Weakness with OA – from antagonist cocontraction?

Smith & Nephew Journey Deuce Bi-compartmental unit) 2 of 3 Michael L. Baird's right knee as shown in x-ray 11 June 2008

This study was of interest to me after working with a patient with significant OA in one knee and one hip.

Heiden TL, Lloyd DG, Ackland TR. Knee extension and flexion weakness is people with knee osteoarthritis: is antagonist cocontraction a factor? J Orthop Sports Phys Ther. 2009;39:807-815.

Why the study matters: Quad weakness is a common impairment for those with knee OA, often impacting their daily lives. There are three possible factors that may contribute to weakness in knee extension and flexion in this population: “muscle atrophy, failure of voluntary muscle activity, and apparent weakness from increased antagonist muscle cocontraction.” In those with knee OA, atrophy has been noted in type 2 and type 1 fibers as well as reduced cross-sectional area for the vastus medialis. Other studies have shown a reduced ability to fully contract during knee extension, which could either be from not being able to recruit all motor units or a reduction in the rate that the motor units discharge. Finally co-contraction may be occurring to stabilize the knee and reduce its translation, thus creating the appearance of weakness.

Hypotheses: 1: participants with knee OA would have reduced knee flexion and extension strength compared to controls; 2: There would be no difference in voluntary activity during MVIC between the participants and controls; and 3: participants with knee OA would have more antagonist cocontraction during MVIC for flexion and extension than controls.

Outcome measures: EMG data taken on the quadriceps, hamstrings, and gastroc, with calculation of cocontraction ratios and net activation.

Subjects/ patients: 54 patients with knee OA (30F, 24M recruited through advertising and outpatient ortho clinic) visible on radiographic film, BMI <35, morning knee stiffness <30 min, did not use an AD, and had not received regular PT in past 12 months or steroid injections in last 6 months. These patients completed the Knee Osteoarthritis Outcomes Survey and were included based on their average score of <70 on the subscales (pain, sx, ADL, QoL). Twenty-seven controls (18F, 9M recruited through advertisements and university mainling lists) were recruited, with exclusion criteria of arthritis. Exclusion criteria for both were neuromuscular disease, cardiovascular disorders or recent surgery or injury to back or lower extremities (within 2 yrs).

Intervention: isometric testing of the involved leg using an isokinetic dynamometer, with three trials of MVIC’s for knee extension, knee flexion, and knee flexion/plantar flexion. They then calculated cocontraction ratios and net activation.

Results: Age and height was not significantly different between groups; KOOS scores were significant on all four subscales. Looking at BMI, extension and flexion strength of the experimental group was significantly less than for the control group, but knee flexion did not differ between treatment and control groups overall. A lack of extension strength was not due to quad inhibition or hamstring cocontraction.

What I would like to know more about: This study examined isometric strength – I would like a follow-up study for dynamic activities as that is where I see the problem in my patient.

How this will affect my clinical practice: For patients with knee OA, I’ll continue to work on strengthening the quads (this is the second study I’ve seen recently for knee OA that emphasized the importance of strengthening), and I may incorporate the KOOS after reviewing information on it.

Picture credit: Smith & Nephew Journey Deuce Bi-compartmental unit) 2 of 3 Michael L. Baird’s right knee as shown in x-ray 11 June 2008, originally uploaded by mikebaird.

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