High-intensity exercise training ameliorates aberrant expression of markers of mitochondrial turnover but not oxidative damage in skeletal muscle of men with essential hypertension
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High-intensity exercise training ameliorates aberrant expression of markers of mitochondrial turnover but not oxidative damage in skeletal muscle of men with essential hypertension. / Fiorenza, Matteo; Gunnarsson, Thomas P; Ehlers, Thomas Svare; Bangsbo, Jens.
In: Acta Physiologica (Print), Vol. 225, No. 3, e13208, 2019.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - High-intensity exercise training ameliorates aberrant expression of markers of mitochondrial turnover but not oxidative damage in skeletal muscle of men with essential hypertension
AU - Fiorenza, Matteo
AU - Gunnarsson, Thomas P
AU - Ehlers, Thomas Svare
AU - Bangsbo, Jens
N1 - CURIS 2019 NEXS 059
PY - 2019
Y1 - 2019
N2 - 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.
AB - 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.
KW - Faculty of Science
KW - Apoptosis
KW - Autophagy
KW - Blood pressure
KW - Endothelium nitric oxide synthase (eNOS)
KW - Mitochondrial biogenesis
KW - Mitochondrial dynamics
KW - Oxidative stress
KW - Reactive oxygen species (ROS)
U2 - 10.1111/apha.13208
DO - 10.1111/apha.13208
M3 - Journal article
C2 - 30339318
VL - 225
JO - Acta Physiologica
JF - Acta Physiologica
SN - 1748-1708
IS - 3
M1 - e13208
ER -
ID: 204085278