Four mature horses were used to test the effects of two doses (50 and
200 mg) of intravenously administered cocaine on hemodynamics and sele
cted indexes of performance [maximal heart rate (HR(max)), treadmill v
elocity at HR(max), treadmill velocity needed to produce a blood lacta
te concentration of 4 mmol/l, maximal mixed venous blood lactate conce
ntration, maximal treadmill work intensity, and test duration] measure
d during an incremental treadmill test. Both doses of cocaine increase
d HR(max) similar to 7% (P < 0.05). Mean arterial pressure was 30 mmHg
greater (P < 0.05) during the 4- to 7-m/s steps of the exercise test
in the 200-mg trial. Neither dose of cocaine had an effect on the resp
onses to exertion of right atrial pressure, right ventricular pressure
, or maximal change in right ventricular pressure over time. Maximal m
ixed venous blood lactate concentration increased 41% (P < 0.05) with
the 50-mg dose and 75% (P < 0.05) with the 200-mg dose during exercise
. Administration of cocaine resulted in decreases (P < 0.05) in the tr
eadmill velocity needed to produce a blood lactate concentration of 4
mmol/l from 6.9 +/- 0.5 and 6.8 +/- 0.9 m/s during the control trials
to 4.4 +/- 0.1 m/s during the 200-mg cocaine trial. Cocaine did not al
ter maximal treadmill work intensity (P > 0.05); however, time to exha
ustion increased by similar to 92 s (15%; P < 0.05) during the 200-mg
trial. The earlier onset of lactate accumulation and the greater maxim
al lactate concentration observed during the cocaine trials may have b
een due to the greater run times during the test or to peripheral vaso
constriction, which may also explain the increase in mean arterial pre
ssure observed during the 200-mg cocaine trial.