Furosemide reduces accumulated oxygen deficit in horses during brief intense exertion

Abstract

Hinchcliff, K. W., K. H. McKeever, W. W. Muir, and R. A. Sams. Furosemide reduces accumulated oxygen deficit in horses during brief intense exertion. J. Appl. Physiol. 81(4): 1550–1554, 1996.—We theorized that furosemide-induced weight reduction would reduce the contribution of anaerobic metabolism to energy expenditure of horses during intense exertion. The effects of furosemide on accumulated O2 deficit and plasma lactate concentration of horses during high-intensity exercise were examined in a three-way balance randomized crossover study. Nine horses completed each of three trials: 1) a control (C) trial, 2) a furosemide-unloaded (FU) trial in which the horse received furosemide 4 h before running, and 3) a furosemide weight-loaded (FL) trial during which the horse received furosemide and carried weight equal to the weight lost after furosemide administration. Horses ran for 2 min at ∼120% maximal O2 consumption. Furosemide (FU) increased O2 consumption (ml ⋅ 2 min−1 ⋅ kg−1) compared with C (268 ± 9 and 257 ± 9, P < 0.05), whereas FL was not different from C (252 ± 8). Accumulated O2 deficit (ml O2 equivalents/kg) was significantly ( P < 0.05) lower during FU (81.2 ± 12.5), but not during FL (96.9 ± 12.4), than during C (91.4 ± 11.5). Rate of increase in blood lactate concentration (mmol ⋅ 2 min−1 ⋅ kg−1) after FU (0.058 ± 0.001), but not after FL (0.061 ± 0.001), was significantly ( P < 0.05) lower than after C (0.061 ± 0.001). Furosemide decreased the accumulated O2 deficit and rate of increase in blood lactate concentration of horses during brief high-intensity exertion. The reduction in accumulated O2 deficit in FU-treated horses was attributable to an increase in the mass-specific rate of O2 consumption during the high-intensity exercise test.