
Lifetime overproduction of circulating angiotensin-(1-7) in rats attenuates the increase in skeletal muscle damage biomarkers after exhaustive exercise
Author(s) -
Lenice Kappes Becker,
Nádia Lúcia Totou,
Mariana Oliveira,
Daniel Barbosa Coelho,
Emerson Cruz de Oliveira,
Daisy MottaSantos,
Emerson Silami Garcia,
Maria José CampagnoleSantos,
Robson Augusto Souza Santos
Publication year - 2019
Publication title -
chinese journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.396
H-Index - 31
eISSN - 2666-0059
pISSN - 0304-4920
DOI - 10.4103/cjp.cjp_57_19
Subject(s) - medicine , endocrinology , skeletal muscle , angiotensin ii , chemistry , lactate dehydrogenase , creatine kinase , glycogen , blood pressure , biochemistry , enzyme
Angiotensin-(1-7) (Ang-[1-7]) can modulate glucose metabolism and protect against muscular damage. The aim of this study was to investigate the influence of lifetime increase of circulating levels of Ang-(1-7) at exhaustive swimming exercise (ESE). Sprague-Dawley (SD) and transgenic rats TGR(A1-7)3292 (TR) which overproduce Ang-(1-7) (2.5-fold increase) were submitted to ESE. The data showed no differences in time to exhaustion (SD: 4.90 ± 1.37 h vs. TR: 5.15 ± 1.15 h), creatine kinase, and transforming growth factor beta (TGF-β). Lactate dehydrogenase (SD: 219.9 ± 12.04 U/L vs. TR: 143.9 ± 35.21 U/L) and α-actinin (SD: 336.7 ± 104.5 U/L vs. TR: 224.6 ± 82.45 U/L) values were significantly lower in TR. There was a significant decrease in the range of blood glucose levels (SD: -41.4 ± 28.32 mg/dl vs. TR: -13.08 ± 39.63 mg/dl) in SD rats. Muscle (SD: 0.06 ± 0.02 mg/g vs. TR: 0.13 ± 0.01 mg/g) and hepatic glycogen (SD: 0.66 ± 0.36 mg/g vs. TG: 2.24 ± 1.85 mg/g) in TR were higher. The TR presented attenuation of the increase in skeletal muscle damage biomarkers and of the changes in glucose metabolism after ESE.