Myocardial O2-extraction rate was studied during exercise induced augmentation of cardiac work in dogs. The O2-extraction rate at rest was 75% of arterial content. Progressive levels of exercise increased the animals' O2-consumption from 7 ml/min-kg up to 91 ml/min-kg. Cardiac output rose from 108 ml/min-kg at rest to 484 ml/min-kg at the highest exercise level. The increase in myocardial O2-consumption from 9 ml/min-100 g at rest up to 57 ml/min-100g at the highest exercise level was met by an increase in coronary flow from 59 to 256 ml/min-100 g and a rise of myocardial AVDO2 from 15 to 22 Vol%. Thus the latter contributed 40% to the augmented myocardial O2-requirements. Coronary venous O2-saturation decreased to 9% saturation during highest levels of exercise. This low value was not the result of a limited coronary dilatory capacity, of inadequate state of exercise training, or of a relative underperfusion of the inner layers of the left ventricle. Thus, augmentation of myocardial O2-extraction rate seems to be a mechanism of physiological relevance during exercise induced elevation of myocardial O2-requirements in dogs and may be explained by capillary recruitment in the myocardium.

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Coronary flow and myocardial oxygen consumption were measured in conscious dogs at rest and during two levels of submaximal treadmill exercise (3 and 7 km/h at 15% grade, respectively) during adaptation to progressive hemodilution with dextran 60. At rest coronary flow increased to more than seven-fold with diminishing hematocrit to 12.5% in order to cover myocardial oxygen consumption which increased from 6.5 +/- 0.3 ml/min with 100 g at hematocrit 47.5% to 13.5 +/- 0.8 ml/min with 100 g at hematocrit 12.5%. The dilatory capacity of the coronary vessels, estimated from the reactive hyperemia after a 12 sec occlusion of the left circumflex coronary artery, dropped from 602% at control to 45% at lowest hematocrit levels. During the superimposed stress of exercise coronary flow and myocardial oxygen consumption increased further, so that the dilatory capacity of the coronaries was exhausted at hematocrit levels between 16 and 22%. Myocardial oxygen consumption per unit of oxygen delivered to peripheral tissues increased substantially with progressive hemodilution. In the presence of the reduced arterial oxygen content the augmented myocardial oxygen demand limits the overall adaptability to hemodilution by an exhaustion of the coronary dilatory capacity.

During progressive normovolemic hemodilution with dextran-60, circulatory functions (cardiac output, oxygen delivery to tissues, arterial pressure and mixed venous oxygen saturation) and total body oxygen consumption were studied in conscious dogs at rest and during two levels of submaximal treadmill exercise. At rest, cardiac output rose continuously with progressive hemodilution. This increase, however, was not sufficient to compensate for the reduced arterial oxygen content. Consequently oxygen delivery fell significantly from 23.3 +/- 1.8 ml/min with kg at hematocrit 47.5% to 15.7 +/- 0.9 ml/min with kg at hematocrit 12.5%. The constant oxygen consumption was maintained by a simultaneous increase in oxygen extraction from blood. During the superimposed stress of exercise, a constant oxygen consumption was maintained between hematocrit ranges of 50 to 15 or 25%, respectively. Again, the increase of cardiac output due to hemodilution did not compensate for the reduced arterial oxygen content and consequently oxygen extraction rate was increased. These data demonstrate that at rest (and even more during submaximal treadmill exercise) the reduced whole blood viscosity or improved fluidity during hemodilution does not initiate an increase in cardiac output that is sufficient to maintain a constant oxygen delivery to the tissues.

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