Oxygen transport and oxyhemoglobin dissociation during prolonged muscular work.

Thomson, J. M.; Dempsey, J A; Chosy, L. W.; Shahidi, Nasrollah T.; Reddan, W. G.

doi:10.1152/jappl.1974.37.5.658

Cited by 56 publications

(24 citation statements)

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“…These results speak against the hypothesis than an exercise-induced tissue hypoxia causes the lactate release seen during exercise in normal subjects, since that lactate release occurs even at venous oxygen pressures that are clearly quite higher than in the present two subjects. The im- portance of tissue hypoxia in lactate production during exercise in man has also been questioned by others (37,38).…”

Section: Discussionmentioning

confidence: 99%

Tissue oxygenation and muscular substrate turnover in two subjects with high hemoglobin oxygen affinity.

Wranne¹,

Berlin²,

Jorfeldt³

et al. 1983

J. Clin. Invest.

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A B S T R A C T Oxygen transport to and substrate turnover in leg muscle were studied at rest and during light and heavy upright bicycle exercise in two brothers with a hereditary hemoglobinopathy associated with high oxygen affinity (P50 = 13 mmHg). Femoral venous oxygen tension was below normal and femoral venous oxygen saturation above normal at rest and during exercise. Thus, the arterial-femoral venous oxygen saturation difference was decreased. Despite a compensatory increase in hemoglobin concentration, the arterial-femoral venous oxygen content difference tended to be below normal at heavy exercise. Approximately 25% of the oxygen was delivered via the abnormal hemoglobin at relative heavy exercise. Arterial lactate levels, lactate release, and muscle lactate concentration were not increased at any level of exercise. Glucose, alanine, pyruvate, and glycerol turnover were essentially normal, but the glycogen and creatine phosphate stores were abnormally depleted at the termination of heavy exercise. The exercise electrocardiogram (ECG) was normal, indicating that myocardial oxygenation was adequate. Muscle-surface oxygen pressure fields were normal at rest (not investigated during exercise). It is concluded that the high oxygen affinity of the hemoglobin in our two subjects did not lead to heart or skeletal muscle hypoxia during heavy exercise, as judged from the ECG and from the leg lactate turnover. Despite the lack of evidence for muscle hypoxia, the subjects experienced leg muscle fatigue and the creatine phosphate and glycogen stores were depleted more than normally.

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Section: Discussionmentioning

confidence: 99%

Tissue oxygenation and muscular substrate turnover in two subjects with high hemoglobin oxygen affinity.

Wranne¹,

Berlin²,

Jorfeldt³

et al. 1983

J. Clin. Invest.

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“…For each test session, eight to twelve samples of human blood were tonometered using gases in the range of measured values for Pa 02 and Pa,co (arterial Po,and Pco2) to validate the blood gas measurements (Thomson, Dempsey, Chosy, Shahidi & Reddan, 1974;Bateman, Musch, Smith & Dempsey, 1980 (R) were calculated in the usual way from mixed expired gas samples. Dead space was estimated from the Bohr equation, and mean 'ideal' alveolar Po, (PA, 02) calculated using the alveolar air equation (Otis, 1964 …”

Section: Gas and Blood Collection Analysis And Calculationsmentioning

confidence: 99%

Exercise‐induced arterial hypoxaemia in healthy human subjects at sea level.

Dempsey¹,

Hanson²,

Henderson³

1984

The Journal of Physiology

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516

376

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SUMMARY1. We determined the incidence of exercise-induced arterial hypoxaemia and its determinants in sixteen highly trained, healthy runners who were capable of achieving and sustaining very high metabolic rates (maximal 02 uptake = 72 + 2 ml kg-' min-or 4-81 + 0-131 min'). Arterial blood gases and acidbase status were determined at each load of a progressive short-term exercise test and repeatedly during constant-load treadmill running while breathing air and during inhalation of mildly hypoxic, hyperoxic, and helium-enriched gases.2. 5. In view of the correction of hypoxaemia with mild hyperoxia and the very high ratios of alveolar ventilation to pulmonary blood flow (PA/C = 4-6) achieved during heavy exercise, we think it unlikely that non-uniformity of the VA/QC distribution or veno-arterial shunt could explain the hypoxaemia observed in most of our subjects. By exclusion, we suggest that hypoxaemia may be attributed to a diffusion limitation secondary to very short red cell transit times in at least a portion of the pulmonary circulation. These excessively short transit times may occur at high metabolic rates 6 PHY 355 J. A. DEMPSEY, P. G. HANSON AND K. S. HENDERSON if pulmonary capillary blood volume has achieved its maximum expansion at a time when pulmonary blood flow continues to increase.6. Considerable individual variations were present in the hyperventilatory response to heavy work. These variations were inconsistently related to corresponding levels of metabolic acidosis and in many cases a compensatory hyperventilation was minimal or absent in the face of substantial acidosis and hypoxaemia. The findings that tidal breaths during heavy exercise often exceeded the maximum flow-volume curve and that hyperventilation was consistently obtained with helium inhalation, suggest that the hyperventilatory response to heavy work is determined to a significant extent by the mechanical load imposed on the chest wall secondary to increased pulmonary impedance.

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“…Cette modification de l'affinité est liée au changement de pH (effet Bohr), puisque P50 IV calculée à partir de P50 (7,40), en tenant compte du pH veineux, est superpo sable à P50 IVm. Ceci rejoint les constata tions de Thomson et al [28]: l'effet-pH est plus actif que l'effet-température sur le glis sement de la CDO, au cours d'un exercice bref; par contre, l'effet-température prédo-A P 50, Ton- mine dans les exercices de longue durée. De toutes façons ces deux facteurs agissent dans le même sens au cours de l'exercice muscu laire.…”

Section: La Concentration Des Lactates Et Des Pyruvates Est éGalementunclassified

“…Thomson et al [28] constatent égale ment ce déplacement in vivo de la CDO, chez des sujets sains soumis à un exercise prolongé d'une intensité égale à 66°/o de leur V°2niax. Ils s'interrogent quant à sa signifi cation physiologique chez le sujet normal, sans donner de réponse.…”

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Corrélation entre modifications de l’affinité de l’hémoglobine pour l’oxygène et métabolisme anaérobie au cours de l’exercice musculaire chez 20 silicotiques

Vanuxem¹,

Fornaris²,

Guillot³

et al. 1979

Respiration

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This study investigated the changes in hemoglobin affinity for oxygen – P50 standard [P50 (7.40)]; P50 in vivo (P50 IV), and 2,3-diphosphoglycerate concentration (2,3-DPG) – and the anaerobic metabolism during a short muscular exercise in 20 silicotic patients. P50 (7. 40) and 2,3-DPG remained unchanged at the end of the exercise but P50 IV increased significantly. A negative correlation was found between the increase in the arterial lactates and the increase in P50 IV. Such a shift to the right of the oxyhemoglobin dissociation curve probably improves the tissular oxygenation and can be regarded as a compensatory mechanism in patients with pulmonary impairment during exercise.

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Oxygen transport and oxyhemoglobin dissociation during prolonged muscular work.

Cited by 56 publications

References 0 publications

Tissue oxygenation and muscular substrate turnover in two subjects with high hemoglobin oxygen affinity.

Tissue oxygenation and muscular substrate turnover in two subjects with high hemoglobin oxygen affinity.

Exercise‐induced arterial hypoxaemia in healthy human subjects at sea level.

Corrélation entre modifications de l’affinité de l’hémoglobine pour l’oxygène et métabolisme anaérobie au cours de l’exercice musculaire chez 20 silicotiques

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