High-intensity exercise training ameliorates aberrant expression of markers of mitochondrial turnover but not oxidative damage in skeletal muscle of men with essential hypertension

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 - 2019/3

Y1 - 2019/3

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 6 weeks of high-intensity interval training (HIIT). Twenty four-hour ambulatory blood pressure, body composition, cardiorespiratory fitness, exercise capacity and skeletal muscle characteristics were examined before and after HIIT. Expression of markers of mitochondrial turnover, anti-oxidant protection and oxidative damage was 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. Expression of markers of anti-oxidant protection was similar in HYP and NORM, whereas oxidative damage was higher in HYP than in 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 protein content. 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 6 weeks of high-intensity interval training (HIIT). Twenty four-hour ambulatory blood pressure, body composition, cardiorespiratory fitness, exercise capacity and skeletal muscle characteristics were examined before and after HIIT. Expression of markers of mitochondrial turnover, anti-oxidant protection and oxidative damage was 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. Expression of markers of anti-oxidant protection was similar in HYP and NORM, whereas oxidative damage was higher in HYP than in 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 protein content. 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

SN - 1748-1708

VL - 225

JO - Acta Physiologica (Print)

JF - Acta Physiologica (Print)

IS - 3

M1 - e13208

ER -