In competitive racing, horses rapidly accelerate to their top speed and probably perform supramaximal work. Therefore, the primary objective of this study was to examine changes in pulmonary vascular pressures of Thoroughbreds with rapid acceleration to supramaximal exercise which could not be sustained for more than 90 s. Right atrial and pulmonary vascular pressures were studied at rest and during supramaximal exercise in 10 healthy, sound, exercise trained Thoroughbred horses. Exercise was performed on separate days without (control) and with frusemide administration 250 mg i.v., 4 h before exercise. The protocol consisted of a warm-up at treadmill speeds of 2 to 6 m/s (trot) for 60 s each followed by 8 m/s (canter) for 60 s. Thereafter, the treadmill was raised to 10% uphill incline and speed accelerated from 8 to 15 m/s in 8 s. None of the horses could sustain exercise at 15 m/s + 10% incline for more than 90 s. Mean right atrial, pulmonary arterial, pulmonary artery wedge and pulmonary capillary pressures increased sharply as horses accelerated rapidly attaining their zenith as speed reached 15 m/s. Peak values of various pressures were maintained only for the first 45 s of exercise at 15 m/s +10% uphill incline. Thereafter, a declining trend emerged and all pressures decreased significantly as exercise duration increased. Although frusemide significantly lowered the magnitude of pulmonary vascular pressures both at rest and during exercise, it did not affect the rapid escalation in pulmonary vascular pressures upon rapid acceleration of horses or their unsteadiness in the latter 45 s of supramaximal exercise. It is suggested that rapid rate of rise of pulmonary capillary blood pressure during a sudden burst of supramaximal exercise may be a crucial factor in precipitating stress failure of pulmonary capillaries and onset of exercise induced pulmonary haemorrhage.