Quadriceps Arthrogenic Muscle Inhibition: Neurophysiological Mechanisms and Possible Therapeutic Interventions
Quadriceps arthrogenic muscle inhibition (AMI) is a near universal finding after knee joint injury, surgery and pathology; leading to marked quadriceps weakness that impairs physical function and may hasten joint degeneration. While AMI has been linked to a number of factors such as articular swelling, inflammation, pain, joint laxity and sensory receptor damage, its underlying neural mechanisms are poorly understood. Furthermore, interventions aimed at reversing AMI have been underdeveloped. As such, the aims of this thesis were to enhance our current understanding of AMI’s neurophysiological mechanisms and investigate the efficacy of three different interventions that may counteract AMI’s deleterious effects. The first study examined the efficacy of cryotherapy in reversing quadriceps AMI caused by experimental knee joint swelling. Healthy participants were randomly assigned to a cryotherapy or a control group. Quadriceps maximum effort voluntary contractions were performed at baseline, after the experimental infusion of saline dextrose into the knee joint and following 20 minutes of cryotherapy or a no intervention control period. Experimental joint swelling led to a significant reduction in knee extensor peak torque, electromyography amplitude and muscle fibre conduction velocity. Compared to the control group, cryotherapy led to a significant increase in knee extensor peak torque and muscle fibre conduction velocity. These findings suggest that cryotherapy may provide a useful adjunct to traditional resistance training in individuals with AMI. Study two explored the effects of experimental joint swelling and cryotherapy on quadriceps corticomotor excitability, short interval intracortical inhibition, intracortical facilitation and intermuscular coherence. Both swelling and cryotherapy led to a significant increase in the area of the quadriceps motor evoked potential but had no significant effect on short interval intracortical inhibition, intracortical facilitation or intermuscular coherence in the β-band. These findings suggest that joint swelling and cryotherapy lead to an increase in quadriceps corticomotor excitability that does not appear to be associated with increased excitability in the primary motor cortex. Study three examined the effects of knee joint aspiration and intraarticular corticosteroid injection on flexion reflex excitability and knee extensor peak torque in individuals with chronic arthritis. Flexion reflex threshold and knee extensor peak torque were measured at baseline, immediately after knee joint aspiration alone and 5 ± 2 and 15 ± 2 days after aspiration and corticosteroid injection. Both flexion reflex threshold and knee extensor peak torque increased immediately after joint aspiration and, to a greater degree, 5 ± 2 and 15 ± 2 days following aspiration and corticosteroid injection, suggesting that swelling and inflammation may increase flexion reflex excitability in humans, as has previously been shown in animals. The notable increase in knee extensor peak torque 15 ± 2 days after aspiration and corticosteroid injection indicates that this may be a clinically useful intervention to reverse AMI in individuals with chronic knee joint arthritis. Study four examined the effects of infrapatellar tendon vibration on knee extensor peak torque and electromyography amplitude in healthy controls, individuals with knee joint osteoarthritis and individuals who had recently undergone anterior cruciate ligament reconstruction. Following prolonged tendon vibration, knee extensor peak torque and electromyography amplitude decreased significantly in healthy controls, but did not change in the osteoarthritis or anterior cruciate ligament reconstruction groups, indicating a dysfunction in the gamma (γ)-loop pathway that may contribute to quadriceps AMI. All participants then attended a second testing session 6 ± 3 days later, where the effects of short duration tendon vibration on knee extensor peak torque and electromyography amplitude were investigated. A series of 12 maximum effort quadriceps contractions was performed under 4 different vibration conditions: 0 Hz, 5 Hz, 80 Hz and 200 Hz. The order of conditions was randomised for each participant and both the participant and tester were blinded to the vibration condition. There was no significant difference in knee extensor peak torque or electromyography amplitude across vibration conditions. As short duration tendon vibration failed to enhance quadriceps muscle activation in populations with an established γ-loop dysfunction, this may indicate an impairment in the afferent portion of the γ-loop or a failure of Ia afferent input to facilitate the quadriceps α-motoneuron pool in the presence of ongoing inhibition from other neural pathways. Findings from this thesis provide important new insights into the neurophysiological mechanisms underlying quadriceps AMI and potential therapeutic interventions that may negate its influence on rehabilitation. These observations will assist in the design of rehabilitation programmes that target AMI directly, helping to minimise muscle atrophy and enhance quadriceps strength gains after knee joint injury, knee surgery and in individuals with chronic knee joint pathology.
Quadriceps inhibition, Knee joint, Arthrogenic, Arthritis, Effusion, Muscle
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