Effects of intracerebroventricular microinjection of L-arginine on exercise capacity and expression of nitric oxide in rat hypothalamus.
- Author:
Jin-Juan XUE
1
;
Hong-Yu LIU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Arginine; administration & dosage; pharmacology; Hippocampus; metabolism; Hypothalamus; metabolism; Lateral Ventricles; Male; Nitric Oxide; metabolism; Physical Conditioning, Animal; Rats; Rats, Sprague-Dawley
- From: Chinese Journal of Applied Physiology 2013;29(2):158-161
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the relationship between nitric oxide (NO) in central nervous system and exercise-induced fatigue stress and to study the effect of L-arginine (L-Arg), as a substrate of nitric oxide, on the exercise capacity and NO content in the exhausted rat brain and blood.
METHODSThrough an implanted cannula, the normal saline or L-Arg was microinjected into rat's intracerebroventrical for consecutive four days. Then an acute exhaustive model (on the speed of 18 m/min, an inclination of 5 degrees) was established with animal treadmill. The time of exercise till exhaustion was recorded, and the total workload was calculated that represented the exercise capacity. Nitrate and nitrite (NO3/NO2-, NOx-) levels in blood, hypothalamus and hippocampus were assayed.
RESULTSBoth the time of exercise till exhaustion and total workload in the LArg group increased respectively by 51.8% and 50.08% (P < 0.05), compared with those in the control. The NOx- content in hypothalamus in the L-Arg group (8.93 +/- 1.83) micromol/g pro was larger than that in the control (4.25 +/- 0.79) micromol/g pro, (P < 0.01). There was no significant difference in NOx- content in brain and hippocampus between the two groups. The total workload was positively correlated with NOx- concentration in hypothalamus (P < 0.01). However, there was no correlation between workload and changes in hippocampus NOx- content at fatigue.
CONCLUSIONIntracerebroventricular microinjection of L-Arg may enhance the exercise capacity and lead to up-regulation of NO by means of L-Arg-NO signal path in the hypothalamus. Hypothalamus may be a key site in brain in the modulation of physiological exercise.