Effect of ubiquinol supplementation on biochemical and oxidative stress indexes after intense exercise in young athletes

Abstract

Objectives: Physical exercise significantly impacts the biochemistry of the organism. Ubiquinone is a key component of the mitochondrial respiratory chain and ubiquinol, its reduced and active form, is an emerging molecule in sport nutrition. The aim of this study was to evaluate the effect of ubiquinol supplementation on biochemical and oxidative stress indexes after an intense bout of exercise. Methods: 21 male young athletes (26 + 5 years of age) were randomized in two groups according to a double blind cross-over study, either supplemented with ubiquinol (200 mg/day) or placebo for 1 month. Blood was withdrawn before and after a single bout of intense exercise (40 min run at 85% maxHR). Physical performance, hematochemical parameters, ubiquinone/ubiquinol plasma content, intracellular reactive oxygen species (ROS) level, mitochondrial membrane depolarization, paraoxonase activity and oxidative DNA damage were analyzed. Results: A single bout of intense exercise produced a significant increase in most hematochemical indexes, in particular CK and Mb while, on the contrary, normalized coenzyme Q 10 plasma content decreased significantly in all subjects. Ubiquinol supplementation prevented exercise-induced CoQ deprivation and decrease in paraoxonase activity. Moreover at a cellular level, in peripheral blood mononuclear cells, ubiquinol supplementation was associated with a significant decrease in cytosolic ROS while mitochondrial membrane potential and oxidative DNA damage remained unchanged. Discussion: Data highlights a very rapid dynamic of CoQ depletion following intense exercise underlying an increased demand by the organism. Ubiquinol supplementation minimized exerciseinduced depletion and enhanced plasma and cellular antioxidant levels but it was not able to improve physical performance indexes or markers of muscular damage.

DNA Damage Following Acute Aerobic Exercise: A Systematic Review and Meta-analysis

“…The most common reason for study exclusion was the exercise protocol not consisting of acute and aerobic exercise. Thirty-nine studies (39) were included in the qualitative analysis, out of which one (1) was excluded due to same sample size [47], one had unpublished data [48], and two (2) due to non-extractable data [36,37], and therefore, thirty five (35) were included in the quantitative analysis.…”

Prolonged oral coenzyme Q10-β-cyclodextrin supplementation increases plasma CoQ10 concentration and skeletal muscle complex I+III activity in young, untrained healthy Thoroughbreds

“…For horses in active exercise training this may lead to improvements in responses to exercise training, delay in the onset of fatigue and enhanced recovery following intense exercise (Cooke et al, 2008; M. Kon et al, 2007; Michihiro Kon et al, 2008; Kwong et al, 2002; Mizuno et al, 2008). During exercise, movement of plasma CoQ 10 into skeletal muscle may increase due to increased metabolic demand (M. Kon et al, 2007; Orlando et al, 2018). This theory is supported by results from a study identifying increased post-exercise intramuscular CoQ 10 content in human athletes orally supplemented with CoQ 10 (Cooke et al, 2008).…”

“…In humans, chronic diseases such as chronic heart failure, hypertension and Parkinson’s disease are characterised by low plasma concentration and tissue CoQ 10 content, with CoQ 10 supplementation shown to improve clinical responses to treatment (Hofman-Bang, Rehnqvist, Swedberg, Wiklund, & Åström, 1995; Jankowski, Korzeniowska, Cieślewicz, & Jabłecka, 2016; Mortensen et al, 2014; Yang et al, 2015). Healthy human athletes have also been found to develop CoQ 10 deficiencies, believed to be due to increased metabolic demand (Cooke et al, 2008; M. Kon et al, 2007; Orlando et al, 2018; Zhou, Zhang, Davie, & Marshall-Gradisnik, 2005). Deficiencies in skeletal muscle CoQ 10 are thought to result in less efficient energy transduction due to decreased ETC activity and suboptimal ATP production (Lenaz et al, 1999), resulting in reduced effective skeletal muscle contractile function and earlier onset of fatigue (Cooke et al, 2008; M. Kon et al, 2007; Michihiro Kon et al, 2008; Kwong et al, 2002; Mizuno et al, 2008).…”

Three Months Monitored Metabolic Fitness Modulates Cardiovascular Risk Factors in Diabetic Patients

“…Paraoxonase-1 (PON-1) paraoxonase and arylesterase activities [12] and oxidized LDL levels by using enzyme-linked immunosorbent assay (ELISA) test (Oxidized LDL ELISA kit; Mercodia, Uppsala, Sweden) were evaluated in plasma. CACs isolation was performed from peripheral blood and microR-NA-21, -126, -130a, and -146a were evaluated [13].…”

“…Peripheral blood mononuclear cells were isolated to quantify DNA damage by using the alkaline version of the Comet Assay [14] and both intracellular ROS levels and mitochondrial membrane potential (MMP) flow-cytometrically (Guava InCyte software; Millipore, Burlington, MA, USA) [15] using 2-7-dichlorodihydro-fluorescein diacetate (DCFH-DA) [12] and 5´,6,6´tetrachloro-1,1´,3,3´-tetraethylbenzimidazolylcarbocyanine iodide (JC-1) [14] fluorescence probes, respectively.…”