Cellular Response To Exercise Induced Oxidative Stress And The Effect Of Diet Composition In Trained Athletes

Abstract

Intense exercise is known to increase free radical production resulting in increased oxidative damage. This results in the up regulation of genes that protect cells against adverse effects of oxidative stress and induces the expression of NADPH ubiquinone oxidoreductase (NQO1) and heme oxygenase-1 (HO1). It has recently been suggested that NQO1 can directly scavenge superoxide radicals. In addition, HO1 has been shown to increase following muscular contractions. However, there are few studies that have examined the effects of dietary fat on exercise-induced oxidative stress. PURPOSE To compare the effects of a low vs. a moderate fat diet on the induction of NQO1, HO1 and uncoupling proteins 2 and 3 (UCP 2 and 3) at rest and in response to an acute bout of high intensity endurance exercise. METHODS In a randomly assigned cross over design, 11 male (27±9y, 68.4±4.9kg, 13±2%, VO2max = 64.7+6.6ml/kg/min) and 10 female (29±7y, 56.2±4.9kg, 21±2%, VO2max = 53.1±5.4ml/kg/min) endurance runners performed a 90-minute run at 65% VO2max immediately followed by a 10K time trial. Four days prior to the exercise bout, participants completed a 2-h run (65% VO2max; designed to lower intramyocellular lipid stores) and were then assigned to either a low (10%) or moderate (35%) fat diet for 3 days. A glycogen loading diet was provided the day before the test to equalize glycogen stores. Using quantitative RT-PCR, the expression of NQO1, HO1 UCP2, and UCP3L was measured in the vastus lateralis (via biopsy) before and after the time trial. RESULTS NQO1 expression was significantly increased (p = 0.025) immediately post exercise and was not affected by diet treatment. HO-1 (p = 0.001) expression was also increased following exercise on the low-fat diet but was attenuated on the moderate fat diet. UCP2 and UCP3 expression was not affected by exercise or diet. CONCLUSIONS Exercise-induced oxidative stress results in the up regulation of HO1 and NQO1 in endurance-trained athletes. Furthermore, the induction of NQO1 may be affected by the amount of dietary fat.