Effect of changes in arterial oxygen content on circulation and physical performance

Ekblom, Björn; Huot, Roger; Stein, Emanuel; Thorstensson, Alf

doi:10.1152/jappl.1975.39.1.71

Cited by 160 publications

(88 citation statements)

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“…This assumption has got experimental support in acute normobaric hypoxia (Stenberg et al 1966;Hartley, Vogel & Landowne, 1973;Ekblom, Huot, Stein & Thorstensson, 1975), which is the condition prevailing in the present study, but not in chronic hypobaric hypoxia, such as after altitude acclimatization (Pugh, 1964;Cerretelli, 1976). In the latter case maximal cardiac output is reduced, so that the decrease of o02,max in hypoxia may be greater than that of Sa°2 as suggested by West et al (1983), even though the shape of the oxygen equilibrium curve may determine the non-linear decrease of V02maX also in chronic hypobaric hypoxia.…”

Section: Discussionmentioning

confidence: 94%

The decrease of maximal oxygen consumption during hypoxia in man: a mirror image of the oxygen equilibrium curve.

Ferretti¹,

Moia²,

Thomet³

et al. 1997

The Journal of Physiology

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1. Endurance athletes (E) undergo a marked reduction of arterial 02 saturation (Sa02) at maximal exercise in normoxia, which disappears when they breathe hyperoxic mixtures. In addition, at a given level of hypoxia, the drop in maximal 02 consumption (T42max) is positively related to the individual normoxic V02,max. 2. These data suggest that the curve relating V02,max to P1I02 may be steeper and perhaps less curved in E than in sedentary subjects (S) with low Vo2 max values because of the greater hypoxaemia in the latter, whence the hypotheses that (i) the relationship between V02 max and PI,02 may be set by the shape of the oxygen equilibrium curve; and (ii) the differences between E and S may be due to the different position on the oxygen equilibrium curve on which these subjects operate. These hypotheses have been tested by performing a systematic comparison of the Vo2 max or 5a,02 VS. PI02 relationships in E and S.3. On ten subjects (five S and five E), V02 max was measured by standard procedure during cycloergometric exercise. Sa°2 was measured by finger-tip infrared oximetry. Arterialized blood P02 (Pa,o2) and Pco2 (Pa,co2) were determined in 80 #1 blood samples from an ear lobe. The subjects breathed ambient air or a N2-02 mixture with an inspired 02 fraction (FIj 02) of 0 30, 0-18, 016, 013 and 0 11, respectively. V2,max was normalized with respect to that obtained at the highest F 02.4. The relationships between Sao02 or normalized I 2,max and FI A (or PL02) had similar shapes, the data for E being systematically below and significantly different from those for S. Linear relationships between 2ao°and normalized '42,max, statistically equal between E and S, were found.5. We conclude that the relationships between either V02,max or Sa.O2 and FI A (or Pa,o2) may indeed be the mirror images of one another, implying a strict link between the decrease of V2,max in hypoxia and the shape of the oxygen equilibrium curve, as hypothesized.The classical non-linear relationship between maximal oxygen consumption (V0, max) and inspired oxygen partial pressure (PI 2) in hypoxia

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Section: Discussionmentioning

confidence: 94%

The decrease of maximal oxygen consumption during hypoxia in man: a mirror image of the oxygen equilibrium curve.

Ferretti¹,

Moia²,

Thomet³

et al. 1997

The Journal of Physiology

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“…Increasing the COHb should have no effect on arterial P02 (4,30). However, as with anemia (31), the capillary and venous Po2 should be decreased at submaximal work rates (4) since the increase in blood flow is compensatory and does not completely adjust for the reduced 02 flow caused by the increased COHb.…”

Section: Resultsmentioning

confidence: 99%

Evidence that diffusion limitation determines oxygen uptake kinetics during exercise in humans.

Koike

Wasserman²,

McKenzie³

et al. 1990

J. Clin. Invest.

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To determine the role of arterial 02 content on the mechanism of muscle 02 utilization, we studied the effect of 2, 11, and 20% carboxyhemoglobin (COHb) on 02 uptake (V02), and CO2 output (VCO2) kinetics in response to 6 min of constant moderate-and heavy-intensity cycle exercise in 10 subjects. Increased COHb did not affect resting heart rate, V02 or VC02. Also, the COHb did not affect the asymptotic V02 in response to exercise. However, V02 and VCO2 kinetics were affected differently. The time constant (TC) of V02 significantly increased with increased COHb for both moderate and heavy work intensities. V02 TC was positively correlated with blood lactate. In contrast, VCO2 TC was negatively correlated with increased COHb for the moderate but unchanged for the heavy work intensity. The gas exchange ratio reflected a smaller increase in CO2 stores and faster VCO2 kinetics relative to V02 with increased COHb. These changes can be explained by compensatory cardiac output (heart rate) increase in response to reduced arterial 02 content. The selective slowing of V02 kinetics, with decreased blood 02 content and increased cardiac output, suggests that 02 is diffusion limited at the levels of exercise studied. (J. Clin. Invest. 1990Invest. . 86:1698Invest. -1706

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“…Maximal exercise performance and oxygen uptake (V O 2 ) are reduced in the hypoxic environment at altitude or with simulated hypobaric or normobaric hypoxia (46,63). On the other hand, oxygen-enriched air [normobaric hyperoxia, increased fraction of inspired oxygen (FI O 2 )] may enhance exercise performance in healthy individuals and, potentially to an even higher extent, in patients with respiratory diseases associated with exercise-induced hypoxemia, such as pulmonary hypertension (PH) (12). Thus studies on the effect of breathing oxygen-enriched air near sea level on exercise performance in healthy individuals and in patients with respiratory disease may help to identify mechanisms involved in exercise limitation in normoxia and in the hypoxic environment at altitude.…”

Section: Introductionmentioning

confidence: 99%

“…Studies revealed that, with acute exposure to hypoxia, the cardiac output was increased at low workloads, along with a higher heart rate, which was attributed to a combined inhibition of ␤-adrenergic and muscarinic receptors (57). At altitude, the maximal work rate, the maximal V O 2 (V O 2max ), heart rate, and cardiac output were all decreased in comparison to sea level (12,74), whereas there was little change in the relationship between these variables (38,49). Whether the reduced maximal cardiac output at altitude is a cause or consequence of the decreased V O 2 remains uncertain (73).…”

Section: Introductionmentioning

confidence: 99%

Effect of hypoxia and hyperoxia on exercise performance in healthy individuals and in patients with pulmonary hypertension: a systematic review

Ulrich

Schneider

Bloch

2017

Journal of Applied Physiology

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Exercise performance is determined by oxygen supply to working muscles and vital organs. In healthy individuals, exercise performance is limited in the hypoxic environment at altitude, when oxygen delivery is diminished due to the reduced alveolar and arterial oxygen partial pressures. In patients with pulmonary hypertension, exercise performance is already reduced near sea level due to impairments of the pulmonary circulation and gas exchange and, presumably, these limitations are more pronounced at altitude. In studies performed near sea level in healthy subjects as well as in patients with pulmonary hypertension (PH) maximal performance during progressive ramp exercise and endurance of submaximal constant load exercise were substantially enhanced by breathing oxygen-enriched air. Both in healthy individuals and in PH-patients these improvements were mediated by a better arterial, muscular and cerebral oxygenation along with a reduced sympathetic excitation, as suggested by the reduced heart rate and alveolar ventilation at submaximal isoloads, and an improved pulmonary gas exchange efficiency, especially in patients with PH. In summary, in healthy individuals and in patients with pulmonary hypertension, alterations in the inspiratory PO2 by exposure to hypobaric hypoxia or normobaric hyperoxia reduce or enhance exercise performance, respectively, by modifying oxygen delivery to the muscles and the brain, by effects on cardiovascular and respiratory control and by alterations in pulmonary gas exchange. The understanding of these physiologic mechanisms helps counselling individuals planning altitude or air travel and prescribing oxygen therapy to patients with pulmonary hypertension. is determined by oxygen supply to working muscles and vital organs. In healthy individuals, exercise performance is limited in the hypoxic environment at altitude, when oxygen delivery is diminished due to the reduced alveolar and arterial oxygen partial pressures. In patients with pulmonary hypertension (PH), exercise performance is already reduced near sea level due to impairments of the pulmonary circulation and gas exchange, and, presumably, these limitations are more pronounced at altitude. In studies performed near sea level in healthy subjects, as well as in patients with PH, maximal performance during progressive ramp exercise and endurance of submaximal constant-load exercise were substantially enhanced by breathing oxygen-enriched air. Both in healthy individuals and in PH patients, these improvements were mediated by a better arterial, muscular, and cerebral oxygenation, along with a reduced sympathetic excitation, as suggested by the reduced heart rate and alveolar ventilation at submaximal isoloads, and an improved pulmonary gas exchange efficiency, especially in patients with PH. In summary, in healthy individuals and in patients with PH, alterations in the inspiratory PO 2 by exposure to hypobaric hypoxia or normobaric hyperoxia reduce or enhance exercise performance, respectively, by modifying oxygen deliv...

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Effect of changes in arterial oxygen content on circulation and physical performance

Cited by 160 publications

References 0 publications

The decrease of maximal oxygen consumption during hypoxia in man: a mirror image of the oxygen equilibrium curve.

The decrease of maximal oxygen consumption during hypoxia in man: a mirror image of the oxygen equilibrium curve.

Evidence that diffusion limitation determines oxygen uptake kinetics during exercise in humans.

Effect of hypoxia and hyperoxia on exercise performance in healthy individuals and in patients with pulmonary hypertension: a systematic review

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