Operation Everest II: maximal oxygen uptake at extreme altitude

1989 ◽  
Vol 66 (5) ◽  
pp. 2446-2453 ◽  
Author(s):  
A. Cymerman ◽  
J. T. Reeves ◽  
J. R. Sutton ◽  
P. B. Rock ◽  
B. M. Groves ◽  
...  
Keyword(s):  
Sea Level ◽  
Chronic Hypoxia ◽  
Rank Order ◽  
Minute Ventilation ◽  
Barometric Pressure ◽  
Arterial Pco2 ◽  
Altitude Exposure ◽  
Extreme Altitude ◽  
Maximum Effort ◽  
Arterial O2 Saturation

Chronic exposure to high altitude reduces maximal O2 uptake (VO2max). At extreme altitudes approaching the summit of Mt. Everest [inspiratory PO2(PIO2) = 43 Torr], mean VO2max have been determined to be 15.3 ml.kg-1.min-1 in two subjects who breathed 14% O2 at 6,300 m on Mt. Everest (West et al., J. Appl. Physiol. 54: 1188–1194, 1983). To provide a more complete description of performance near the limits of human tolerance to chronic hypoxia, we measured VO2max in volunteers in an altitude chamber before, during, and after a 40-day decompression to a barometric pressure (PB) of 240 Torr (PIO2 = 43 Torr). In five of eight subjects studied at sea level and PB of 464, 347, 289, and 240 Torr, VO2max was reduced from 4.13 to 1.17 l/min (49.1–15.3 ml.kg-1.min-1) in agreement with the prior study. Although the range decreased, the rank order among the subjects was preserved. Arterial O2 saturation at maximum effort decreased (46% by ear oximetry), but minute ventilation, respiratory frequency, and tidal volume did not. The highest minute ventilation (201 l/min BTPS) was observed at PB of 464 Torr. Arterial PCO2 in three subjects at PB of 240 Torr, at rest, and with maximum effort, averaged 10.3 and 9.6 Torr, respectively. Sustained hyperventilation was crucial to exercise performance during chronic, severe hypoxemia. VO2max was lower after altitude exposure compared with initial sea level values, indicating that exposure had not improved sea level exercise capacity.

Effects of sleep state on ventilatory acclimatization to hypoxia in humans

1984 ◽  
Vol 57 (4) ◽  
pp. 1089-1096 ◽  
Author(s):  
A. D. Berssenbrugge ◽  
J. A. Dempsey ◽  
J. B. Skatrud
Keyword(s):  
Eye Movement ◽  
Chronic Hypoxia ◽  
Minute Ventilation ◽  
Barometric Pressure ◽  
Nrem Sleep ◽  
Hypoxic Exposure ◽  
Adult Males ◽  
Sleep State ◽  
Co2 Partial Pressure ◽  
Arterial O2 Saturation

We assessed the influence of sleep state on ventilatory acclimatization to hypoxia. Ventilation, arterial O2 saturation (SaO2), and arterial acid-base status were monitored in healthy adult males during wakefulness, nonrapid-eye-movement (NREM) sleep, and rapid-eye-movement (REM) sleep in normoxia [barometric pressure (PB) = 740 Torr] and over 4 continuous days of hypobaric hypoxia (PB = 455 Torr). The relative hypoventilation observed during sleep compared with wakefulness in normoxia was also observed during all stages of hypoxic acclimatization. The characteristic time-dependent changes associated with acclimatization to chronic hypoxia were similar during wakefulness and all sleep states: 1) arterial CO2 partial pressure (PaCO2) decreased 27–31% by night 4 with approximately half of this fall occurring acutely (0.3–3 h hypoxia); 2) minute ventilation increased progressively with duration of hypoxic exposure including increased levels of hyperventilation throughout the initial night of sleep in hypoxia; 3) SaO2 was lowest acutely and gradually increased coincident with the progressive hyperventilation; and 4) pHa increased acutely and remained unchanged despite additional hyperventilation due to a compensatory reduction in [HCO3-]a. In addition, in the acclimatized subject hyperventilation persisted following acute restoration of normoxia, and this continued hyperventilation was similar in magnitude during both wakefulness and NREM sleep. These results indicate that suprapontine influences on ventilatory control associated with the state of wakefulness are not required in the process of ventilatory acclimatization to chronic hypoxia.

Oxygen transport to exercising leg in chronic hypoxia

1988 ◽  
Vol 65 (6) ◽  
pp. 2592-2597 ◽  
Author(s):  
P. R. Bender ◽  
B. M. Groves ◽  
R. E. McCullough ◽  
R. G. McCullough ◽  
S. Y. Huang ◽  
...  
Keyword(s):  
Blood Flow ◽  
Sea Level ◽  
Chronic Hypoxia ◽  
Peripheral Resistance ◽  
Hemoglobin Concentration ◽  
Barometric Pressure ◽  
Ambient Air ◽  
Leg Blood Flow ◽  
State Cycle ◽  
O2 Delivery

Residence at high altitude could be accompanied by adaptations that alter the mechanisms of O2 delivery to exercising muscle. Seven sea level resident males, aged 22 +/- 1 yr, performed moderate to near-maximal steady-state cycle exercise at sea level in normoxia [inspired PO2 (PIO2) 150 Torr] and acute hypobaric hypoxia (barometric pressure, 445 Torr; PIO2, 83 Torr), and after 18 days' residence on Pikes Peak (4,300 m) while breathing ambient air (PIO2, 86 Torr) and air similar to that at sea level (35% O2, PIO2, 144 Torr). In both hypoxia and normoxia, after acclimatization the femoral arterial-iliac venous O2 content difference, hemoglobin concentration, and arterial O2 content, were higher than before acclimatization, but the venous PO2 (PVO2) was unchanged. Thermodilution leg blood flow was lower but calculated arterial O2 delivery and leg VO2 similar in hypoxia after vs. before acclimatization. Mean arterial pressure (MAP) and total peripheral resistance in hypoxia were greater after, than before, acclimatization. We concluded that acclimatization did not increase O2 delivery but rather maintained delivery via increased arterial oxygenation and decreased leg blood flow. The maintenance of PVO2 and the higher MAP after acclimatization suggested matching of O2 delivery to tissue O2 demands, with vasoconstriction possibly contributing to the decreased flow.

Time course of augmentation and depression of hypoxic ventilatory responses at altitude

1994 ◽  
Vol 77 (1) ◽  
pp. 313-316 ◽  
Author(s):  
M. Sato ◽  
J. W. Severinghaus ◽  
P. Bickler
Keyword(s):  
Pulse Oximetry ◽  
Sea Level ◽  
Time Course ◽  
Ventilatory Response ◽  
Barometric Pressure ◽  
Hypoxic Ventilatory Response ◽  
Set Point ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Arterial O2 Saturation

Hypoxic ventilatory response (HVR) and hypoxic ventilatory depression (HVD) were measured in six subjects before, during, and after 12 days at 3,810-m altitude (barometric pressure approximately 488 Torr) with and without 15 min of preoxygenation. HVR was tested by 5-min isocapnic steps to 75% arterial O2 saturation measured by pulse oximetry (Spo2) at an isocapnic PCO2 (P*CO2) chosen to set hyperoxic resting ventilation to 140 ml.kg-1.min-1. Hypercapnic ventilatory response (HCVR, 1.min-1.Torr-1) was tested at ambient and high SPO2 6–8 min after a 6- to 10-Torr step increase of end-tidal PCO2 (PETCO2) above P*CO2. HCVR was independent of preoxygenation and was not significantly increased at altitude (when corrected to delta logPCO2). Preoxygenated HVR rose from -1.13 +/- 0.23 (SE) l.min-1.%SPO2(-1) at sea level to -2.17 +/- 0.13 by altitude day 12, without reaching a plateau, and returned to control after return to sea level for 4 days. Ambient HVR was measured at P*CO2 by step reduction of SPO2 from its ambient value (86–91%) to approximately 75%. Ambient HVR slope was not significantly less, but ventilation at equal levels of SPO2 and PCO2 was lower by 13.3 +/- 2.4 l/min on day 2 (SPO2 = 86.2 +/- 2.3) and by 5.9 +/- 3.5 l/min on day 12 (SPO2 = 91.0 +/- 1.5; P < 0.05). This lower ventilation was estimated (from HCVR) to be equivalent to an elevation of the central chemoreceptor PCO2 set point of 9.2 +/- 2.1 Torr on day 2 and 4.5 +/- 1.3 on day 12.(ABSTRACT TRUNCATED AT 250 WORDS)

Augmented hypoxic ventilatory response in men at altitude

1992 ◽  
Vol 73 (1) ◽  
pp. 101-107 ◽  
Author(s):  
M. Sato ◽  
J. W. Severinghaus ◽  
F. L. Powell ◽  
F. D. Xu ◽  
M. J. Spellman
Keyword(s):  
Sea Level ◽  
Ventilatory Response ◽  
Hypoxic Ventilatory Response ◽  
Co2 Response ◽  
Altitude Exposure ◽  
Arterial Ph ◽  
Ventilatory Drive ◽  
Normal Males ◽  
End Tidal ◽  
Arterial O2 Saturation

To test the hypothesis that the hypoxic ventilatory response (HVR) of an individual is a constant unaffected by acclimatization, isocapnic 5-min step HVR, as delta VI/delta SaO2 (l.min-1.%-1, where VI is inspired ventilation and SaO2 is arterial O2 saturation), was tested in six normal males at sea level (SL), after 1–5 days at 3,810-m altitude (AL1-3), and three times over 1 wk after altitude exposure (PAL1-3). Equal medullary central ventilatory drive was sought at both altitudes by testing HVR after greater than 15 min of hyperoxia to eliminate possible ambient hypoxic ventilatory depression (HVD), choosing for isocapnia a P′CO2 (end tidal) elevated sufficiently to drive hyperoxic VI to 140 ml.kg-1.min-1. Mean P′CO2 was 45.4 +/- 1.7 Torr at SL and 33.3 +/- 1.8 Torr on AL3, compared with the respective resting control end-tidal PCO2 of 42.3 +/- 2.0 and 30.8 +/- 2.6 Torr. SL HVR of 0.91 +/- 0.38 was unchanged on AL1 (30 +/- 18 h) at 1.04 +/- 0.37 but rose (P less than 0.05) to 1.27 +/- 0.57 on AL2 (3.2 +/- 0.8 days) and 1.46 +/- 0.59 on AL3 (4.8 +/- 0.4 days) and remained high on PAL1 at 1.44 +/- 0.54 and PAL2 at 1.37 +/- 0.78 but not on PAL3 (days 4–7). HVR was independent of test SaO2 (range 60–90%). Hyperoxic HCVR (CO2 response) was increased on AL3 and PAL1. Arterial pH at congruent to 65% SaO2 was 7.378 +/- 0.019 at SL, 7.44 +/- 0.018 on AL2, and 7.412 +/- 0.023 on AL3.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Muscle tissue adaptations of high-altitude natives to training in chronic hypoxia or acute normoxia

1996 ◽  
Vol 81 (5) ◽  
pp. 1946-1951 ◽  
Author(s):  
D. Desplanches ◽  
H. Hoppeler ◽  
L. Tüscher ◽  
M. H. Mayet ◽  
H. Spielvogel ◽  
...  
Keyword(s):  
High Altitude ◽  
Sea Level ◽  
Muscle Tissue ◽  
Chronic Hypoxia ◽  
Citrate Synthase ◽  
Vastus Lateralis ◽  
Training Session ◽  
Barometric Pressure ◽  
Vastus Lateralis Muscle ◽  
High Altitude Natives

Desplanches, D., H. Hoppeler, L. Tüscher, M. H. Mayet, H. Spielvogel, G. Ferretti, B. Kayser, M. Leuenberger, A. Grünenfelder, and R. Favier. Muscle tissue adaptations of high-altitude natives to training in chronic hypoxia or acute normoxia. J. Appl. Physiol. 81(5): 1946–1951, 1996.—Twenty healthy high-altitude natives, residents of La Paz, Bolivia (3,600 m), participated in 6 wk of endurance exercise training on bicycle ergometers, 5 times/wk, 30 min/session, as previously described in normoxia-trained sea-level natives (H. Hoppeler, H. Howald, K. E. Conley, S. L. Lindstedt, H. Claassen, P. Vock, and E. R. Weibel. J. Appl. Physiol. 59: 320–327, 1985). A first group of 10 subjects was trained in chronic hypoxia (HT; barometric pressure = 500 mmHg; inspired O2fraction = 0.209); a second group of 10 subjects was trained in acute normoxia (NT; barometric pressure = 500 mmHg; inspired O2 fraction = 0.314). The workloads were adjusted to ∼70% of peak O2 consumption (V˙o 2 peak) measured either in hypoxia for the HT group or in normoxia for the NT group.V˙o 2 peak determination and biopsies of the vastus lateralis muscle were taken before and after the training program.V˙o 2 peak in the HT group was increased (14%) in a way similar to that in NT sea-level natives with the same protocol. Moreover,V˙o 2 peak in the NT group was not further increased by additional O2 delivery during the training session. HT or NT induced similar increases in muscle capillary-to-fiber ratio (26%) and capillary density (19%) as well as in the volume density of total mitochondria and citrate synthase activity (45%). It is concluded that high-altitude natives have a reduced capillarity and muscle tissue oxidative capacity; however, their training response is similar to that of sea-level residents, independent of whether training is carried out in hypobaric hypoxia or hypobaric normoxia.

Maximal work capacity of women during acute hypoxia

1979 ◽  
Vol 47 (6) ◽  
pp. 1223-1227 ◽  
Author(s):  
J. A. Wagner ◽  
D. S. Miles ◽  
S. M. Horvath ◽  
J. A. Reyburn
Keyword(s):  
Oxygen Uptake ◽  
Sea Level ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Work Capacity ◽  
Men And Women ◽  
Oxygen Pulse ◽  
Altitude Exposure ◽  
Plasma Volume Shifts ◽  
Bicycle Work

Six healthy women (22--34 yr of age) performed maximal bicycle work in a hypobaric chamber at sea level and at simulated altitudes of 2,130 and 3,050 m (barometric pressures, 758, 586, and 523 Torr). Maximal oxygen uptake (VO2max) decreased 10 and 15% from sea-level values at 2,130 and 3,050 m, respectively. At these altitudes minute ventilation (VEBTPS) increased 17 and 22% respectively, a consequence of increased respiratory rate (fR). Respiratory exchange ratios increased 10 and 14%, and oxygen pulse decreased 9 and 12%, respectively, at 2,130 and 3,050 m. Maximal blood lactates, heart rates, cardiac outputs, and plasma volume shifts were unaffected by these altitudes. Although during maximal work the percentage increases in VEBTPS, fR, and R that resulted from altitude exposure were greater in women than those previously reported for men, the decrements in VO2max were comparable to those in men. The results show that relative to their performance at sea level, men and women have equal ability to perform maximal work at altitudes up to 3,050 m.

Mechanisms of improved arterial oxygenation after peripheral chemoreceptor stimulation during hypoxic exercise

1993 ◽  
Vol 74 (4) ◽  
pp. 1666-1671 ◽  
Author(s):  
R. Naeije ◽  
C. Melot ◽  
G. Niset ◽  
M. Delcroix ◽  
P. D. Wagner
Keyword(s):  
Minute Ventilation ◽  
Right Heart Catheterization ◽  
Heart Catheterization ◽  
Peripheral Chemoreceptor ◽  
Pulmonary Hemodynamics ◽  
Arterial Pco2 ◽  
Fractional Concentration ◽  
Before And After ◽  
Arterial O2 Saturation ◽  
Hypoxic Exercise

Almitrine, a peripheral chemoreceptor agonist, has been reported to increase arterial O2 saturation (SaO2) without changing minute ventilation (VE) during hypoxic exercise (Giesbrecht et al. J. Appl. Physiol. 70: 1770–1774, 1991). To explain this finding, we studied pulmonary hemodynamics (right heart catheterization) and gas exchange (multiple inert gas elimination technique) in six healthy volunteers at rest and during heavy exercise in normobaric normoxia (fractional concentration of O2 in inspired air 0.21) or hypoxia (fractional concentration of O2 in inspired air 0.125), before and after 75 mg of almitrine taken orally. During normoxic exercise, at a mean O2 uptake (VO2) of 4.0 l/min, almitrine increased arterial PO2 (PaO2) (P < 0.05), SaO2 (P < 0.01), and VE (P < 0.05) and decreased arterial PCO2 (P < 0.01), without affecting pulmonary hemodynamics or ventilation-perfusion distributions. During hypoxic exercise, at a mean VO2 of 3.0 l/min, almitrine increased SaO2 (P < 0.01) and VE (P < 0.01) and decreased arterial PCO2 (P < 0.05), with no effect on PaO2 or on ventilation-perfusion distributions and with a slight pulmonary vasoconstriction (P < 0.01). Almitrine during hypoxia did not affect cardiac output or calculated O2 diffusing capacity, but it did increase the slope of the VE/VO2 relationship (P < 0.01). We conclude that during hypoxic exercise, a pharmacological stimulation of the peripheral chemoreceptors improves SaO2 but not PaO2 by means of increased ventilation and an associated leftward shift of the oxyhemoglobin dissociation curve.

Adrenergic status of humans during prolonged exposure to the altitude of 6,542 m

1994 ◽  
Vol 76 (3) ◽  
pp. 1055-1059 ◽  
Author(s):  
A. M. Antezana ◽  
R. Kacimi ◽  
J. L. Le Trong ◽  
M. Marchal ◽  
I. Abousahl ◽  
...  
Keyword(s):  
Adrenergic Receptors ◽  
Prolonged Exposure ◽  
Plasma Norepinephrine ◽  
Maximal Heart Rate ◽  
Maximal Dose ◽  
Chronotropic Response ◽  
Altitude Exposure ◽  
Extreme Altitude ◽  
Arterial O2 Saturation ◽  
Made In

Plasma norepinephrine (NE) concentration increases with altitude exposure while maximal heart rate (HR) and chronotropic response to isoproterenol (IP) are blunted. Downregulation of cardiac beta-adrenergic receptors (beta-AR) has been evoked to explain this phenomenon. Chronotropic response was studied at extreme altitude in 10 subjects (4 women, 6 men; aged 35 +/- 6 yr). Observations were made in normoxia (N) and after 1 (H1) and 3 (H3) wk at 6,542 m. Acclimatization was accomplished by gradual climbing from 4,000 to 6,542 m over 10 days. Plasma NE was obtained at rest and during submaximal exercise. Successive doses of IP (0.02, 0.04, and 0.06 microgram/kg-1.min-1) were infused for 5 min each. Density and affinity of lymphocyte beta 2-AR were also measured. Increase in HR for maximal dose of IP decreased from 57 +/- 12 to 34 +/- 7 and 37 +/- 10 min-1 in H1 and H3, respectively (P < 0.001 for both). IP dose for which HR rises by 25 min-1 (I25) increased from 27 +/- 5 in N to 42 +/- 10 and 43 +/- 17 ng.kg-1.min-1 in H1 and H3, respectively (P < 0.001 for both). Arterial O2 saturation at rest was 98 +/- 2% in N, 72 +/- 6% in H1 (P < 0.001), and 79 +/- 5% in H3 (P < 0.001). The chronotropic response was neither restored nor further attenuated after 3 wk at 6,542 m. Plasma NE levels at rest and during exercise were higher at 6,542 m than values obtained in previous studies at 4,350 and 4,800 m.(ABSTRACT TRUNCATED AT 250 WORDS)

Maximal exercise performance in chronic hypoxia and acute normoxia in high-altitude natives

1995 ◽  
Vol 78 (5) ◽  
pp. 1868-1874 ◽  
Author(s):  
R. Favier ◽  
H. Spielvogel ◽  
D. Desplanches ◽  
G. Ferretti ◽  
B. Kayser ◽  
...  
Keyword(s):  
High Altitude ◽  
Chronic Hypoxia ◽  
Acute Hypoxia ◽  
Bicycle Ergometer ◽  
La Paz ◽  
Altitude Exposure ◽  
Exercise Ventilation ◽  
High Altitude Natives ◽  
The Difference ◽  
Arterial O2 Saturation

Maximal O2 uptake (VO2max) was determined on a bicycle ergometer in chronic hypoxia (CH) and during acute exposure to normoxia (AN) in 50 healthy young men who were born and had lived at 3,600 m altitude (La Paz, Bolivia). VO2max was significantly improved (approximately 8%) by AN. However, the difference in VO2max measured in CH and AN (delta VO2max) was lower than that reported in sea-level natives (SN) who exercised in chronic normoxia and acute hypoxia. It is shown that high-altitude natives (HN) and SN have a similar VO2max in normoxia, but highlanders can attain a greater VO2max when O2 availability is reduced by altitude exposure. In addition, in HN, the higher the subject's VO2max in hypoxia, the smaller his delta VO2max. These results contrast with the data obtained in 14 lowlanders acclimatized to high altitude who showed that their delta VO2max was positively related to their VO2max in hypoxia, as previously reported in SN who exercised in acute hypoxia (A. J. Young, A. Cymerman, and R. L. Burse. Eur. J. Appl. Physiol. Occup. Physiol. 54: 12–15, 1985). Furthermore, arterial O2 saturation of HN behaved differently from acclimatized lowland natives, inasmuch as it fell less during exercise both in CH and AN. HN with high aerobic capacity display a lower exercise ventilation and a reduced arterial saturation, which could explain their inability to improve VO2max with normoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Improvement in lung diffusion by endothelin A receptor blockade at high altitude

2012 ◽  
Vol 112 (1) ◽  
pp. 20-25 ◽  
Author(s):  
Claire de Bisschop ◽  
Jean-Benoit Martinot ◽  
Gil Leurquin-Sterk ◽  
Vitalie Faoro ◽  
Hervé Guénard ◽  
...  
Keyword(s):  
High Altitude ◽  
Sea Level ◽  
Exercise Capacity ◽  
Barometric Pressure ◽  
Membrane Component ◽  
Alveolar Volume ◽  
Double Blind ◽  
Lung Diffusion ◽  
Endothelin A Receptor ◽  
Endothelin A

Lung diffusing capacity has been reported variably in high-altitude newcomers and may be in relation to different pulmonary vascular resistance (PVR). Twenty-two healthy volunteers were investigated at sea level and at 5,050 m before and after random double-blind intake of the endothelin A receptor blocker sitaxsentan (100 mg/day) vs. a placebo during 1 wk. PVR was estimated by Doppler echocardiography, and exercise capacity by maximal oxygen uptake (V̇o2 max). The diffusing capacities for nitric oxide (DLNO) and carbon monoxide (DLCO) were measured using a single-breath method before and 30 min after maximal exercise. The membrane component of DLCO (Dm) and capillary volume (Vc) was calculated with corrections for hemoglobin, alveolar volume, and barometric pressure. Altitude exposure was associated with unchanged DLCO, DLNO, and Dm but a slight decrease in Vc. Exercise at altitude decreased DLNO and Dm. Sitaxsentan intake improved V̇o2 max together with an increase in resting and postexercise DLNO and Dm. Sitaxsentan-induced decrease in PVR was inversely correlated to DLNO. Both DLCO and DLNO were correlated to V̇o2 max at sea level ( r = 0.41–0.42, P < 0.1) and more so at altitude ( r = 0.56–0.59, P < 0.05). Pharmacological pulmonary vasodilation improves the membrane component of lung diffusion in high-altitude newcomers, which may contribute to exercise capacity.

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