The Influence of Quercetin on Exercise Performance and Muscle Mitochondria. Part 4

Despite all of its promised potential, quercetin has not shown the striking effects in human clinical trials that were predicted from the in vitro or animal studies; at best, the human trials have shown only modest effect at lowering inflammation, and other studies have demonstrated no effect.
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Quercetin is extensively transformed in the gastrointestinal tract and liver and, once absorbed, rapidly metabolized into glucuronides and sulfate conjugates that are excreted with the bile. Some evidence exists that quercetin metabolites accumu¬late in the plasma albumin and that activated macrophages at the site of inflamed arteries can deconjugate these metabolites, recreating active quercetin that in turn suppresses foam cell formation. This form of ad hoc protective action would not be measured via the common parameters by which cardiovas-cular risk is assessed. Measuring quercetin’s protection of vascu¬lature structure may require histological examination of tissue rather than the simple monitoring of blood chemistry.

The prolonged and intensive physical exertion by endurance athletes and the resulting inflammation, oxidative stress, and lower immune protection leaves them at high risk of URTI. Athletes have been utilized as subjects in numerous clinical trials using a range of nutritional supplements including, zinc, omega-3 fats, plant sterols, antioxidants, N-acetyl-cysteine, glutamine, and others. To date, most of these trials have been disappointments. Only in recent trials have quercetin, EGCG, and omega-3 fats yielded promising results.

This information has obvious implications to our clinical practices. Dosing quercetin in combination with green tea and fish oil may increase its effectiveness.

Some of the studies about quercetin’s effect on exercise perfor¬mance have paid particular attention to the effect on mitochon¬dria and suggest a novel clinical use: increasing mitochondrial function within cells. If this proves true, then quercetin may not only be useful to increase performance, but also potentially to treat fatigue of mitochondrial origin.

For competitive athletes, even minuscule changes in performance may mean the difference between winning and losing; for researchers, however, these very small changes are difficult to perceive and prove. The effects of quercetin on performance in elite athletes were judged as modest at best. When the researchers tried a parallel clinical trial on untrained individuals, they produced more dramatic results.
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We should learn a number of things from these studies and bring them to our clinical practices. It is readily apparent that we must be cautious in translating animal studies to humans. Quercetin, like a number of other phytonutrients, appears to work better in mice than men. Oral supplementation of quer¬cetin to mice produces increases in serum concentrations, albeit at much higher doses, that are not replicated in human trials. Significant results seen in animal studies do not guarantee similar action in humans.

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