Antagonist muscle coactivation

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Coactivation of antagonist muscles is involved in many types of joint movements [147,148]. Antagonist muscle coactivation could be important for several reasons: to protect ligaments at the end-range of joint motion [149,150], to ensure a homogeneous distribution of compression forces over the articular surfaces of the joint [i5i], and to increase joint stiffness thereby providing protection against external impact forces as well as enhancing the stiffness of the entire limb [152]. In addition, maximal antagonist muscle strength may play an important role in the execution of fast, ballistic limb movements. Thus, high eccentric antagonist strength allows for a shortened phase of limb deceleration, thereby increasing the time available for limb acceleration, with a resulting rise in maximal movement velocity [153].

Coactivation is elevated during either of two states: when uncertainty exists in the required task, or during anticipation of compensatory muscle forces [147]. During maximal coactivation, the monosynaptic excitatory pathway (Ia) as well as the disynaptic reciprocal inhibitory pathway (Ib) are exposed to spinal inhibition via descending supraspinal pathways

[154.155]. The increase in muscle and joint stiffness mainly results from a direct activation from the CNS with the cerebellum playing an important role in switching from reciprocal activation to coactivation

It is not well known whether strength training per se may induce altered patterns of antagonist coactiva-tion. Intuitively, a decrease in antagonist coactivation would seem desirable, as this would cause net joint moment (agonist joint moment minus antagonist joint moment) to increase. However, as implied above a decrease antagonist muscle coactivation may not be optimal for the integrity of the joint. Antagonist coactivation has been reported to decrease [77a, 158], increase [151] or remain unchanged [43,5o,76a,77a,i35,i57,i59,

160] in response to strength training. Häkkinen and coworkers [77a] found that coactivation of the lateral hamstring muscle during maximal isometric contraction of the quadriceps femoris was elevated in old subjects (70 years) compared to middle-aged subjects (40 years). However, after 6 months of heavy resistance-training coactivation decreased in the old subjects to reach a level similar to that recorded for the middle-aged subjects, which in turn did not change during the course of training [77a]. Given that antagonist coactivation is markedly elevated when uncertainty exists in the motor task, subjects may occasionally demonstrate very high levels of coactivation during the initial round of experiments. This may, at least in part, explain the decrease in antagonist coactivation that has been observed with training. To minimize this potential problem, conditioning tests could be conducted prior to the round of actual pretraining testing.

Interestingly, a differential change in antagonist motor pattern in terms of a selective decrease in medial (semitendinosus) but unchanged lateral (biceps femoris) hamstring EMG activity was observed in maximal isolated knee extension in response to 14 weeks of heavy-resistance training, involving isolated knee extension and squat exercises [ 157]. This adaptation indicates an important aspect of motor reprogramming, as it potentially counteracts excessive internal tibia rotation which otherwise may give rise to elevated stress forces in the anterior cruciate ligament (ACL) during active knee extension [150,161].

To obtain a valid measure of antagonist muscle coactivation it is crucial to ensure that the antagonist EMG signal is not contaminated by the EMG activity of adjacent agonist muscles, as a result of EMG crosstalk between electrode pairs [162,163]. The amount of cross-talk between two given EMG signals can be quantified by use of cross-correlation analysis [66,102]. Using a wide range of time phase shifts (i.e. from t=0 to t = ±50ms) and long record lengths (> 1500 data points), the peak cross-correlation coefficient raised to the second power, Rxy(t)2, may be taken to represent the percentage cross-talk between electrode sites [102]. Based on this methodology low levels of EMG cross-talk (4-6%) were demonstrated between adjacent quadriceps (agonist) and hamstring (antagonist) muscles in maximal isolated knee extension [164], although substantially higher values have also been reported [162]. Importantly, the level of cross-talk will depend strictly on the specific measuring set-up used, with electrode size and distance between electrodes being the most critical factors. The above findings therefore indicate that it may be possible, with careful experimental procedures, to minimize the magnitude of EMG cross-talk between antagonist and agonist muscles.

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