To evaluate the effect of different levels of arterial oxygen content on hemodynamic parameters during exercise nine subjects performed submaximal bicycle or treadmill exercise and maximal treadmill exercise under three different experimental conditions: 1) breathing room air (control); 2) breathing 50% oxygen (hyperoxia); 3) after rebreathing a carbon monoxide gas mixture (hypoxia). Maximal oxygen consumption (Vo2 max) was significantly higher in hyperoxia (4.99 1/min) and significantly lower in hypoxia (3.80 1/min) than in the control experiment (4.43 1/min). Physical performance changes in parallel with Vo2 max. Maximal cardiac output (Qmax) was similar in hyperoxia as in control but was significantly lower in hypoxia mainly due to a decreased stroke volume. A correlation was found between Vo2 max and transported oxygen, i.e., Cao2 times Amax, thus suggesting that central circulation is an important limiting factor for human maximal aerobic power. During submaximal work HR was decreased in hyperoxia and increased in hypoxia. Corresponding Q values were unchanged except for a reduction during high submaximal exercise in hyperoxia.
EKBLOM, B. and R. HUOT. Rel-ponse to .rubmaximal and malcimal exercise at different levels of carboxyhemoglobin. Acta physiol. scand. 1972. 86. 474-482. Five subjects performed submaximal and maximal bicycle and maximal treadmill exercise in normalcy and after carbon monoxide inhalation, giving different levels of carboxyhemoglobin ( C O H b ) in the blood. During maximal treadmill exercise work time on a fixed work load and maximal oxygen uptake were decreased with increasing level of C O H b ( r = 0.79 and r = 0.85, respectively). Peak blood lactate concentration and pulmonary ventilation were unchanged. Highest measured heart rate was lower in parallell with the increased C O H b level compared to control studies. During submaximal work heart rate was increased and oxygen uptake was unchanged at the various levels of COHb. At low submasimal work loads blood lactate concentrations and oxygen deficit was unchanged but increased as work load and COHb-level increased.K e y words: Submaximal and maximal work; carbon monoxide; oxygen uptake; heart rate; lactate concentration ; pulmonary ventilation; physical performance.The physical performance capacity and maximal oxygen uptake (oo,) can be affected by altering factors in the oxygen transport system. When arterial oxygen content is reduced, as during acute hypoxia, the amount of oxygen offered to the tissues during maximal exercise is reduced. The maximal cardiac output is not changed compared to normoxia, and therefore max v0, is decreased in parallell with the decreased hemoglobin oxygen saturation (Sternberg et al. 1966). Partial blocking of the hemoglobin ( H b ) by carbon monoxide (CO) can induce a similar reduction in the arterial oxygen content but without affecting the arterial oxygen tension. The aim of the present study was to explore some of the effects of carboxyhemoglobin (COI-Ib) on the cardio respiratory system during submaximal and maximal exercise. Of special interest was the maximal work level. It is a well-known fact that the capacity for physical work requiring large muscle groups for longer than 2 to 3 min depends mainly on aerobic metabolism. If oxygen transport capacity of the blood is one of the main limiting factors in such work situations, reduction of this capacity should be correlated with reduction of physical work performance and max ooz.Fellowship from the Samuel hlcLaughlin Foundation.Roger Huot is on leave from L'Institute de Cardiologie de Montreal, supported by a
This research was supported by the Réseau Québécois de recherche sur le médicament (RQRM); the Blueprint for Pharmacy in collaboration with Pfizer Canada; and the Cercle du Doyen of the Faculty of Pharmacy, University of Montreal. The study sponsors were not involved in the study design, data collection, data interpretation, the writing of the article, or the decision to submit the report for publication. Chartrand received a scholarship from the Fonds de Recherche du Québec en Santé (FRQ-S), the Réseau Québécois de recherche sur l'usage des médicaments with Pfizer, and the Faculty of Pharmacy, University of Montreal. Guénette holds a Junior-1 Clinician Researcher Award from the FRQ-S in partnership with the Société québécoise d'hypertension artérielle. Williamson holds a Junior-1 Career Award from the FRQ-S. Côté reported being a medical speaker for Bayer, Boehringer Ingelheim Canada, and Pfizer Canada. The other authors reported no conflicts of interest. Study concept and design were contributed by Lalonde, Chartrand, and Martin. Chartrand, Martin, and Lalonde collected the data, along with Brouillette, Côté, Huot, Landry, Martineau, Perreault, Williamson, and White-Guay. Data interpretation was performed by Chartrand, Gagnon, and Lalonde, along with Guénette and Martin. The manuscript was primarily written by Chartrand, along with Guénette and Lalonde, and revised by Chartrand, Guénette, and Lalonde, along with the other authors. A portion of this study's results was presented at the 4th RQRM Annual Meeting on September 22-23, 2014, in Orford, Quebec, Canada, in the form of an abstract, which was published in the Journal of Population Therapeutics and Clinical Pharmacology, 2014;21(2):e312.
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