess hemodynamic responses to lower body negative pressure (LBNP) to -45 torr with selective cardiac parasympathetic (using atropine sulphate), sympathetic efferent (using metoprolol tartrate), and combined (atropine+metoprolol) blockade prior to and following 8 months of endurance exercise training in eight young men. Training resulted in significant increases of maximal oxygen uptake (27%) and blood volume (16%) and a decrease of baseline heart rate (HR, from 66 +/- 4 to 57 +/- 4 bpm). This training related bradycardia was exclusively determined by an enhanced vagal tone as there was no significant difference in intrinsic HR pre- to post-training and only atropine (pre: 100 +/- 3 vs post: 101 +/- 3 bpm), not metoprolol (pre: 56 +/- 3 vs post: 49 +/- 4 bpm), abolished the HR difference. The reflex tachycardia in the control experiment was significantly diminished following training. However, the increase in HR at LBNP -45 torr between pre- and post-training was similar after either atropine (+13 +/- 2 vs +14 +/- 1 bpm) or metoprolol (+8 +/- 1 vs +8 +/- 1 bpm). Reflex tachycardia was greater during atropine than metoprolol blockade and the sum of the HR increase during selective blockade (21 and 22 bpm) was greater when compared with the control (no blockade, 16 +/- 2 vs 11 +/- 2 bpm). There was no difference pre- to post-training in SV or Qc response to -45 torr LBNP during the control condition. However, selective beta 1-receptor blockade resulted in a greater decrease in SV to -45 torr LBNP post-training compared to pre-training (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Reflex increase in blood pressure induced by leg compression in man.

1. We tested the hypotheses that the increase in mean arterial pressure with the application of external leg compression in man is (i) blocked with epidural anaesthesia, and (ii) dependent upon the level of external pressure applied, the quantity of leg muscle mass compressed and the vascular volume of the leg. Fourteen healthy subjects were fitted with an anti-shock trouser garment to provide three levels (30, 60 and 90 mmHg) of leg compression, while cephalad translocation of fluid was prevented by upper-thigh cuffs inflated to a supra-systolic pressure. Cardiovascular responses were recorded during leg compression before and after the administration of epidural anaesthesia in eight subjects, while blood pressure responses from six subjects were compared with their single leg pressor response. 2. Both mean arterial and diastolic pressures were elevated with increasing leg compression, with no changes in heart rate, cardiac output, thoracic impedance, and central venous pressure. The leg compression-induced blood pressure increases were abolished by epidural anaesthesia. Furthermore, when only one leg was compressed at 90 mmHg, the pressor response was less than that elicited from compression of both legs at the same external pressure. Changes in vascular volume of the leg did not influence the pressor response to leg compression. 3. The results indicate that the mean arterial pressure increases in response to external compression of the legs and that a reflex mechanism, mediated by muscle afferent nerves, is involved. The response is dependent upon both the changes in intramuscular pressure and the quantity of muscle mass compressed.

Adult↗
PubMed1994

Altered thermoregulatory responses after 15 days of head-down tilt.

To determine whether extended exposure to a simulation of microgravity alters thermoregulatory reflex control of skin blood flow, six adult males (mean age 40 +/- 2 yr) were exposed to 15 days of 6 degrees head-down tilt (HDT). On an ambulatory control day before HDT exposure and on HDT day 15, the core temperature of each subject was increased by 0.5-1.0 degree C by whole body heating with a water-perfused suit. Mean skin temperature, oral temperature (Tor), mean arterial pressure, and forearm blood flow were measured throughout the protocol. Forearm vascular conductance (FVC) was calculated from the ratio of forearm blood flow to mean arterial pressure. After HDT exposure, the Tor threshold at which reflex thermally induced increases in FVC began was elevated (36.87 +/- 0.06 to 37.00 +/- 0.09 degrees C; P = 0.043), whereas the slope of the Tor-FVC relationship after this threshold was reduced (13.7 +/- 2.3 to 9.5 +/- 1.1 FVC units/degrees C; P = 0.038). Moreover, normothermic FVC and FVC at the highest common Tor between pre- and post-HDT trials were reduced after HDT (normothermic: 4.2 +/- 0.5 to 3.0 +/- 0.4 ml.100 ml-1.min-1.100 mmHg-1, P = 0.04; hyperthermic: 12.4 +/- 1.0 to 7.8 +/- 0.7 ml.100 ml-1.min-1.100 mmHg-1, P < 0.001). These data suggest that HDT exposure reduces thermoregulatory responses to heat stress. The mechanisms resulting in such an impaired thermoregulatory response are unknown but are likely related to the relative dehydration that accompanies this exposure.

Adult↗