Lifetime overproduction of circulating angiotensin‑(1‑7) in rats attenuates the increase in skeletal muscle damage biomarkers after exhaustive exercise.

Abstract

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.