Effects of eccentric treadmill exercise on inflammatory gene expression in human skeletal muscle.
The present study examined the skeletal muscle expression of several genes related to the inflammatory process before and after a bout of downhill running. Twenty-nine males between the ages of 18 and 35 years performed a 45-min downhill (-17.5%) treadmill protocol at 60% of maximal oxygen consumption. Venous bloods samples and muscle biopsy samples from the vastus lateralis were donated prior to and at 3-h and 24-h postexercise, along with ratings of perceived muscle soreness. Serum creatine kinase (CK) was determined, as was skeletal muscle gene expression of interleukin (IL)-6, IL-8, IL-12 (p35), tumor necrosis factor-alpha (TNF-alpha), IL-1beta, cyclooxygenase 2 (COX2), and nuclear factor kappa B (NFkB) (p105/p50). Gene expression was analyzed using RT-PCR and compared with a standard housekeeping gene (beta-actin). Data were analyzed for statistical differences using multivariate analysis of variance with univariate follow-up. In addition, Pearson correlations were conducted to determine if any significant relationship exists between any of these transcripts and both CK and muscle soreness. Significant (p < 0.05) up-regulations in IL-6, IL-8, and COX2 mRNA expression were observed compared with baseline, whereas no significant changes for IL-12, IL-1beta, TNF-alpha, or NFkB were noted. Significant increases in IL-6 mRNA were observed at 3 h (p < 0.001) and 24 h (p = 0.043), whereas significant increases in IL-8 (p = 0.001) and COX2 (p = 0.046) mRNA were observed at 3-h postexercise. In addition, muscle soreness was significantly correlated with IL-8 at 24 h (r = -0.370; p = 0.048), whereas CK was significantly related to NFkB at baseline (r = -0.460; p = 0.012). These data indicate that increases in the mRNA expression of IL-6, IL-8, and COX2 occur in the vastus lateralis as a result of damaging eccentric exercise in young, recreationally trained males. Further, it appears that IL-8 transcription may play some role in inhibiting postexercise muscle soreness, possibly through regulation of angiogenesis.
Buford
Thomas W
TW
Exercise and Biochemical Nutrition Laboratory, Baylor University, Waco, TX 76798, USA.
Cooke
Matthew B
MB
Shelmadine
Brian D
BD
Hudson
Geoffrey M
GM
Redd
Liz
L
Willoughby
Darryn S
DS
D000293:Adolescent; D000328:Adult; D052283:Creatine Kinase, MM Form / Q000097:blood; D051546:Cyclooxygenase 2 / Q000235:genetics; D015444:Exercise; D005786:Gene Expression Regulation; D006801:Humans; D007249:Inflammation / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D018836:Inflammation Mediators / Q000378:metabolism*; D007378:Interleukins / Q000235:genetics; D008297:Male; D009119:Muscle Contraction / Q000235:genetics*; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000473:pathology; D016328:NF-kappa B / Q000235:genetics; D012333:RNA, Messenger / Q000378:metabolism*; D012420:Running; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics; D055815:Young Adult
D018836:Inflammation Mediators; D007378:Interleukins; D016328:NF-kappa B; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D052283:Creatine Kinase, MM Form