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Sir_Lukasz - tutaj chodzi o kwestię wrazliwosci insulinowej, której rozwój mogą niektore antyoksydanty blokowac (jesli dobrze pamiętam). Są badania ktoreto potwierdzają. Ja jak najbardziej widze miejsce dla zywnosci zawierającej antyoksydanty - okolotreningowo, ale nie widzę juz np sensu dorzucania 500mg wit C, czy innych wynalazkow specjalnie z suplementu.
Antyoksydanty na pewno nie bedą utrudniac regeneracji - więc to nie ona jest miarą werfikujacą ew ich wady
Zmieniony przez - faftaq w dniu 2010-04-16 10:19:37
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nie czytalem,
ale nie wydaje mi się.
spotkalem sie natomiast z podobnym dotego ponizej wnioskami:
Antioxidants prevent health-promoting effects of physical exercise in humans.
Ristow M, Zarse K, Oberbach A, Klöting N, Birringer M, Kiehntopf M, Stumvoll M, Kahn CR, Blüher M.
Department of Human Nutrition, Institute of Nutrition, University of Jena, Jena D-07743, Germany. [email protected]
Exercise promotes longevity and ameliorates type 2 diabetes mellitus and insulin resistance. However, exercise also increases mitochondrial formation of presumably harmful reactive oxygen species (ROS). Antioxidants are widely used as supplements but whether they affect the health-promoting effects of exercise is unknown. We evaluated the effects of a combination of vitamin C (1000 mg/day) and vitamin E (400 IU/day) on insulin sensitivity as measured by glucose infusion rates (GIR) during a hyperinsulinemic, euglycemic clamp in previously untrained (n = 19) and pretrained (n = 20) healthy young men. Before and after a 4 week intervention of physical exercise, GIR was determined, and muscle biopsies for gene expression analyses as well as plasma samples were obtained to compare changes over baseline and potential influences of vitamins on exercise effects. Exercise increased parameters of insulin sensitivity (GIR and plasma adiponectin) only in the absence of antioxidants in both previously untrained (P < 0.001) and pretrained (P < 0.001) individuals. This was paralleled by increased expression of ROS-sensitive transcriptional regulators of insulin sensitivity and ROS defense capacity, peroxisome-proliferator-activated receptor gamma (PPARgamma), and PPARgamma coactivators PGC1alpha and PGC1beta only in the absence of antioxidants (P < 0.001 for all). Molecular mediators of endogenous ROS defense (superoxide dismutases 1 and 2; glutathione peroxidase) were also induced by exercise, and this effect too was blocked by antioxidant supplementation. Consistent with the concept of mitohormesis, exercise-induced oxidative stress ameliorates insulin resistance and causes an adaptive response promoting endogenous antioxidant defense capacity. Supplementation with antioxidants may preclude these health-promoting effects of exercise in humans.