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Nitric oxide synthase inhibition in Thoroughbred horses augments O 2 extraction at rest and submaximal exercise, but not during short‐term maximal exercise
Author(s) -
MANOHAR M.,
GOETZ T. E.,
HASSAN A. S.
Publication year - 2006
Publication title -
equine veterinary journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.82
H-Index - 87
eISSN - 2042-3306
pISSN - 0425-1644
DOI - 10.1111/j.2042-3306.2006.tb05591.x
Subject(s) - anaerobic exercise , exertion , venous blood , nitric oxide synthase , medicine , arterial blood , chemistry , endocrinology , metabolism , anesthesia , nitric oxide , physical therapy
Summary Reason for performing study: Work is required to establish the role of endogenous nitric oxide (NO) in metabolism of resting and exercising horses. Objectives: To examine the effects of NO synthase inhibition on O 2 extraction and anaerobic metabolism at rest, and during submaximal and maximal exertion. Methods: Placebo and NO synthase inhibition (with Nω‐nitro‐L‐arginine methyl ester [ l ‐NAME] administered at 20 mg/kg bwt i.v.) studies were performed in random order, 7 days apart on 7 healthy, exercise‐trained Thoroughbred horses at rest and during incremental exercise leading to 120 sec of maximal exertion at 14 m/sec on a 3.5% uphill grade. Results: At rest, NO synthase inhibition significantly augmented the arterial to mixed‐venous blood O 2 content gradient and O 2 extraction as mixed‐venous blood O 2 tension and saturation decreased significantly. While NO synthase inhibition did not affect arterial blood‐gas tensions in exercising horses, the exercise‐induced increment in haemoglobin concentration and arterial O 2 content was attenuated. In the l ‐NAME study, during submaximal exercise, mixed‐venous blood O 2 tension and haemoglobin‐O 2 saturation decreased to a greater extent causing O 2 extraction to increase significantly. During maximal exertion, arterial hypoxaemia, desaturation of haemoglobin and hypercapnia of a similar magnitude developed in both treatments. Also, the changes in mixed‐venous blood O 2 tension and haemoglobin‐O 2 saturation, arterial to mixed‐venous blood O 2 content gradient, O 2 extraction and markers of anaerobic metabolism (lactate and ammonia production, and metabolic acidosis) were not different from those in the placebo study. Conclusion: Endogenous NO production augments O 2 extraction at rest and during submaximal exertion, but not the during short‐term maximal exercise. Also, NO synthase inhibition does not affect anaerobic metabolism at rest or during exertion. Potential relevance: It is unlikely that endogenous NO release modifies aerobic or anaerobic metabolism in horses performing short‐term maximal exertion.