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J P Richalet

Publications and source records attributed to J P Richalet.

At least 19 recordsLinked to original sources
PubMed2006

Characterisation of the ventilatory response to hypoxia in a model of transgenic anemic mice.

Both polycythemia and the increase in hypoxic ventilatory response (HVR) are considered as important factors of acclimatization to hypoxia. The objective of this study was to characterise the ventilation pattern at different inspired oxygen fraction in a model of chronic anemic mice. These mice have a targeted disruption in the 5' untranslated region of the Epo gene that reduces Epo expression such that the homozygous animal is severely anemic. Ventilation in normoxia in Epo-TAg(h) mice was significantly greater than in wild type, and the difference was mainly due to a higher tidal volume. HVR was higher in Epo-TAg(h) mice at every FIO2 suggesting a higher chemosensitivity. Resting oxygen consumption was maintained in anemic mice. Maximal oxygen consumption was 30% lower while hemoglobin was 60% lower in anemic mice compared to wild type. This small decrease in maximal oxygen consumption is probably due a greater cardiac output and/or a better tissue oxygen extraction and would allow these anemic mice to acclimatize to hypoxia in spite of low oxygen carrying capacity. In conclusion, Epo-TAg(h) anemic mice showed increased ventilation and hypoxic ventilatory response. However, whether these adaptations will contribute to acclimatization in chronic hypoxia remains to be determined.

Anemia↗
PubMed2006

Heart rate variability and performance at two different altitudes in well-trained swimmers.

UNLABELLED: The aim of this study was to compare the effects of training at two different altitudes on heart rate variability (HRV) and performance in well-trained swimmers. Eight national-level male swimmers (age = 17.0 +/- 1.8 yrs, weight = 67.0 +/- 6.6 kg, height = 180.4 +/- 7.2 cm, V(O2max) = 60.4 +/- 4.0 ml.min(-1). kg(-1)) trained 17 days at 1200 m altitude (T1200), then, after 6 weeks of moderate training at sea level, reproduced the same training plan at 1850 m (T1850). The training was mainly aerobic with 86 % and 84 % < or = anaerobic threshold for T 1200 and T1850, respectively. Four HRV analysis tests were performed during T1200 and T1850, respectively (pre-test = day 0, test 2 = day 5, test 3 = day 11, post-test = day 17), in supine and standing position. Performance was measured over a 2000-m freestyle test at the altitude of 1200 m. A difference in HRV changes was observed between the two altitudes: during T1200, addition of parasympathetic and sympathetic activity in supine (TP(SU)) (p < 0.05) and standing (TP(ST)) (p < 0.05) position, supine parasympathetic activity (HF(SU)) (p < 0.05), and standing sympathetic activity (LF(ST)) (p < 0.05) were increased and the 2000-m performance was improved (p < 0.05) whereas none of these parameters was changed during T1850. Change in performance was correlated with increase in HF(SU) (r = 0.73; p < 0.05) and tended towards correlation with increase in LF(ST) (r = 0.73; p = 0.06). CONCLUSION: the same training loads induced a positive effect on HRV and performance at 1200 m but not at 1850 m. This may be the consequence of greater stress due to an interaction between greater hypoxic stimulus and the same training loads. These results highlight two opposing effects: aerobic training increases, whereas hypoxia decreases HF(SU), due to the correlation between HRV and changes in performance during altitude training.

Adolescent↗
PubMed2005

Time course of ventilatory acclimatisation to hypoxia in a model of anemic transgenic mice.

We questioned the assumption that polycythemia is essential for adaptation to chronic hypoxia. Thus, the objective of our study was to determine if anemic Epo-TAg(h) mice could survive in hypoxia despite low oxygen carrying capacity. We explored the possibility that ventilatory acclimatisation is involved in the strategy used by anemic transgenic mice to adapt to chronic hypoxia. Epo-TAg(h) and Wild Type mice were exposed during 2 weeks at a barometric pressure of 450 Torr. After 1, 5 and 14 days of exposure, ventilation at different inspired oxygen fraction was measured in both groups. Ventilation during acclimatisation to hypoxia was significantly greater in Epo-TAg(h) than in Wild Type. The difference was mainly due to a higher tidal volume that could explain a higher arterial PO2 in Epo-TAg(h) mice. Epo-Tag(h) mice did not develop right ventricle hypertrophy after 2 weeks of exposure to hypoxia while Wild Type did. Hemoglobin concentration was 60% lower in anemic mice versus Wild Type after acclimatisation. In conclusion, ventilatory acclimatisation contributed to the adaptation of Epo-Tag(h) mice in chronic hypoxia despite low arterial oxygen carrying capacity.

Acclimatization↗
PubMed2002

Parathyroid hormone concentrations during and after two periods of high intensity exercise with and without an intervening recovery period.

The purpose of this study was to examine the effect of a recovery period between two periods of exercise on bone metabolism and related hormones. Concentrations of serum parathyroid hormone ([PTH]), plasma ionized calcium ([Ca(2+)]) and total calcium were measured. A group of 12 healthy men aged 20-27 years participated in this study. They took part in two exercise protocols (P(1) and P(2)) on two separate weeks. The exercise in P(1) comprised two successive periods of 21 min each at 70% and 85% of maximal oxygen uptake; P(2) comprised two periods of exercise at the same intensities but separated by 40 min of recovery. Venous blood samples were collected 1 day before the sessions (control), before each protocol, during (7th and 21st min), at the end (42nd min in P(1) and 82nd min in P(2)) and after 24 h of recovery. The [PTH] was significantly elevated during the two protocols ( P<0.01), remained raised in P(1) after 24 h of recovery ( P<0.05) and was significantly lower ( P<0.01) at the end of P(2) when compared to P(1). The [Ca(2+)] decreased significantly during and at the end of the two protocols ( P<0.01) and had returned to control values after 24 h of recovery. Plasma lactate concentration increased during the two protocols ( P<0.01) and returned to control values after recovery. These results indicate firstly that [Ca(2+)] decreases during continuous exercise as [PTH] increases and remains raised after 24 h of recovery, secondly that a recovery period between two periods of exercise attenuates the variations in [Ca(2+)] and [PTH], and thirdly that recovery may have anabolic effects on bone. However, the small physiological changes observed prevent us from forming any firm conclusion about this.

Adult↗
PubMed2002

Effect of intermittent hypoxia on cardiovascular function, adrenoceptors and muscarinic receptors in Wistar rats.

The usual model of intermittent hypoxia (sleep apnoea) corresponds to repeated episodes of hypoxia from a few seconds to a few hours interspersed with episodes of normoxia. The aim of this study was to evaluate in rats the effect of two periods of intermittent exposure for 2 months to hypoxia (IHX1, 24 h in hypoxia (428 Torr), 24 h in normoxia; IHX2, 48 h in hypoxia (428 Torr), 24 h in normoxia) as a new model of hypoxia simulating intermittent exposure to high altitude experienced by Andean miners. We assessed the haematological parameters, time course of resting heart rate and systolic blood pressure. We also evaluated the expression of adrenergic and muscarinic receptors. IHX1 and IHX2 produced an increase in haematocrit, haemoglobin concentration and mean corpuscular volume as previously seen in most hypoxic models. IHX1 and IHX2 induced a similar sustained elevation of systolic blood pressure (132 +/- 2 and 135 +/- 3 mmHg, respectively, vs. the control level of 121 +/- 16 mmHg) after 10 days of exposure without change in heart rate. Right ventricular (RV) hypertrophy (225 +/- 13 and 268 +/- 15 mg g(-1), vs. 178 +/- 7 mg g(-1) and downregulation of alpha1-adrenoceptor (RV: 127 +/- 21 and 94 +/- 16 fmol mg(-1) vs. 157 +/- 8 fmol mg(-1); left ventricle (LV): 141 +/- 5 and 126 +/- 9 fmol mg(-1) vs. 152 +/- 5 fmol mg(-1)) have been found in both groups, with right ventricular hypertrophy being greater and alpha1-adrenoceptor density being lower in IHX2 than in HX1 groups. These data indicate that both parameters are related to the time of exposure to hypoxia. IHX1 and IHX2 produced the same magnitude of upregulation of muscarinic receptors (LV, 60%; RV, 40%), and no change in beta-adrenoceptors. In conclusion, exposure to intermittent hypoxia led to polycythaemia and RV hypertrophy as observed in other types of hypoxia. A specific cardiovascular response was seen, that is an increase in blood pressure without change in heart rate, which was different from the one observed in episodic and chronic hypoxia. Furthermore, this model involved specific modifications of alpha1-adrenergic and muscarinic expression.

Animals↗
PubMed2002

Nasal peak inspiratory flow at altitude.

The present study investigated whether there are changes in nasal peak inspiratory flow (NPIF) during hypobaric hypoxia under controlled environmental conditions. During operation Everest III (COMEX '97), eight subjects ascended to a simulated altitude of 8,848 m in a hypobaric chamber. NPIF was recorded at simulated altitudes of 0 m, 5,000 m and 8,000 m. Oral peak inspiratory and expiratory flow (OPIF, OPEF) were also measured. Ambient air temperature and humidity were controlled. NPIF increased by a mean +/- SD of 16 +/- 12% from sea level to 8,000 m, whereas OPIF increased by 47 +/- 14%. NPIF rose by 0.085 +/- 0.03 L x s(-1) per kilometre of ascent (p<0.05), significantly less than the rise in OPIF and OPEF of 0.35 +/- 0.10 and 0.33 +/- 0.04 L x s(-1) per kilometre (p<0.0005). Nasal peak inspiratory flow rises with ascent to altitude. The rise in nasal peak inspiratory flow with altitude was far less than oral peak inspiratory flow and less than the predicted rise according to changes in air density. This suggests flow limitation at the nose, and occurs under controlled environmental conditions, refuting the hypothesis that nasal blockage at altitude is due to the inhalation of cold, dry air. Further work is needed to determine if nasal blockage limits activity at altitude.

Adult↗
PubMed2001

Operation Everest III (Comex'97): the effect of simulated sever hypobaric hypoxia on lipid peroxidation and antioxidant defence systems in human blood at rest and after maximal exercise.

Eight subjects were placed in a decompression chamber for 31 days at pressures from sea level (SL) to 8848 m altitude equivalent. Whole blood lipid peroxidation (LP) was increased at 6000 m by a mean of 23% (P<0.05), at 8000 m by 79% (P<0.01) and at 8848 m by 94% (P<0.01). (All figures are means.) Two days after return to sea level (RSL), it remained high, by 81% (P<0.01), while corresponding erythrocyte GSH/GSSG ratios decreased by 31, 46, 49, 48%, respectively (each P<0.01). Erythrocyte SOD and plasma ascorbate did not change significantly. At sea level, maximal exercise induced a 49% increase in LP (P<0.01), and a 27% decrease in erythrocyte GSH/GSSG ratio relative to resting values (P<0.05). At 6000 m, the LP was enhanced further from 23 (P<0.05) to 66% (P<0.01), and after RSL from 81 (P<0.01) to 232% (P<0.01), while pre-exercise GSH/GSSG ratios did not change significantly. Exercise did not change plasma ascorbate relative to sea level or to 6000 m, but decreased after RSL by 32% (P<0.01). These findings suggest that oxidative stress is induced by prolonged hypobaric hypoxia, and is maintained by rapid return to sea level, similar to the post-hypoxic re-oxygenation process. It is increased by physical exercise.

Acclimatization↗
PubMed2001

The scientific observatories on Mont Blanc.

Since the first ascent of Mont Blanc by Jacques Balmat and Dr. Michel-Gabriel Paccard in 1786, numerous scientific events have taken place on the highest peak of Europe. Horace Benédict de Saussure, since his first ascent in 1787, made numerous observations on barometric pressure, temperature, geology, and mountain sickness on Mont Blanc. Over the next 100 years, scientists and physicians climbed Mont Blanc and made many interesting although anecdotal reports. Science on Mont Blanc exploded at the end of the 19th century. A major player at that time was Joseph Vallot (1854-1925), who constructed an observatory in 1890 at 4,358 m on the Rochers des Bosses and then moved it in 1898 to a better location at 4,350 m. There Vallot and invited scientists made observations over more than 30 years: studies in geology, glaciology, astronomy, cartography, meteorology, botany, physiology and medicine were performed and published in the seven volumes of the Annales de l'Observatoire du Mont Blanc, between 1893 and 1917, and in the Comptes Rendus de l'Académie des Sciences. While Jules Janssen and Xaver Imfeld were preparing the construction of the new observatory on the top of Mont Blanc, Dr. Jacottet died in 1891 at the Observatoire Vallot from a disease that was clearly attributed by Dr. Egli-Sinclair to the effect of high altitude. This was probably the first case of high altitude pulmonary edema documented by an autopsy and suspected to be directly due to high altitude. Extensive studies on ventilation were made from 1886 to 1900. Increase in ventilation with altitude was documented, with the phenomenon of "ventilatory acclimatization." Paul Bert's theories on the role of oxygen in acute mountain sickness were confirmed in 1903 and 1904 by studying the effects of oxygen inhalation. In 1913, Vallot documented for the first time the decrease in physical performance at the top of Mont Blanc using squirrels. After that pioneering era, few studies were done until 1984, when a team of the Association pour la Recherche en Physiologie de l'Environnement (ARPE) renovated the observatory and started to organize annual scientific expeditions.

Altitude Sickness↗
PubMed2001

Differential alterations in cardiac adrenergic signaling in chronic hypoxia or norepinephrine infusion.

Norepinephrine (NE)-induced desensitization of the adrenergic receptor pathway may mimic the effects of hypoxia on cardiac adrenoceptors. The mechanisms involved in this desensitization were evaluated in male Wistar rats kept in a hypobaric chamber (380 Torr) and in rats infused with NE (0.3 mg. kg(-1). h(-1)) for 21 days. Because NE treatment resulted in left ventricular (LV) hypertrophy, whereas hypoxia resulted in right (RV) hypertrophy, the selective hypertrophic response of hypoxia and NE was also evaluated. In hypoxia, alpha(1)-adrenergic receptors (AR) density increased by 35%, only in the LV. In NE, alpha(1)-AR density decreased by 43% in the RV. Both hypoxia and NE decreased beta-AR density. No difference was found in receptor apparent affinity. Stimulated maximal activity of adenylate cyclase decreased in both ventricles with hypoxia (LV, 41%; RV, 36%) but only in LV with NE infusion (42%). The functional activities of G(i) and G(s) proteins in cardiac membranes were assessed by incubation with pertussis toxin (PT) and cholera toxin (CT). PT had an important effect in abolishing the decrease in isoproterenol-induced stimulation of adenylate cyclase in hypoxia; however, pretreatment of the NE ventricle cells with PT failed to restore this stimulation. Although CT attenuates the basal activity of adenylate cyclase in the RV and the isoproterenol-stimulated activity in the LV, pretreatment of NE or hypoxic cardiac membranes with CT has a less clear effect on the adenylate cyclase pathway. The present study has demonstrated that 1) NE does not mimic the effects of hypoxia at the cellular level, i.e., hypoxia has specific effects on cardiac adrenergic signaling, and 2) changes in alpha- and beta-adrenergic pathways are chamber specific and may depend on the type of stimulation (hypoxia or adrenergic).

Adenylate Cyclase Toxin↗
PubMed2001

Myocardial adrenergic and cholinergic receptor function in hypoxia: correlation with O(2) transport in exercise.

The time course of changes in rat myocardial alpha(1)- and beta-adrenoceptors and of muscarinic cholinergic (M-Ach) receptor characteristics was studied parallel with the changes in exercise systemic O(2) transport during a 21-day period of hypoxia (barometric pressure 380 Torr) to assess the effects of receptor modification during acclimatization on maximal exercise capacity. Hypoxia resulted in polycythemia, pulmonary hypertension, right ventricular hypertrophy, and transient left ventricular weight loss. Maximal O(2) consumption at 30 min of hypoxia was reduced to 60% of the normoxic value and remained unchanged. This was partly due to a gradual decrease in maximal cardiac output and heart rate (HR(max)), which offset the increase in blood O(2) content. HR(max) correlated positively (r = 0.994) with beta-adrenoceptor density and negatively (r = -0.964) with M-Ach-receptor density, suggesting that HR(max) reduction results from intrinsic changes in myocardial receptor characteristics leading to reduced responses to adrenergic stimulation and elevated responses to cholinergic stimulation. alpha-Adrenoceptor density in both ventricles increased initially to eventually fall below normoxic values. The dissociation between the different patterns of right and left ventricular weight and the similar pattern of alpha-adrenoceptor change in both ventricles do not support a role for these receptors on right ventricular myocardial hypertrophy.

Acclimatization↗
PubMed2001

Exercise training alters the effect of chronic hypoxia on myocardial adrenergic and muscarinic receptor number.

Chronic hypoxic exposure results in elevated sympathetic activity leading to downregulation of myocardial alpha(1)- and beta-adrenoceptors (alpha(1)-AR, beta-AR). On the other hand, it has been shown that sympathetic activity is reduced by exercise training. The objective of this study was to determine whether exercise training could modify the changes in receptor expression associated with acclimatization. Four groups of rats were studied: normoxic sedentary rats (NS), rats living and training in normoxia (NTN), sedentary rats living in hypoxia (HS, inspired PO(2) = 110 Torr), and rats living and training in hypoxia (HTH, inspired PO(2) = 110 Torr). Training consisted of running in a treadmill at 80% of maximal O(2) uptake during 10 wk. Myocardial receptor density was measured by radioactive ligand binding. Right ventricular (RV) hypertrophy occurred in HS but not in HTH. No effect of exercise was detected in RV weight of normoxic rats. Acclimatization to hypoxia (HS vs. NS) resulted in a decrease in both alpha(1)- and beta-AR density, whereas muscarinic receptor (M-Ach) expression increased. Hypoxic exercise training (HS vs. HTH) moderated beta-AR downregulation and M-Ach upregulation and prevented the fall in alpha(1)-AR density. Normoxic training (NS vs. NTN) did not change beta-AR density. On the other hand, densities of alpha(1)-AR in both ventricles as well as RV M-Ach increased in NTN vs. NS. The data show that exercise training in hypoxia 1) prevents RV hypertrophy, 2) suppresses the downregulation of alpha(1)-AR in the left ventricle (LV) and RV, and 3) attenuates the changes in both beta-AR and M-Ach receptor density in LV and RV. Exercise training in normoxia increases M-Ach receptor expression in the RV.

Animals↗
PubMed2001

Response of nitric oxide pathway to L-arginine infusion at the altitude of 4,350 m.

It was hypothesized that hypoxia may inhibit nitric oxide (NO) production by reducing the availability of endothelial NO synthase (NOS III) substrate. To evaluate the effect of L-arginine on the NO release in high altitude, 11 subjects were infused with L-arginine (0.5 g x kg(-1)) during 30 min in normoxia and after 36 h at 4,350 m (hypoxia). The L-citrulline and cyclic guanosine monophosphate (cGMP) concentrations were measured to investigate NO synthesis and guanylyl cyclase activity respectively. L-citrulline concentration, arterial oxygen saturation (Sa,O2), systemic blood pressure, heart rate and acute mountain sickness (AMS) score were measured at rest and 15, 30 and 45 min after starting infusion. The results showed that baseline L-citrulline was lower in hypoxia (p<0.05). L-arginine infusion increased L-citrulline concentration in both conditions. However, in hypoxia L-citrulline concentration remained lower than in normoxia (p<0.05). The concentration of cGMP was lower in hypoxia (p<0.05). In hypoxia, Sa,O2 increased from 15 min after the start of the infusion to 45 min (p<0.05). Blood pressure and heart rate were not affected by L-arginine infusion. Subjects who experienced symptoms of AMS showed a slight decrease in AMS score with L-arginine. The decreased L-citrulline suggests a hypoxia-induced impairment of nitric oxide synthase III or a decrease in L-arginine availability. The improvement of arterial oxygen saturation by pretreatment with L-arginine could be ascribed to an enhancement of the ventilation/perfusion ratio. Collectively, these results are consistent with a decrease in nitric oxide production in hypoxia that could be antagonized by supplying nitric oxide synthase cosubstrate.

Adult↗
PubMed2001

Doppler study of middle cerebral artery blood flow velocity and cerebral autoregulation during a simulated ascent of Mount Everest.

OBJECTIVE: To explore cerebral hemodynamics in 8 healthy volunteers in a hypobaric chamber up to the altitude of Mount Everest after a progressive stepwise decompression to 8,848 m. METHODS: Physiological, clinical, and transcranial Doppler data were collected after at least 3 days at 5,000, 6,000, and 7,000 m and within 4 hours of reaching 8,000 m and returning to sea level. RESULTS: Three subjects were excluded at 8,000 and 8,848 m because of acute neurological deficits. Heart rate increased; mean arterial pressure remained stable; PaO2 and PaCO2 decreased with altitude; hemoglobin (Hb) and hematocrit (Ht) increased; arterial O2 content decreased over 6,000 m; middle cerebral artery blood flow velocity (MCAv) increased only during acute exposure to 8,000 m; and the corresponding pulsatility (PI) and resistivity indices (RI) decreased over 5,000 m. PI and RI correlated with heart rate. The transient hyperemic response (THR) of MCAv to common carotid compression was depressed at 8,000 m. CONCLUSIONS: At 8,000 m, the increase in MCAv seemed to reflect the normal hemodynamic response to acute hypoxia. The decrease of THR at this altitude could be an indication of impaired cerebral autoregulation. The role of impaired cerebral autoregulation in the genesis of acute neurologic deficits, observed at 8,000 m and above in 3 subjects, remains speculative.

Adult↗
PubMed2000

Operation Everest III: energy and water balance.

We hypothesized that hypoxia decreases energy intake and increases total energy requirement and, additionally, that decreased barometric pressure increases total water requirement. Energy and water balance was studied over 31 days in a hypobaric chamber at 452-253 Torr (corresponding to 4,500-8,848 m altitude), after 7 days acclimatization at 4,350 m. Subjects were eight men, age 27+/-4 years (mean+/-SD), body mass index 22.9+/-1.5 kg/m2. Food and water intake was measured with weighed dietary records, energy expenditure and water loss with labelled water. Insensible water loss was calculated as total water loss minus urinary and faecal water loss. Energy intake at normoxia was 13.6+/-1.8 MJ/d. Energy intake decreased from 10.4+/-2.1 to 8.3+/-1.9 MJ/d (P<0.001) and energy expenditure from 13.3+/-1.6 to 12.1+/-1.8 MJ/d (P<0.001) over the first and second 15-day intervals of progressive hypoxia. Absolute insensible water loss did not change (1.67+/-0.26 and 1.66+/-0.37 l/d), however, adjusted for energy expenditure it increased with ambient pressure reduction (P<0.05). In conclusion, hypoxia induced a negative energy balance, mainly by a reduction of energy intake. Overall insensible water loss was unchanged because the increase in respiratory evaporative water loss was counterbalanced by a decrease in metabolic rate that probably limited the hypoxia-induced increase in ventilation.

Acclimatization↗
PubMed2000

Operation Everest III: role of plasma volume expansion on VO(2)(max) during prolonged high-altitude exposure.

We hypothesize that plasma volume decrease (DeltaPV) induced by high-altitude (HA) exposure and intense exercise is involved in the limitation of maximal O(2) uptake (VO(2)(max)) at HA. Eight male subjects were decompressed for 31 days in a hypobaric chamber to the barometric equivalent of Mt. Everest (8,848 m). Maximal exercise was performed with and without plasma volume expansion (PVX, 219-292 ml) during exercise, at sea level (SL), at HA (370 mmHg, equivalent to 6, 000 m after 10-12 days) and after return to SL (RSL, 1-3 days). Plasma volume (PV) was determined at rest at SL, HA, and RSL by Evans blue dilution. PV was decreased by 26% (P < 0.01) at HA and was 10% higher at RSL than at SL. Exercise-induced DeltaPV was reduced both by PVX and HA (P < 0.05). Compared with SL, VO(2)(max) was decreased by 58 and 11% at HA and RSL, respectively. VO(2)(max) was enhanced by PVX at HA (+9%, P < 0.05) but not at SL or RSL. The more PV was decreased at HA, the more VO(2)(max) was improved by PVX (P < 0.05). At exhaustion, plasma renin and aldosterone were not modified at HA compared with SL but were higher at RSL, whereas plasma atrial natriuretic factor was lower at HA. The present results suggest that PV contributes to the limitation of VO(2)(max) during acclimatization to HA. RSL-induced PVX, which may be due to increased activity of the renin-aldosterone system, could also influence the recovery of VO(2)(max).

Adult↗
PubMed2000

Peripheral chemoreflex function in hyperoxia following ventilatory acclimatization to altitude.

After a period of ventilatory acclimatization to high altitude (VAH), a degree of hyperventilation persists after relief of the hypoxic stimulus. This is likely, in part, to reflect the altered acid-base status, but it may also arise, in part, from the development during VAH of a component of carotid body (CB) activity that cannot be entirely suppressed by hyperoxia. To test this hypothesis, eight volunteers undergoing a simulated ascent of Mount Everest in a hypobaric chamber were acutely exposed to 30 min of hyperoxia at various stages of acclimatization. For the second 10 min of this exposure, the subjects were given an infusion of the CB inhibitor, dopamine (3 microg. kg(-1). min(-1)). Although there was both a significant rise in ventilation (P < 0.001) and a fall in end-tidal PCO(2) (P < 0.001) with VAH, there was no progressive effect of dopamine infusion on these variables with VAH. These results do not support a role for CB in generating the persistent hyperventilation that remains in hyperoxia after VAH.

Acclimatization↗
PubMed2000

Operation Everest III (Comex '97): modifications of cardiac function secondary to altitude-induced hypoxia. An echocardiographic and Doppler study.

During Operation Everest III (Comex '97), to assess the consequences of altitude-induced hypoxia, eight volunteers were decompressed in a hypobaric chamber, with a decompression profile simulating the climb of Mount Everest. Cardiac function was assessed using a combination of M-mode and two-dimensional echocardiography, with continuous and pulsed Doppler at 5,000, 7,000, and 8,000 m as well as 2 d after return to sea level (RSL). On simulated ascent to altitude, aortic and left atrial diameters, left ventricular (LV) diameters, and right ventricular (RV) end-systolic diameter fell regularly. Heart rate (HR) increased at all altitudes accompanied by a decrease in stroke volume; in total, cardiac output (Q) remained unchanged. LV filling was assessed on transmitral and pulmonary venous flow profiles. Mitral peak E velocity decreased, peak A velocity increased, and E/A ratio decreased. Pulmonary venous flow velocities showed a decreased peak D velocity, a decreased peak S velocity, and a reduction of the D/S ratio. Systolic pulmonary arterial pressure (Ppa) showed a progressive and constant increase, as seen on the elevation of the right ventricular/right atrial (RV/RA) gradient pressure from 19.0 +/- 2.4 mm Hg at sea level up to 40.1 +/- 3.3 mm Hg at 8,000 m (p < 0.05), and remained elevated 2 d after recompression to sea level (SL) (not significant). In conclusion, this study confirmed the elevation of pulmonary pressures and the preservation of LV contractility secondary to altitude-induced hypoxia. It demonstrated a modification of the LV filling pattern, with a decreased early filling and a greater contribution of the atrial contraction, without elevation of LV end-diastolic pressure.

Adult↗