Effect of increased intracardiac and arterial pressure on plasma vasopressin in humans

1984 ◽  
Vol 246 (5) ◽  
pp. H647-H651 ◽  
Author(s):  
S. R. Goldsmith ◽  
A. W. Cowley ◽  
G. S. Francis ◽  
J. N. Cohn

The effects of loading cardiopulmonary and sinoaortic baroreceptors on plasma arginine vasopressin (AVP) levels were examined in 18 healthy young adults after a mild water restriction. Cardiopulmonary receptors were acutely loaded by volume expansion which increased central venous pressure (CVP) from 4.7 +/- 1.9 to 7.3 +/- 2.2 mmHg but did not change mean arterial blood pressure (MAP). Both receptor groups were acutely loaded by applications of lower body positive pressure, which induced a comparable increase in CVP and, in addition, raised MAP from 85 +/- 6.7 to 93 +/- 6.8 mmHg (P less than 0.001). There was evidence of reflex activation as forearm blood flow and heart rate increased during volume expansion while the increase in heart rate was blocked during lower body positive pressure. Neither intervention significantly altered the control AVP level of 4.6 +/- 1.4 pg/ml. An investigation of more prolonged stimulation of cardiopulmonary receptors was carried out using 1 h of head-down tilt. Again, despite increases in CVP (5.1 +/- 1.3 to 9.0 +/- 1.4 mmHg, P less than 0.005), AVP (5.7 +/- 2.4 pg/ml) did not decrease. MAP did not change during head-down tilt. There were no changes in osmolality throughout any of the studies. AVP levels in humans are therefore not responsive to moderate isosmotic loading of the cardiopulmonary and sinoaortic baroreceptors under conditions of mild water restriction.

1988 ◽  
Vol 65 (3) ◽  
pp. 1226-1230 ◽  
Author(s):  
S. R. Goldsmith

Increases in central venous pressure and arterial pressure have been reported to have variable effects on normal arginine vasopressin (AVP) levels in healthy humans. To test the hypothesis that baroreceptor suppression of AVP secretion might be more likely if AVP were subjected to a prior osmotic stimulus, we investigated the response of plasma AVP to increased central venous pressure and mean arterial pressure after hypertonic saline in six normal volunteers. Plasma AVP, serum osmolality, heart rate, central venous pressure, mean arterial pressure, and pulse pressure were assessed before and after a 0.06 ml.kg-1.min-1-infusion of 5% saline give over 90 min and then after 10 min of 30 degrees head-down tilt and 10 min of head-down tilt plus lower-body positive pressure. Hypertonic saline increased plasma AVP. After head-down tilt, which did not change heart rate, pulse pressure, or mean arterial pressure but did increase central venous pressure, plasma AVP fell. Heart rate, pulse pressure, and central venous pressure were unchanged from head-down tilt values during lower-body positive pressure, whereas mean arterial pressure increased. Plasma AVP during lower-body positive pressure was not different from that during tilt. Osmolality increased during the saline infusion but was stable throughout the remainder of the study. These data therefore suggest that an osmotically stimulated plasma AVP level can be suppressed by baroreflex activation. Either the low-pressure cardiopulmonary receptors (subjected to a rise in central venous pressure during head-down tilt) or the sinoaortic baroreceptors (subjected to hydrostatic effects during head-down tilt) could have been responsible for the suppression of AVP.(ABSTRACT TRUNCATED AT 250 WORDS)


Sports ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 51
Author(s):  
Daniel Fleckenstein ◽  
Olaf Ueberschär ◽  
Jan C. Wüstenfeld ◽  
Peter Rüdrich ◽  
Bernd Wolfarth

Lower body positive pressure treadmills (LBPPTs) as a strategy to reduce musculoskeletal load are becoming more common as part of sports conditioning, although the requisite physiological parameters are unclear. To elucidate their role, ten well-trained runners (30.2 ± 3.4 years; VO2max: 60.3 ± 4.2 mL kg−1 min−1) ran at 70% of their individual velocity at VO2max (vVO2max) on a LBPPT at 80% body weight support (80% BWSet) and 90% body weight support (90% BWSet), at 0%, 2% and 7% incline. Oxygen consumption (VO2), heart rate (HR) and blood lactate accumulation (LA) were monitored. It was found that an increase in incline led to increased VO2 values of 6.8 ± 0.8 mL kg−1 min−1 (0% vs. 7%, p < 0.001) and 5.4 ± 0.8 mL kg−1 min−1 (2% vs. 7%, p < 0.001). Between 80% BWSet and 90% BWSet, there were VO2 differences of 3.3 ± 0.2 mL kg−1 min−1 (p < 0.001). HR increased with incline by 12 ± 2 bpm (0% vs. 7%, p < 0.05) and 10 ± 2 bpm (2% vs. 7%, p < 0.05). From 80% BWSet to 90% BWSet, HR increases of 6 ± 1 bpm (p < 0.001) were observed. Additionally, LA values showed differences of 0.10 ± 0.02 mmol l−1 between 80% BWSet and 90% BWSet. Those results suggest that on a LBPPT, a 2% incline (at 70% vVO2max) is not yet sufficient to produce significant physiological changes in VO2, HR and LA—as opposed to running on conventional treadmills, where significant changes are measured. However, a 7% incline increases VO2 and HR significantly. Bringing together physiological and biomechanical factors from previous studies into this practical context, it appears that a 7% incline (at 80% BWSet) may be used to keep VO2 and HR load unchanged as compared to unsupported running, while biomechanical stress is substantially reduced.


1993 ◽  
Vol 265 (1) ◽  
pp. H69-H73 ◽  
Author(s):  
X. Shi ◽  
C. G. Crandall ◽  
P. B. Raven

Fourteen healthy young men were exposed to progressive increases in lower body positive pressure (LBPP) from 0 to 40 Torr in the supine position. Central venous pressure (CVP) increased 1.09 mmHg (P < 0.05) at 5 Torr LBPP. Between 20 and 40 Torr LBPP CVP increased 0.85 mmHg, resulting in a total increase of 2.06 mmHg (P < 0.05). During 0–20 Torr LBPP mean arterial pressure (MAP) increased from 86 to 89 mmHg with a slope of 0.15 mmHg/Torr LBPP. Stroke volume and cardiac output were significantly increased at 20 Torr LBPP. Beyond 20 Torr LBPP, MAP increased to 95 mmHg at 40 Torr (P < 0.05) with a slope of 0.32 mmHg/Torr LBPP. Forearm blood flow increased above rest at 40 Torr LBPP (P< 0.05). However, neither peripheral nor forearm vascular resistance decreased significantly from rest. Despite the significant increases in MAP, heart rate was unchanged above 20 Torr LBPP. These data suggest that LBPP produces increases in CVP at 0–20 Torr by translocation of blood volume from the legs to the thorax. At LBPP > 20 Torr, further increases in CVP and MAP were produced by other mechanisms possibly related to an activation of intramuscular pressure-sensitive receptors.


2007 ◽  
Vol 293 (1) ◽  
pp. H670-H676 ◽  
Author(s):  
Takeshi Nishiyasu ◽  
Shigeko Hayashida ◽  
Asami Kitano ◽  
Kei Nagashima ◽  
Masashi Ichinose

We tested the hypothesis that peripheral vascular responses (in the lower and upper limbs) to application of lower body positive pressure (LBPP) are dependent on the posture of the subjects. We measured heart rate, stroke volume, mean arterial pressure, leg and forearm blood flow (using the Doppler ultrasound technique), and leg (LVC) and forearm (FVC) vascular conductance in 11 subjects (9 men, 2 women) without and with LBPP (25 and 50 mmHg) in supine and upright postures. Mean arterial pressure increased in proportion to increases in LBPP and was greater in supine than in upright subjects. Heart rate was unchanged when LBPP was applied to supine subjects but was reduced in upright ones. Leg blood flow and LVC were both reduced by LBPP in supine subjects [LVC: 4.8 (SD 4.0), 3.6 (SD 3.5), and 1.4 (SD 1.8) ml·min−1·mmHg−1 before LBPP and during 25 and 50 mmHg LBPP, respectively; P < 0.05] but were increased in upright ones [LVC: 2.0 (SD 1.2), 3.4 (SD 3.4), and 3.0 (SD 2.0) ml·min−1·mmHg−1, respectively; P < 0.05]. Forearm blood flow and FVC both declined when LBPP was applied to supine subjects [FVC: 1.3 (SD 0.6), 1.0 (SD 0.4), and 0.9 (SD 0.6) ml· min−1·mmHg−1, respectively; P < 0.05] but remained unchanged in upright ones [FVC: 0.7 (SD 0.4), 0.7 (SD 0.4), and 0.6 (SD 0.5) ml·min−1·mmHg−1, respectively]. Together, these findings indicate that the leg vascular response to application of LBPP is posture dependent and that the response differs in the lower and upper limbs when subjects assume an upright posture.


2018 ◽  
Vol 27 (3) ◽  
pp. 224-229 ◽  
Author(s):  
Ben J. Lee ◽  
Charles Douglas Thake

Context: Anecdotal reports suggest elite sports clubs combine lower-body positive-pressure rehabilitation with a hypoxic stimulus to maintain or increase physiological and metabolic strain, which are reduced during lower-body positive pressure. However, the effects of hypoxia on cardiovascular and metabolic response during lower-body positive-pressure rehabilitation are unknown. Objective: Evaluate the use of normobaric hypoxia as a means to increase physiological strain during body-weight-supported (BWS) running. Design: Crossover study. Setting: Controlled laboratory. Participants: Seven familiarized males (mean (SD): age, 20 (1) y; height, 1.77 (0.05) m; mass, 69.4 (5.1) kg; hemoglobin, 15.2 (0.8) g·dL−1) completed a normoxic and hypoxic (fraction of inspired oxygen [O2] = 0.14) trial, during which they ran at 8 km·h−1 on an AlterG™ treadmill with 0%, 30%, and 60% BWS in a randomized order for 10 minutes interspersed with 5 minutes of recovery. Main Outcome Measures: Arterial O2 saturation, heart rate, O2 delivery, and measurements of metabolic strain via indirect calorimetry. Results: Hypoxic exercise reduced hemoglobin O2 saturation and elevated heart rate at each level of BWS compared with normoxia. However, the reduction in hemoglobin O2 saturation was attenuated at 60% BWS compared with 0% and 30%, and consequently, O2 delivery was better maintained at 60% BWS. Conclusion: Hypoxia is a practically useful means of increasing physiological strain during BWS rehabilitation. In light of the maintenance of hemoglobin O2 saturation and O2 delivery at increasing levels of BWS, fixed hemoglobin saturations rather than a fixed altitude are recommended to maintain an aerobic stimulus.


2006 ◽  
Vol 101 (3) ◽  
pp. 771-777 ◽  
Author(s):  
Adnan Cutuk ◽  
Eli R. Groppo ◽  
Edward J. Quigley ◽  
Klane W. White ◽  
Robert A. Pedowitz ◽  
...  

The purpose of this study is to assess cardiovascular responses to lower body positive pressure (LBPP) and to examine the effects of LBPP unloading on gait mechanics during treadmill ambulation. We hypothesized that LBPP allows comfortable unloading of the body with minimal impact on the cardiovascular system and gait parameters. Fifteen healthy male and female subjects (22–55 yr) volunteered for the study. Nine underwent noninvasive cardiovascular studies while standing and ambulating upright in LBPP, and six completed a gait analysis protocol. During stance, heart rate decreased significantly from 83 ± 3 beats/min in ambient pressure to 73 ± 3 beats/min at 50 mmHg LBPP ( P < 0.05). During ambulation in LBPP at 3 mph (1.34 m/s), heart rate decreased significantly from 99 ± 4 beats/min in ambient pressure to 84 ± 2 beats/min at 50 mmHg LBPP ( P < 0.009). Blood pressure, brain oxygenation, blood flow velocity through the middle cerebral artery, and head skin microvascular blood flow did not change significantly with LBPP. As allowed by LBPP, ambulating at 60 and 20% body weight decreased ground reaction force ( P < 0.05), whereas knee and ankle sagittal ranges of motion remained unaffected. In conclusion, ambulating in LBPP has no adverse impact on the systemic and head cardiovascular parameters while producing significant unweighting and minimal alterations in gait kinematics. Therefore, ambulating within LBPP is potentially a new and safe rehabilitation tool for patients to reduce loads on lower body musculoskeletal structures while preserving gait mechanics.


2013 ◽  
pp. 653-662 ◽  
Author(s):  
T. SOTA ◽  
S. MATSUO ◽  
Y. UCHIDA ◽  
H. HAGINO ◽  
Y. KAWAI

This study was undertaken to investigate the effects of lower body positive pressure (LBPP) on cardiovascular responses during a 15-min walking trial in young (22.1±0.4 years) and elderly women (67.8±1.1 years). The application of 20 mm Hg LBPP reduced ground reaction forces by 31.2±0.5 kgw in both groups. We hypothesized that cardiovascular responses to LBPP during walking were different between the young and elderly subjects. Applying 20 mm Hg of LBPP increased diastolic and mean blood pressure but not systolic blood pressure in both groups. LBPP-induced reduction in heart rate (HR) occurred more quickly in the young group compared to the elderly group (p<0.05). Applying LBPP also decreased double product (systolic blood pressure x HR) in both groups, suggesting that LBPP reduces myocardial oxygen consumption during exercise. These results suggest that heart rate responses to LBPP during exercise vary with increasing age.


1993 ◽  
Vol 265 (3) ◽  
pp. H918-H922 ◽  
Author(s):  
X. Shi ◽  
J. T. Potts ◽  
B. H. Foresman ◽  
P. B. Raven

Lower body positive pressure (LBPP) was applied at 4 and 30 Torr to increase central venous pressure (CVP). CVP increased with LBPP (r = 0.55, P < 0.01), and the increases were significant at 4 and 30 Torr (7.4 and 7.8 mmHg) from the control (6.0 mmHg). During LBPP cardiac output increased, which was significantly related to the increase in CVP (r = 0.63, P < 0.01). The carotid baroreflex was elicited by trains of neck pressure and suction from 40 to -65 Torr. The carotid-cardiac and carotid-vasomotor baroreflex responses were assessed by determining the maximal gains of heart rate (HR) interval and intraradial mean arterial pressure (MAP) to changes in carotid sinus pressure using a logistic model. The carotid-cardiac and carotid-vasomotor baroreflex gains were negatively related to LBPP, and at 30 Torr, both gains (5.6 ms/mmHg and -0.14 mmHg/mmHg) were significantly smaller than the control (12.4 ms/mmHg and -0.24 mmHg/mmHg). The decreases in carotid-cardiac and carotid-vasomotor baroreflex sensitivity during LBPP were primarily associated with the increases in CVP (r = -0.52, P < 0.01, and r = -0.74, P < 0.01, respectively). These data suggest that the increases in CVP and/or central blood volume diminish the sensitivity of the carotid baroreflex control of HR and MAP by enhancing the tonic inhibitory influence from the cardiopulmonary baroreceptors.


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