Chronic swimming training counteracts sucrose intake increase induced by water deprivation and central angiotensin II

Angiotensin II (ANG II) induces water intake, sodium appetite and, more recently, its effects on sucrose intake have become interest. Chronic swimming training reduce plasma ANG II levels, basal sucrose intake, but not water intake. Therefore, this study investigated the chronic effect of swimming training on water and sucrose intake induced by 24-hour water deprivation or central injection of ANG II. Male Wistar rats from different cohorts remained sedentary (SED) or underwent swimming training (TR - 1 hour/day, 5 times/week, for 8 weeks, without additional load). Chronic effects of swimming and/or a sedentary lifestyle were checked three days after the end of the exercise protocol by two experiments. Experiment 1: WD-RP (water deprivation-partial rehydration protocol) to check water and sucrose solution intake. Experiment 2 and 3: Involvement of central ANG II (0.4 nmol/μl) and its antagonists (AT1 - losartan (50 nmol/μl) and AT2 - PD 123,319 (30 nmol/μl) in sucrose solution intake. Chronic swimming training prevented the increase in sucrose intake - but not water intake - induced by either water deprivation or central ANG II administration. Both angiotensinergic receptors (AT1 and AT2) are involved on basal sucrose intake (in both sedentary and trained rats) as well as in ANG II-induced sucrose intake (in sedentary rats). These findings suggest that ANG II plays an significant role in regulating sucrose intake, regardless of whether the animals were sedentary or trained. However, this mechanism appears attenuated in trained animals, suggesting that swimming training may activate unidentified pathways that limit ANG II-dependent sucrose intake.