WISE-2005: adrenergic responses of women following 56-days, 6° head-down bed rest with or without exercise countermeasures

2007 ◽  
Vol 293 (6) ◽  
pp. R2343-R2352 ◽  
Author(s):  
Heather Edgell ◽  
Kathryn A. Zuj ◽  
Danielle K. Greaves ◽  
J. Kevin Shoemaker ◽  
Marc-Antoine Custaud ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Orthostatic Intolerance ◽  
Lower Body Negative Pressure ◽  
Peripheral Resistance ◽  
Resistance Index ◽  
Cardiovascular Responses ◽  
Bed Rest ◽  
Nutritional Supplement ◽  
Exercise Group ◽  
Adrenergic Stimulation

We tested the hypotheses that women completing 56 days, 6° head-down bed-rest (HDBR) would have changes in sensitivity of cardiovascular responses to adrenergic receptor stimulation and that frequent aerobic and resistive exercise would prevent these changes. Twenty-four women, eight controls, eight exercisers (lower body negative pressure treadmill and flywheel resistance exercise), and eight receiving nutritional supplement but no exercise were studied in baseline and during administration of the β-agonist isoproterenol (ISO) and the α- and β-agonist norepinephrine (NOR). In the control and nutrition groups, HDBR increased heart rate (HR) and reduced stroke volume (SV), and there was a significantly greater increase in HR with ISO after HDBR. In contrast, the HR and SV of the exercise group were unchanged from pre-HDBR. After HDBR, leg vascular resistance (LVR) was greater than pre-HDBR in the exercise group but reduced in control and nutrition. LVR was reduced with ISO and increased with NOR. Changes in total peripheral resistance were similar to those of LVR but of smaller magnitude, perhaps because changes in cerebrovascular resistance index were directionally opposite to those of LVR. There were no changes in sensitivity of the vascular resistance responses to adrenergic stimulation. The HR response might reflect a change in sensitivity or a necessary response to the reduction in SV after HDBR in control and nutrition groups. The reduced peripheral vascular resistance after HDBR might help to explain orthostatic intolerance in women. Exercise was an effective countermeasure to the HDBR effects.

scholarly journals Regulation of muscle sympathetic nerve activity after bed rest deconditioning

2001 ◽  
Vol 280 (5) ◽  
pp. H2230-H2239 ◽  
Author(s):  
James A. Pawelczyk ◽  
Julie H. Zuckerman ◽  
C. Gunnar Blomqvist ◽  
Benjamin D. Levine
Keyword(s):  
Vascular Resistance ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Orthostatic Intolerance ◽  
Lower Body Negative Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Bed Rest ◽  
Orthostatic Tolerance ◽  
Nerve Activity ◽  
Stimulus Response

Cardiovascular deconditioning reduces orthostatic tolerance. To determine whether changes in autonomic function might produce this effect, we developed stimulus-response curves relating limb vascular resistance, muscle sympathetic nerve activity (MSNA), and pulmonary capillary wedge pressure (PCWP) with seven subjects before and after 18 days of −6° head-down bed rest. Both lower body negative pressure (LBNP; −15 and −30 mmHg) and rapid saline infusion (15 and 30 ml/kg body wt) were used to produce a wide variation in PCWP. Orthostatic tolerance was assessed with graded LBNP to presyncope. Bed rest reduced LBNP tolerance from 23.9 ± 2.1 to 21.2 ± 1.5 min, respectively (means ± SE, P= 0.02). The MSNA-PCWP relationship was unchanged after bed rest, though at any stage of the LBNP protocol PCWP was lower, and MSNA was greater. Thus bed rest deconditioning produced hypovolemia, causing a shift in operating point on the stimulus-response curve. The relationship between limb vascular resistance and MSNA was not significantly altered after bed rest. We conclude that bed rest deconditioning does not alter reflex control of MSNA, but may produce orthostatic intolerance through a combination of hypovolemia and cardiac atrophy.

WISE 2005: responses of women to sublingual nitroglycerin before and after 56 days of 6° head-down bed rest

2012 ◽  
Vol 113 (3) ◽  
pp. 434-441 ◽  
Author(s):  
K. A. Zuj ◽  
H. Edgell ◽  
J. K. Shoemaker ◽  
M. A. Custaud ◽  
P. Arbeille ◽  
...  
Keyword(s):  
Blood Flow ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Femoral Artery ◽  
Peripheral Resistance ◽  
Resistance Index ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Bed Rest ◽  
Sublingual Nitroglycerin

This study tested the hypothesis that cardiovascular effects of sublingual nitroglycerin (NG) would be exaggerated after 56 days of 6° head-down bed rest (HDBR) in women, and that an aerobic and resistive exercise countermeasure (EX, n = 8) would reduce the effect compared with HDBR without exercise (CON, n = 7). Middle cerebral artery maximal blood flow velocity (CBFV), cardiac stroke volume (SV), and superficial femoral artery blood flow (Doppler ultrasound) were recorded at baseline rest and for 5 min following 0.3 mg sublingual NG. Post-HDBR, NG caused greater increases in heart rate (HR) in CON compared with EX (+24.9 ± 7.7 and +18.8 ± 6.6 beats/min, respectively, P < 0.0001). The increase in HR combined with reductions in SV to maintain cardiac output. Systolic, mean, and pulse pressures were reduced 5–10 mmHg by NG, but total peripheral resistance was only slightly reduced at 3 min after NG. Reductions in CBFV of −12.5 ± 3.8 cm/s were seen after NG, but a reduction in the Doppler resistance index suggested dilation of the middle cerebral artery with no differences after HDBR. The femoral artery dilated with NG and blood flow was reduced ∼50% with the appearance of large negative waves suggesting a marked increase in downstream resistance, but there were no effects of HDBR. In general, responses of women to NG were not altered by HDBR; the greater increase in HR in CON but not EX was probably a consequence of cardiovascular deconditioning. These results contrast with the hypothesis and a previous investigation of men after HDBR by revealing no change in cardiovascular responses to exogenous nitric oxide.

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).

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)

scholarly journals LBNP exercise protects aerobic capacity and sprint speed of female twins during 30 days of bed rest

2009 ◽  
Vol 106 (3) ◽  
pp. 919-928 ◽  
Author(s):  
Stuart M. C. Lee ◽  
Suzanne M. Schneider ◽  
Wanda L. Boda ◽  
Donald E. Watenpaugh ◽  
Brandon R. Macias ◽  
...  
Keyword(s):  
Treadmill Exercise ◽  
Lower Body Negative Pressure ◽  
Bed Rest ◽  
Exercise Group ◽  
Peak Oxygen Consumption ◽  
Control Group ◽  
Treadmill Test ◽  
Sprint Speed ◽  
Long Duration ◽  
Volitional Fatigue

We have shown previously that treadmill exercise within lower body negative pressure (LBNPex) maintains upright exercise capacity (peak oxygen consumption, V̇o2peak) in men after 5, 15, and 30 days of bed rest (BR). We hypothesized that LBNPex protects treadmill V̇o2peak and sprint speed in women during a 30-day BR. Seven sets of female monozygous twins volunteered to participate. Within each twin set, one was randomly assigned to a control group (Con) and performed no countermeasures, and the other was assigned to an exercise group (Ex) and performed a 40-min interval (40–80% pre-BR V̇o2peak) LBNPex (51 ± 5 mmHg) protocol, plus 5 min of static LBNP, 6 days per week. Before and immediately after BR, subjects completed a 30.5-m sprint test and an upright graded treadmill test to volitional fatigue. These results in women were compared with previously reported reductions in V̇o2peak and sprint speed in male twins after BR. In women, sprint speed (−8 ± 2%) and V̇o2peak (−6 ± 2%) were not different after BR in the Ex group. In contrast, both sprint speed (−24 ± 5%) and V̇o2peak (−16 ± 3%) were significantly less after BR in the Con group. The effect of BR on sprint speed and V̇o2peak after BR was not different between women and men. We conclude that treadmill exercise within LBNP protects against BR-induced reductions in V̇o2peak and sprint speed in women and should prove effective during long-duration spaceflight.

Cardiovascular Response to Orthostatic Stress: Effects of Exercise Training Modality

1995 ◽  
Vol 20 (2) ◽  
pp. 240-254 ◽  
Author(s):  
Gabrielle K. Savard ◽  
Mark A. Stonehouse
Keyword(s):  
Exercise Training ◽  
Vascular Resistance ◽  
Orthostatic Intolerance ◽  
Lower Body Negative Pressure ◽  
Cardiovascular Response ◽  
Group Differences ◽  
Peripheral Vascular ◽  
Baroreflex Control ◽  
Stress Effects ◽  
Training Modality

The effects of exercise training posture on cardiovascular and baroreflex responses to orthostatic challenge were assessed in highly trained cyclists (CT, n = 8) and swimmers (ST, n = 8), and in untrained men (UT, n = 8). CT demonstrated the lowest orthostatic tolerance to lower body negative pressure (LBNP, 0 to −50 mmHg), with only 3 subjects completing the full LBNP procedure; 5 UT and all ST completed the testing. During LBNP, stroke volume (SV) decreases were similar in CT and ST, but greater than in UT. Mean pulse pressure and systemic vascular resistance (SVR) were reduced in CT relative to ST and UT at the highest levels of LBNP; the slope of the ΔSVR/ΔZ0 and ΔSVR/ΔSV relationships in CT, used to assess peripheral vascular baroreflex function, were attenuated relative to the other groups. There were no between-group differences in the heart rate response to LBNP. The greater incidence of orthostatic intolerance observed in upright-versus supine-trained athletes during passive LBNP was linked to attenuated baroreflex control of peripheral vascular resistance. Key words: arterial baroreflex, arterial pressure, cardiopulmonary baroreceptor, endurance training, vascular resistance

Cerebral critical closing pressure and CO2 responses during the progression toward syncope

2013 ◽  
Vol 114 (6) ◽  
pp. 801-807 ◽  
Author(s):  
K. A. Zuj ◽  
P. Arbeille ◽  
J. K. Shoemaker ◽  
R. L. Hughson
Keyword(s):  
Lower Body Negative Pressure ◽  
Resistance Index ◽  
Bed Rest ◽  
Tolerance Test ◽  
Cerebral Hypoperfusion ◽  
Cerebrovascular Resistance ◽  
Critical Closing Pressure ◽  
Cerebral Blood Velocity ◽  
End Tidal ◽  
Closing Pressure

Syncope from sustained orthostasis results from cerebral hypoperfusion associated with reductions in arterial pressure at the level of the brain (BPMCA) and reductions in arterial CO2 as reflected by end-tidal values (PetCO2). It was hypothesized that reductions in PetCO2 increase cerebrovascular tone before a drop in BPMCA that ultimately leads to syncope. Twelve men (21–42 yr of age) completed an orthostatic tolerance test consisting of head-up tilt and progressive lower body negative pressure to presyncope, before and after completing 5 days of continuous head-down bed rest (HDBR). Cerebral blood velocity (CBFV), BPMCA, and PetCO2 were continuously recorded throughout the test. Cerebrovascular indicators, cerebrovascular resistance, critical closing pressure (CrCP), and resistance area product (RAP), were calculated. Comparing from supine baseline to 6–10 min after the start of tilt, there were reductions in CBFV, PetCO2, BPMCA, and CrCP, an increase in RAP, and no change in cerebrovascular resistance index. Over the final 15 min before syncope in the pre-HDBR tests, CBFV and CrCP were significantly related to changes in PetCO2 ( r = 0.69 ± 0.17 and r = 0.63 ± 0.20, respectively), and BPMCA, which was not reduced until the last minute of the test, was correlated with a reduction in RAP ( r = 0.91 ± 0.09). Post-HDBR, tilt tolerance was markedly reduced, and changes in CBFV were dominated by a greater reduction in BPMCA with no relationships to PetCO2. Therefore, pre-HDBR, changes in PetCO2 with orthostasis contributed to increases in cerebrovascular tone and reductions in CBFV during the progression toward syncope, whereas, after 5 days of HDBR, orthostatic responses were dominated by changes in BPMCA.

scholarly journals Presyncopal cardiac contractility and autonomic activity in young healthy males

2009 ◽  
pp. 827-833
Author(s):  
E Grasser ◽  
N Goswami ◽  
H Hinghofer-Szalkay
Keyword(s):  
Blood Pressure ◽  
Lower Body Negative Pressure ◽  
Nervous Activity ◽  
Cardiac Contractility ◽  
Peripheral Resistance ◽  
Resistance Index ◽  
Left Ventricular ◽  
Orthostatic Stress ◽  
Frequency Variation ◽  
Healthy Humans

We investigated non-invasively cardiac contractility and autonomic nervous activity during presyncopal orthostatic stress induced in healthy humans. A graded orthostatic stress (GOS) paradigm, consisting of head-up tilt (HUT) combined with lower body negative pressure (LBNP) of increasing magnitude, was used to reach a presyncopal end-point in 15 healthy adults. Continuous beat-to-beat hemodynamic and autonomic parameters were recorded. From supine control (C1) to presyncope (PS), total peripheral resistance index (TPRI) decreased from 2300±500 to 1910±320 dyne*s*m²/cm^5 (p=0.004), index of contractility (IC) from 59±14 to 27±6 1000/s (p<0.0001), left ventricular working index (LVWI) from 5.2±1.3 vs. 3.6±0.6 mmHg*L/(min*m²) (p=0.0001) and acceleration index (ACI) from 65±18 vs. 54±15 100/s² (p=0.04). Low frequency variation of diastolic blood pressure (LFnudBP) increased from 51±14 to 67±11 % (p=0.0006) and of systolic blood pressure (LFnusBP) from 50±6 vs. 67±8 % (p<0.0001). High frequency variation of RR-interval (HFms²RRI) decreased from 385±320 to 38±43 ms² (p=0.001). From late GOS (G3) to PS, TPRI decreased from 2540±640 to 1910±320 dyne*s*m²/cm^5 (p=0.003), IC from 35±6 to 27±6 1000/s (p=0.003), LVWI from 4.6±0.9 to 3.6±0.6 mmHg*L/(min/m²) (p=0.003), LFnusBP from 71±8 to 67±8 % (p=0.03), LFmmHg²dBP from 6.6±4.0 to 4.8±2.9 mmHg² (p=0.0001), LFmmHg²sBP from 9.7±7.8 to 7.4±4.8 mmHg² (p=0.01). HFnuRRI increased from 19±8 to 28±13 % (p=0.008). Myocardial contractility indices and parameters of sympathetic activity were reduced in the presyncopal state, while parasympathic activity was increased. This suggests a decrease in cardiac contractility during orthostatically induced presyncope in healthy subjects.

Lower body negative pressure exercise plus brief postexercise lower body negative pressure improve post-bed rest orthostatic tolerance

2007 ◽  
Vol 103 (6) ◽  
pp. 1964-1972 ◽  
Author(s):  
Donald E. Watenpaugh ◽  
Deborah D. O'Leary ◽  
Suzanne M. Schneider ◽  
Stuart M. C. Lee ◽  
Brandon R. Macias ◽  
...  
Keyword(s):  
Negative Pressure ◽  
Acute Exercise ◽  
Treadmill Exercise ◽  
Orthostatic Intolerance ◽  
Lower Body Negative Pressure ◽  
Bed Rest ◽  
Orthostatic Tolerance ◽  
Lower Body ◽  
Before And After ◽  
Head Up Tilt

Orthostatic intolerance follows actual weightlessness and weightlessness simulated by bed rest. Orthostasis immediately after acute exercise imposes greater cardiovascular stress than orthostasis without prior exercise. We hypothesized that 5 min/day of simulated orthostasis [supine lower body negative pressure (LBNP)] immediately following LBNP exercise maintains orthostatic tolerance during bed rest. Identical twins (14 women, 16 men) underwent 30 days of 6° head-down tilt bed rest. One of each pair was randomly selected as a control, and their sibling performed 40 min/day of treadmill exercise while supine in 53 mmHg (SD 4) [7.05 kPa (SD 0.50)] LBNP. LBNP continued for 5 min after exercise stopped. Head-up tilt at 60° plus graded LBNP assessed orthostatic tolerance before and after bed rest. Hemodynamic measurements accompanied these tests. Bed rest decreased orthostatic tolerance time to a greater extent in control [34% (SD 10)] than in countermeasure subjects [13% (SD 20); P < 0.004]. Controls exhibited cardiac stroke volume reduction and relative cardioacceleration typically seen after bed rest, yet no such changes occurred in the countermeasure group. These findings demonstrate that 40 min/day of supine LBNP treadmill exercise followed immediately by 5 min of resting LBNP attenuates, but does not fully prevent, the orthostatic intolerance associated with 30 days of bed rest. We speculate that longer postexercise LBNP may improve results. Together with our earlier related studies, these ground-based results support spaceflight evaluation of postexercise orthostatic stress as a time-efficient countermeasure against postflight orthostatic intolerance.

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