Work capacity in acute exposures to altitude.

Dill, D. B.; Myhre, Gunnar; Phillips, E E; Brown, Darine F.

doi:10.1152/jappl.1966.21.4.1168

Cited by 27 publications

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“…This demonstrates the presence of a time-dependent component lasting several days. In acute hypoxia, varying from a few minutes with hypoxic gas breathing to 10-60 min at 462 mmHg in a hypobaric chamber, some authors have reported no consistent lowering of the peak heart rate [4,27], whereas others found a consistent and significant decrease [28]. Subjects studied at 3823 m for 50 h experienced a 7 % reduction in maximal heart rate [29].…”

Section: Discussionmentioning

confidence: 98%

Heart rate response to hypoxic exercise: role of dopamine D2-receptors and effect of oxygen supplementation

et al. 2001

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This study examined the effects of dopamine D(2)-receptor blockade on the early decrease in maximal heart rate at high altitude (4559 m). We also attempted to clarify the time-dependent component of this reduction and the extent to which it is reversed by oxygen breathing. Twelve subjects performed two consecutive maximal exercise tests, without and with oxygen supplementation respectively, at sea level and after 1, 3 and 5 days at altitude. On each study day, domperidone (30 mg; n=6) or no medication (n=6) was given 1 h before the first exercise session. Compared with sea level, hypoxia progressively decreased the maximal heart rate from day 1 and onwards; also, hypoxia by itself increased plasma noradrenaline levels after maximal exercise. Domperidone further increased maximal noradrenaline concentrations, but had no effect on maximal heart rate. On each study day at altitude, oxygen breathing completely reversed the decrease in maximal heart rate to values not different from those at sea level. In conclusion, dopamine D(2)-receptor blockade with domperidone demonstrates that hypoxic exercise in humans activates D(2)-receptors, resulting in a decrease in circulating levels of noradrenaline. However, dopamine D(2)-receptors are not involved in the hypoxia-induced decrease in the maximal heart rate. These data suggest that receptor uncoupling, and not down-regulation, of cardiac adrenoreceptors, is responsible for the early decrease in heart rate at maximal hypoxic exercise.

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Section: Discussionmentioning

confidence: 98%

Heart rate response to hypoxic exercise: role of dopamine D2-receptors and effect of oxygen supplementation

et al. 2001

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“…In contrast, short explosive efforts, relying mainly on anaerobic metabolic pathways, are not, or much less, affected by hypoxia (Kayser et al, 1994;Roach et al, 2000;Calbet et al, 2003b;Amann and Calbet, 2008). Aerobic capacity of moderately trained individuals is decreased during both acute and chronic exposure to altitude (Dill et al, 1966;Boutellier et al, 1982;Calbet et al, 2003a;Lundby et al, 2004;Lundby et al, 2006) by *1% for each 100 m ascended *1500 m above sea level (Buskirk et al, 1967;Fulco et al, 1998). This decrease is not only more rapid at more severe hypoxia, but subjects with higher sea-level aerobic capacity also suffer earlier, that is, at lower altitudes (*600 m), and from a greater loss compared with untrained individuals (Gore et al, 1996;Ferretti et al, 1997;Roach et al, 2000;Wehrlin and Hallen, 2005).…”

Section: Introductionmentioning

confidence: 99%

Nervous System Function during Exercise in Hypoxia

Amann

Kayser

2009

High Altitude Medicine & Biology

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Aerobic exercise capacity decreases with exposure to hypoxia. This article focuses on the effects of hypoxia on nervous system function and the potential consequences for the exercising human. Emphasis is put on somatosensory muscle afferents due to their crucial role in the reflex inhibition of muscle activation and in cardiorespiratory reflex control during exercise. We review the evidence of hypoxia influences on muscle afferents and discuss important consequences for exercise performance. Efferent (motor) nerves are less affected at altitude and are thought to stay fairly functional even in severe levels of arterial hypoxemia. Altitude also alters autonomic nervous system functions, which are thought to play an important role in the regulation of cardiac output and ventilation. Finally, the consequences of hypoxia-induced cortical adaptations and dysfunctions are evaluated in terms of neurotransmitter turnover, brain electrical activity, and cortical excitability. Even though the cessation of exercise or the reduction of exercise intensity, when reaching maximum performance, implies reduced motor recruitment by the nervous system, the mechanisms that lead to the de-recruitment of active muscle are still not well understood. In moderate hypoxia, muscle afferents appear to play an important role, whereas in severe hypoxia brain oxygenation may play a more important role.

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“…Their model predicts a 25% reduction from 1,600 to 4,350 m for subjects in this study, well above 15.5%. Reports based on a few subjects have noted that VO 2 max was higher upon acute (30 min) altitude exposure when compared with several days of acclimatization in spite of higher V E during exercise in the latter (8,9). Perhaps, a longer exposure (e.g., to 24 h) to 455 mmHg prior to exercise in this study would have reduced VO 2 max toward the predicted value.…”

Section: Discussionmentioning

confidence: 50%

“…Maher et al (22) reported a 32% reduction on day 2 which returned minimally after remaining 10 days at 458 mmHg. Average data from Dill et al (9) showed a 15% decrease at 455 mmHg in four subjects after less than 1 h. Reeves et al (29) reported an insignificant drop in five young males on the second day after ascent from 734 to 530 mmHg, suggesting that the altitude may have been too low to induce sufficient hypocapnia because the PaO 2 measured in two subjects was near 60 mmHg, the threshold of hypoxemia required for V E to respond (28). The range in values of V E STPD attenuation in these reports indicates that it depends on the magnitude of the (11) pressure change, the length of the time and the rate of the pressure drop before measurements are made, the subjects' hypoxic chemosensitivity, and the intensity of the exercise where measurements are made.…”

Section: Discussionmentioning

confidence: 99%

“…Observations after acute exposures have been reported by Stenberg et al (31) and Elliott et al (10); their data show that in spite of the early increase of V E BTPS at 462 and 406 mmHg, respectively, the V E STPD/VO 2 ratio was lower than at sea level during steady-state submaximal workloads and at VO 2 max by ≈20%. Other reports contain serial measurements after 1-3 days and later after acclimatization (9,14,22,29). Lower resting V E STPD during the first day at altitude compared with pre-ascent and subsequent measurements 3-4 days later have also been reported, suggesting early transient hypoxic ventilatory depression and progressive hypocapnia (16).…”

Section: Introductionmentioning

confidence: 99%

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V_ESTPD as a measure of ventilatory acclimatization to hypobaric hypoxia

Loeppky

Sheard

Salgado

et al. 2016

Physiology International

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This study compared the ventilation response to an incremental ergometer exercise at two altitudes: 633 mmHg (resident altitude = 1,600 m) and following acute decompression to 455 mmHg (≈4,350 m altitude) in eight male cyclists and runners. At 455 mmHg, the V E STPD at RER <1.0 was significantly lower and the V E BTPS was higher because of higher breathing frequency; at VO 2 max, both V E STPD and V E BTPS were not significantly different. As percent of VO 2 max, the V E BTPS was nearly identical and V E STPD was 30% lower throughout the exercise at 455 mmHg. The lower V E STPD at lower pressure differs from two classical studies of acclimatized subjects (Silver Hut and OEII), where V E STPD at submaximal workloads was maintained or increased above that at sea level. The lower V E STPD at 455 mmHg in unacclimatized subjects at submaximal workloads results from acute respiratory alkalosis due to the initial fall in HbO 2 (≈0.17 pHa units), reduction in PACO 2 (≈5 mmHg) and higher PAO 2 throughout the exercise, which are partially pre-established during acclimatization. Regression equations from these studies predict V E STPD from VO 2 and P B in unacclimatized and acclimatized subjects. The attainment of ventilatory acclimatization to altitude can be estimated from the measured vs. predicted difference in V E STPD at low workloads after arrival at altitude.

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Work capacity in acute exposures to altitude.

Cited by 27 publications

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Heart rate response to hypoxic exercise: role of dopamine D2-receptors and effect of oxygen supplementation

Heart rate response to hypoxic exercise: role of dopamine D2-receptors and effect of oxygen supplementation

Nervous System Function during Exercise in Hypoxia

V_ESTPD as a measure of ventilatory acclimatization to hypobaric hypoxia

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Work capacity in acute exposures to altitude.

Cited by 27 publications

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Heart rate response to hypoxic exercise: role of dopamine D2-receptors and effect of oxygen supplementation

Heart rate response to hypoxic exercise: role of dopamine D2-receptors and effect of oxygen supplementation

Nervous System Function during Exercise in Hypoxia

VESTPD as a measure of ventilatory acclimatization to hypobaric hypoxia

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Resources

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V_ESTPD as a measure of ventilatory acclimatization to hypobaric hypoxia