Reflex and intrinsic changes induced by fatigue of human elbow extensor muscles

Fatigue-induced changes in intrinsic and reflex properties of human elbow e xtensor muscles and the underlying mechanisms for fatigue compensation were investigated. The elbow joint was perturbed using small-amplitude and pseu dorandom movement patterns while subjects maintained steady levels of mean joint extension torque. Intrinsic and reflex properties were identified sim ultaneously 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 int ermittent voluntary isometric (submaximal) exercise, and a rest period of 1 0 min was taken to allow the fatigued muscles to recover from acute fatigue effects. Identical experimental and data analysis procedures were used bef ore and after fatigue. Our findings were that after fatigue, joint stiffnes s was significantly reduced at higher torque levels, presumably reflecting the reduced force-generating. capacity of fatigued muscles. Conversely, joi nt viscosity was increased after fatigue potentially because of the reduced crossbridge detachment rate and prolonged relaxation associated with intra cellular acidosis accompanying fatigue. Static stretch reflex gain decrease d 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, fibers. For matched pre- an d postfatigue torque levels, dynamic reflexes contributed relatively more t orque after fatigue, displaying hh,her dynamic reflex gains and larger dyna mic electromyographic responses elicited by the controlled small-amplitude. position perturbations. These changes appear to counteract the fatigue-ind uced reductions in joint stiffness and static reflex gain. The compensatory responses could be partly due to the effects of increasing the number of a ctive motoneurons innervating the fatiguing muscles. This shift in operatin g point gave rise to significant compensation for the. loss of contractile force. The compensation could also be due to fusimotor adjustment, which co uld make the dynamic reflex gain much less sensitive to fatigue than intrin sic stiffness. In short, the reduced contribution from intrinsic stiffness to joint torque was compensated by increased contribution from dynamic stre tch reflexes after fatigue.