On spinal mechanisms for reflex control in man modulation of Ia-afferent excitation with changes in muscle length, activation level and fatigue

Abstract: To control muscle force, neural activation has to take alterations in muscle mechanics into account. This thesis assesses modulations in excitatory efficacy of Ia-afferents during muscle length changes at different levels of voluntary activation and during fatigue. Excitatory efficacy of Iaafferents was inferred from modulations in the Hoffmann reflex (Hreflex) elicited in the triceps surae. The H-reflex is affected by the excitability of the motoneurones, as well as presynaptic inhibition of Iaafferents. The latter can be induced by primary afferent depolarization (PAD) and homosynaptic post activation depression (HPAD) within the terminal. The H-reflex was depressed with increasing velocities of passive plantar flexor lengthening and was smaller during passive muscle lengthening than when the muscles were isometric or undergoing passive shortening. The depression was probably induced by a peripheral mechanism since it was present at a latency too short for supra-spinal involvement. The rapid modulation and the velocity dependency suggest that during muscle lengthening, muscle spindle firing may have induced HPAD in the Ia-terminal. The H-reflex increased from passive to active lengthening, whereas it remained unchanged from passive to active shortening. Despite similar neural activation during the active tasks, the H-reflex was lower during muscle lengthening than shortening, indicating more presynaptic inhibition during lengthening. When Iaafferents were conditioned by electrical stimulation to emulate muscle spindle activation, the H-reflex was depressed only during passive shortening. No depression of the H-reflex during active shortening implies that HPAD was already present in the active condition. The lack of increase in the H-reflex from passive to active shortening may thus be caused by muscle spindle activation reducing the efficacy of Ia-excitation in the active muscle via HPAD. During fatigue from maximal voluntary intermittent isometric plantar flexor actions, both central and peripheral fatigue developed. The stronger the subjects and the higher their ability to fully activate the plantar flexors, the greater was the amount of peripheral fatigue. After the first bout, presynaptic inhibition had increased, most likely due to HPAD. During the fatigue protocol, the amount of presynaptic inhibition decreased slightly, either due to decreased PAD-mediated inhibition or due to less HPAD as a result of reduced muscle spindle firing. Having two separate mechanisms, independently capable of modulating the efficacy of Iaafferents, provides the central nervous system with a high flexibility for regulating motoneurone excitability.