On the mechanisms that limit oxygen uptake during exercise in acute and chronic hypoxia: role of muscle mass

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On the mechanisms that limit oxygen uptake during exercise in acute and chronic hypoxia: role of muscle mass. / Calbet, José A L; Rådegran, Göran; Boushel, Robert; Saltin, Bengt.

I: Journal of Physiology, Bind 587, Nr. Pt 2, 2009, s. 477-90.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Calbet, JAL, Rådegran, G, Boushel, R & Saltin, B 2009, 'On the mechanisms that limit oxygen uptake during exercise in acute and chronic hypoxia: role of muscle mass', Journal of Physiology, bind 587, nr. Pt 2, s. 477-90. https://doi.org/10.1113/jphysiol.2008.162271

APA

Calbet, J. A. L., Rådegran, G., Boushel, R., & Saltin, B. (2009). On the mechanisms that limit oxygen uptake during exercise in acute and chronic hypoxia: role of muscle mass. Journal of Physiology, 587(Pt 2), 477-90. https://doi.org/10.1113/jphysiol.2008.162271

Vancouver

Calbet JAL, Rådegran G, Boushel R, Saltin B. On the mechanisms that limit oxygen uptake during exercise in acute and chronic hypoxia: role of muscle mass. Journal of Physiology. 2009;587(Pt 2):477-90. https://doi.org/10.1113/jphysiol.2008.162271

Author

Calbet, José A L ; Rådegran, Göran ; Boushel, Robert ; Saltin, Bengt. / On the mechanisms that limit oxygen uptake during exercise in acute and chronic hypoxia: role of muscle mass. I: Journal of Physiology. 2009 ; Bind 587, Nr. Pt 2. s. 477-90.

Bibtex

@article{b03854c0787611df928f000ea68e967b,
title = "On the mechanisms that limit oxygen uptake during exercise in acute and chronic hypoxia: role of muscle mass",
abstract = "Peak aerobic power in humans (VO2,peak) is markedly affected by inspired O2 tension (FIO2). The question to be answered in this study is what factor plays a major role in the limitation of muscle peak VO2 in hypoxia: arterial O2 partial pressure (Pa,O2) or O2 content (Ca,O2)? Thus, cardiac output (dye dilution with Cardio-green), leg blood flow (thermodilution), intra-arterial blood pressure and femoral arterial-to-venous differences in blood gases were determined in nine lowlanders studied during incremental exercise using a large (two-legged cycle ergometer exercise: Bike) and a small (one-legged knee extension exercise: Knee)muscle mass in normoxia, acute hypoxia (AH) (FIO2 = 0.105) and after 9 weeks of residence at 5260 m (CH). Reducing the size of the active muscle mass blunted by 62% the effect of hypoxia on VO2,peak in AH and abolished completely the effect of hypoxia on VO2,peak after altitude acclimatization. Acclimatization improved Bike peak exercise Pa,O2 from 34 +/- 1 in AH to 45 +/- 1 mmHg in CH(P <0.05) and Knee Pa,O2 from 38 +/- 1 to 55 +/- 2 mmHg(P <0.05). Peak cardiac output and leg blood flow were reduced in hypoxia only during Bike. Acute hypoxia resulted in reduction of systemic O2 delivery (46 and 21%) and leg O2 delivery (47 and 26%) during Bike and Knee, respectively, almost matching the corresponding reduction in VO2,peak. Altitude acclimatization restored fully peak systemic and leg O(2) delivery in CH (2.69 +/- 0.27 and 1.28 +/- 0.11 l min(-1), respectively) to sea level values (2.65 +/- 0.15 and 1.16 +/- 0.11 l min(-1), respectively) during Knee, but not during Bike. During Knee in CH, leg oxygen delivery was similar to normoxia and, therefore, also VO2,peak in spite of a Pa,O2 of 55 mmHg. Reducing the size of the active mass improves pulmonary gas exchange during hypoxic exercise, attenuates the Bohr effect on oxygen uploading at the lungs and preserves sea level convective O2 transport to the active muscles. Thus, the altitude-acclimatized human has potentially a similar exercising capacity as at sea level when the exercise model allows for an adequate oxygen delivery (blood flow x Ca,O2), with only a minor role of Pa,O2 per se, when Pa,O2 is more than 55 mmHg.",
author = "Calbet, {Jos{\'e} A L} and G{\"o}ran R{\aa}degran and Robert Boushel and Bengt Saltin",
note = "Keywords: Acclimatization; Acute Disease; Adult; Altitude; Anoxia; Blood Pressure; Carbon Dioxide; Cardiac Output; Catecholamines; Chronic Disease; Exercise; Exercise Test; Female; Femoral Vein; Humans; Leg; Male; Muscle, Skeletal; Oxygen; Partial Pressure; Pulmonary Gas Exchange; Pulmonary Ventilation; Regional Blood Flow; Young Adult",
year = "2009",
doi = "10.1113/jphysiol.2008.162271",
language = "English",
volume = "587",
pages = "477--90",
journal = "The Journal of Physiology",
issn = "0022-3751",
publisher = "Wiley-Blackwell",
number = "Pt 2",

}

RIS

TY - JOUR

T1 - On the mechanisms that limit oxygen uptake during exercise in acute and chronic hypoxia: role of muscle mass

AU - Calbet, José A L

AU - Rådegran, Göran

AU - Boushel, Robert

AU - Saltin, Bengt

N1 - Keywords: Acclimatization; Acute Disease; Adult; Altitude; Anoxia; Blood Pressure; Carbon Dioxide; Cardiac Output; Catecholamines; Chronic Disease; Exercise; Exercise Test; Female; Femoral Vein; Humans; Leg; Male; Muscle, Skeletal; Oxygen; Partial Pressure; Pulmonary Gas Exchange; Pulmonary Ventilation; Regional Blood Flow; Young Adult

PY - 2009

Y1 - 2009

N2 - Peak aerobic power in humans (VO2,peak) is markedly affected by inspired O2 tension (FIO2). The question to be answered in this study is what factor plays a major role in the limitation of muscle peak VO2 in hypoxia: arterial O2 partial pressure (Pa,O2) or O2 content (Ca,O2)? Thus, cardiac output (dye dilution with Cardio-green), leg blood flow (thermodilution), intra-arterial blood pressure and femoral arterial-to-venous differences in blood gases were determined in nine lowlanders studied during incremental exercise using a large (two-legged cycle ergometer exercise: Bike) and a small (one-legged knee extension exercise: Knee)muscle mass in normoxia, acute hypoxia (AH) (FIO2 = 0.105) and after 9 weeks of residence at 5260 m (CH). Reducing the size of the active muscle mass blunted by 62% the effect of hypoxia on VO2,peak in AH and abolished completely the effect of hypoxia on VO2,peak after altitude acclimatization. Acclimatization improved Bike peak exercise Pa,O2 from 34 +/- 1 in AH to 45 +/- 1 mmHg in CH(P <0.05) and Knee Pa,O2 from 38 +/- 1 to 55 +/- 2 mmHg(P <0.05). Peak cardiac output and leg blood flow were reduced in hypoxia only during Bike. Acute hypoxia resulted in reduction of systemic O2 delivery (46 and 21%) and leg O2 delivery (47 and 26%) during Bike and Knee, respectively, almost matching the corresponding reduction in VO2,peak. Altitude acclimatization restored fully peak systemic and leg O(2) delivery in CH (2.69 +/- 0.27 and 1.28 +/- 0.11 l min(-1), respectively) to sea level values (2.65 +/- 0.15 and 1.16 +/- 0.11 l min(-1), respectively) during Knee, but not during Bike. During Knee in CH, leg oxygen delivery was similar to normoxia and, therefore, also VO2,peak in spite of a Pa,O2 of 55 mmHg. Reducing the size of the active mass improves pulmonary gas exchange during hypoxic exercise, attenuates the Bohr effect on oxygen uploading at the lungs and preserves sea level convective O2 transport to the active muscles. Thus, the altitude-acclimatized human has potentially a similar exercising capacity as at sea level when the exercise model allows for an adequate oxygen delivery (blood flow x Ca,O2), with only a minor role of Pa,O2 per se, when Pa,O2 is more than 55 mmHg.

AB - Peak aerobic power in humans (VO2,peak) is markedly affected by inspired O2 tension (FIO2). The question to be answered in this study is what factor plays a major role in the limitation of muscle peak VO2 in hypoxia: arterial O2 partial pressure (Pa,O2) or O2 content (Ca,O2)? Thus, cardiac output (dye dilution with Cardio-green), leg blood flow (thermodilution), intra-arterial blood pressure and femoral arterial-to-venous differences in blood gases were determined in nine lowlanders studied during incremental exercise using a large (two-legged cycle ergometer exercise: Bike) and a small (one-legged knee extension exercise: Knee)muscle mass in normoxia, acute hypoxia (AH) (FIO2 = 0.105) and after 9 weeks of residence at 5260 m (CH). Reducing the size of the active muscle mass blunted by 62% the effect of hypoxia on VO2,peak in AH and abolished completely the effect of hypoxia on VO2,peak after altitude acclimatization. Acclimatization improved Bike peak exercise Pa,O2 from 34 +/- 1 in AH to 45 +/- 1 mmHg in CH(P <0.05) and Knee Pa,O2 from 38 +/- 1 to 55 +/- 2 mmHg(P <0.05). Peak cardiac output and leg blood flow were reduced in hypoxia only during Bike. Acute hypoxia resulted in reduction of systemic O2 delivery (46 and 21%) and leg O2 delivery (47 and 26%) during Bike and Knee, respectively, almost matching the corresponding reduction in VO2,peak. Altitude acclimatization restored fully peak systemic and leg O(2) delivery in CH (2.69 +/- 0.27 and 1.28 +/- 0.11 l min(-1), respectively) to sea level values (2.65 +/- 0.15 and 1.16 +/- 0.11 l min(-1), respectively) during Knee, but not during Bike. During Knee in CH, leg oxygen delivery was similar to normoxia and, therefore, also VO2,peak in spite of a Pa,O2 of 55 mmHg. Reducing the size of the active mass improves pulmonary gas exchange during hypoxic exercise, attenuates the Bohr effect on oxygen uploading at the lungs and preserves sea level convective O2 transport to the active muscles. Thus, the altitude-acclimatized human has potentially a similar exercising capacity as at sea level when the exercise model allows for an adequate oxygen delivery (blood flow x Ca,O2), with only a minor role of Pa,O2 per se, when Pa,O2 is more than 55 mmHg.

U2 - 10.1113/jphysiol.2008.162271

DO - 10.1113/jphysiol.2008.162271

M3 - Journal article

C2 - 19047206

VL - 587

SP - 477

EP - 490

JO - The Journal of Physiology

JF - The Journal of Physiology

SN - 0022-3751

IS - Pt 2

ER -

ID: 20321684