The study was designed to test the hypothesis that a moderate decrease in upper body oxygen consumption observed during crossclamping of the thoracic aorta represents tissue hypoxia (possibly as a result of microcirculatory disorders) and results in adenosine triphosphate homeostasis disturbances. We averaged phosphorus 31-nuclear magnetic resonance spectroscopy measurements for 10 minutes with the use of a surface coil on the left ventricle and on the deltoid muscle during a 1-hour period before aortic crossclamping, during aortic crossclamping, and after aortic unclamping. Skeletal muscle creatine phosphate levels decreased 3.1% (p < 0.01), whereas the ratio of creatine phosphate to adenosine triphosphate decreased 2.2% (p < 0.05); glycolytic intermediates increased 70% (p < 0.01) and intracellular inorganic phosphate decreased 9% (p < 0.01). Myocardial creatine phosphate decreased 15% (p < 0.01), whereas the ratio of creatine phosphate to adenosine triphosphate decreased 5.3% (p < 0.01); glycolytic intermediates did not change, but intracellular inorganic phosphate almost doubled (p < 0.05). These data suggest that observations of reduced upper body oxygen consumption after aortic crossclamping are consistent with the effects of skeletal muscle hypoxia. Changes in myocardial metabolites may result from transient ischemia caused by the increased wall stress.