Hypoxic ventilatory response in successful extreme altitude climbers

Bernardi, Luciano; Schneider, Annette; Pomidori, Luca; Paolucci, Emily M.; Cogo, Annalisa

doi:10.1183/09031936.06.00015805

Cited by 60 publications

(62 citation statements)

References 29 publications

(37 reference statements)

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“…However, the actual mechanism for any HVR protection remains unknown, and some argue that a strong HVR may form a negative response due to diminishing ventilatory reserve (Bernardi et al, 2006). Ainslie and Poulin (2004) reported that, across individuals, a higher AHVR during acute poikilocapnic hypoxia was associated with a decrease in the acute hypoxic cerebral blood flow response, but propose that this may be due to the hyperventilation already inducing a hypocapnic-induced cerebral vasoconstriction and dampening the possibility for further responsiveness.…”

Section: Discussionmentioning

confidence: 99%

“…Ventilation rapidly increases upon acute hypoxic exposure, and this hypoxic ventilatory response (HVR) is generally presumed to enable better performance at altitude by maintaining arterial oxygen saturation levels (Schoene et al, 1984;Masuyama et al, 1986). Alternatively, a strong HVR has also been proposed to be a negative adaptation that reduces ventilatory reserve at altitude (Bernardi et al, 2006), while hyperventilation and the resultant hypocapnia may reduce cerebral blood flow (Poulin et al, 2002;Ainslie and Poulin, 2004).…”

Section: Introductionmentioning

confidence: 99%

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Ventilatory Chemosensitivity, Cerebral and Muscle Oxygenation, and Total Hemoglobin Mass Before and After a 72-Day Mt. Everest Expedition

Cheung

Mutanen²,

Karinen³

et al. 2014

High Altitude Medicine & Biology

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, cerebral and muscle oxygenation, and total hemoglobin mass before and after a 72-day Mt. Everest expedition. High Alt Med Biol 15:331-340, 2014.-Background: We investigated the effects of chronic hypobaric hypoxic acclimatization, performed over the course of a 72-day self-supported Everest expedition, on ventilatory chemosensitivity, arterial saturation, and tissue oxygenation adaptation along with total hemoglobin mass (tHb-mass) in nine experienced climbers (age 37 -6 years, _ VO 2peak 55 -7 mL$kg). Methods: Exercise-hypoxia tolerance was tested using a constant treadmill exercise of 5.5 km$h -1 at 3.8% grade (mimicking exertion at altitude) with 3-min steps of progressive normobaric poikilocapnic hypoxia. Breath-by-breath ventilatory responses, Spo 2 , and cerebral (frontal cortex) and active muscle (vastus lateralis) oxygenation were measured throughout. Acute hypoxic ventilatory response (AHVR) was determined by linear regression slope of ventilation vs. Spo 2 . PRE and POST (< 15 days) expedition, tHb-mass was measured using carbon monoxide-rebreathing. Results: Post-expedition, exercise-hypoxia tolerance improved (11:32 -3:57 to 16:30 -2:09 min, p < 0.01). AHVR was elevated (1.25 -0.33 to 1.63 -0.38 L$min -1. % -1 Spo 2 , p < 0.05). Spo 2 decreased throughout exercise-hypoxia in both trials, but was preserved at higher values at 4800 m post-expedition. Cerebral oxygenation decreased progressively with increasing exercise-hypoxia in both trials, with a lower level of deoxyhemoglobin POST at 2400, 3500 and 4800 m. Muscle oxygenation also decreased throughout exercisehypoxia, with similar patterns PRE and POST. No relationship was observed between the slope of AHVR and cerebral or muscle oxygenation either PRE or POST. Absolute tHb-mass response exhibited great individual variation with a nonsignificant 5.4% increasing trend post-expedition (975 -154 g PRE and 1025 -124 g POST, p = 0.17). Conclusions: We conclude that adaptation to chronic hypoxia during a climbing expedition to Mt. Everest will increase hypoxic tolerance, AHVR, and cerebral but not muscle oxygenation, as measured during simulated acute hypoxia at sea level. However, tHb-mass did not increase significantly and improvement in cerebral oxygenation was not associated with the change in AHVR.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Ventilatory Chemosensitivity, Cerebral and Muscle Oxygenation, and Total Hemoglobin Mass Before and After a 72-Day Mt. Everest Expedition

Cheung

Mutanen²,

Karinen³

et al. 2014

High Altitude Medicine & Biology

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“…In this context, observations from the 2004 Everest-K2 Italian Expedition are of interest. That is, those climbers who reached the summit without oxygen evidenced a lower restingV E and hypoxic ventilatory responsiveness (HVR, V E − SpO 2 ) during acclimatization (Bernardi et al, 2006); it being proposed that a less sensitive HVR at HA might increase BR and therefore reduce dyspnea to allow sustainableV E 's in the extreme hypoxia at the summit. It should be noted that the observations of Bernardi and coworkers are in contrast those of Schoene et al (1984) who observed a better climbing performance in those subjects with a higher HVR at HA.…”

Section: Ventilatory Limitation and Dyspneic Sensationmentioning

confidence: 99%

Exercise intolerance at high altitude (5050m): Critical power and W′

Valli¹,

Cogo²,

Passino³

et al. 2011

Respiratory Physiology & Neurobiology

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a b s t r a c tThe relationship between work rate (WR) and its tolerable duration (t LIM ) has not been investigated at high altitude (HA). At HA (5050 m) and at sea level (SL), six subjects therefore performed symptomlimited cycle-ergometry: an incremental test (IET) and three constant-WR tests (% of IET WR max , HA and SL respectively: WR 1 70 ± 8%, 74 ± 7%; WR 2 86 ± 14%, 88 ± 10%; WR 3 105 ± 13%, 104 ± 9%). The power asymptote (CP) and curvature constant (W ) of the hyperbolic WR-t LIM relationship were reduced at HA compared to SL (CP: 81 ± 21 vs. 123 ± 38 W; W : 7.2 ± 2.9 vs. 13.1 ± 4.3 kJ). HA breathing reserve (estimated maximum voluntary ventilation minus end-exercise ventilation) was also compromised (WR 1 : 25 ± 25 vs. 50 ± 18 l min −1 ; WR 2 : 4 ± 23 vs. 38 ± 23 l min −1 ; WR 3 : −3 ± 18 vs. 32 ± 24 l min −1 ) with nearmaximal dyspnea levels (Borg) (WR 1 : 7.2 ± 1.2 vs. 4.8 ± 1.3; WR 2 : 8.8 ± 0.8 vs. 5.3 ± 1.2; WR 3 : 9.3 ± 1.0 vs. 5.3 ± 1.5). The CP reduction is consistent with a reduced O 2 availability; that of W with reduced muscle-venous O 2 storage, exacerbated by ventilatory limitation and dyspnea.

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“…Exposure to hypoxia [e.g., high altitude; (Bernardi et al 2006;Forster et al 1971;Reeves et al 1993;Sato et al 1994) or intermittent hypoxia (Ainslie et al 2003;Garcia et al 2000;Katayama et al 1998;Levine et al 1992;Mahamed and Duffin 2001;Ricart et al 2000)] results in an elevated ventilatory sensitivity to hypoxia and subsequent hypocapnia. Studies have shown that, despite an elevation in ventilatory chemosensitivity following intermittent hypoxic exposure (IHE), there are no related gas exchange alterations during maximal exercise (Foster et al 2005;Katayama et al 2001); these findings point to a lack of ''carry-over'' effect of a hypoxic-induced elevation in ventilatory chemosensitivity on respiratory responses to normoxic exercise.…”

Section: Introductionmentioning

confidence: 99%

Effects of intermittent hypoxia on SaO2, cerebral and muscle oxygenation during maximal exercise in athletes with exercise-induced hypoxemia

Marshall

Hamlin

Hellemans³

et al. 2007

Eur J Appl Physiol

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In a placebo-controlled study, the effects of intermittent hypoxic exposures (IHE) or a placebo control for 10 days, were examined on the extent of exercise-induced hypoxemia (EIH), cerebral and muscle oxygenation (near-infrared spectroscopy) and VO(2peak). Eight athletes who had previously displayed EIH (fall in saturation of arterial oxygen (SaO(2)) of >4% from rest) during an incremental maximal exercise test, volunteered for the present research. Prior to (baseline), and 2 days following (post) the IHE or placebo, an incremental maximal exercise test was performed whilst SaO(2), heart rate, cerebral and muscle oxygenation and respiratory gas exchange were measured continuously. After IHE, but not placebo, EIH was less pronounced at VO(2peak) (IHE group, SaO(2) at VO(2peak) baseline 91.23 +/- 1.10%, post 94.10 +/- 2.19%; P < 0.01, mean +/- SD). This reduction was reflected in an increased ventilation (NS), a lower end-tidal CO(2) (P < 0.01), and lowered cerebral TOI during heavy exercise (90% VO(2peak): -6.1 +/- 6.0 Delta%, P = 0.04). Conversely, muscle tHb at maximal exercise, was increased (2.4 +/- 1.8 DeltamicroM, P = 0.01, mean +/- 95 CL) following IHE, whilst de-oxygenated Hb at 90% of VO(2peak) was reduced (-0.9 +/- 0.8 DeltamicroM, P = 0.02). These data indicate that exposure to IHE can attenuate the degree of EIH. Despite a potential compromise in cerebral oxygenation, exposure to IHE may induce some positive physiological adaptations at the muscle tissue level. We speculate that the unchanged VO(2peak) following IHE might reflect a balance between these central (cerebral) and peripheral (muscle) adaptations.

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Hypoxic ventilatory response in successful extreme altitude climbers

Cited by 60 publications

References 29 publications

Ventilatory Chemosensitivity, Cerebral and Muscle Oxygenation, and Total Hemoglobin Mass Before and After a 72-Day Mt. Everest Expedition

Ventilatory Chemosensitivity, Cerebral and Muscle Oxygenation, and Total Hemoglobin Mass Before and After a 72-Day Mt. Everest Expedition

Exercise intolerance at high altitude (5050m): Critical power and W′

Effects of intermittent hypoxia on SaO2, cerebral and muscle oxygenation during maximal exercise in athletes with exercise-induced hypoxemia

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