The effect of joint velocity on the contribution of the antagonist musculature to knee stiffness and laxity

Abstract

The electromyographic (EMG) coactivation patterns of the knee flexors and extensors when acting as antagonists were studied as a function of limb velocity to assess their contribution to joint stiffness and laxity. Normalized antagonist coactivation patterns developed from surface EMG recordings from the hamstrings and quadriceps during maximal effort isokinetic extension and flexion, respectively, demonstrated characteristic variations as the joint velocity increased from 15 deg/sec up to 240 deg/sec. The two-tailed t-test (P less than 0.01) was performed on the data obtained from eight normal knees. The results indicate that both hamstrings and quadriceps demonstrate a significant increase (greater than 100%) in their antagonist coactivation pattern during the final 40 degrees of fast extension and flexion movements, respectively, as limb velocity increases. A minor decrease in antagonist activity of the hamstrings (24%) and quadriceps (8%) was evident during the initial phase of the extension and flexion movements, respectively, as joint velocity increased. We concluded that as limb velocity is increased, there is a substantial reflexive (unintentional) increase in the contribution of the antagonist musculature to joint stiffness and reduction of laxity. The results also suggest that strength training of the hamstrings (rather than quadriceps) should be considered as a modality for conservative treatment of ACL deficiencies, as well as an adjunct to surgical reconstruction. Such training can also reduce the risk of high performance athletes in a reflexive manner by increasing joint stiffness.

Antagonist moment of force during maximal knee extension in pubertal boys: effects of quadriceps fatigue

“…This can be attributed to the fact the knee extensors generate very low moments of force near extension ( Table 2). The above support previous EMG findings ( Baratta et al 1988;Hagood et al 1990;Solomonow et al 1987) indicating that the hamstrings may play an active role in maintaining joint stability, when the knee approaches knee extension. On the basis of this result, it can be suggested that the evaluation of the knee extensor isokinetic performance at various angular positions in children should take into consideration the antagonist hamstrings effect.…”

“…The antagonist activity of the hamstrings during maximal isokinetic efforts of the knee extensors has been extensively examined in adults (Aagaard et al 2000; Baratta et al 1988;Bobbert and Harlaar 1992;Hagood et al 1990;Kellis 1998;Solomonow et al 1987) and has been attributed to the stabilizing effect of these muscles in order to protect the knee from injury (Baratta et al 1988; Kellis and Baltzopoulos 1998;Psek and Cafarelli 1993;Solomonow et al 1987). Fewer studies examined the antagonist activity in children (Kellis and Unnithan 1999) and have not found significant differences in the normalized antagonist hamstring electromyographic (EMG) signal between children and adults.…”

Effects of Age, Power Output, and Cadence on Energy Expenditure and Lower Limb Antagonist Muscle Coactivation During Cycling

“…In summary, for our older participants, cycling at the higher cadence was metabolically more demanding but it was not accompanied by greater co-activation of antagonists about the knee and ankle compared to young individuals. Unlike results of studies on walking and stair negotiation, our results indicate that older adults may not be relying on increased antagonist co-activation to provide joint stabilization to compensate for increased joint laxity and reduced muscular strength when cycling at higher cadences (Hagood, Solomonow, Baratta, Zhou, & D'Ambrosia, 1990;Hortobágyi & DeVita, 2006). The physiological and mechanical demands of the cycling task increase with power output.…”

The force–velocity relationship of the human soleus muscle during submaximal voluntary lengthening actions

“…The reported magnitude of antagonist activation varies widely and may be influenced by many factors, such as the joint tested (for example, Behm and Sale 1996;Pousson et al 1999;Snow et al 1995), joint angle (Aagaard et al 2000a;Snow et al 1993Snow et al , 1995Solomonow et al 1986), angular velocity (Behm and Sale 1996;Carpentier et al 1996;Hagood et al 1990), training history (Amiridis et al 1996;Amiridis and Morlon 1995) and/or the functional demands of the task (Doorenbosch et al 1995). Inconsistencies in methodological procedures and the problems associated with calculating muscle forces in vivo make it difficult to accurately quantify the influence of antagonist co-activation on the resultant joint torque (Kellis 1998).…”