scholarly journals Effects of head-down-tilt bed rest on cerebral hemodynamics during orthostatic stress

1997 ◽  
Vol 83 (6) ◽  
pp. 2139-2145 ◽  
Author(s):  
Rong Zhang ◽  
Julie H. Zuckerman ◽  
James A. Pawelczyk ◽  
Benjamin D. Levine
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Autoregulation ◽  
Orthostatic Intolerance ◽  
Bed Rest ◽  
Cerebral Hemodynamics ◽  
Orthostatic Stress ◽  
Orthostatic Tolerance ◽  
Mean Velocity ◽  
Significant Difference

Zhang, Rong, Julie H. Zuckerman, James A. Pawelczyk, and Benjamin D. Levine. Effects of head-down-tilt bed rest on cerebral hemodynamics during orthostatic stress. J. Appl. Physiol. 83(6): 2139–2145, 1997.—Our aim was to determine whether the adaptation to simulated microgravity (μG) impairs regulation of cerebral blood flow (CBF) during orthostatic stress and contributes to orthostatic intolerance. Twelve healthy subjects (aged 24 ± 5 yr) underwent 2 wk of −6° head-down-tilt (HDT) bed rest to simulate hemodynamic changes that occur when humans are exposed to μG. CBF velocity in the middle cerebral artery (transcranial Doppler), blood pressure, cardiac output (acetylene rebreathing), and forearm blood flow were measured at each level of a ramped protocol of lower body negative pressure (LBNP; −15, −30, and −40 mmHg × 5 min, −50 mmHg × 3 min, then −10 mmHg every 3 min to presyncope) before and after bed rest. Orthostatic tolerance was assessed by using the cumulative stress index (CSI; mmHg × minutes) for the LBNP protocol. After bed rest, each individual’s orthostatic tolerance was reduced, with the group CSI decreased by 24% associated with greater decreases in cardiac output and greater increases in systemic vascular resistance at each level of LBNP. Before bed rest, mean CBF velocity decreased by 14, 10, and 45% at −40 mmHg, −50 mmHg, and maximal LBNP, respectively. After bed rest, mean velocity decreased by 16% at −30 mmHg and by 21, 35, and 39% at −40 mmHg, −50 mmHg, and maximal LBNP, respectively. Compared with pre-bed rest, post-bed-rest mean velocity was less by 11, 10, and 21% at −30, −40, and −50 mmHg, respectively. However, there was no significant difference at maximal LBNP. We conclude that cerebral autoregulation during orthostatic stress is impaired by adaptation to simulated μG as evidenced by an earlier and greater fall in CBF velocity during LBNP. We speculate that impairment of cerebral autoregulation may contribute to the reduced orthostatic tolerance after bed rest.

Exercise plus volume loading prevents orthostatic intolerance but not reduction in cerebral blood flow velocity after bed rest

2012 ◽  
Vol 302 (2) ◽  
pp. H489-H497 ◽  
Author(s):  
Sung-Moon Jeong ◽  
Shigeki Shibata ◽  
Benjamin D. Levine ◽  
Rong Zhang
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Blood Flow Velocity ◽  
Orthostatic Intolerance ◽  
Bed Rest ◽  
Left Ventricular ◽  
Stress Index ◽  
Control Group ◽  
Orthostatic Tolerance ◽  
Volume Loading

This study tested the hypothesis that reduction in cerebral blood flow (CBF) during orthostatic stress after bed rest can be ameliorated with volume loading, exercise, or both. Transcranial Doppler was used to measure changes in CBF velocity during lower body negative pressure (LBNP) before and after an 18-day bed rest in 33 healthy subjects. Subjects were assigned into four groups with similar age and sex: 1) supine cycling during bed rest (Exercise group; n = 7), 2) volume loading with Dextran infusion after bed rest to restore reduced left ventricular filling pressure (Dextran group; n = 7), 3) exercise combined with volume loading to prevent orthostatic intolerance (Ex-Dex group; n = 7), and 4) a control group ( n = 12). LBNP tolerance was measured using a cumulative stress index (CSI). After bed rest, CBF velocity was reduced at a lower level of LBNP in the Control group, and the magnitude of reduction was greater in the Ex-Dex group. However, reduction in orthostatic tolerance was prevented in the Ex-Dex group. Notably, volume loading alone prevented greater reductions in CBF velocity after bed rest, but CSI was reduced still by 25%. Finally, decreases in CBF velocity during LBNP were correlated with reduction in cardiac output under all conditions ( r2 = 0.86; P = < 0.001). Taken together, these findings demonstrate that volume loading alone can ameliorate reductions in CBF during LBNP. However, the lack of associations between changes in CBF velocity and orthostatic tolerance suggests that reductions in CBF during LBNP under steady-state conditions by itself are unlikely to be a primary factor leading to orthostatic intolerance.

Alterations in autonomic function and cerebral hemodynamics to orthostatic challenge following a mountain marathon

2007 ◽  
Vol 103 (1) ◽  
pp. 88-96 ◽  
Author(s):  
Carissa Murrell ◽  
Luke Wilson ◽  
James D. Cotter ◽  
Samuel Lucas ◽  
Shigehiko Ogoh ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Cerebral Autoregulation ◽  
Prolonged Exercise ◽  
Autonomic Function ◽  
Orthostatic Intolerance ◽  
Low Frequency ◽  
Time Domain Analysis ◽  
Cerebral Hemodynamics ◽  
Cerebral Hypoperfusion ◽  
Baroreflex Control

We examined potential mechanisms (autonomic function, hypotension, and cerebral hypoperfusion) responsible for orthostatic intolerance following prolonged exercise. Autonomic function and cerebral hemodynamics were monitored in seven athletes pre-, post- (<4 h), and 48 h following a mountain marathon [42.2 km; cumulative gain ∼1,000 m; ∼15°C; completion time, 261 ± 27 (SD) min]. In each condition, middle cerebral artery blood velocity (MCAv), blood pressure (BP), heart rate (HR), and cardiac output (Modelflow) were measured continuously before and during a 6-min stand. Measurements of HR and BP variability and time-domain analysis were used as an index of sympathovagal balance and baroreflex sensitivity (BRS). Cerebral autoregulation was assessed using transfer-function gain and phase shift in BP and MCAv. Hypotension was evident following the marathon during supine rest and on standing despite increased sympathetic and reduced parasympathetic control, and elevations in HR and cardiac output. On standing, following the marathon, there was less elevation in normalized low-frequency HR variability ( P < 0.05), indicating attenuated sympathetic activation. MCAv was maintained while supine but reduced during orthostasis postmarathon [−10.4 ± 9.8% pre- vs. −15.4 ± 9.9% postmarathon (%change from supine); P < 0.05]; such reductions were related to an attenuation in BRS ( r = 0.81; P < 0.05). Cerebral autoregulation was unchanged following the marathon. These findings indicate that following prolonged exercise, hypotension and postural reductions in autonomic function or baroreflex control, or both, rather than a compromise in cerebral autoregulation, may place the brain at risk of hypoperfusion. Such changes may be critical factors in collapse following prolonged exercise.

Interruption of cardiac output does not affect short-term growth and metabolic rate in day 3 and 4 chick embryos

2000 ◽  
Vol 203 (24) ◽  
pp. 3831-3838 ◽  
Author(s):  
W.W. Burggren ◽  
S.J. Warburton ◽  
M.D. Slivkoff
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Body Mass ◽  
Regression Line ◽  
Heart Beat ◽  
Chick Embryos ◽  
Simple Diffusion ◽  
Significant Difference ◽  
Vertebrate Embryos ◽  
Cervical Flexure

The heart beat of vertebrate embryos has been assumed to begin when convective bulk transport by blood takes over from transport by simple diffusion. To test this hypothesis, we measured eye growth, cervical flexure and rates of oxygen consumption (V(O2)) in day 3–4 chick embryos denied cardiac output by ligation of the outflow tract and compared them with those of embryos with an intact cardiovascular system.Eye diameter, used as the index for embryonic growth, increased at a rate of approximately 4.5-5 % h(−)(1) during the observation period. There was no significant difference (P&gt;0.1) in the rate of increase in eye diameter between control (egg opened), sham-ligated (ligature present but not tied) and ligated embryos. Similarly, the normal progression of cervical flexure was not significantly altered by ligation (P&gt;0.1). V(O2) (ml O(2)g(−)(1)h(−)(1)) at 38 degrees C, measured by closed respirometry, was not significantly different (P&gt;0.1) on day 3 in sham-ligated (14.5+/−1.9 ml O(2)g(−)(1)h(−)(1)) and ligated 17.6+/−1.8 ml O(2)g(−)(1)h(−)(1)) embryos. Similarly, on day 4, V(O2) in sham-ligated and ligated embryos was statistically the same (sham-ligated 10. 5+/−2.9 ml O(2)g(−)(1)h(−)(1); ligated 9.7+/−2.9 ml O(2)g(−)(1)h(−)(1)). Expressed as a linear function of body mass (M), V(O2) in sham-ligated embryos was described by the equation V(O2)=−0.48M+24.06 (r(2)=0.36, N=18, P&lt;0.01), while V(O2) in ligated embryos was described by the equation V(O2)=−0.53M+23.32 (r(2)=0.38, N=16, P&lt;0.01). The regression line describing the relationship between body mass and V(O2) for pooled sham-ligated and ligated embryos (the two populations being statistically identical) was V(O2)=−0.47M+23.24. The slope of this regression line, which was significantly different from zero (r(2)=0.30, N=34, P&lt;0.01), was similar to slopes calculated from previous studies over the same range of body mass.Collectively, these data indicate that growth and V(O2) are not dependent upon cardiac output and the convective blood flow it generates. Thus, early chick embryos join those of the zebrafish, clawed frog and axolotl in developing a heart beat and blood flow hours or days before required for convective oxygen and nutrient transport. We speculate that angiogenesis is the most likely role for the early development of a heart beat in vertebrate embryos.

Abstract 2197: The Multi-System Effect of Exercise Training During Prolonged Bed Rest Deconditioning: An Integrated Approach to Countermeasure Development for the Heart, Lungs, Muscle and Bones

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Jeffrey Hastings ◽  
Eric Pacini ◽  
Felix Krainski ◽  
Shigeki Shibata ◽  
Manish Jain ◽  
...  
Keyword(s):  
Exercise Training ◽  
Exercise Capacity ◽  
Orthostatic Intolerance ◽  
Lower Body Negative Pressure ◽  
Bed Rest ◽  
Orthostatic Tolerance ◽  
Volume Loading ◽  
System Effect ◽  
Cardiac Atrophy ◽  
South Central

We propose to prevent the cardiac atrophy and orthostatic intolerance associated with prolonged bed rest using rowing ergometry/resistance training with aggressive volume loading on the day of testing. We hypothesize that prevention of cardiac atrophy will forestall cardiovascular deconditioning, leading to preserved exercise capacity and orthostatic tolerance. Twenty-four healthy subjects, ages 20 –55, were enrolled with 8 randomized to training (EX), 8 with training and volume loading (VOL), and 8 as sedentary (SED) controls. Testing included maximal upright exercise, orthostatic tolerance via graded lower body negative pressure (LBNP), cardiac MRI, as well as invasive cardiac pressure-volume measurements, performed at baseline and at the end of 5 weeks of 6° head down bedrest. Upright exercise capacity was preserved with training as measured by peak workrate and VO2max (EX/VOL: pre 195±46W, 34±7 ml/kg/min; post 202±42W, 33±4 ml/kg/min) but deteriorated in SED group (pre 171±55W, 34±8 ml/kg/min; post 145±51W, 27±7 ml/kg/min). MRI derived mass (% change: +6.3±9.9% EX/VOL vs. −5.5±3.7% SED) was increased by training. Exercise training appears to preserve LV chamber compliance (stiffness constants: EX/VOL: pre= 0.035±0.021, post = 0.036±0.029; SED: pre= 0.020±0.011, post = 0.028±0.007). Training also preserves hemodynamic variables measured at −40mmHg of LBNP, including stroke volume (EX: pre 44±12; post 38±9 ml, VOL: pre 49±30; post 45±29 ml, SED: pre 35±5; post 24±8 ml ). These preliminary data support our hypothesis that an optimized training program consisting of dynamic and resistance exercise can prevent part of the multisystem atrophy and orthostatic intolerance associated with prolonged bed rest. This defines a specific countermeasure that is practical, safe, and effective against the cardiovascular, muscle and bone deconditioning associated with prolonged bed rest. This information is relevant not only for astronauts exposed to long duration spaceflight, but also for patients with chronic reductions in physical activity, and those with disease processes that alter cardiac stiffness such as obesity, hypertension, heart failure or ischemic heart disease, plus normal aging and osteoporosis. This research has received full or partial funding support from the American Heart Association, AHA South Central Affiliate (Arkansas, New Mexico, Oklahoma & Texas).

scholarly journals Effect of intermittent hypoxic training on orthostatic tolerance in humans before and after simulated microgravity

2020 ◽  
Author(s):  
VP Katuntsev ◽  
TV Sukhostavtseva ◽  
AN Kotov ◽  
MV Baranov
Keyword(s):  
Orthostatic Intolerance ◽  
Bed Rest ◽  
Daily Basis ◽  
Tilt Test ◽  
Control Group ◽  
Orthostatic Tolerance ◽  
Pronounced Increase ◽  
Intermittent Hypoxic Training ◽  
Hypoxic Training ◽  
Before And After

Reduced orthostatic tolerance (OT) is a serious concern facing space medicine. This work sought to evaluate the effects of intermittent hypoxic training (IHT) on OT in humans before and after 3 days of head-down bed rest (HDBR) used to model microgravity. The study was carried out in 16 male volunteers aged 18 to 40 years and included 2 series of experiments with 11-day and 21-day IHT administered on a daily basis. During the first IHT session, the concentration of oxygen in the inspired gas mixture was 10%; for other sessions it was adjusted to 9%. OT was assessed by a 20-minute-long orthostatic tilt test (OTT) conducted before and after HDBR. Before HDBR, orthostatic intolerance was observed in 3 participants, while after HDBR, it was observed in 9 of 16 volunteers (p < 0.05). During OTT conducted after HDBR, the heart rate (HR) exceeded control values by 26.8% (p < 0.01). Preexposure to any of the applied IHT regimens led to a reduction in the number of volunteers with orthostatic intolerance. After the 11-day IHT program, there was a less pronounced increase in HR during OTT before HDBR; with the extended IHT regimen, less pronounced changes were observed for HR, systolic, diastolic and mean blood pressure (BP). The increase in HR during OTT after HDBR was significantly lower in the group that had completed the 11-day IHT program, while BP remained stable. The changes in HR and systolic BP were less pronounced in the group that had completed the 21-day IHT program than in the control group (p < 0.05). Thus, IHT reduced the risk of orthostatic disorders and mitigated changes in cardiovascular parameters during the orthostatic test.

Effects of 18 days of bed rest on leg and arm venous properties

2004 ◽  
Vol 96 (3) ◽  
pp. 840-847 ◽  
Author(s):  
M. W. P. Bleeker ◽  
P. C. E. De Groot ◽  
J. A. Pawelczyk ◽  
M. T. E. Hopman ◽  
B. D. Levine
Keyword(s):  
Orthostatic Intolerance ◽  
Lower Body Negative Pressure ◽  
Bed Rest ◽  
Venous Occlusion ◽  
Stress Index ◽  
Orthostatic Tolerance ◽  
Venous Compliance ◽  
Venous Flow ◽  
Gravitational Gradients ◽  
Small Change

Venous function may be altered by bed rest deconditioning. Yet the contribution of altered venous compliance to the orthostatic intolerance observed after bed rest is uncertain. The purpose of this study was to assess the effect of 18 days of bed rest on leg and arm (respectively large and small change in gravitational gradients and use patterns) venous properties. We hypothesized that the magnitude of these venous changes would be related to orthostatic intolerance. Eleven healthy subjects (10 men, 1 woman) participated in the study. Before (pre) and after (post) 18 days of 6° head-down tilt bed rest, strain gauge venous occlusion plethysmography was used to assess limb venous vascular characteristics. Leg venous compliance was significantly decreased after bed rest (pre: 0.048 ± 0.007 ml·100 ml-1·mmHg-1, post: 0.033 ± 0.007 ml·100 ml-1·mmHg-1; P < 0.01), whereas arm compliance did not change. Leg venous flow resistance increased significantly after bed rest (pre: 1.73 ± 1.08 mmHg·ml-1·100 ml·min, post: 3.10 ± 1.00 mmHg·ml-1·100 ml·min; P < 0.05). Maximal lower body negative pressure tolerance, which was expressed as cumulative stress index (pressure·time), decreased in all subjects after bed rest (pre: 932 mmHg·min, post: 747 mmHg·min). The decrease in orthostatic tolerance was not related to changes in leg venous compliance. In conclusion, this study demonstrates that after bed rest, leg venous compliance is reduced and leg venous outflow resistance is enhanced. However, these changes are not related to measures of orthostatic tolerance; therefore, alterations in venous compliance do not to play a major role in orthostatic intolerance after 18 days of head-down tilt bed rest.

Microgravity and orthostatic intolerance: carotid hemodynamics and peripheral responses

1993 ◽  
Vol 264 (2) ◽  
pp. H588-H594 ◽  
Author(s):  
P. J. Lacolley ◽  
B. M. Pannier ◽  
J. L. Cuche ◽  
J. S. Hermida ◽  
S. Laurent ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Orthostatic Intolerance ◽  
Lower Body Negative Pressure ◽  
Cold Pressor Test ◽  
Systolic Pressure ◽  
Cold Pressor ◽  
Bed Rest ◽  
Plasma Norepinephrine ◽  
Tangential Tension

A ground-based model [24 h of bed rest (BR) with head-down tilt (HDT)] was used to investigate the cardiovascular deconditioning responsible for orthostatic intolerance, frequently observed after weightlessness flights. This experimental deconditioning is shown to be distinguished by an increase of mean blood pressure (P < 0.05), with increased total peripheral resistances (TPRs). Systolic tangential tension of the carotid arterial wall, cardiac output and frequency (spectral analysis), and plasma norepinephrine and epinephrine were not significantly altered, while plasma dopamine was increased (P < 0.05). Cardiovascular homeostasis was challenged before and after 24 h of BR with HDT through -40 mmHg lower body negative pressure (LBNP). Systolic tangential tension of the carotid wall was decreased, with a decrease of systolic pressure and cardiac output; increased heart rate was likely due to an increase of sympathetic drive with a decrease of vagal braking. The overall picture was not changed after 24 h of BR with HDT, except for a lack of increase of TPRs: their increase (+13.7%, P < 0.05) before was no longer observed after (-2.6%) 24 h of BR with HDT. This apparent deficiency cannot be explained. However, a heterogeneity in the response of TPR should be considered because the magnitude of the increase of blood pressure to cold pressor test was the same after 24 h of BR with HDT as it was before.(ABSTRACT TRUNCATED AT 250 WORDS)

Leg crossing with muscle tensing, a physical counter-manoeuvre to prevent syncope, enhances leg blood flow

2007 ◽  
Vol 112 (3) ◽  
pp. 193-201 ◽  
Author(s):  
Jan T. Groothuis ◽  
Nynke van Dijk ◽  
Walter ter Woerds ◽  
Wouter Wieling ◽  
Maria T. E. Hopman
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Orthostatic Intolerance ◽  
Peripheral Resistance ◽  
Haemodynamic Effects ◽  
Vascular Conductance ◽  
Leg Blood Flow ◽  
Head Up Tilt

In patients with orthostatic intolerance, the mechanisms to maintain BP (blood pressure) fail. A physical counter-manoeuvre to postpone or even prevent orthostatic intolerance in these patients is leg crossing combined with muscle tensing. Although the central haemodynamic effects of physical counter-manoeuvres are well documented, not much is known about the peripheral haemodynamic events. Therefore the purpose of the present study was to examine the peripheral haemodynamic effects of leg crossing combined with muscle tensing during 70° head-up tilt. Healthy subjects (n=13) were monitored for 10 min in the supine position followed by 10 min in 70° head-up tilt and, finally, for 2 min of leg crossing with muscle tensing in 70° head-up tilt. MAP (mean arterial BP), heart rate, stroke volume, cardiac output and total peripheral resistance were measured continuously by Portapres. Leg blood flow was measured using Doppler ultrasound. Leg vascular conductance was calculated as leg blood flow/MAP. A significant increase in MAP (13 mmHg), stroke volume (27%) and cardiac output (18%), a significant decrease in heart rate (−5 beats/min) and no change in total peripheral resistance during the physical counter-manoeuvre were observed when compared with baseline 70° head-up tilt. A significant increase in leg blood flow (325 ml/min) and leg vascular conductance (2.9 arbitrary units) were seen during the physical counter-manoeuvre when compared with baseline 70° head-up tilt. In conclusion, the present study indicates that the physical counter-manoeuvre of leg crossing combined with muscle tensing clearly enhances leg blood flow and, at the same time, elevates MAP.

Single-breath breath-holding estimate of pulmonary blood flow in man: comparison with direct Fick cardiac output

1989 ◽  
Vol 76 (6) ◽  
pp. 673-676 ◽  
Author(s):  
A. H. Kendrick ◽  
A. Rozkovec ◽  
M. Papouchado ◽  
J. West ◽  
G. Laszlo
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Pulmonary Blood Flow ◽  
Hold Time ◽  
Normal Subjects ◽  
Breath Holding ◽  
Breath Hold ◽  
Single Breath ◽  
Significant Difference ◽  
Cardiac Disorders

1. Resting pulmonary blood flow (Q.), using the uptake of the soluble inert gas Freon-22 and an indirect estimate of lung tissue volume, has been estimated during breath-holding (Q.c) and compared with direct Fick cardiac output (Q.f) in 16 patients with various cardiac disorders. 2. The effect of breath-hold time was investigated by comparing Q.c estimated using 6 and 10 s of breath-holding in 17 patients. Repeatability was assessed by duplicate measurements of Q.c in the patients and in six normal subjects. 3. Q.c tended to overestimate Q.f, the bias and error being 0.09 l/min and 0.59, respectively. The coefficient of repeatability for Q.c in the patients was 0.75 l/min and in the normal subjects was 0.66 1/min. For Q.f it was 0.72 l/min. There was no significant difference in Q.c measured at the two breath-hold times. 4. The technique is simple to perform, and provides a rapid estimate of Q., monitoring acute and chronic changes in cardiac output in normal subjects and patients with cardiac disease.

Alterations in cerebral autoregulation and cerebral blood flow velocity during acute hypoxia: rest and exercise

2007 ◽  
Vol 292 (2) ◽  
pp. H976-H983 ◽  
Author(s):  
Philip N. Ainslie ◽  
Alice Barach ◽  
Carissa Murrell ◽  
Mike Hamlin ◽  
John Hellemans ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Cerebral Autoregulation ◽  
Cerebral Oxygenation ◽  
Cerebral Blood Flow Velocity ◽  
Arterial Blood ◽  
Cerebrovascular Function ◽  
Hypoxic Exercise

We examined the relationship between changes in cardiorespiratory and cerebrovascular function in 14 healthy volunteers with and without hypoxia [arterial O2 saturation (SaO2) ∼80%] at rest and during 60–70% maximal oxygen uptake steady-state cycling exercise. During all procedures, ventilation, end-tidal gases, heart rate (HR), arterial blood pressure (BP; Finometer) cardiac output (Modelflow), muscle and cerebral oxygenation (near-infrared spectroscopy), and middle cerebral artery blood flow velocity (MCAV; transcranial Doppler ultrasound) were measured continuously. The effect of hypoxia on dynamic cerebral autoregulation was assessed with transfer function gain and phase shift in mean BP and MCAV. At rest, hypoxia resulted in increases in ventilation, progressive hypocapnia, and general sympathoexcitation (i.e., elevated HR and cardiac output); these responses were more marked during hypoxic exercise ( P < 0.05 vs. rest) and were also reflected in elevation of the slopes of the linear regressions of ventilation, HR, and cardiac output with SaO2 ( P < 0.05 vs. rest). MCAV was maintained during hypoxic exercise, despite marked hypocapnia (44.1 ± 2.9 to 36.3 ± 4.2 Torr; P < 0.05). Conversely, hypoxia both at rest and during exercise decreased cerebral oxygenation compared with muscle. The low-frequency phase between MCAV and mean BP was lowered during hypoxic exercise, indicating impairment in cerebral autoregulation. These data indicate that increases in cerebral neurogenic activity and/or sympathoexcitation during hypoxic exercise can potentially outbalance the hypocapnia-induced lowering of MCAV. Despite maintaining MCAV, such hypoxic exercise can potentially compromise cerebral autoregulation and oxygenation.

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