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Received April 20, 2004
Revised May 17, 2004
Accepted after revision May 24, 2004
1 University of Copenhagen
2 Royal Melbourne Institute of Technology
3 University of Copenhagen, The Panum Institute
4 University of Uppsala
5 Karolinska University Hospital
6 Semper Foods AB
* To whom correspondence should be addressed. E-mail: cfischer{at}rh.dk.
Contracting human skeletal muscle is a major contributor to the exercise-induced increase of plasma interleukin-6 (IL-6). Though antioxidants have been shown to attenuate the exercise-induced increase of plasma IL-6, it is unknown whether antioxidants inhibit transcription, translation or translocation of IL-6 within contracting human skeletal muscle. Using a single-blind placebo-controlled design with randomisation, young healthy men received an oral supplementation with either a combination of ascorbic acid 500 mg day-1 and RRR-
-tocopherol 400 IU day-1 (Treatment, n = 7), or placebo (Control, n = 7). After 28 days of supplementation, the subjects performed three hours of dynamic two-legged knee-extensor exercise at 50% of their individual maximal power output. Muscle biopsies from vastus lateralis were obtained at rest (0 h), immediately post exercise (3 h) and after three hours of recovery (6 h). Leg blood flow was measured using Doppler ultrasonography. Plasma IL-6 concentration was measured in blood sampled from the femoral artery and vein. The net release of IL-6 was calculated using Fick's principle. Plasma vitamin C and E concentrations were elevated in Treatment compared to Control. Plasma 8-iso-prostaglandin F2, a marker of lipid peroxidation, increased in response to exercise in Control, but not in Treatment. In both Control and Treatment skeletal muscle IL-6 mRNA and protein levels increased from 0 h to 3 h. In contrast, the net release of IL-6 from the leg, which increased during exercise with a peak at 3.5 h in Control, was completely blunted during exercise in Treatment. The arterial plasma IL-6 concentration from 3 h to 4 h, where the arterial IL-6 levels peaked in both groups, was ~50% lower in the Treatment group compared to the Control (7.9 pg ml-1, CI 6.0-10.7 pg ml-1, at 3.5 h in Treatment versus 19.7 pg ml-1, CI 13.8-29.4 pg ml-1, at 3.5 h in Control, P < 0.05 between groups). Moreover, plasma IL-1ra, C-reactive protein and cortisol levels all increased after the exercise in Control, but not in Treatment. In conclusion, our results show that supplementation with vitamin C and E attenuated the systemic IL-6 response to exercise primarily via inhibition of the IL-6 protein release from the contracting skeletal muscle per se.
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