Key result
Angiotensin 1-7 overproduction in rats reduces post-exercise lactate dehydrogenase by ~35% and attenuates muscle damage.
Why the study?
Angiotensin-(1-7) can modulate glucose metabolism and protect against muscular damage, but the influence of lifetime increased circulating levels during exhaustive swimming exercise was unknown.
Does lifetime overproduction of circulating angiotensin-(1-7) attenuate skeletal muscle damage and alter glucose metabolism after exhaustive exercise in rats?
Does lifetime overproduction of circulating angiotensin-(1-7) attenuate skeletal muscle damage and alter glucose metabolism after exhaustive exercise in rats?
Absolute Event Rate: 143.9% vs 219.9%
Lifetime overproduction of Ang-(1-7) in rats attenuates skeletal muscle damage biomarkers and preserves glycogen stores following exhaustive exercise.
May attenuate exercise-induced muscle damage in rats; hypothesis-generating, leaves open human translation.
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.
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Oliveira et al. (2019) studied Skeletal muscle damage after exhaustive exercise. Lifetime overproduction of circulating Ang-(1-7) vs. Sprague-Dawley (SD) rats was evaluated on Lactate dehydrogenase (LDH) levels. Lifetime overproduction of Ang-(1-7) in rats attenuated skeletal muscle damage after exhaustive exercise, with significantly lower lactate dehydrogenase (143.9 vs 219.9 U/L) compared to controls.
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