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

Abstract

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, upregulated 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. K E Y W O R D S apoptosis, autophagy, endothelium nitric oxide synthase (eNOS), mitochondrial biogenesis, mitochondrial dynamics, oxidative stress

High-Intensity Interval Training Decreases Muscle Sympathetic Nerve Activity in Men With Essential Hypertension and in Normotensive Controls

“…It is notable that the hypertensive group did not improve theirVO 2 -max during the training intervention, which is in contrast to the normotensive group and to previous observations in similar patient groups implementing 10-20-30 cycling training (Fiorenza et al, 2019;Gunnarsson et al, 2020). ThatVO 2 -max did not improve with training in the hypertensive individuals of the present study is not easily explained as 7-8 weeks of 10-20-30 training improved thė VO 2 -max in trained runners (Gunnarsson and Bangsbo, 2012;Gliemann et al, 2015).…”

Efficacy of 10‐20‐30 training versus moderate‐intensity continuous training on HbA1c, body composition and maximum oxygen uptake in male patients with type 2 diabetes: A randomized controlled trial

“…In various patient groups, 10‐20‐30 training conducted as cycling lowered blood pressure and fat mass and increased fat‐free mass and V˙O 2 max, with a high compliance . Furthermore, 10‐20‐30 training decreased blood pressure and lipid profile and increased V˙O 2 max and performance in trained individuals .…”

“…An emerging exercise modality is 10‐20‐30 training, consisting of repeated 10‐second sprints followed by 30 and 20 seconds of low and moderate‐intensity exercise, respectively, eliciting a high aerobic and anaerobic load . 10‐20‐30 training elicits an average heart rate (HR) response similar to traditional HIIT (80%–95% of HR peak ) in patients with T2D, and higher than MICT (60%–80% of HR peak ) and SIT (~ 70% of HR peak ) .…”

Exercise and cardiovascular diseases

“…Hypertensive individuals demonstrate anomalous muscle mitochondrial turnover and amplified oxidative damage. However, high‐intensity exercise training showed that hypertension‐related impairments can be partly reversed 27 . We need more personalized research on physical activity; however, individualized approaches are often cost‐intensive.…”