TY - JOUR
T1 - Exercise and NSAIDs
T2 - effect on muscle protein synthesis in patients with knee osteoarthritis
AU - Petersen, Susanne Germann
AU - Miller, Ben F
AU - Hansen, Mette
AU - Kjaer, Michael
AU - Holm, Lars
PY - 2011/3
Y1 - 2011/3
N2 - Purpose: The purpose of this study was to determine muscle and tendon protein fractional synthesis rates (FSR) at rest and after a one-legged kicking exercise in patients with knee osteoarthritis (OA) receiving either placebo or nonsteroidal anti-inflammatory drugs (NSAIDs). Methods: Twenty patients with knee OA (50-70 yr) were enrolled. For each of the 3 days before the exercise intervention, 9 patients were administered NSAIDs (1200 mg), and 11 patients were administered placebo in a double-blinded manner. Each patient performed 60 min of one-legged kicking at 55% of workload maximum while the contralateral leg remained rested. Twenty-four hours after exercise, we determined circulating concentrations of inflammatory parameters and measured FSR of myofibrillar and sarcoplasmic protein fractions of vastus lateralis muscle and patellar tendon collagen protein by the direct incorporation method using a flooding dose of C/C-proline. Results: Circulating levels of prostaglandin F2α were lower in the NSAID group compared with the placebo group (P < 0.05). There was an overall significant effect of exercise on FSR in muscle myofibrillar (P = 0.003) and sarcoplasmic protein (P = 0.026) but not in tendon collagen protein (P = 0.52). No overall significant effect of the drug was seen on either of the tissue protein fractions (P > 0.05) or on the interaction between the drug and exercise on FSR in tendon collagen (P = 0.21), muscle myofibrillar (P = 0.68), or sarcoplasmic protein, FSR (P = 0.16). Conclusion: In elderly patients with knee OA, an acute bout of moderate exercise significantly increases FSR of muscle myofibrillar and sarcoplasmic protein, but not tendon collagen, 24 h after exercise. NSAID administration in patients with knee OA reduced the level of circulating prostaglandin F2α but did not diminish the exercise-induced response of muscle contractile protein FSR. However, we cannot exclude that a minor inhibition of muscle sarcoplasmic proteins may have been present with NSAID treatment. This study suggests that muscle hypertrophy after long-term training is not influenced by NSAIDs.
AB - Purpose: The purpose of this study was to determine muscle and tendon protein fractional synthesis rates (FSR) at rest and after a one-legged kicking exercise in patients with knee osteoarthritis (OA) receiving either placebo or nonsteroidal anti-inflammatory drugs (NSAIDs). Methods: Twenty patients with knee OA (50-70 yr) were enrolled. For each of the 3 days before the exercise intervention, 9 patients were administered NSAIDs (1200 mg), and 11 patients were administered placebo in a double-blinded manner. Each patient performed 60 min of one-legged kicking at 55% of workload maximum while the contralateral leg remained rested. Twenty-four hours after exercise, we determined circulating concentrations of inflammatory parameters and measured FSR of myofibrillar and sarcoplasmic protein fractions of vastus lateralis muscle and patellar tendon collagen protein by the direct incorporation method using a flooding dose of C/C-proline. Results: Circulating levels of prostaglandin F2α were lower in the NSAID group compared with the placebo group (P < 0.05). There was an overall significant effect of exercise on FSR in muscle myofibrillar (P = 0.003) and sarcoplasmic protein (P = 0.026) but not in tendon collagen protein (P = 0.52). No overall significant effect of the drug was seen on either of the tissue protein fractions (P > 0.05) or on the interaction between the drug and exercise on FSR in tendon collagen (P = 0.21), muscle myofibrillar (P = 0.68), or sarcoplasmic protein, FSR (P = 0.16). Conclusion: In elderly patients with knee OA, an acute bout of moderate exercise significantly increases FSR of muscle myofibrillar and sarcoplasmic protein, but not tendon collagen, 24 h after exercise. NSAID administration in patients with knee OA reduced the level of circulating prostaglandin F2α but did not diminish the exercise-induced response of muscle contractile protein FSR. However, we cannot exclude that a minor inhibition of muscle sarcoplasmic proteins may have been present with NSAID treatment. This study suggests that muscle hypertrophy after long-term training is not influenced by NSAIDs.
U2 - http://dx.doi.org/10.1249/MSS.0b013e3181f27375
DO - http://dx.doi.org/10.1249/MSS.0b013e3181f27375
M3 - Journal article
SN - 0195-9131
VL - 43
SP - 425
EP - 431
JO - Medicine and Science in Sports and Exercise
JF - Medicine and Science in Sports and Exercise
IS - 3
ER -