The applicants plan to study the regulatory mechanisms underlying compensation for the loss of contractile force that develops in severe neuromuscular fatigue. They propose six specific objectives to determine the mechanisms and characteristics of force regulation in normal human elbow muscles. First, they plan to characterize the dynamic relation between the stretch reflexes evoked in flexor muscles during the application of white noise angular perturbation at the elbow, when the subject establishes predetermined background torque. Using cross correlational techniques to relate the angular input to torque (or EMG) output, the applicants will derive impulse and frequency response descriptors of joint dynamic behavior in the normal and then in the fatigued state. Fatigue will be induced by sequence of near maximal voluntary contractions with duty cycle 4-1 over a period of several minutes. This protocol typically induces as much as 50-60% loss and contractile force. These data will allow the applicants to derive accurate comparisons of joint compliance and EMG responses before and after fatigue. To estimate changes in the intrinsic mechanical properties of muscle before and after fatigue the applicants plan to use a combination of rapid steps in which mechanical characteristics of muscle may be visualized prior to reflex or voluntary intervention, and electrical stimulation of elbow flexor muscles which would override reflex actions. These studies will allow the applicants to estimate the degree of changes in muscle contractile force, from which estimates of open loop feedback gain can be derived. These estimates of feedback force will then be compared with others derived from experimentally induced increases in force, which are mediated by electrical stimulation of a small number of motor axons within the muscle. Finally to determine which neurophysiological pathways are involved, they plan to examine the effects of conditioning soleus H reflexes by 1b heteronymous input derived from stimulation of the medial gastrocnemius muscle nerve. These conditioning effects will be evaluated before and after neuromuscular fatigue. If fatigue related effects impact 1b pathway gain then the magnitude of the conditioning stimulus should be enhanced. These studies should help in understanding the force regulatory mechanisms which are especially relevant to fatigue compensation but may well apply in a variety of neurological and neuromuscular disorders.
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