Norepinephrine and epinephrine responses during orthostatic intolerance in healthy elderly men

In young individuals, orthostatic intolerance is associated with marked increases in plasma epinephrine (EPI) concentrations and attenuated rises in plasma norepinephrine (NE) concentrations. This study investigated the cardiovascular, EPI and NE responses of healthy elderly males during orthostatic stress. Twelve men (68 +/- 1 yr) with a recent history of orthostatic hypotension and who exhibited orthostatic intolerance (HYPO) during 90 degrees head-up tilt (HUT) were compared with 12 men (69 +/- 1 yr) without a history of orthostatic hypotension and who remained normotensive (NORMO) throughout 90 degrees HUT. Beat-by-beat recordings of heart rate (HR), mean (MAP), systolic (SBP), diastolic (DBP), and pulse (PP) pressures were made throughout 90 degrees HUT. Blood samples obtained during supine rest and 90 degrees HUT were analyzed for changes in EPI and NE concentrations, hematocrit, hemoglobin and plasma volume. Compared to supine rest, orthostatic intolerance was characterized by significant reductions (p < 0.0001) in MAP, SBP, DBP, and PP. The HR, MAP, SBP, DBP, and PP at the termination of 90 degrees HUT was significantly lower (p < 0.0001) for HYPO than NORMO. The 90 degrees HUT position resulted in significant increases (p < 0.01) in NE for both HYPO and NORMO, with the rise in NE significantly lower (p < 0.05) in HYPO. There were no differences between groups regarding EPI concentrations at the termination of 90 degrees HUT. These results suggest that the magnitude of arterial pressure (AP) reduction does not influence the EPI response during orthostasis in healthy elderly men. However, marked reductions in AP, leading to orthostatic intolerance, are associated with inadequate increases in NE in these individuals.     

Reliability of orthostatic responses in healthy men aged between 65 and 75 years

The purpose of this study was to investigate the short-, medium- and long-term reproducibility of cardiovascular responses during 90 degrees head-up tilt (HUT) in healthy older men. Twenty-eight healthy male subjects aged 69 (95% confidence intervals, 68-70) years participated in the study. Eight subjects underwent duplicate 90 degrees HUT tests on consecutive days, while 20 subjects underwent four 90 degrees HUT tests performed at baseline, and after 1 week, 1 month and 1 year. Following a 20-min supine resting period, each subject was rapidly tilted to the upright vertical position (90 degrees HUT) and remained in that position for 15 min. Beat-by-beat recordings of mean (MAP), systolic (SBP) and diastolic (DBP) pressures were made via Finapres, while heart rate (HR) was monitored continuously from an electrocardiogram. No significant test-retest differences (P > 0.05) were observed for the changes in HR, MAP, SBP or DBP during 90 degrees HUT. These measurements demonstrated high reproducibility (intraclass correlation coefficient, r = 0.91-0.99, P < 0.05). The supine resting and tilted HR, MAP, SBP and DBP over the 1-week, 1-month and 1-year period were not significantly different (P > 0.05) from baseline, and demonstrated high reproducibility (intraclass correlation coefficient, r = 0.82-0.98, P < 0.05). The results of this study demonstrate that in healthy older men, cardiovascular responses during orthostasis are highly reproducible, and this reproducibility is maintained over a 12-month period. These findings demonstrate that the 90 degrees HUT test offers a reproducible method of monitoring longitudinal orthostatic responses in healthy older men.     

Prone sleeping impairs circulatory control during sleep in healthy term infants: implications for SIDS

STUDY OBJECTIVES: To determine the effects of sleeping position on development of circulatory control in infants over the first 6 months of postnatal age (PNA). DESIGN: Effects of sleeping position, sleep state and PNA on beat-beat heart rate (HR) and mean arterial pressure (MAP) responses to a head-up tilt (HUT) were assessed during sleep in infants at 2-4 wks, 2-3 mo and 5-6 mo PNA. MEASUREMENTS: Daytime polysomnography was performed on 20 full-term infants (12 F/8 M) and MAP was recorded continuously and noninvasively (Finometer). HUTs of 15 degrees were performed during active sleep (AS) and quiet sleep (QS) in both the prone and supine sleeping positions. MAP and HR data were expressed as the percentage change from baseline, and responses were divided into initial, middle and late phases. RESULTS: In the supine position HUT usually resulted in an initial increase (P < 0.05) in HR and MAP, followed by decreases (P < 0.05) in HR and MAP in the middle phase; subsequently HR and MAP returned to baseline in the late phase. By contrast, in the prone position the initial HUT-induced rises in HR and MAP were usually absent, and at 2-3 mo MAP actually decreased (P < 0.05); subsequently HR but not MAP returned to baseline. At 2-3 mo, MAP was lower (P < 0.05) in prone than supine sleeping throughout the HUT. CONCLUSIONS: Prone sleeping alters MAP responses to a HUT during QS at 2-3 mo PNA. Decreased autonomic responsiveness may contribute to the increased risk for SIDS of infants sleeping in the prone position.     

Pregnancy decreases GABAergic inhibition of the hypothalamic paraventricular nucleus

Depressor responses to peripheral or central infusion of Angiotensin II type 1 (AT₁) receptor antagonists (AT₁X) are greater in pregnant (P) compared to nonpregnant (NP) animals. AT₁ and ionotropic excitatory amino acid (EAA) receptors contribute to pressor responses to GABA_A receptor blockade with bicuculline (Bic) in the paraventricular nucleus (PVN) of male rats. Therefore, we hypothesized that GABAergic inhibition is decreased and AT₁ receptors play a greater excitatory role in the PVN of P versus NP rats. Unilateral microinjection of Bic was performed before (Bic₁), after AT₁X (Bic₂), and after AT₁X + EAA blockade (kynurenate, Kyn) (Bic₃) in the PVN. Increases in mean arterial pressure (MAP: NP = 20 ± 2; P = 12 ± 2 mmHg), heart rate (HR: NP = 57 ± 6; P = 19 ± 6 beats/min) and renal sympathetic nerve activity (RSNA: NP = 70 ± 9; P = 33 ± 7%) due to Bic (Bic₁) were attenuated in P rats. Responses to AT₁X and Kyn alone were insignificant in both groups. In NP rats, AT₁X attenuated (+ 12 ± 4 mmHg), and AT₁X + Kyn further decreased the pressor response to Bic in the PVN (+ 6 ± 2 mmHg). In P rats AT₁X reduced the pressor response to Bic (+ 5 ± 1 mm Hg), and Kyn had no additional effect (+ 3 ± 1 mmHg). Effects of PVN Bic to alter the autospectra of RSNA were suppressed by prior AT₁X and Kyn in both groups. Thus, tonic GABAergic inhibition is decreased and the contribution of AT₁ receptors in the PVN may be greater in P rats.     

Increased hypoxic ventilatory response during hypovolemic stress imposed through head-up-tilt and lower-body negative pressure

The aim of this study was to quantify the influence of head-up-tilt (HUT) on the isocapnic hypoxic ventilatory response (HVR) in man, and to investigate the effect of orthostatic blood shifts separately from other gravitational effects by the application of lower-body negative pressure (LBNP) with subjects in a horizontal position. HVR was measured in 15 subjects during passive HUT from 0° to 85° as well as during −7° head-down-tilt and while they were in a sitting position. In a subgroup of eight subjects the effect of 85° HUT was compared to a corresponding LBNP of −70 mbar on HVR. Moreover, by imposing graded HUT (7°, 15°, 30°, 50°) and LBNP (−15, −30 mbar) we studied the effect of low-level orthostatic stress on HVR. Ventilation, end-tidal partial pressure of CO₂, heart rate and blood pressure were recorded continuously for 1 min before, and during HVR. HVR was significantly increased by ≅50% through both 85° HUT and −70 mbar LBNP as compared to 0° and 0 mbar, respectively, at unchanged mean arterial pressure. Low-level HUT and LBNP had no effect on HVR. It was concluded that the orthostatic HVR increase may be attributable to caudal blood shifts (i.e., central hypovolemia). This HVR increase requires a pronounced hypovolemic stress but no decrease in arterial blood pressure. It is suggested that a central interaction of arterial and cardiopulmonary baroreceptors is underlying this response. Their separate contribution remains to be assessed. Accepted: 14 October 1999     

Carotid-cardiac baroreflex function does not influence blood pressure regulation during head-up tilt in humans

The influence of the carotid-cardiac baroreflex on blood pressure regulation was evaluated during supine rest and 40 degrees head-up tilt (HUT) in 9 healthy young subjects with and without full cardiac vagal blockade. The carotid baroreflex responsiveness, or maximal gain (G(MAX)), was assessed from the beat-to-beat changes in heart rate (HR) and mean arterial pressure (MAP) by the variable neck pressure and suction technique ranging in pressure from +40 to -80 Torr, with and without glycopyrrolate (12.0 +/- 1.0 microg/kg body weight; mean +/- SE). In the supine position, glycopyrrolate increased the HR to 91 +/- 3 bpm, from 54 +/- 3; MAP to 89 +/- 2 mmHg, from 76 +/- 2; and cardiac output to 6.8 +/- 0.3 l.min(-1), from 4.9 +/- 0.3 (P < 0.05). The G(MAX) of the carotid baroreflex control of HR was reduced to -0.06 +/- 0.01 bpm.mmHg(-1), from -0.30 +/- 0.02 (P < 0.05) with no significant effect on the G(MAX) of the carotid baroreflex control of MAP. During HUT the carotid baroreflex control of MAP was unchanged, though the G(MAX) of the carotid baroreflex control of HR was increased (P < 0.05). During HUT, central blood volume, assessed by electrical thoracic admittance, and total vascular conductance were decreased with and without glycopyrrolate. Furthermore, glycopyrrolate reduced G(MAX) of the carotid baroreflex control of HR during HUT (P < 0.05) with no significant effect on G(MAX) of the carotid baroreflex control of MAP. These data suggest that during supine rest and HUT-induced decreases in central blood volume, the carotid baroreflex control of HR is mediated primarily via parasympathetic activity. Furthermore, the maintenance of arterial blood pressure during postural stress is primarily mediated by arterial and cardiopulmonary reflex regulation of sympathetic activity and its effects on the systemic vasculature.     

Renal sympathetic nerve activity is increased in monosodium glutamate induced hyperadipose rats

The literature suggests that both obesity and hypertension are associated with increased sympathetic nerve activity. In the present study we evaluated the renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP) and heart rate (HR) in hyperadipose rats induced by neonatal administration of monosodium glutamate (MSG). Neonatal Wistar male rats were injected with MSG (4 mg/g body weight ID) or equimolar saline (control) for 5 days. At 90th day, all rats were anesthetized (urethane 1.4 g/kg) and prepared for MAP, HR and renal sympathetic nerve activity recordings. The anesthetized MSG rats presented baseline hypertension and increased baseline RSNA compared with control. Our results suggest the involvement of the renal sympathetic nervous system in the physiopathology of the MSG obesity.     

A comparative assessment of two techniques for investigating initial cardiovascular reflexes under acute orthostatic stress

The physiological differences between active and passive changes in posture have been previously established. This study determined the extent of the differences in the initial cardiovascular responses to the passive head-up tilt (HUT) and the active squat-stand test (SST). Eleven females and 13 males underwent one +75° HUT and one SST. Beat-to-beat diastolic blood pressure (DBP), systolic blood pressure (SBP), mean arterial pressure (MAP) and heart rate (HR) were determined non-invasively. Data were recorded 10 s prior to (control) and 30 s after tilt or stand (event). Blood pressure and HR responses were analysed by calculating the deviation from control at 10 s (T10), 20 s (T20) and 30 s (T30) after the onset of each test. The DBP response (reflecting changes in systemic vascular resistance) at T10 was –10 (2) mmHg [mean (SEM)] for the HUT and –25 (2) mmHg for the SST (P<0.01). DBP returned to control levels by T30 for the HUT, but remained depressed for the SST. MAP responses directly reflected these changes in DBP. HR significantly increased from control values (P<0.001) for the HUT [+14 (1) bpm] and the SST [+16 (1) bpm], and remained elevated for the entire 30-s period for both tests. This study demonstrates that although the magnitude of the initial blood pressure decrease is greater for the active SST compared with the passive HUT, the reflex compensatory response is no different, making the SST a greater challenge for the cardiovascular reflexes.     

Reproducibility of the alterations in circulation and cerebral oxygenation from supine rest to head-up tilt.

Cardiovascular stability, as affected by several diseases, may be assessed by head-up tilt testing. Follow-up studies are essential in both evaluating interventions and assessing progression. However, data on the reproducibility of the changes in circulatory status and cerebral oxygenation provoked by head-up tilt testing are fundamental to follow-up studies. The aim of this study was, therefore, to assess the reproducibility of the alterations in stroke volume (SV), mean arterial pressure (MAP), as well as oxygenated ([O2Hb]) and deoxygenated haemoglobin ([HHb]) concentration in cerebral tissue from supine rest (SUP) to head-up tilt (HUT). SV was calculated by Modelflow, a pulse contour method, from the finger arterial pressure wave measured by Portapres, the portable version of Finapres. [O2Hb] and [HHb] were measured using near-infrared spectroscopy (NIRS). Ten healthy individuals visited the laboratory on two different days. On both days, they underwent 10 min SUP followed by 10 min 70 degrees HUT twice. SV decreased, which was (in part) compensated for by an increased heart rate, while MAP increased slightly during HUT compared with SUP. Although [HHb] increased during HUT, no presyncope symptoms were experienced. The circulatory variables (SV, HR and MAP) as well as [HHb] showed an acceptably small systematic and random error as well as reproducibility error compared with the observed difference between HUT and SUP and were similar between and within visits. Therefore, it is concluded that MAP measured by Portapres and SV calculated by Modelflow as well as HHb measured by NIRS seem to be reproducible and may therefore be used in follow-up studies.     

Effect of hydration on some orthostatic and haematological responses to head-up tilt

Summary Experiments were undertaken to determine the effects of hydration status on a) orthostatic responses, and on b), relative changes in intravascular volume and protein content, during 70 head-up tilt (HUT). Six men underwent 45 min of HUT, preceded by 45 min supine, first dehydrated, and again 105 min later after rehydration with water. Heart rate was consistently lower following rehydration (p<0.01), while supine diastolic pressure was higher (p<0.02). Systolic pressure fell during dehydrated HUT (p<0.01), but not during rehydrated HUT. Postural haemoconcentration, which was reduced after rehydration (p<0.001), was accompanied by a decrease in intravascular albumin content (p<0.05). Two subjects experienced severe presyncopal symptoms during dehydrated HUT, but not during rehydrated HUT. Thus, it appears that rehydration after fluid restriction improves orthostatic tolerance. Furthermore, extravascular hydration status may be more important than intravascular hydration status in determining orthostatic tolerance.     

Effects of inspiratory impedance on hemodynamic responses to a squat–stand test in human volunteers: implications for treatment of orthostatic hypotension

Recent studies in our laboratory demonstrated that spontaneous breathing through an inspiratory impedance threshold device (ITD) increased heart rate (HR), stroke volume (SV), cardiac output (Q), and mean arterial blood pressure (MAP) in supine human subjects. In this study, we tested the effectiveness of an ITD as a countermeasure against development of orthostatic hypotension, provoked using a squat-to-stand test (SST). Using a prospective, randomized blinded protocol, 18 healthy, normotensive volunteers (9 males, 9 females) completed two-counterbalanced 6-min SST protocols with and without (sham) an ITD set to open at 0.7 kPa (7-cm H₂O) pressure. HR, SV, Q, total peripheral resistance (TPR), and MAP were assessed noninvasively with infrared finger photoplethysmography. Symptoms were recorded on a 5-point scale (1=normal; 5=faint) of subject perceived rating (SPR). The reduction in TPR produced by SST (–35±5 %) was not affected by the ITD. Reduction in MAP with ITD during the transient phase of the SST (–3.6±0.5 kPa or –27±4 mmHg) was less (P=0.03) than that measured while breathing through a sham device (–4.8±0.4 kPa or –36±3 mmHg) despite similar (P<0.926) elevations in HR of 15±2 bpm. SV (+2±4 %) and Q (+22±5 %) with the ITD were higher (P<0.04) than SV (–8±4 %) and Q (+10±6 %) without the ITD. SPR was 1.4±0.1 with ITD compared to 2.0±0.2 with the sham device (P<0.04). This reduction in orthostatic symptoms with application of an ITD during the SST was associated with higher MAP, SV and Q. Our results demonstrate the potential application of an ITD as a countermeasure against orthostatic hypotension.     

Modulation of arterial baroreflex dynamic response during mild orthostatic stress in humans

We tested the hypothesis that in humans, carotid-baroreflex dynamic responses (evaluated by examining the time course of the carotid-baroreflex-induced alterations in muscle sympathetic nerve activity (MSNA), mean arterial blood pressure (MAP) and heart rate (HR)) would be altered during mild orthostatic stress in ways that serve to limit orthostatic hypotension. In 12 healthy subjects (10 male, 2 female), 5-s periods of neck pressure (NP) (50 mmHg) and neck suction (NS) (− 60 mmHg) were used to evaluate carotid baroreflex function at rest (CON) and during lower body negative pressure (LBNP) (−15 mmHg). During LBNP (as compared with CON) (a) the augmentations in MSNA and MAP elicited by NP were greater, (b) the NS-induced period of MSNA suppression was, if anything, shorter, (c) the peak decrement in MAP elicited by NS, although not different in amplitude, occurred earlier and recovered to its initial level more quickly after NS, and (d) the HR responses to NP and NS were greater. These results suggest that during mild orthostatic stress, carotid-baroreflex dynamic responses are modulated in ways that should help maintain blood pressure and limit orthostatic hypotension.     

Cardiovascular and catecholamine responses to static exercise in partially curarized humans

Neural control of the circulation was evaluated during static exercise in 19 subjects by the determination of heart rate (HR), mean arterial pressure (MAP), cardiac output (CO) and plasma catecholamines. Influence from central command was evaluated during contractions with weakened muscles following partial curarization and reflex influence from metaboreceptors was assessed by post-exercise muscle ischaemia. Static handgrip increased HR and more so MAP and CO and MAP remained elevated during post-exercise muscle ischaemia. With partial curarization plasma catecholamines were also increased (P<0.05). Two-leg extension increased all variables and during post-exercise muscle ischaemia elevations of HR, MAP and CO were maintained (P<0.05). With partial curarization HR, MAP and plasma noradrenaline were even greater during the contraction. With the involvement of both legs during static exercise, reflex influence from the muscles elevated blood pressure by way of HR and CO and the importance of central command was detectable for HR and MAP as plasma catecholamines became elevated. However, the results indicate a separation between a central command influence on HR and CO related to an increase in plasma catecholamines during a handgrip, while the reflex influence on blood pressure was directed towards total peripheral resistance.     

Sympathoinhibition to Bezold–Jarisch reflex is attenuated in protein malnourished rats

Malnutrition affects cardiovascular reflexes, including chemoreflex and baroreflex. In this study we assessed the hypothesis that malnourishment changes the responses in mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) evoked from Bezold–Jarisch reflex (BJR). Fischer rats were fed diets containing either (6% malnourished or 14% control) protein for 35 days after weaning. There were no differences in baseline MAP (102 ± 4 vs. 95 ± 3 mmHg) whereas higher baseline HR (478 ± 18 vs. 360 ± 11 bpm; P < 0.05,) and reduced sympathoinhibition (ΔRSNA = −54 ± 9 vs. −84 ± 7%; P = 0.0208) to BJR activation were found in malnourished rats. We conclude that malnutrition affects the sympathetic control of BJR.     

Coordination of the EEG and the heart rate of preterm neonates during quiet sleep

Aim of this study was to confirm that EEG bursts are associated with heart rate (HR) accelerations, and to investigate the synchronicity between quadratic phase couplings (QPC) courses of the EEG and HR before and during burst activity during quiet sleep in preterm newborns. The time-courses of QPC between frequency components of the EEG ([0.25–1.0 Hz] ↔ [4.0–6.0 Hz]) as well as between the Mayer–Traube–Hering (MTH) wave and the frequency component of the HR associated to the respiratory sinus arrhythmia (RSA) ([0.02–0.15 Hz] ↔ [0.4–1.5 Hz]) were investigated in five preterm neonates. During quiet sleep, the EEG alternates between burst and interburst activity. The burst onsets were used to trigger an averaging procedure for the EEG, HR, and QPC courses. It can be demonstrated that the envelopes of the EEG rise after the burst onset accompanied by an acceleration of HR before or at the burst maximum. The QPC courses show that the HR's QPC increases before or at the burst onset whereas the increase of the EEG's QPC is delayed. The synchronous changes of EEG and HR as well as of the corresponding QPC courses indicate a coupling between cortical, thalamocortical and neurovegetative brain structures. Such a coupling might be mediated by the MTH waves in the blood pressure.     

Is the association between depression and blunted cardiovascular stress reactions mediated by perceptions of stress?

Symptoms of depression are related to blunted cardiovascular reactions to acute stress tasks. However, it is unclear what factors might mediate this association and whether blunted responses are specific to mental stress tasks or are also evident with other forms of stress. The present study assessed cardiovascular reactivity to both mental and postural stress and the role of background stress exposure and stress perception. Undergraduate students (N = 119, 81 females) were screened for depressive symptoms using the Beck Depression Inventory. Twenty-six participants with probable depression and 26 non-depressed controls underwent cardiovascular stress testing. Heart rate (HR), systolic (SBP) and diastolic (DBP) blood pressure were measured at rest and in response to a 5 min orthostatic challenge and an 8 min mental arithmetic task. Stress exposure was measured using the Undergraduate Stress Questionnaire. Perceptions of general life stress were assessed using the Perceived Stress Scale (PSS) and perceptions of the stress task impact were measured using Threat Appraisal (TA). Symptoms of depression were associated with blunted HR, F(2,98) = 5.26, p = .010, η² = .097, and SBP, F(2,98) = 6.47, p = .008, η² = .117, reactions to the mental stress but not to postural challenge. HR reactions were mediated by PSS score, while both PSS score and TA emerged independently as mediators of SBP reactions. These results confirm a negative relationship between depressive symptoms and cardiovascular reactions to acute stress, suggest that this association may be stress task-specific, and may be mediated by perceptions of stress.     

Whole-body heating decreases skin vascular response to low orthostatic stress in the lower extremities

To elucidate the influence of heat stress on cutaneous vascular response in the lower extremities during orthostatic stress, a head-up tilt (HUT) test at angles of 15 degrees, 30 degrees, 45 degrees, and 60 degrees for 4 min each was conducted under normothermic control conditions followed by whole-body heat stress produced by a hot water-perfused suit in healthy volunteers. Skin blood flows (SkBF) in the forearm, thigh, and calf were monitored using laser-Doppler flowmetry throughout the experiment. Furthermore, to elucidate the effects of increased core and local skin temperatures on the local vascular response in calf skin under increasing orthostatic stress, the thigh was occluded at 20, 30, 50, 70, and 80 mmHg with a cuff in both the normothermic condition and the whole-body or local heating condition. Significant decreases in forearm SkBF during HUT were observed at an angle of 60 degrees during normothermia and at 30 degrees or more during heating. SkBF in the thigh and calf was decreased significantly by HUT at 15 degrees and above during normothermia, and there was no significant reduction of SkBF in these sites during HUT at the lower angles (15 degrees -45 degrees ) during whole-body heating. Significant decreases of calf SkBF were observed at cuff pressures of 20 mmHg and above during normothermia and of 30 mmHg and above during whole-body and local heating, respectively. These results suggest that SkBF in the lower extremities shows a marked reduction compared with the upper extremities during low orthostatic stress in normothermia, and the enhanced skin vasoconstrictor response in the lower extremities is diminished by both whole-body and local heat stress.     

Chronic inhibition of standing behaviour alters baroreceptor reflex function in rats

Aim: To investigate whether daily orthostatic stress during development is an important factor affecting arterial baroreceptor reflex function, we examined the effect of chronic inhibition of upright standing behaviour on the baroreceptor reflex function in rats. Methods: Upright standing behaviour was chronically inhibited during the developmental period between 3 and 8 weeks of age in Sprague–Dawley rats and heart rate (HR) and aortic nerve activity in response to increased and decreased mean arterial pressure (MAP) was measured after the treatment period. Results: The baroreceptor cardiac gain in the rats grown without standing behaviour was significantly lower than the control rats grown in a normal commercial cage (1.0 ± 0.1 beats min^?1 mmHg^?1 vs. 1.6 ± 0.2 beatsmin^?1 mmHg^?1, P < 0.05). The range of HR change in the MAP–HR functional curve was also lowered by chronic inhibition of orthostatic behaviour (56.2 ± 5.9 beats min^?1) compared with that of the control rats (76.8 ± 6.9 beats min^?1, P < 0.05). However the aortic afferent function remained normal after the treatment period, indicating that the attenuated baroreceptor reflex function may be due to other mechanisms involving functional alterations in the cardiovascular centres, efferents and/or peripheral organs. Body weight and adrenal weight were not affected by the inhibition of orthostatic behaviour, suggesting that the animals were not exposed to specific stress by this treatment. Conclusion: These results indicate that active haemodynamic changes induced by orthostatic behaviour are an important factor for setting the basal level of reflex function during development. Moreover, our experimental model may be useful for studying mechanisms of attenuated baroreceptor reflex observed after exposure to a chronic inactive condition.     

Effects of aging on the cerebrovascular orthostatic response

When healthy subjects stand up, it is associated with a reduction in cerebral blood velocity and oxygenation although cerebral autoregulation would be considered to prevent a decrease in cerebral perfusion. Aging is associated with a higher incidence of falls, and in the elderly falls may occur particularly during the adaptation to postural change. This study evaluated the cerebrovascular adaptation to postural change in 15 healthy younger (YNG) vs. 15 older (OLD) subjects by recordings of the near-infrared spectroscopy-determined cerebral oxygenation (cO₂Hb) and the transcranial Doppler-determined mean middle cerebral artery blood velocity (MCA V_mean). In OLD (59 (52-65) years) vs. YNG (29 (27-33) years), the initial postural decline in mean arterial pressure (−52 ± 3% vs. −67 ± 3%), cO₂Hb (−3.4 ± 2.5 μmol l⁻¹ vs. −5.3 ± 1.7 μmol l⁻¹) and MCA V_mean (−16 ± 4% vs. −29 ± 3%) was smaller. The decline in MCA V_mean was related to the reduction in MAP. During prolonged orthostatic stress, the decline in MCA V_meanand cO₂Hb in OLD remained smaller. We conclude that with healthy aging the postural reduction in cerebral perfusion becomes less prominent.     

Heart rate variability and baroreceptor sensitivity following exercise-induced hyperthermia in endurance trained men

We evaluated the effect of exercise-induced hyperthermia (EIH) on autonomic nervous system (ANS) function in the early (<80 min) and late (24 and 48 h) stages of recovery. Eight males underwent three repeated 6 min 70° head-up tilts (HUT1, HUT2 and HUT3), each separated by 10-min supine rest in a non-exercise/non-heat stress control state (NHS). On a separate day, three 6 min 70° HUT were performed following EIH (esophageal temperature ≥40°C) and repeated after 24 and 48 h of recovery. Heart rate, stroke volume (SV), mean arterial pressure and cardiac output ([(Q)\dot] \dot{Q} ) were evaluated during the last min prior to a change in posture. Responses to 70° HUT were compared to the same challenge performed without prior exercise and under a NHS condition. Relative to NHS, [(Q)\dot] \dot{Q} was maintained during the repeated HUT’s following EIH, despite significant reductions in SV and sustained elevations in esophageal temperature (p < 0.05). The preserved [(Q)\dot] \dot{Q} appears to be due to increased HR (HUT1: NRS = 76 ± 3 beats min⁻¹, EIH = 126 ± 6 beats min⁻¹) stemming from modulation of the ANS toward sympathetic dominance. Parasympathetic withdrawal was evidenced by a reduction in root mean squared successive difference (i.e., HUT1: NHS = 66 ± 12 ms, EIH = 9 ± 1 ms) of heart rate variability and paralleled by a reduction in baroreceptor sensitivity for all HUT’s following EIH (p < 0.05). Despite significant modulation in ANS activity, Q is maintained and participants do not become orthostatic intolerant/syncopal during the short-term recovery period following EIH. Normal ANS and cardiovascular function is restored following 24 h of recovery.