Stevens Jennifer E, Pathare Neeti C, Tillman Susan M, Scarborough Mark T, Gibbs C Parker, Shah Prithvi, Jayaraman Arun, Walter Glenn A, Vandenborne Krista
Department of Physical Therapy, University of Florida, P.O. Box 100154, Gainesville, Florida 32610, USA.
J Orthop Res. 2006 Aug;24(8):1729-36. doi: 10.1002/jor.20153.
Muscle atrophy is clearly related to a loss of muscle torque, but the reduction in muscle size cannot entirely account for the decrease in muscle torque. Reduced neural input to muscle has been proposed to account for much of the remaining torque deficits after disuse or immobilization. The purpose of this investigation was to assess the relative contributions of voluntary muscle activation failure and muscle atrophy to loss of plantarflexor muscle torque after immobilization. Nine subjects (ages 19-23) years with unilateral ankle malleolar fractures were treated by open reduction-internal fixation and 7 weeks of cast immobilization. Subjects participated in 10 weeks of rehabilitation that focused on both strength and endurance of the plantarflexors. Magnetic resonance imaging, isometric plantarflexor muscle torque and activation (interpolated twitch technique) measurements were performed at 0, 5, and 10 weeks of rehabilitation. Following immobilization, voluntary muscle activation (56.8 +/- 16.3%), maximal cross-sectional area (CSA) (35.3 +/- 7.6 cm(2)), and peak torque (26.2 +/- 12.7 N-m) were all significantly decreased ( p < 0.0056) compared to the uninvolved limb (98.0 +/- 2.3%, 48.0 +/- 6.8 cm(2), and 105.2 +/- 27.0 N-m, respectively). During 10 weeks of rehabilitation, muscle activation alone accounted for 56.1% of the variance in torque ( p < 0.01) and muscle CSA alone accounted for 35.5% of the variance in torque ( p < 0.01). Together, CSA and muscle activation accounted for 61.5% of the variance in torque ( p < 0.01). The greatest gains in muscle activation were made during the first 5 weeks of rehabilitation. Both increases in voluntary muscle activation and muscle hypertrophy contributed to the recovery in muscle strength following immobilization, with large gains in activation during the first 5 weeks of rehabilitation. In contrast, muscle CSA showed fairly comparable gains throughout both the early and later phase of rehabilitation.
肌肉萎缩显然与肌肉扭矩的丧失有关,但肌肉大小的减小并不能完全解释肌肉扭矩的下降。有人提出,肌肉神经输入减少是废用或固定后剩余扭矩不足的主要原因。本研究的目的是评估自愿性肌肉激活失败和肌肉萎缩对固定后跖屈肌扭矩丧失的相对贡献。9名(年龄19 - 23岁)单侧踝关节骨折的受试者接受了切开复位内固定治疗,并进行了7周的石膏固定。受试者参与了为期10周的康复训练,重点是跖屈肌的力量和耐力。在康复的第0、5和10周进行了磁共振成像、等长跖屈肌扭矩和激活(插值抽搐技术)测量。固定后,与未受伤肢体(分别为98.0±2.3%、48.0±6.8 cm²和105.2±27.0 N·m)相比,自愿性肌肉激活(56.8±16.3%)、最大横截面积(CSA)(3�.3±7.6 cm²)和峰值扭矩(26.2±12.7 N·m)均显著降低(p < 0.0056)。在10周的康复过程中,仅肌肉激活就占扭矩变化的56.1%(p < 0.01),仅肌肉CSA占扭矩变化的35.5%(p < 0.01)。CSA和肌肉激活共同占扭矩变化的61.5%(p < 0.01)。肌肉激活的最大增加发生在康复的前5周。自愿性肌肉激活的增加和肌肉肥大都有助于固定后肌肉力量的恢复,在康复的前5周激活有大幅增加。相比之下,肌肉CSA在康复的早期和后期阶段的增加相当。