Abstract
High intensity interval training (HIIT) is characterized by vigorous exercise with short rest intervals. Hydrogen peroxide (H2O2) plays a key role in muscle adaptation. This study aimed to evaluate whether HIIT promotes similar H2O2 formation via O2 consumption (electron leakage) in three skeletal muscles with different twitch characteristics. Rats were assigned to two groups: sedentary (n=10) and HIIT (n=10, swimming training). We collected the tibialis anterior (TA-fast), gastrocnemius (GAST-fast/slow) and soleus (SOL-slow) muscles. The fibers were analyzed for mitochondrial respiration, H2O2 production and citrate synthase (CS) activity. A multi-substrate (glycerol phosphate (G3P), pyruvate, malate, glutamate and succinate) approach was used to analyze the mitochondria in permeabilized fibers. Compared to the control group, oxygen flow coupled to ATP synthesis, complex I and complex II was higher in the TA of the HIIT group by 1.5-, 3.0- and 2.7-fold, respectively. In contrast, oxygen consumed by mitochondrial glycerol phosphate dehydrogenase (mGPdH) was 30% lower. Surprisingly, the oxygen flow coupled to ATP synthesis was 42% lower after HIIT in the SOL. Moreover, oxygen flow coupled to ATP synthesis and complex II was higher by 1.4- and 2.7-fold in the GAST of the HIIT group. After HIIT, CS activity increased 1.3-fold in the TA, and H2O2 production was 1.3-fold higher in the TA at sites containing mGPdH. No significant differences in H2O2 production were detected in the SOL. Surprisingly, HIIT increased H2O2 production in the GAST via complex II, phosphorylation, oligomycin and antimycin by 1.6-, 1.8-, 2.2-, and 2.2-fold, respectively. Electron leakage was 3.3-fold higher in the TA with G3P and 1.8-fold higher in the GAST with multiple substrates. Unexpectedly, the HIIT protocol induced different respiration and electron leakage responses in different types of muscle.
Highlights
The World Health Organization has stated that physical inactivity is the fourth leading risk factor for global mortality (6% of deaths worldwide), which is equivalent to approximately 3.2 million deaths per year [1]
In previous work [15], we demonstrated that High intensity interval training (HIIT) resulted in high endurance and low mitochondrial glycerol phosphate dehydrogenase activity
The effect of HIIT on mitochondrial respiration, which is supported by mitochondrial glycerol phosphate dehydrogenase (mGPdH) activity and multiple substrates, was not measured in different muscles
Summary
The World Health Organization has stated that physical inactivity is the fourth leading risk factor for global mortality (6% of deaths worldwide), which is equivalent to approximately 3.2 million deaths per year [1]. HIIT protocols shorten the total time spent on physical activity while producing the same work load [3, 4]. This training strategy is currently applied in humans as an alternative exercise intervention in different disease conditions, such as heart failure, hypertension, type II diabetes, obesity and chronic obstructive pulmonary disease [5,6,7,8,9,10]. In previous work [15], we demonstrated that HIIT resulted in high endurance and low mitochondrial glycerol phosphate dehydrogenase (mGPdH) activity. Decreased mGPdH activity has been previously demonstrated] 15], but the mitochondrial ROS production rate was not evaluated, and the effects of HIIT protocols on hydrogen peroxide (H2O2) generation are unknown
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