Abstract
AimExercise training induces adaptations in muscle and other tissue mitochondrial metabolism, dynamics, and oxidative phosphorylation capacity. Mitochondrial fatty acid oxidation was shown to be pivotal for the anti‐inflammatory status of immune cells. We hypothesize that exercise training can exert effects influence mitochondrial fatty acid metabolism in peripheral blood mononuclear cells (PBMCs). The aim was to investigate the effect of exercise on the fatty acid oxidation‐dependent respiration in PBMCs.DesignTwelve fasted or fed volunteers first performed incremental‐load exercise tests to exhaustion on a cycle ergometer to determine the optimal workload ensuring maximal health benefits in volunteers with a sedentary lifestyle. In addition, the same volunteers performed 60 min of low‐intensity constant‐load exercise.ResultsIn the incremental‐load exercise, the maximal whole‐body fat oxidation rate measured by indirect calorimetry was reached at the fasted state already at a 50 W workload. At the 75–175 W workloads, the contribution of fat oxidation significantly decreased to only 11%, the heart rate increased to 185 BPM, and the study participants reached exhaustion. These results show that low‐intensity exercise (50W) is optimal for maximal whole‐body fat utilization. After low‐intensity exercise, the ROUTINE mitochondrial respiration, as well as fatty acid oxidation‐dependent respiration in PBMCs at LEAK and OXPHOS states, were significantly increased by 31%, 65%, and 76%, respectively. In addition, during 60 min of low‐intensity (50W) exercise, a 2‐fold higher lipolysis rate was observed and 13.5 ± 0.9 g of fat was metabolized, which was 57% more than the amount of fat that was metabolized during the incremental‐load exercise.ConclusionsIn individuals with a sedentary lifestyle participating in a bicycle ergometry exercise program, maximal lipolysis and whole‐body fat oxidation rate is reached in a fasted state during low‐intensity exercise. For the first time, it was demonstrated that low‐intensity exercise improves bioenergetics and increases fatty acid oxidation in PBMCs and may contribute to the anti‐inflammatory phenotype.
Highlights
Obesity is a major public health problem that affects over 600 million adults worldwide, and physical activity is the most important intervention for the weight management, and for the prevention of metabolic and cardiovascular diseases (Golbidi & Laher, 2012; MacLeod, Terada, Chahal, & Boule, 2013; Malin et al, 2013; Sacre et al, 2014)
Metabolic adaptation in the immune cells is necessary to modulate immune cell functions as they are intricately coupled with intracellular metabolism (Fuller, Summers, & Valentine, 2017)
After low-intensity constant-load exercise the complex IV-linked respiration rate in peripheral blood mononuclear cells (PBMCs) was comparable with respiration rate before exercise, indicating that overall mitochondrial electron transfer system capacity is not changed after exercise. These results indicate that low-intensity constant load-exercise improves mitochondrial fatty acid oxidation in PBMCs
Summary
Obesity is a major public health problem that affects over 600 million adults worldwide, and physical activity is the most important intervention for the weight management, and for the prevention of metabolic and cardiovascular diseases (Golbidi & Laher, 2012; MacLeod, Terada, Chahal, & Boule, 2013; Malin et al, 2013; Sacre et al, 2014). Adaptive response to training is primarily translated into increased muscle endurance, enhanced vascular functions, and metabolism oxidative capacity. Most of the findings related to mitochondrial bioenergetics are clearly evidenced in skeletal muscle, it is poorly studied in other cell types. Results regarding exercise effects on mitochondrial function in PBMCs are inconclusive. Training increased the mitochondrial biogenesis and improved the antioxidant capacity of mitochondria in well-trained individual PBMCs (Busquets-Cortes et al, 2017). The mitochondrial function of PBMCs did not reflect interval training-induced changes in muscle mitochondria of young healthy men (Hedges et al, 2019). We hypothesize that exercise training can affect cell functionality and, thereby, can exert some effects on mitochondrial energy metabolism that have not been described in PBMCs
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