Mitochondria‐specific antioxidant supplementation does not influence endurance exercise training‐induced adaptations in circulating angiogenic cells, skeletal muscle oxidative capacity or maximal oxygen uptake

Abstract

Antioxidants have been shown to improve endothelial function and cardiovascular outcomes. However, the effects of antioxidants on exercise training-induced vascular adaptations remain elusive. General acting antioxidants combined with exercise have not impacted circulating angiogenic cells (CACs). We investigated whether mitochondria-specific antioxidant (MitoQ) supplementation would affect the response to 3 weeks of endurance exercise training on CD3 , CD3 /CD31 , CD14 /CD31 , CD31 , CD34 /VEGFR2 and CD62E peripheral blood mononuclear cells (PBMCs), muscle mitochondrial capacity, and maximal oxygen uptake (VO2 max ) in healthy men aged 22.1 ± 0.7 years, with a body mass index of 26.9 ± 0.9 kg m , and 24.8 ± 1.3% body fat. Analysis of main effects revealed that training induced 33, 105 and 285% increases in CD14 /CD31 , CD62E and CD34 /VEGFR2 CACs, respectively, and reduced CD3 /CD31 PBMCs by 14%. There was no effect of MitoQ on CAC levels. Also independent of MitoQ supplementation, exercise training significantly increased quadriceps muscle mitochondrial capacity by 24% and VO2 max by roughly 7%. In conclusion, endurance exercise training induced increases in multiple CAC types, and this adaptation is not modified by MitoQ supplementation. Furthermore, we demonstrate that a mitochondrial-targeted antioxidant does not influence skeletal muscle or whole-body aerobic adaptations to exercise training.

A mitochondrial‐targeted antioxidant improves myofilament Ca2+ sensitivity during prolonged low frequency force depression at low

“…The use of mitochondrial specific antioxidants is a step forward for controlling oxidant activity in specific cellular compartments without drastically affecting overall cellular redox state, different cellular functions and muscle adaptation to exercise (Shill et al . ).…”

“…glucose uptake, Sandström et al 2006; force development, Andrade et al 1998; and adaptation to exercise training, Kavdia, 2011), the use of antioxidants supplementation needs to be well deliberated to avoid blunting of ROS signalling. The use of mitochondrial specific antioxidants is a step forward for controlling oxidant activity in specific cellular compartments without drastically affecting overall cellular redox state, different cellular functions and muscle adaptation to exercise (Shill et al 2016).…”

Redox homeostasis and age‐related deficits in neuromuscular integrity and function

“…Although there is a large amount of evidence to suggest that MitoQ administration provides beneficial effects, recent studies in the field of muscle metabolism have shown that MitoQ was found to have no effect on exercise-induced adaptations in muscle oxidative capacity in humans. 308 Similarly, in the context of musculoskeletal ageing, MitoQ intervention in old mice failed to rescue the loss of muscle mass and function associated with ageing of skeletal muscle. 39 Overall, targeted antioxidant compounds such as SS-31 and MitoQ are clearly useful from a mechanistic perspective; however, the ability to translate these findings in a human context remains less clear.…”

Catalase overexpression modulates metabolic parameters in a new ‘stress-less’ leptin-deficient mouse model

“…Increases in fat mass, manifested as an increase in white adipose tissue (WAT), increases oxidative stress/oxidant production and results in an obese phenotype [11] characterized by a BMI (Body Mass Index) ≥ 30kg/m 2 [12]. The obese phenotype is accompanied by mitochondrial dysfunction and increased lipid peroxidation in adipose tissue, further leading to the dysfunction of other metabolic tissues such as liver, muscle, [11, 13] gut, and brain [14]. …”