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The Journal of Neurophysiology Vol. 86 No. 3 September 2001, pp. 1086-1094
Copyright ©2001 by the American Physiological Society
1Sensory Motor Performance Program, Rehabilitation Institute of Chicago; and 2Department of Physical Medicine and Rehabilitation, 3Department of Orthopaedic Surgery, 4Department of Biomedical Engineering, and 5Department of Physiology, Northwestern University, Chicago, Illinois 60611
Zhang, Li-Qun and
W. Zev Rymer.
Reflex and Intrinsic Changes Induced by Fatigue of Human Elbow
Extensor Muscles. J. Neurophysiol. 86: 1086-1094, 2001. 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 bag2 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.
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