The hemodynamic effects of daily treadmill exercise were evaluated in hamsters with experimental thiamine deficiency to test the hypothesis that increased energy consumption might be a contributory factor in the pathogenesis of beriberi heart disease. Daily exercise enhanced thiamine deficiency and was manifested by earlier development of symptoms of neuropathy compared to non-exercised animals. Hemodynamics of exercised thiamine deficient animals were characterized by significantly lower O2 consumption, lower cardiac output, and lower left ventricular minute work, compared to exercised, pair-fed control animals. Left ventricular end-diastolic pressure was slightly but not significantly higher in thiamine deficient animals. Left ventricular function, therefore, was depressed in this group. There was no evidence of hyperkinetic circulation, cardiomegaly or congestive heart failure. Neuropathy and depressed ventricular function, characteristic of pure thiamine deficiency, were observed in the absence of high cardiac output or high output failure, the pathogenesis of which may require other unknown factors.