Effect of anti-inflammatory medication on the running-induced rise in patella tendon collagen synthesis in humans
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Effect of anti-inflammatory medication on the running-induced rise in patella tendon collagen synthesis in humans. / Christensen, Britt; Dandanell, Sune; Kjaer, Michael; Langberg, Henning.
I: Journal of Applied Physiology, Bind 110, Nr. 1, 2011, s. 137-41.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › fagfællebedømt
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TY - JOUR
T1 - Effect of anti-inflammatory medication on the running-induced rise in patella tendon collagen synthesis in humans
AU - Christensen, Britt
AU - Dandanell, Sune
AU - Kjaer, Michael
AU - Langberg, Henning
PY - 2011
Y1 - 2011
N2 - NSAIDs are widely used in the treatment of inflammatory diseases as well as of tendon diseases associated with pain in sports and labor. However, the effect of NSAID intake, and thus blockade of PGE(2) production, on the tendon tissue adaptation is unknown. The purpose of the present study was to elucidate the possible effects of NSAID intake on healthy tendon collagen turnover in relation to a strenuous bout of endurance exercise. Fifteen healthy young men were randomly assigned into two experimental groups, with one group receiving indomethacin (oral 2 × 100 mg Confortid daily for 7 days; NSAID; n = 7) and a placebo group (n = 8). Both groups were exposed to a prolonged bout of running (36 km). The collagen synthesis NH2-terminal propeptide of type I (PINP) and PGE2 concentrations were measured before and 72 h following the run in the patella tendon by microdialysis. The peritendinous concentrations of PINP increased significantly in the placebo group as a result of the run, as shown previously. PGE2 levels were significantly decreased 72 h after the run compared with basal levels in the subjects treated with NSAID and unchanged in the placebo group. The NSAID intake abolished the adaptive increase in collagen synthesis in the patella tendon found in the placebo group in response to the prolonged exercise (P <0.05). The present study demonstrates that intake of NSAID decreased interstitial PGE2 and abolished the exercise-induced adaptive increase in collagen synthesis in human tendons.
AB - NSAIDs are widely used in the treatment of inflammatory diseases as well as of tendon diseases associated with pain in sports and labor. However, the effect of NSAID intake, and thus blockade of PGE(2) production, on the tendon tissue adaptation is unknown. The purpose of the present study was to elucidate the possible effects of NSAID intake on healthy tendon collagen turnover in relation to a strenuous bout of endurance exercise. Fifteen healthy young men were randomly assigned into two experimental groups, with one group receiving indomethacin (oral 2 × 100 mg Confortid daily for 7 days; NSAID; n = 7) and a placebo group (n = 8). Both groups were exposed to a prolonged bout of running (36 km). The collagen synthesis NH2-terminal propeptide of type I (PINP) and PGE2 concentrations were measured before and 72 h following the run in the patella tendon by microdialysis. The peritendinous concentrations of PINP increased significantly in the placebo group as a result of the run, as shown previously. PGE2 levels were significantly decreased 72 h after the run compared with basal levels in the subjects treated with NSAID and unchanged in the placebo group. The NSAID intake abolished the adaptive increase in collagen synthesis in the patella tendon found in the placebo group in response to the prolonged exercise (P <0.05). The present study demonstrates that intake of NSAID decreased interstitial PGE2 and abolished the exercise-induced adaptive increase in collagen synthesis in human tendons.
KW - Adult
KW - Anti-Inflammatory Agents, Non-Steroidal
KW - Collagen
KW - Dinoprostone
KW - Dose-Response Relationship, Drug
KW - Female
KW - Humans
KW - Indomethacin
KW - Male
KW - Patellar Ligament
KW - Physical Endurance
KW - Running
KW - Up-Regulation
U2 - 10.1152/japplphysiol.00942.2010
DO - 10.1152/japplphysiol.00942.2010
M3 - Journal article
C2 - 21030675
VL - 110
SP - 137
EP - 141
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
SN - 8750-7587
IS - 1
ER -
ID: 38363716