Full length articleDifferences in lower extremity muscular coactivation during postural control between healthy and obese adults
Introduction
During postural control, young adults produce a net torque at the ankle joint by activating both agonist and antagonist muscles to maintain body stabilization [1]. The simultaneous activation of agonist and antagonist muscles around a joint, which is defined as muscle coactivation [2], is designed to allow an agonist to work fluently [1] and to increase joint stabilization during refined motor performance [3]. In older adults, studies have reported increased levels of muscle coactivation between the soleus and the tibialis anterior during static postural control tests compared to young adults [[4], [5], [6]]. Increased muscle coactivation at the ankle level in older adults has been suggested to be a compensatory mechanism for enhancing postural control stability, resulting in increased joint stiffness [3,7,8]. However, other studies have reported a correlation between high muscle coactivation and low postural control stability [8,9], which may be explained by the following: first, strong muscle activation has been associated with an increased risk of excessive energy expenditure [7], resulting in fatigue, which could potentially lead to an increased risk of postural instability; and second, excessive muscle coactivation increases postural rigidity and might restrict dynamic postural control [8].
Several authors have shown that obesity is associated with a deterioration in postural control, resulting in an increase in center of pressure (CoP) oscillations during quiet standing [10,11]. Deteriorations in this functional capacity could lead to increase risks of falls, which may reduce obese adults’ autonomy [12]. Postural control alterations in obese adults have been explained by the increased mechanical demands related to an increased body mass and by the non-negligible proportion of body mass that is further from the axis of rotation (i.e., the ankle joint, assuming an inverted pendulum model) [11,13,14]. Recently, we reported that obese individuals showed similar relative force values for the ankle plantar and dorsal flexor muscles to those for non-obese individuals, suggesting that the primary source of imbalance in obese individuals is not associated with a lack of strength but is instead associated with increased muscle activity in the plantar flexors of the ankle [10]. This phenomenon is due to the increased stimulation of the plantar flexors in obese individuals, to counteract the anterior postural instability. However, we did not investigate ankle muscle coactivation in obese individuals, which may provide further indications regarding the underlying mechanisms through which postural control alterations occur in obese individuals.
To our knowledge, only the study of Tomlinson et al. [15] has investigated ankle muscle coactivation during maximal isometric contraction in obese adults, indicating that obesity does not affect antagonist coactivation during this task. However, this study did not evaluate ankle muscle coactivation during postural control testing, nor did examine the relationships that may exist between ankle muscle coactivation and body weight which is a strong predictor of postural control stability [16]. Thus, the objectives of this study were to evaluate the effects of an excessive body weight on muscle coactivation at the ankle level during static and dynamic postural control and to analyze the relationships between ankle muscle coactivation, CoP parameters and body weight in obese adults. We hypothesize that an excessive body weight is associated with increased ankle muscle coactivation during static and dynamic postural control tasks, and the level of muscle coactivation and CoP parameters are positively correlated with body weight in obese adults.
Section snippets
Participants
Forty participants, recruited from our university and from an obesity treatment center, were divided into two groups (Table 1) according to their body mass index (BMI, Kg/m²). The non-obese control group (CG; age = 32.5 ± 7.6 years; BMI = 22.4 ± 2.2 Kg/m²) included 20 normal-weight adults and the obese group (OG; age = 34.2 ± 5.6 years; BMI = 38.6 ± 4.1 Kg/m²) included 20 obese adults. Participants were excluded from the study if they had a history of cardiovascular disorders, diabetes,
Result
Participants’ characteristics are shown in Table 1.
Discussion
This is the first study that measured the effect of obesity on muscle coactivation at the ankle joint under quiet standing and dynamic postural control capacities. The study provides three major findings. First, an excessive body weight is associated with altered CoP parameters during static and dynamic postural control trials. Second, obesity induces higher ankle muscle coactivation during upright standing tasks. Finally, during these tasks coactivation index of SOL/TA is significantly
Conclusion
Obesity increases muscle coactivation of the soleus and tibialis anterior muscles at the ankle joint to counteract obesity-related constraints during postural regulation. However, high levels of muscle coactivation may reduce the performance of the agonist muscle, increase postural rigidity and could confound future development of fatigue. For these reasons, muscle coactivation could not be considered as a good adaptation since it is associated with negative consequences that could impact other
Declaration of Competing Interest
The authors declare no conflict of interest.
Acknowledgements
We would like to thank the patients of the reeducation center François Gallouedec (Le Mans, France) and the students of Le Mans University for their acceptance to participate in this study.
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