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Research Article Free access | 10.1172/JCI107416
Division of Medicine, Boston University School of Medicine, Boston City Hospital, Boston, Massachusetts 02118
Cardiology Division, Boston University Medical Service, Boston City Hospital, Boston, Massachusetts 02118
Departments of Medicine and Clinical Research, University Hospital, Boston, Massachusetts 02118
Find articles by Liang, C. in: JCI | PubMed | Google Scholar
Division of Medicine, Boston University School of Medicine, Boston City Hospital, Boston, Massachusetts 02118
Cardiology Division, Boston University Medical Service, Boston City Hospital, Boston, Massachusetts 02118
Departments of Medicine and Clinical Research, University Hospital, Boston, Massachusetts 02118
Find articles by Hood, W. in: JCI | PubMed | Google Scholar
Published September 1, 1973 - More info
Both electrically induced exercise and infusion of 2,4-dinitrophenol (DNP) increased oxygen consumption and tissue metabolism in chloralose-anesthetized dogs. Cardiac output increased with oxygen consumption at the same rate in both experimental conditions. The increase in cardiac output induced by exercise was, as expected, accompanied by increases in both lactate-to-pyruvate ratio and “excess lactate” in arterial blood. However, these parameters did not increase after DNP infusion until the rate of oxygen consumption had increased four- to fivefold, perhaps due to facilitation of mitochondrial electron transport by DNP. Anaerobic tissue metabolism therefore probably did not contribute significantly to increased cardiac output during the mild-to-moderate tissue hypermetabolism induced by DNP. The increased cardiac output may have been the result of metabolic changes common to both exercise and DNP infusion; muscular activity alone may not have been the primary determinant of the cardiac output response during exercise.