Journal of Applied Physiology
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J Appl Physiol 91: 891-896, 2001;
8750-7587/01 $5.00
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Vol. 91, Issue 2, 891-896, August 2001

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

Casey A. Kindig, Paul McDonough, Howard H. Erickson, and David C. Poole

Departments of Anatomy and Physiology and Kinesiology, Kansas State University, Manhattan, Kansas 66506-5602

There is evidence that oxidative enzyme inertia plays a major role in limiting/setting the O2 uptake (VO2) response at the transition to higher metabolic rates and also that nitric oxide (NO) competitively inhibits VO2 within the electron transport chain. To investigate whether NO is important in setting the dynamic response of VO2 at the onset of high-intensity (heavy-domain) running in horses, five geldings were run on a treadmill across speed transitions from 3 m/s to speeds corresponding to 80% of peak VO2 with and without nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor (20 mg/kg; order randomized). L-NAME did not alter (both P > 0.05) baseline (3 m/s, 15.4 ± 0.3 and 16.2 ± 0.5 l/min for control and L-NAME, respectively) or end-exercise VO2 (56.9 ± 5.1 and 55.2 ± 5.8 l/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), despite no change in the gain of VO2 (P > 0.05). The faster on-kinetic response was confirmed independent of modeling by reduced time to 50, 63, and 75% of overall VO2 response (all P < 0.05). In addition, onset of the VO2 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 O2 deficit was attenuated (both P < 0.05) in the L-NAME compared with the control trial. Acceleration of the VO2 kinetics by L-NAME suggests that NO inhibition of mitochondrial VO2 may contribute, in part, to the intrinsic metabolic inertia evidenced at the transition to higher metabolic rates in the horse.

nitric oxide; nitric oxide synthase inhibition; oxygen uptake slow component; oxygen deficit; nitro-L-arginine methyl ester


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