High-intensity exercise training ameliorates aberrant expression of markers of mitochondrial turnover but not oxidative damage in skeletal muscle o…
Authors of this article are:
Fiorenza M, Gunnarsson TP, Ehlers TS, Bangsbo J.
A summary of the article is shown below:
AIM: To examine whether hypertensive individuals exhibit altered muscle mitochondrial turnover and redox homeostasis compared with healthy normotensive counterparts, and whether the antihypertensive effect of high-intensity exercise training is associated with improved mitochondrial quality and enhanced anti-oxidant defence.METHODS: In a cross-sectional and longitudinal parallel design, 24 essential hypertensive (HYP) and 13 healthy normotensive (NORM) men completed six weeks of high-intensity interval training (HIIT). 24-h ambulatory blood pressure, body composition, cardiorespiratory fitness, exercise capacity and skeletal muscle characteristics were examined before and after HIIT. Protein levels of markers of mitochondrial turnover, anti-oxidant protection and oxidative damage were determined in vastus lateralis muscle biopsies. Muscle protein levels of eNOS and VEGF, and muscle capillarity were also evaluated.RESULTS: At baseline, HYP exhibited lower expression of markers of mitochondrial volume/biogenesis, mitochondrial fusion/fission and autophagy along with depressed eNOS expression compared with NORM. Content of markers of anti-oxidant protection was similar in HYP and NORM, whereas oxidative damage was higher in HYP than NORM. In HYP, HIIT lowered blood pressure, improved body composition, cardiorespiratory fitness and exercise capacity, up-regulated markers of mitochondrial volume/biogenesis and autophagy and increased eNOS and VEGF expression. Furthermore, in HYP, HIIT induced divergent responses in markers of mitochondrial fusion and anti-oxidant protection, did not affect markers of mitochondrial fission, and increased apoptotic susceptibility and oxidative damage.CONCLUSION: The present results indicate aberrant muscle mitochondrial turnover and augmented oxidative damage in hypertensive individuals. High-intensity exercise training can partly reverse hypertension-related impairments in muscle mitochondrial turnover, but not redox imbalance. This article is protected by copyright. All rights reserved.This article is protected by copyright. All rights reserved.
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This article is a good source of information and a good way to become familiar with topics such as:
apoptosis;autophagy;blood pressure;endothelium nitric oxide synthase (eNOS);mitochondrial biogenesis;mitochondrial dynamics;oxidative stress;reactive oxygen species (ROS)
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