Does exogenous coenzyme Q10 affect aerobic capacity in endurance athletes?
Weston SB, Zhou S, Weatherby RP, Robson SJ
The effect of orally supplemented coenzyme Q10 (CoQ10) on plasma CoQ10 concentration and aerobic capacity in endurance athletes was evaluated. Eighteen volunteer male road cyclists and triathletes, 8 in a CoQ10 supplementation group (QG) and 10 in a placebo group (PG), successfully completed the experimental protocol. Subjects were evaluated during and following graded cycling exercise tests, which were performed before and after 28 days of supplementation with 1 mg.kg-1.day-1 of CoQ10 or placebo. The presupplementation plasma CoQ10 concentration was significantly increased from 0.91 +/- 0.13 microgram.ml-1 to 1.97 +/- 0.27 microgram.ml-1 in QG following supplementation (p < .05). However, the CoQ10 supplementation regime had no consistently significant effect on oxygen uptake, anaerobic and respiratory compensation thresholds, blood lactate, glucose and triglyceride kinetics, heart rate, and blood pressure during and after graded cycling to exhaustion.
The effect of lifelong oral supplementation with ubiquinone Q10 (10 mg/kg/day) was examined in Sprague-Dawley rats and C57/B17 mice. There were no significant differences in survival or life-span found in either rats or mice. Histopathologic examination o f different rat tissues showed no differences between the groups. In Q10 supplemented rats, plasma and liver Q10 levels were 2.6 to 8.4 times higher at all age points than in control rats. Interestingly, in supplemented rats the Q9 levels also were signif icantly higher (p<0.05) in plasma and liver at ages 18 and 24 months. Neither Q9 nor Q10 levels were affected by supplementation in kidney, heart, or brain tissues. In spite of the significant changes in plasma and liver ubiquinone concentrations, life long Q10 supplementation did not prolong or shorten the lifespan of either rats or mice. Lonnrot K,et al;Biochem Mol Biol Int 1998 Apr;44(4):727-737
Energy metabolism defects in Huntington's disease and effects of coenzyme Q10.
Neurology Service, Massachusetts General Hospital and Harvard Medical School, Boston 02114, USA.
We investigated whether the Huntington's disease (HD) gene mutation may produce either primary or secondary effects on energy metabolism. 31P magnetic resonance spectroscopy demonstrated a significant decrease in the phosphocreatine
to inorganic phosphate ratio in resting muscle of 8 patients as compared with 8 control subjects. The cerebrospinal fluid lactate-pyruvate ratio was significantly increased in 15 patients as compared with 13 control subjects. Lactate concentrations assessed using 1H magnetic resonance spectroscopy are increased in Huntington's disease cerebral cortex. Treatment with coenzyme Q10, an essential cofactor of the electron transport chain, resulted in significant decreases in cortical lactate concentrations in 18 patients, which reversed following withdrawal of therapy. These findings provide evidence for a generalized energy defect in Huntington's disease, and suggest a possible therapy.