Hemodynamic and hormonal responses to lower body negative pressure in men with varying profiles of strength and aerobic power

Hemodynamic, cardiac, and hormonal responses to lower-body negative pressure (LBNP) were examined in 24 healthy men to test the hypothesis that responsiveness of reflex control of blood pressure during orthostatic challenge is associated with interactions between strength and aerobic power. Subjects underwent treadmill tests to determine peak oxygen uptake ( O_2max) and isokinetic dynamometer tests to determine knee extensor strength. Based on predetermined criteria, subjects were classified into one of four fitness profiles of six subjects each, matched for age, height, and body mass: (a) low strength/average aerobic fitness, (b) low strength/high aerobic fitness, (c) high strength/average aerobic fitness, and (d) high strength/high aerobic fitness. Following 90 min of 0.11 rad (6°) head-down tilt (HDT), each subject underwent graded LBNP to –6.7 kPa or presyncope, with maximal duration 15 min, while hemodynamic, cardiac, and hormonal responses were measured. All groups exhibited typical hemodynamic, hormonal, and fluid shift responses during LBNP, with no intergroup differences between high and low strength characteristics. Subjects with high aerobic power exhibited greater (P < 0.05) stroke volume and lower (P < 0.05) heart rate, vascular peripheral resistance, and mean arterial pressure during rest, HDT, and LBNP. Seven subjects, distributed among the four fitness profiles, became presyncopal. These subjects showed greatest reduction in mean arterial pressure during LBNP, had greater elevations in vasopressin, and lesser increases in heart rate and peripheral resistance. Neither O_2max nor leg strength were associated with fall in arterial pressure or with syncopal episodes. We conclude that interactions between aerobic and strength fitness characteristics do not influence responses to LBNP challenge.     

Amélioration de la perfusion des organes vitaux par la valve d’impédance inspiratoire et le concept de pompe respiratoire : rationnel physiologique et application clinique

Objective

In this article, we review the effects of the respiratory pump to improve vital organ perfusion by the use of an inspiratory threshold device.

Data sources

Medline and MeSH database.

Study selection

All papers with a level of proof of I to III have been used.

Data extraction

The analysis of the papers has focused on the physiological modifications induced by intrathoracic pressure regulation.

Data synthesis

Primary function of breathing is to provide gas exchange. Studies of the mechanisms involved in animals and humans provide the physiological underpinnings for “the other side of breathing”: to increase circulation to the heart and brain. We describe studies that focus on the fundamental relationship between the generation of negative intrathoracic pressure during inspiration through a low-level of resistance created by an impedance threshold device and the physiologic effects of a respiratory pump. A decrease in intrathoracic pressure during inspiration through a fixed resistance resulting in an intrathoracic pressure of −7 cmH₂O has multiple physiological benefits including: enhanced venous return, cardiac stroke volume and aortic blood pressure; lower intracranial pressure; resetting of the cardiac baroreflex; elevated cerebral blood flow oscillations and increased tissue blood flow/pressure gradient.

Conclusion

The clinical and animal studies support the use of the intrathoracic pump to treat different clinical conditions: hemorrhagic shock, orthostatic hypotension, septic shock, and cardiac arrest.     

Effect of G-suit protection on carotid-cardiac baroreflex function

INTRODUCTION: To test the hypothesis that G-suit inflation could increase cardiac chronotropic responses to baroreceptor stimulation and enhance baroreflex buffering of BP, the carotid-cardiac baroreflex response of 12 subjects was measured across two levels of lower body negative pressure (LBNP = 0 and 50 mm Hg) and two levels of G-suit inflation (0 and 50 mm Hg) in random order. METHODS: Carotid-cardiac baroreflex stimulation was delivered via a silastic neck pressure cuff and responsiveness quantified by determination of the maximum slope of the stimulus-response function between R-R intervals (ms) and their respective carotid distending pressures (mmHg). RESULTS: Mean +/- SE baseline control baroreflex responsiveness was 3.8+/-0.4 ms x mm Hg(-1). LBNP reduced the baroreflex response to 2.7+/-0.4 ms x mm Hg(-1), but G-suit inflation with LBNP restored the baroreflex response to 4.3+/-0.6 ms x mm Hg(-1). CONCLUSIONS: These results suggest that, in addition to increased venous return and elevated peripheral resistance, G-suit inflation may provide protection against the debilitating effects of blood distribution to the lower extremities during orthostatic challenges such as standing or high +Gz acceleration by increasing cardiovascular responsiveness to carotid baroreceptor stimulation.     

Effect of simulated weightlessness on exercise-induced anaerobic threshold

Ventilation (VE), CO2 output (VCO2), oxygen uptake (VO2), respiratory exchange ratio (R), and the ventilatory equivalents for VO2 and VCO2 were measured during graded exercise before and after 10 d of continuous bed rest (BR) in the -6 degrees head-down position to determine the effect of deconditioning on the anaerobic threshold (AT), i.e., the highest workrate or VO2 which was achieved without evidence of lactic acidosis, as judged from the profile of ventilatory and gas exchange responses. Ten healthy male subjects performed a supine graded cycle ergometer test before (pre) and after (post) BR which consisted of 4 min of unloaded pedaling at 60 rpm followed by an increased workrate of 15 W X min-1 until volitional fatigue (max). VE, VCO2, VO2, R, VE/VO2 and VE/VCO2 were measured every 30 s and used collectively to identify the AT. Plasma (PV) and blood (BV) volumes were measured pre- and post-BR by T-1824. Following BR, VO2max decreased from 2.42 +/- 0.17 to 2.25 +/- 0.13 L X min-1 (7.0%, p less than 0.05). BR significantly (p less than 0.05) reduced the AT from 1.26 +/- 0.09 to 0.95 +/- 0.05 L X min-1 VO2; from 52.2 +/- 2.0 to 42.6 +/- 1.6% VO2max; and from 93 +/- 9 to 65 +/- 6 W. A correlation coefficient (r) of -0.11 (NS) was found between the change in VO2max and change in AT. A decrease in BV of 8.8% (p less than 0.05) was due to the 11.0% reduction in PV; red cell volume remained constant.(ABSTRACT TRUNCATED AT 250 WORDS)     

Blood pressure measurement for accurate assessment of patient status in emergency medical settings

Obtaining blood pressure measurements with traditional sphygomanometry that are insensitive and nonspecific can fail to provide an accurate assessment of patient status, particularly in specific clinical scenarios of acute reduction in central blood volume such as hemorrhage or orthostatic testing. This paper provides a review of newly emerging monitoring technologies that are being developed and integrated to improve patient diagnosis by using collection and feature extraction in real time of arterial waveforms by machine-learning algorithms. With assessment of continuous, noninvasively measured arterial waveforms, machine-learning algorithms have been developed with the capability to predict cardiovascular collapse with > 96% accuracy and a correlation of 0.89 between the time of predicted and actual cardiovascular collapse (e.g., shock, syncope) using a human model of progressive central hypovolemia. The resulting capability to obtain earlier predictions of imminent hemodynamic instability has significant implications for effective countermeasure applications by the aeromedical community. The ability to obtain real-time, continuous information about changes in features and patterns of arterial waveforms in addition to standard blood pressure provides for the first time the capability to assess the status of circulatory blood volume of the patient and can be used to diagnose progression toward development of syncope or overt shock, or guide fluid resuscitation.     

Potential benefits of maximal exercise just prior to return from weightlessness

The purpose of this study was to determine whether performance of a single maximal bout of exercise during weightlessness within hours of return to earth would enhance recovery of aerobic fitness and physical work capacities under a 1G environment. Ten healthy men (36-51 yr) underwent maximal supine exercise followed by upright maximal exercise before and after a 10-d bedrest period in the 6 degrees headdown position. A graded maximal supine cycle ergometer test was performed before and at the end of bedrest to simulate exercise during weightlessness. Following 3 h of resumption of the upright posture from the supine exercise test, a second maximal exercise test was performed on a treadmill to measure work capacity under conditions of 1G. Compared to before bedrest, peak VO2 decreased (p less than 0.05) by 8.7% and peak HR increased (p less than 0.05) by 5.6% in the supine cycle test at the end of bedrest. However, there were no significant changes in peak VO2 and peak HR in the upright treadmill test following bedrest. These data, based on a simulation, suggest that one bout of maximal leg exercise prior to return from 10 d of weightlessness may be adequate to restore preflight aerobic fitness and physical work capacity.     

Effects of exposure to simulated microgravity on neuronal catecholamine release and blood pressure responses to norepinephrine and angiotensin

We tested the hypothesis that exposure to microgravity reduces the neuronal release of catecholamines and blood pressure responses to norepinephrine and angiotensin. Eight men underwent 30 days of 6° head-down tilt (HDT) bedrest to simulate exposure to microgravity. Plasma norepinephrine and mean arterial blood pressure (MAP) were measured before and after a cold pressor test (CPT) and graded norepinephrine infusion (8, 16 and 32 ng/kg/min) on day 6 of a baseline control period (C6) and on days 14 and 27 of HDT. MAP and plasma angiotensin II (Ang-II) were measured during graded Ang-II infusion (1, 2 and 4 ng/kg/min) on C8 and days 16 and 29 of HDT. Baseline total circulating norepinephrine was reduced from 1017 ng during the baseline control period to 610 ng at day 14 and 673 ng at day 27 of HDT, confirming a hypoadrenergic state. An elevation of norepinephrine (+178 ng) to the CPT during the baseline control period was eliminated by HDT days 14 and 27. During norepinephrine infusion, similar elevations in plasma norepinephrine (7.7 pg/ml/ng/kg/min) caused similar elevations in MAP (0.12 mmHg/ng/kg/min) across all test days. Ang-II infusion produced higher levels of plasma Ang-II during HDT (47.3 pg/ml) than during baseline control (35.5 pg/ml), while producing similar corresponding elevations in blood pressure. While vascular responsiveness to norepinephrine appears unaffected, impaired neuronal release of norepinephrine and reduced vascular responsiveness to Ang-II might contribute to the lessened capacity to vasoconstrict after spaceflight. The time course of alterations indicates effects that occur within two weeks of exposure.     

Carotid-cardiac baroreflex response and LBNP tolerance following resistance training.

The purpose of this study was to examine the effect of lower body resistance training on cardiovascular control mechanisms and blood pressure maintenance during an orthostatic challenge. Lower body negative pressure (LBNP) tolerance, carotid-cardiac baroreflex function (using neck chamber pressure), and calf compliance were measured in eight healthy males before and after 19 wk of knee extension and leg press training. Resistance training sessions consisted of four or five sets of 6-12 repetitions of each exercise, performed two times per week. Training increased strength 25 +/- 3 (SE)% (P = 0.0003) and 31 +/- 6% (P = 0.0004), respectively, for the leg press and knee extension exercises. Average fiber size in biopsy samples of m. vastus lateralis increased 21 +/- 5% (P = 0.0014). Resistance training had no significant effect on LBNP tolerance. However, calf compliance decreased in five of the seven subjects measured, with the group average changing from 4.4 +/- 0.6 ml.mm Hg-1 to 3.9 +/- 0.3 ml.mm Hg-1 (P = 0.3826). The stimulus-response relationship of the carotid-cardiac baroreflex response shifted to the left on the carotid pressure axis as indicated by a reduction of 6 mm Hg in baseline systolic blood pressure (P = 0.0471). In addition, maximum slope increased from 5.4 +/- 1.3 ms.mm Hg-1 before training to 6.6 +/- 1.6 ms.mm Hg-1 after training (P = 0.0141). Our results suggest the possibility that high resistance, lower extremity exercise training can cause a chronic increase in sensitivity and resetting of the carotid-cardiac baroreflex.(ABSTRACT TRUNCATED AT 250 WORDS)     

Human autonomic and cerebrovascular responses to inspiratory impedance

BACKGROUND: We evaluated the influence of breathing through an inspiratory Impedance Threshold Device (ITD) on autonomic neural and cerebrovascular function. METHODS: Eight subjects breathed through a sham ITD (0 cmH2O) and an active ITD (-7 cmH2O) in the supine position. We recorded the ECG, finger photoplethysmographic arterial pressure, cerebral blood flow velocity, and muscle sympathetic nerve activity (MSNA). In a randomized, counterbalanced design, subjects breathed spontaneously and also breathed at a set cadence of 15 breaths/min (0.25 Hz) for 3 minutes each. Data were analyzed in both time and frequency domains. RESULTS: Breathing through the active ITD increased mean arterial pressure by approximately 5 mm Hg, heart rate by 2 bpm, and mean cerebral blood flow velocity by 10% (p<0.05) with no effect on MSNA or estimates of vagal-cardiac control (p>0.05). The active ITD did not affect oscillations of interbeat R-R intervals, arterial pressures, or cerebral flow velocities within the low frequency (LF) domain of the power spectrum (p>0.05). Cross spectral analysis revealed no effect of the active ITD on transfer function magnitudes among arterial pressures and R-R intervals, or between arterial pressures and cerebral blood flow velocities at the LF (p>0.05). CONCLUSIONS: Our results demonstrate that the ITD increases arterial pressure, heart rate, and cerebral blood flow velocity independent of changes in autonomic cardiovascular control or dynamic cerebral autoregulation. Use of an active ITD in situations of acute central hypovolemia, such as during hemorrhage, may slow the progression to hemodynamic instability in bleeding patients who retain the ability to ventilate spontaneously and robustly.