Department of Orthopaedic Surgery, Faculty of Health Sciences, Institute of Sports Medicine, Bispebjerg Hospital and Centre for Healthy Ageing, University of Copenhagen, Copenhagen, Denmark.
Med Sci Sports Exerc. 2011 Mar;43(3):425-31. doi: 10.1249/MSS.0b013e3181f27375.
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).
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 13C/12C-proline.
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).
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.
本研究旨在确定接受非甾体抗炎药（NSAIDs）或安慰剂治疗的膝骨关节炎（OA）患者在休息和单腿踢腿运动后的肌肉和肌腱蛋白合成率（FSR）。
共纳入 20 例膝 OA 患者（50-70 岁）。在运动干预前的 3 天中，每天有 9 例患者接受 NSAIDs（1200mg），11 例患者接受双盲安慰剂治疗。每位患者以 55%最大工作负荷进行 60 分钟的单腿踢腿运动，同时对侧腿部保持休息。运动后 24 小时，我们通过直接掺入法测定循环中炎症参数的浓度，并测量股外侧肌肌原纤维和肌浆蛋白以及髌腱胶原蛋白的 FSR。该方法使用 13C/12C-脯氨酸的 flooding 剂量。
与安慰剂组相比，NSAID 组的前列腺素 F2α 循环水平较低（P<0.05）。运动对肌肉肌原纤维（P=0.003）和肌浆蛋白（P=0.026）的 FSR 有总体显著影响，但对肌腱胶原蛋白无显著影响（P=0.52）。药物对两种组织蛋白分数（P>0.05）或对药物与运动对肌腱胶原（P=0.21）、肌肉肌原纤维（P=0.68）或肌浆蛋白 FSR（P=0.16）的相互作用均无总体显著影响。
在老年膝骨关节炎患者中，单次中等强度运动可显著增加肌肉肌原纤维和肌浆蛋白的 FSR，但对肌腱胶原蛋白无影响，运动后 24 小时即可观察到。膝骨关节炎患者接受 NSAIDs 治疗可降低循环中前列腺素 F2α 的水平，但不会减弱运动引起的肌肉收缩蛋白 FSR 反应。然而，我们不能排除 NSAIDs 治疗可能会轻微抑制肌肉肌浆蛋白。本研究表明，长期训练后的肌肉肥大不受 NSAIDs 影响。
