Cerebral blood flow velocity response induced by a 70-hPa Valsalva manoeuvre associated with normo- and hypergravity in humans.

Anti-G straining manoeuvres, derived from the Valsalva manoeuvre (VM), are physiological methods for protecting fighter pilots against positive accelerations (+Gz). The aim of this study was to investigate the effects of a standard VM on cerebral haemodynamics, in normo- and hypergravity. In six healthy male volunteers, we investigated the cerebral blood flow velocity response induced by a 10-s, 70-hPa (52.5 mmHg) VM, under normogravity, +2, +3 and +4 Gz acceleration plateaus. Mean blood flow velocity [formula: see text] in middle cerebral artery was monitored by transcranial Doppler velocimetry. In normogravity, no significant variation in [formula: see text] was observed at the onset of VM. After a maximal period of 1.2 s, while VM was sustained, [formula: see text] decreased significantly (P < 0.05). Following the end of the manoeuvre [formula: see text] did not change significantly. When the expiratory pressure had returned to the control value, [formula: see text] was transiently increased (P < 0.05) before returning to control values. During hypergravity, [formula: see text] was significantly decreased at +3 and +4 Gz (P < 0.05) before the onset of VM. While performing VM under +Gz, the main difference compared to the normogravity condition was a significant increase of [formula: see text] (P < 0.05) at the onset of the manoeuvre. Our findings would suggest that when performed under +Gz stress, a 70-hPa VM can transiently improve cerebral haemodynamics. However, when VM is sustained for more than 1.2 s it results in a lasting decrease of cerebral perfusion which may lower +Gz tolerance.

Simulation of cardiovascular response to lower body negative pressure from 0 to -40 mmHg.

This paper presents a mathematical model for simulation of the human cardiovascular response to lower body negative pressure (LBNP) up to -40 mmHg both under normal conditions and when arterial baroreflex sensitivity or leg blood capacity (LBC) is altered. Development of the model assumes that the LBNP response could be explained solely on the bases of 1) blood volume redistribution, 2) left ventricular end-diastolic filling, 3) interaction between left ventricle and peripheral circulation, and 4) modulations of peripheral resistances and heart rate by arterial and cardiopulmonary baroreflexes. The model reproduced well experimental data obtained both under normal conditions and during complete autonomic blockade; thus it is validated for simulation of the cardiovascular response from 0 to -40 mmHg LBNP. We tested the ability of the model to simulate the changes in LBNP response due to a reduction in LBC. To assess these changes experimentally, six healthy men were subjected to LBNP of -15, -30, and -38 mmHg with and without wearing elastic compression stockings. Stockings significantly reduced LBC (from 3.9 +/- 0.3 to 1.8 +/- 0.4 ml/100 ml tissue at -38 mmHg LBNP; P < 0.01) and attenuated the change in heart rate (from 23 +/- 4 to 8 +/- 3% at -38 mmHg LBNP; P < 0.05). The model accurately reproduced this result. The model is useful for assessing the influence of LBC or other parameters such as arterial baroreflex sensitivity in diminishing the orthostatic tolerance of humans after spaceflight, bed rest, or endurance training.

Response of human cerebral blood flow to +Gz accelerations.

Intolerance symptoms associated with high sustained +Gz (head to foot) accelerations are attributed to lack of cerebral perfusion. To determine the response of cerebral circulation to +Gz stress, cerebral blood flow (CBF) was measured in humans with the transcranial Doppler method while cephalic arterial blood pressure was calculated simultaneously using a photoplethysmographic technique. Nine volunteers performed four randomized centrifuge runs at +2 to +5 Gz with a 0.4-G/s onset rate for 30 s. Compared with the control values, for +2-, +3-, +4-, and +5-Gz profiles, CBF was reduced by 19 +/- 7, 26 +/- 8, 49 +/- 26, and 61 +/- 29% (SD), respectively, at the end of the onset and by 18 +/- 4, 21 +/- 11, 27 +/- 7, and 47 +/- 29%, respectively, in the last 20 s of the plateau of acceleration. At the end of the onset and during the plateau of +Gz acceleration, CBF was less reduced than cephalic arterial blood pressure, suggesting that some mechanisms would occur to maintain cerebral perfusion under +Gz stress. These protective mechanisms are likely due to a siphon effect and/or an autoregulatory compensation.

Physiological considerations concerning positive pressure breathing (PBG) during +Gz.

The ability to tolerate +Gz radial acceleration depends primarily on the maintenance of sufficient head level arterial pressure and cerebral blood flow to prevent the occurrence of blackout and G-induced loss of consciousness (G-LOC). Because of the hydrostatic effect on the heart-to-head blood column during +Gz acceleration, if exposures to higher +Gz levels are to be tolerated, either the column must be shortened or arterial pressure at heart level must be elevated. This paper is an overview of the effect and concomitant side effects of positive pressure breathing (PBG) as a means to increase arterial pressure at the heart, and, indirectly, at the cerebral level. However, before doing that, it is necessary to summarise the different ways for increasing arterial pressure to obtain tolerance to increasing +Gz loads.

Rapid decompression of a transport aircraft cabin: protection against hypoxia.

The hypoxic hazard after rapid decompression in transport aircraft was evaluated as a function of the current means of protection, including the role of the inhaled oxygen fraction (FIO2) prior to decompression. The decompressions were made in 2 s; the initial altitude was 8,000 ft and the final altitude was 16,000-45,000 ft. The physiological measurements were arterial oxygen saturation, heart rate, ventilatory frequency, and gaseous analysis in the mask. Results show that FIO2 prior to decompression is not very significant, but the delay before donning the oxygen system seems to be the most limiting factor against tolerance to hypoxia.

Fluid shifts and endocrine responses during lower body negative pressure and dynamic arm exercise.

The use of lower body negative pressure (LBNP) is proposed as a means of reducing the effect of spaceflight on body water loss by stimulation of renin angiotensin aldosterone system (RAAS) activity. Seven subjects were successively submitted to LBNP exposure, arm cranking physical exercise, and to a combination of both procedures (LBNP + arm cranking) in order to check whether this combination enhances RAAS activity. The results showed that exposure to 40 min of LBNP to a level of -40 mm Hg was a more potent stimulus for renin secretion than submaximal and maximal arm cranking. The combination of LBNP with exercise does not further enhance the RAAS activity induced by LBNP alone. These data suggest that the fluid shift toward the lower body induced by LBNP counteracts triggering of renin secretion due to physical exercise.

Effect of hypoxia on heart glycogen utilization during exercise.

An investigation was made into the effects of physical exercise upon heart glycogen change in rats exposed to decreased barometric pressure in hypobaric chamber simulating the effects of 3,000 m and 5,000 m altitude. Blood and cardiac tissue samples were examined after 1 h and 5 h of treadmill running at sea level and at 3,000 m, and after 1 h at 5,000 m. At sea level, cardiac glycogen level showed a classic biphasic evolution which was not affected by running. At 3,000 m, 1 h of running promoted an initial increase of 16% from control values, while a secondary decrease of 15% was measured after 5 h of running. Running for 1 h at 5,000 m induced a total depletion in cardiac glycogen level, the latter being depressed by 90% from control values. Free fatty acid (FFA) plasma level was increased by physical exercise at all barometric pressures, but the response was gradually enhanced by hypoxia. These data indicate that heart glycogen utilization during prolonged physical exercise is stimulated by acute altitude exposure, which suppresses the sparing effect observed at sea level upon dependence of enhanced FFA availability. The great differences in cardiac glycogen utilization support the views that enhanced glycogenolysis during hypoxia is promoted by different parameters, thus affecting various pathways. The slight decrease at 3,000 m suggests a moderate increase in anaerobic metabolism while the exhaustion observed after 1 h of running at 5,000 m indicates a decrease in cellular respiration response and enhanced heart anaerobic metabolism.