Mitochondrial-targeted Antioxidant (MitoQ) Ingestion Acutely Blunts Vo2max In Physically Inactive Females

Background: Cardiorespiratory fitness (i.e., VO2max) is directly related to chronic disease risk and is lower in non-exercising individuals. Accumulation of reactive oxygen species (ROS) is also linked to the development of chronic disease yet the role of ROS in regulating VO2max and cardiopulmonary physiology during exercise is currently unknown. Purpose: To determine the acute effects of a mitochondrial targeting antioxidant (MitoQ) on cardiopulmonary and hemodynamic responses to maximal exercise. Methods: Nine (n = 9) physically inactive females (age 47 ± 22 years and BMI 28.5 ± 3.8 kg/m2) performed two trials (Placebo and MitoQ) in a double-blind randomized cross-over design. In both trials, participants performed an exercise protocol consisting of three-minute stages at submaximal workloads followed by a ramp protocol to volitional exhaustion. Participants received either Placebo or MitoQ (80 mg) 1 h prior to exercise. Indirect calorimetry, blood pressure, heart rate, blood lactate and rating of perceived exertion (RPE) were collected throughout the duration of the exercise bout. Results: VO2max was higher (p = 0.03) during Placebo (23.5 ± 5.7 mL•kg•min-1) compared to MitoQ (21.0 ± 6.6 mL•kg•min-1). Maximal ventilation was also higher (p = 0.02) in Placebo (82.4 ± 17.7 L/min) compared to MitoQ (75.0 ± 16.8 L/min). Maximal tidal volume was higher (p = 0.02) in Placebo (1.97 ± 0.35 L/min) than MitoQ (1.83 ± 0.40 L/min) whereas maximal breathing frequency was not different (p > 0.05) between Placebo (44.9 ± 7.0 Br/min) and MitoQ (43.6 ± 5.0 Br/min). Maximal heart rate, blood pressure, and blood lactate were not different between trials (p > 0.05). Conclusion: An acute dose of a mitochondrial targeted antioxidant blunted VO2max, which was primarily mediated by inhibition of ventilatory function. These data suggest that the acute accumulation of exercise-induced ROS are necessary for maximal aerobic capacity. Further research is warranted on ROS-related antioxidant cell signaling cascades, and how they relate to optimizing mitochondrial function during exercise.