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1 Copenhagen Muscle Research Centre, Denmark2 Department of Infectious Diseases, Rigshospitalet University Hospital of Copenhagen, Denmark3 Skeletal Muscle Research Group, School of Medical Sciences, Royal Melbourne Institute of Technology, Victoria, Australia4 Department of Medical Anatomy, The Panum Institute, University of Copenhagen, Denmark5 Clinical Nutrition Research, Department of Public Health and Caring Sciences/Geriatrics, University of Uppsala, Sweden6 Division of Clinical Chemistry, Karolinska University Hospital, Sweden7 Research and Quality Department, Semper Foods AB, Stockholm, Sweden
Contracting human skeletal muscle is a major contributor to the exercise-induced increase of plasma interleukin-6 (IL-6). Although 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 randomization, young healthy men received an oral supplementation with either a combination of ascorbic acid (500 mg day–1) and RRR-
-tocopherol (400 i.u. day–1) (Treatment, n= 7), or placebo (Control, n= 7). After 28 days of supplementation, the subjects performed 3 h 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 3 h 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 between 0 and 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 to 4 h, when the arterial IL-6 levels peaked in both groups, was 
50% lower in the Treatment group compared to Control (Treatment versus Control: 7.9 pg ml–1, 95% confidence interval (CI) 6.0–10.7 pg ml–1, versus 19.7 pg ml–1, CI 13.8–29.4 pg ml–1, at 3.5 h, P < 0.05 between groups). Moreover, plasma interleukin-1 receptor antagonist (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 vitamins 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.
(Received 20 April 2004;
accepted after revision 24 May 2004;
first published online 28 May 2004)
Corresponding author C. P. Fischer: Department of Infectious Diseases, Rigshospitalet University Hospital of Copenhagen, Denmark. Email: cfischer{at}rh.dk
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