Effect of L-NAME on oxygen uptake kinetics during heavy-intensity exercisein the horse

There is evidence that oxidative enzyme inertia plays a major role in limit ing/setting the O-2 uptake ((V) over dot (O2)) response at the transition t o higher metabolic rates and also that nitric oxide (NO) competitively inhi bits (V) over dot (O2) within the electron transport chain. To investigate whether NO is important in setting the dynamic response of (V) over dot (O2 ) at the onset of high-intensity (heavy-domain) running in horses, five gel dings were run on a treadmill across speed transitions from 3 m/s to speeds corresponding to 80% of peak (V) over dot (O2) with and without nitro-L-ar ginine methyl ester (L-NAME), an NO synthase inhibitor (20 mg/kg; order ran domized). L-NAME did not alter (both P > 0.05) baseline (3 m/s, 15.4 +/- 0. 3 and 16.2 +/- 0.5 1/min for control and L-NAME, respectively) or end-exerc ise (V) over dot (O2) (56.9 +/- 5.1 and 55.2 +/- 5.8 1/min for control and L-NAME, respectively). However, in the L-NAME trial, the primary on-kinetic response was significantly (P < 0.05) faster (i.e., reduced time constant, 27.0 +/- 2.7 and 18.7 +/- 3.0 s for control and L-NAME, respectively), des pite no change in the gain of (V) over dot (O2) (P > 0.05). The faster on-k inetic response was confirmed independent of modeling by reduced time to 50 , 63, and 75% of overall (V) over dot (O2) response (all P > 0.05). In addi tion, onset of the (V) over dot (O2) slow component occurred earlier (124.6 +/- 11.2 and 65.0 +/- 6.6 s for control and L-NAME, respectively), and the magnitude of the O-2 deficit was attenuated (both P < 0.05) in the L-NAME compared with the control trial. Acceleration of the (V) over dot (O2) kine tics by L-NAME suggests that NO inhibition of mitochondrial (V) over dot (O 2) may contribute, in part, to the intrinsic metabolic inertia evidenced at the transition to higher metabolic rates in the horse.