This study intended to determine if persons with different severities of knee OA utilized altered muscle coordination strategies at the knee during walking that would result in higher co-contraction values. Consistent with previous literature we found higher levels of antagonistic activity in the pathological groups during walking (Hortobagyi et al., 2005
; Lewek et al., 2006
; Ramsey et al., 2007
; Rudolph et al., 2007
; Schmitt and Rudolph, 2007
). However, in the current study, we analyzed subjects with varying degrees of knee OA, as well as different walking conditions. From this study we discerned that faster walking speeds resulted in higher co-contraction values for all groups. We also concluded that irrespective of speed, subjects with knee OA utilized control strategies that resulted in higher levels of antagonistic muscle activity.
The fact that differences were seen at the control speed (1.0 m/s) and differences were significant when analyzed with respect to speed, suggests that differences in co-contraction seen in individuals with OA are related to intrinsic differences, not merely artifacts of different freely chosen walking speeds. Studies evaluating kinematic and kinetic gait parameters in persons with knee OA have found that walking speed significantly influences results (Bejek et al., 2006
). Similar alterations in gait parameters have also been found in persons with hip OA (Mockel et al., 2003
). For this reason, it was important that we ascertain if muscle activation patterns change in response to external moments and forces that are associated with different walking speeds and not to pathology. While controlling walking speed reduces differences in joint kinematics and kinetics that may be related to freely chosen walking speed, it may still alter control strategies. In order to ensure all subjects would be able to achieve the control walking speed, we chose a value for the control speed that was closer to the self-selected speed in the severe group. This resulted in subjects in the control group reducing their normal walking speed, and subjects with severe OA potentially increasing their walking speed to achieve 1.0 m/s. While this may confound the results, using speed as a covariate at the self-selected and fast walking speeds removes the effect of different walking speeds, and highlights individual differences in co-activation strategies. Using this method, it appears that persons with knee OA utilize a coordination strategy that results in higher CCI values independent of the speed at which they walk.
Previous authors have also suggested that reduction in walking speed may be a compensatory method utilized to reduce joint loading at the knee (Mundermann et al., 2004
). While reducing walking speed has been suggested as a mechanism to reduce compressive forces (Robon et al., 2000
), magnitude of external reaction forces (Bejek et al., 2006
) and muscle activity associated with knee motion (Chiu and Wang, 2007
; Liu et al., 2008
), alterations in walking speed did not account for the differences in CCI seen in this study. While mean CCI values were higher at the fast walking speed for all the groups, the fact that significant differences were found when speed was used as a covariate at the self-selected speed suggests that the reduction in self-selected walking speed in persons with OA does not effectively reduce antagonistic muscle activity to normal levels. This is a very important finding and contrasts with the suggestion that a reduction in walking speed is a mechanism to reduce joint load (Mundermann et al., 2004
). Slower walking speed may reduce the reaction forces and moments at the knee joint and may reduce co-contraction within a group of persons when compared to their faster walking speed. However, the magnitude of co-contraction seems to be dependent on the presence or absence of knee OA, and not by the speed at which subjects walk.
Frequently, persons with knee OA will demonstrate an increase in joint laxity and a reduction in dynamic stability of the knee during walking (Fitzgerald et al., 2004
; Rudolph et al., 2007
). The increased levels of co-contraction that persons with knee OA use may reflect an internal strategy to maximize stability during walking. While this may be a method to improve joint stability, it may also result in inefficient or metabolically demanding gait patterns (Unnithan et al., 1996
) that may expedite the disease process (Griffin and Guilak, 2005
; Piscoya et al., 2005
). Since the increased co-contraction was seen at the 1.0 m/s walking speed, it demonstrated that this may occur even at slower walking speeds.
While both OA groups showed significant differences in CCI versus the control group at 1.0 m/s, only the moderate group was significantly higher than the control group at the self-selected walking speed. Although the CCI values were higher in the severe group than the control group, it did not reach significant levels. Given that EMG signals can be affected by a multitude of external factors (such as body mass or skin movement (De Luca, 1997
) and our lower sample size of subjects with severe OA, the potential for Type II statistical error exists. Although significant differences did not exist for all groups at all conditions, the fact that the OA groups had larger values for all EMG variables should not be overlooked. We think this is an important finding and we feel that, given a larger sample size and BMI matched subjects, more of the results would achieve statistical significance. Even though these limitations exist, subjects with severe OA may not utilize higher levels of co-contraction at the self-selected or fast walking speed. Previous investigations have found that while subjects with lower grades of arthritis have higher anterior/posterior and rotational joint laxity, subjects with severe OA show levels of laxity similar to control groups (Wada et al., 1996
). The laxity in the moderate OA group may be the result of decreased cartilage tissue or diminished meniscal support, whereas subjects with severe OA may have increased osteophytes and higher friction at the articulating surface. This would reduce the need for extra-articular muscular support and subsequently reduce the CCI in this group.
One limitation with this methodology is that differences in voluntary contraction during MVIC may result in inflated differences in CCI or individual muscle activity during walking. Because all subjects were encouraged to maximally contract their muscles during MVIC collection we do not feel that this was an issue with our study. They were given verbal, tactile as well as visual motivation by showing them the magnitude of the EMG signal during contraction. The same investigator was responsible for conducting all of the MVIC trials for all of the subjects. In addition, previous research has shown that there is also no difference in voluntary activation of the quadriceps between persons with and without knee OA (Lewek et al., 2004b
). We feel that the use of MVIC during our data collection provided a valid measure of a persons’ maximal force generating ability.
We have demonstrated that subjects with knee OA utilize different coordination strategies than persons without radiographic evidence of knee OA. Subjects with OA have higher antagonistic muscle activity during walking at control (1.0 m/s), self-selected and fast walking speeds. The fact that significant differences were seen when the effect of speed was removed suggests that coordination strategies resulting in higher CCI values are a result of the disease process and not due to differences in walking speed. While the current study advances the knowledge about differences in coordination strategies at the knee, it does not resolve whether these neuromuscular alterations will induce mechanical changes (such as joint space narrowing) or are a result of mechanical changes in the knee. Future research should address the potential of higher co-contraction to lead to degenerative changes at the knee joint by incorporating a longitudinal experimental design.