title: Exercise reverses peripheral insulin resistance in trained L-NAME-hypertensive rats.
abstract: Several studies have demonstrated an increase in peripheral resistance to insulin associated with hypertension. To assess the hemodynamic and metabolic effects of exercise training, normotensive and N(omega)-nitro-L-arginine methyl ester (L-NAME)-hypertensive male Wistar rats were submitted to low-intensity treadmill exercise training for 10 weeks and compared with their sedentary controls. Blood pressure signals were obtained and processed with a data acquisition system (CODAS, 1 kHz) to evaluate mean arterial pressure, heart rate, autonomic control of heart rate, and baroreflex sensitivity. Exercise training induced a nonsignificant 6.5-mm Hg decrease in mean arterial pressure in trained hypertensive rats (163+/-9 mm Hg) compared with sedentary hypertensive rats (169.5+/-5. 5 mm Hg). The hypertensive groups showed impairment of baroreflex function in response to changes in arterial pressure compared with sedentary controls. Furthermore, exercise training improved the tachycardic response to decreasing arterial pressure and reduced intrinsic heart rate in trained control rats compared with all other groups. Sedentary hypertensive rats presented a decrease in body weight compared with normotensive animals. Basal evaluation of the glucose/insulin ratio showed increased insulin resistance in sedentary (28.4+/-3) and trained (23.5+/-2.7) hypertensive rats compared with sedentary control rats (40.5+/-3). However, the glucose/insulin ratio evaluated during the exercise session in trained rats showed an improvement in insulin resistance (54.5+/-5 for control rats and 44+/-9 for hypertensive rats). In conclusion, L-NAME-induced hypertension is accompanied by an increase in insulin resistance in rats. The improvement in peripheral insulin sensitivity during exercise and the body weight gain observed in trained hypertensive rats may support the positive role of physical activity in the management of hypertension.
authors.affiliation: Laboratory of Cardiovascular Physiology, Department of Physiology, Basic and Health Science Institute, University of Rio Grande do Sul, Brazil.
authors.forename: K
authors.initials: K
authors.lastname: De Angelis Lobo d'Avila
authors.forename: G
authors.initials: G
authors.lastname: Gadonski
authors.forename: J
authors.initials: J
authors.lastname: Fang
authors.forename: P
authors.initials: P
authors.lastname: Dall'Ago
authors.forename: V L
authors.initials: VL
authors.lastname: Albuquerque
authors.forename: L R
authors.initials: LR
authors.lastname: Peixoto
authors.forename: T G
authors.initials: TG
authors.lastname: Fernandes
authors.forename: M C
authors.initials: MC
authors.lastname: Irigoyen
mesh_terms: D000818:Animals; D006973:Hypertension / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology*; D007333:Insulin Resistance; D008297:Male; D019331:NG-Nitroarginine Methyl Ester; D010805:Physical Conditioning, Animal; D011311:Pressoreceptors / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D013564:Sympathetic Nervous System / Q000503:physiopathology*
chemical_list: D019331:NG-Nitroarginine Methyl Ester