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1 Faculty of Medicine, Nimes-Montpellier, EA2992, Dynamique des Incoherences Cardio-vasculaires, Nimes, France; Faculty of Sciences, Avignon, JE 2426, Physiologie des Adaptations Cardio-vasculaires a l'exercice, Avignon, France
2 Faculty of Sciences, Avignon, JE 2426, Physiologie des Adaptations Cardio-vasculaires a l'exercice, Avignon, France
3 Faculty of Sciences, Avignon, JE 2426, Physiologie des Adaptations Cardio-vasculaires a l'exercice, Avignon, France; Faculty of Medicine, Nimes-Montpellier, EA2992, Dynamique des Incoherences Cardio-vasculaires, Nimes, France
4 Faculty of Medicine, Nimes-Montpellier, EA2992, Dynamique des Incoherences Cardio-vasculaires, Nimes, France
* To whom correspondence should be addressed. E-mail: philippe.obert{at}univ-avignon.fr.
This study was designed to test the hypothesis that the previously demonstrated training-induced improvement of the endothelium vasodilator function would be blunted under conditions of chronic hypoxia exposure as a result of deleterious effects of hypoxia per se on the nitric oxide (NO) pathway. Sea level native rats were randomly assigned to N (living in normoxia), NT (living and training 5 days per week for 5 weeks in normoxia), CH (living in hypoxia, 2800 m) and CHT (living and training 5 days per week for 5 weeks in hypoxia, 2800 m) groups. Concentration response curves to acetylcholine (ACh) (10-9 - 10-4 M) with or without L-arginine (10-3 - 10-5 M) and/or L-NAME (10-5 M) were assessed on aortic isolated rings. The main finding was that chronic hypoxia severely depressed maximal ACh-responses of aortic rings in both sedentary and trained groups. However, chronic hypoxia did not interfere with training-induced increases in maximal ACh-responses, considering that maximal ACh-vasorelaxation was improved in CHT rats to the same extent as in NT rats when both groups were directly compared to their sedentary counterparts. It should be pointed out that the vasodilator response to ACh was restored in CH and CHT rats to the level obtained in N and NT rats respectively, by an in vitro L-arginine addition. A hypoxia-induced decrease in L-arginine bioavailability resulting from acclimatization at altitude may be involved in this limitation of the NO pathway in CH and CHT rats. These results are of importance for aerobic performance as the specific vascular adaptations to training at altitude could contribute to limit peripheral vasodilatation and subsequently blood flow during exercise.
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