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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
Author(s) -
Fiorenza Matteo,
Gunnarsson Thomas P.,
Ehlers Thomas S.,
Bangsbo Jens
Publication year - 2019
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/apha.13208
Subject(s) - mitochondrial biogenesis , cardiorespiratory fitness , medicine , skeletal muscle , endocrinology , mitochondrial fission , oxidative stress , mitochondrion , tfam , enos , oxidative phosphorylation , biology , nitric oxide synthase , microbiology and biotechnology , biochemistry , nitric oxide
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.