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Mitochondrial-targeted antioxidant ingestion acutely blunts VO2max in physically inactive females.

ABSTRACT: To determine the acute effects of a mitochondrial targeting antioxidant (MitoQ) on the metabolic response during exercise. Nine (n = 9) physically inactive females (age 47 ± 22 years) performed two trials (Placebo and MitoQ) in a double-blind randomized cross-over design. In both trials, participants performed an exercise protocol consisting of 3-min 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 and cardiovascular measurements were collected throughout the duration of the exercise bout. Submaximal metabolic and cardiovascular variables were not different between trials (p > 0.05). 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 cardiovascular variables and blood lactate were not different between trials (p > 0.05). An acute dose of MitoQ blunted VO2max , which was primarily mediated by impairment of ventilatory function. These data suggest that the acute accumulation of exercise-induced mitochondrial reactive oxygen species (mtROS) are necessary for maximal aerobic capacity. Further research is warranted on mtROS-antioxidant cell signaling cascades, and how they relate to mitochondrial function during exercise.

SUBMITTER: Hughes RP

PROVIDER: S-EPMC10703545 | biostudies-literature | 2023 Dec

REPOSITORIES: biostudies-literature

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Mitochondrial-targeted antioxidant ingestion acutely blunts VO<sub>2max</sub> in physically inactive females.

Hughes Ryan P RP Carlini Nicholas A NA Fleenor Bradley S BS Harber Matthew P MP

Physiological reports 20231201 23

<h4>Purpose</h4>To determine the acute effects of a mitochondrial targeting antioxidant (MitoQ) on the metabolic response during exercise.<h4>Methods</h4>Nine (n = 9) physically inactive females (age 47 ± 22 years) performed two trials (Placebo and MitoQ) in a double-blind randomized cross-over design. In both trials, participants performed an exercise protocol consisting of 3-min stages at submaximal workloads followed by a ramp protocol to volitional exhaustion. Participants received either Pl ...[more]

PMID: 38061764

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Project description:ObjectivesWe investigated the effect of reducing mitochondrial oxidative stress by the mitochondrial-targeted antioxidant peptide SS-31 in hypertensive cardiomyopathy.BackgroundOxidative stress has been implicated in hypertensive cardiovascular diseases. Mitochondria and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase have been proposed as primary sites of reactive oxygen species (ROS) generation.MethodsThe mitochondrial targeted antioxidant peptide SS-31 was used to determine the role of mitochondrial oxidative stress in angiotensin II (Ang)-induced cardiomyopathy as well as in Gαq overexpressing mice with heart failure.ResultsAng induces mitochondrial ROS in neonatal cardiomyocytes, which is prevented by SS-31, but not the nontargeted antioxidant N-acetyl cysteine (NAC). Continuous administration of Ang for 4 weeks in mice significantly increased both systolic and diastolic blood pressure, and this was not affected by SS-31 treatment. Ang was associated with up-regulation of NADPH oxidase 4 (NOX4) expression and increased cardiac mitochondrial protein oxidative damage, and induced the signaling for mitochondrial biogenesis. Reducing mitochondrial ROS by SS-31 substantially attenuated Ang-induced NOX4 up-regulation, mitochondrial oxidative damage, up-regulation of mitochondrial biogenesis, and phosphorylation of p38 mitogen-activated protein kinase and prevented apoptosis, concomitant with amelioration of Ang-induced cardiac hypertrophy, diastolic dysfunction, and fibrosis, despite the absence of blood pressure-lowering effect. The NAC did not show any beneficial effect. The SS-31 administration for 4 weeks also partially rescued the heart failure phenotype of Gαq overexpressing mice.ConclusionsMitochondrial targeted peptide SS-31 ameliorates cardiomyopathy resulting from prolonged Ang stimulation as well as Gαq overexpression, suggesting its potential clinical application for target organ protection in hypertensive cardiovascular diseases.

Dataset Information

Mitochondrial-targeted antioxidant ingestion acutely blunts VO2max in physically inactive females.

Publications

Mitochondrial-targeted antioxidant ingestion acutely blunts VO<sub>2max</sub> in physically inactive females.

Similar Datasets

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