Zhang L Q, Rymer W Z
Sensory Motor Performance Program, Rehabilitation Institute of Chicago, Northwestern University, Chicago, IL 60611, USA.
J Neurophysiol. 2001 Sep;86(3):1086-94. doi: 10.1152/jn.2001.86.3.1086.
Fatigue-induced changes in intrinsic and reflex properties of human elbow extensor muscles and the underlying mechanisms for fatigue compensation were investigated. The elbow joint was perturbed using small-amplitude and pseudorandom movement patterns while subjects maintained steady levels of mean joint extension torque. Intrinsic and reflex properties were identified simultaneously using a nonlinear delay differential equation model. Intrinsic joint properties were characterized by measures of joint stiffness, viscous damping, and limb inertia and reflex properties characterized by measures of dynamic and static reflex gains. Fatigue was induced using 15 min of intermittent voluntary isometric (submaximal) exercise, and a rest period of 10 min was taken to allow the fatigued muscles to recover from acute fatigue effects. Identical experimental and data analysis procedures were used before and after fatigue. Our findings were that after fatigue, joint stiffness was significantly reduced at higher torque levels, presumably reflecting the reduced force-generating capacity of fatigued muscles. Conversely, joint viscosity was increased after fatigue potentially because of the reduced crossbridge detachment rate and prolonged relaxation associated with intracellular acidosis accompanying fatigue. Static stretch reflex gain decreased significantly at higher torque levels after fatigue, indicating that the isometric fatiguing exercise might be associated with a preferential change in properties of spindle chain fibers and bag(2) fibers. For matched pre- and postfatigue torque levels, dynamic reflexes contributed relatively more torque after fatigue, displaying higher dynamic reflex gains and larger dynamic electromyographic responses elicited by the controlled small-amplitude position perturbations. These changes appear to counteract the fatigue-induced reductions in joint stiffness and static reflex gain. The compensatory responses could be partly due to the effects of increasing the number of active motoneurons innervating the fatiguing muscles. This shift in operating point gave rise to significant compensation for the loss of contractile force. The compensation could also be due to fusimotor adjustment, which could make the dynamic reflex gain much less sensitive to fatigue than intrinsic stiffness. In short, the reduced contribution from intrinsic stiffness to joint torque was compensated by increased contribution from dynamic stretch reflexes after fatigue.
研究了疲劳引起的人体肘部伸肌内在和反射特性的变化以及疲劳补偿的潜在机制。在受试者保持平均关节伸展扭矩稳定水平的同时，使用小幅度伪随机运动模式扰动肘关节。使用非线性延迟微分方程模型同时识别内在和反射特性。内在关节特性通过关节刚度、粘性阻尼和肢体惯性的测量来表征，反射特性通过动态和静态反射增益的测量来表征。通过15分钟的间歇性自愿等长（次最大）运动诱导疲劳，并休息10分钟以使疲劳肌肉从急性疲劳效应中恢复。在疲劳前后使用相同的实验和数据分析程序。我们的研究结果表明，疲劳后，在较高扭矩水平下关节刚度显著降低，这可能反映了疲劳肌肉产生力的能力下降。相反，疲劳后关节粘性增加，这可能是由于疲劳伴随的细胞内酸中毒导致横桥解离速率降低和松弛延长。疲劳后，在较高扭矩水平下静态牵张反射增益显著降低，这表明等长疲劳运动可能与纺锤链纤维和袋状（2）纤维特性的优先变化有关。对于疲劳前后匹配的扭矩水平，疲劳后动态反射贡献的扭矩相对更多，表现出更高的动态反射增益和由受控小幅度位置扰动引起的更大动态肌电图反应。这些变化似乎抵消了疲劳引起的关节刚度和静态反射增益的降低。这种补偿反应可能部分归因于支配疲劳肌肉的活性运动神经元数量增加的影响。这种工作点的转变对收缩力的损失产生了显著补偿。这种补偿也可能归因于肌梭运动调节，这可以使动态反射增益比内在刚度对疲劳的敏感性低得多。简而言之，疲劳后内在刚度对关节扭矩的贡献减少，由动态牵张反射的贡献增加所补偿。
