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. 2025 Nov 6;53(2):456–465. doi: 10.1111/joor.70086

Jaw Muscle Electromyographic Response to Whole‐Body Postural Perturbation

Akari Shibagaki 1, Yosuke Tomita 2, Yoshitaka Suzuki 1, Kazuo Okura 1, Masamitsu Oshima 1, Jaime Fabillar Jr 1, Yoshizo Matsuka 1,✉
PMCID: PMC12813513  PMID: 41199584

ABSTRACT

Background

While whole‐body postural control requires integration of the sensorimotor system, the involvement of jaw muscle activity in this control remains unclear.

Objective

This study aimed to clarify the relationship between jaw muscle activity and whole‐body postural stability by measuring jaw‐opening and closing muscle activities, as well as whole‐body postural sway during postural perturbations with two different levels of predictability.

Methods

Twelve healthy adults (7 males, 5 females; median age 21.0 years) underwent vertical perturbations by holding a bar at shoulder height. In the cued condition (C‐cond), the participants were given a 3‐s countdown before the bar was loaded with 3% of their body weight, whereas in the uncued condition (U‐cond), the load was applied without prior cueing. Jaw‐closing (masseter) and jaw‐opening (anterior suprahyoid) muscle activities were measured using surface electromyography (EMG). Bar dynamics and center‐of‐foot‐pressure (COP) were assessed with motion capture and a force plate. Bar‐drop distances, EMG activity, and the proportion of trials with muscle activity exceeding baseline were compared between conditions using the Wilcoxon signed‐rank test, Friedman, Mann–Whitney U and chi‐square tests, as appropriate, with Bonferroni corrections.

Results

Vertical bar displacement was greater in the U‐cond compared with the C‐cond (−46.0 mm vs. −27.4 mm, the Wilcoxon signed‐rank test, p < 0.05). Left anterior suprahyoid activity exceeded baseline in 91.7% of uncued trials versus 58.3% in cued trials (the chi‐square test with the Bonferroni correction applied, adjusted p < 0.05). COP displacement increased when masseter and anterior suprahyoid muscle activity exceeded baseline in the U‐cond (the Mann–Whitney U test with Bonferroni correction, adjusted p < 0.05).

Conclusion

Increased activation of jaw‐opening muscles during uncued perturbations compared with cued perturbations suggests that anterior suprahyoid muscles are recruited for postural control, supporting their involvement in maintaining stability.

Keywords: center of pressure, electromyography, masseter muscles, postural control, postural perturbation, suprahyoid muscles

Graphical abstract illustrating the relationship between jaw muscle activity and whole‐body postural stability in healthy adults. Increased activation of the anterior suprahyoid muscles was observed under uncued postural perturbations compared with cued perturbations, suggesting their recruitment for postural control.

graphic file with name JOOR-53-456-g005.jpg

1. Introduction

Postural control is essential for maintaining posture at rest and during movement, requiring integration of sensory inputs from the somatosensory, visual, and vestibular systems [1]. Impaired postural control can compromise daily activities and is associated with increased fall risk, reduced social participation, and higher mortality rates [2]. While trunk and lower‐limb muscle activity are key contributors to postural stability [3, 4], jaw muscles—although primarily used for mastication and swallowing—may also play a role in postural adjustments. Jaw clenching enhances whole‐body stability by activating jaw‐closing muscles, promoting earlier anticipatory postural activity, increasing trunk and limb activation [5], and reducing anterior–posterior body sway [6, 7], possibly by facilitating soleus and tibialis anterior H‐reflexes [8, 9]. Gum chewing in quiet standing conditions also improves stability [10]. Therefore, jaw motor tasks are associated with changes in trunk and limb muscle activity for whole‐body posture control.

Previous studies have examined the relationship between stomatognathic functions (e.g., jaw clenching, chewing) and postural control, mainly under predictable perturbations or voluntary movements. Although studies on the interaction between postural control and the stomatognathic system focused on jaw‐closing muscle activity, evidence suggests that jaw‐closing muscle activity occurs during postural tasks without occlusal contact. For example, jaw clenching is not always observed during sports activities [11, 12]. Similarly, during dynamic exercises such as weightlifting, where strong skeletal muscle force is exerted, occlusal contact is absent, and both the jaw‐opening and jaw‐closing muscles contract simultaneously [13]. Furthermore, head stability under predictable perturbation conditions does not differ significantly according to clenching status [14]. These findings suggest that jaw‐closing muscles alone cannot fully explain stomatognathic contributions to posture, highlighting the need to also observe jaw‐opening muscles.

Postural control is influenced by the predictability of perturbations, with unpredictable perturbations typically producing larger center‐of‐mass (COM) and center‐of‐foot‐pressure (COP) displacements and greater compensatory activation of trunk and lower‐limb muscles compared with predictable perturbations [15, 16]. However, no studies have examined how jaw muscles, including jaw‐opening muscles, contribute to whole‐body postural control under unpredictable timing. Therefore, this study aimed to clarify the relationship between jaw muscle activity and whole‐body postural stability by measuring jaw‐opening and closing muscle activities, as well as whole‐body postural sway during postural perturbations with two different levels of predictability. To address this aim, we compared cued and uncued perturbation conditions to examine: (1) the relationship between predictability and muscle activity before and after perturbations, and (2) the relationship between the presence or absence of muscle activity exceeding quiet‐standing levels and postural sway. We hypothesised that COP and jaw muscle activity responses would differ between cued and uncued perturbation conditions.

2. Methods

2.1. Participants

The participants were right‐handed, healthy young adults from Takasaki University of Health and Welfare. Individuals with neurological, musculoskeletal, or cardiovascular diseases, as well as those with shoulder or lumbar pain, were excluded. Written informed consent was obtained after providing an explanation of the study procedures and potential risks. The study was approved by the Ethics Committee of Takasaki University of Health and Welfare (approval no. 2253) and was conducted in accordance with the principles of the Declaration of Helsinki.

The required sample size was calculated using G*Power software (version 3.1.9.7; Heinrich Heine University, Germany) [17]. A priori power analysis for the Wilcoxon signed‐rank test (matched pairs) was performed with an effect size of 0.973, as reported by Sako et al. [14], with an alpha level of 0.05 and a power of 0.80. This analysis indicated that a minimum of 11 participants was required.

2.2. Experiment Setting

The participants were instructed to stand on a force platform (BP400600; AMTI, USA) with their feet shoulder‐width apart. The COP position, defined as the point location of the ground reaction force vector, was calculated from forces and moments measured using the force platform. Foot positions were marked on the platform to standardise their placement during the experiment. In the initial position, the participants held an 80 cm‐long exercise bar with both shoulders flexed at 90° and the elbow joints fully extended. A trained assistant manually applied a series of vertical perturbations in the sagittal plane to the middle of the bar by adding a load equivalent to 3% of each participant's body weight to induce the perturbation [14]. The participants were instructed to maintain the bar height and orientation as stable as possible for approximately 5 s (Figure 1A).

FIGURE 1.

FIGURE 1

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(A) Experimental settings. The participants were instructed to stand on a force platform with their feet shoulder‐width apart. In the initial position, the participants held an 80 cm‐long exercise bar with both shoulders flexed to 90° and the elbow joints fully extended. The weight of the bar was adjusted to be 3% of the participant's body weight. The participants wore an eye mask and headphones to restrict visual and auditory input in the U‐cond. (B) Vertical displacement of the bar in the C‐ and U‐conds. Compared with the C‐cond, the vertical displacement is significantly greater in the U‐cond (−27.36 [−40.12 to −15.68] mm vs. −46.03 [−53.36 to −34.75] mm, p = 0.0039, Wilcoxon signed‐rank test, p < 0.05, **p < 0.01). (C) COP displacement in the anterior–posterior direction (COPAP, where positive and negative values indicate forward and backward displacement, respectively) does not differ significantly between C‐ and U‐cond (36.10 [26.78–64.11] mm vs. 36.31 [29.02–49.49] mm). C‐cond, cued condition; COP, center‐of‐foot‐pressure; U‐cond, uncued condition.

For each participant, electromyography (EMG) was recorded from the bilateral masseter (MA) and anterior suprahyoid (ASH) muscles at a sampling rate of 2000 Hz (Ultium, Noraxon). Skin preparation included shaving and cleansing with alcohol wipes before electrode placement. Two disposable surface electrodes (32 mm; Inspad S; Medical Next, Japan) were trimmed to approximately 20 mm in diameter and placed 20 mm apart. The electrode placement sites—the thickest part of the MA [5] and the anterior head of the suprahyoid muscle complex (ASH) [18]—were confirmed by observing muscle activation during a movement corresponding to the primary function of each muscle. Before the experiment, we verified distinct activation for each muscle to minimise signal contamination.

Kinematic data were recorded using inertial measurement units (IMUs; myoMOTION, Noraxon, USA) at a sampling rate of 100 Hz. Sixteen IMU sensors were attached to the head, upper arms, forearms, hands, cervical vertebrae, 12th thoracic vertebra, lower thorax, pelvis, thighs, shanks, and feet of each participant. Reflective motion capture markers were placed at both ends of the bar, and their three‐dimensional positions were recorded using a VICON system at a sampling rate of 100 Hz per marker (VICON Vero 2.2, Oxford Metrics, UK).

All measurements were performed in a laboratory at Takasaki University of Health and Welfare with one participant and three research assistants present. One assistant operated the measurement equipment, the second managed the experimental conditions and monitored for abnormalities, and the third released the bar at the predetermined timing and applied perturbations. No announcements or background noise that could disturb the participants were permitted, and no conversation took place except for questions regarding fatigue and the countdown for perturbations.

2.3. Experiment Procedures

The experiment consisted of two conditions: a cued condition (C‐cond), in which the participants could predict the perturbation timing using visual and auditory cues (3‐s countdown), and an uncued condition (U‐cond), in which the participants wore an eye mask and headphones to restrict visual and auditory input, making the timing unpredictable. An experimental assistant supported the bar with an attached weight while the participant stood upright, facing forward with feet shoulder‐width apart, shoulders flexed at 90°, elbows fully extended, and lightly gripping the bar. The assistant then released the bar, and the participants were instructed to maintain its horizontal position upon perceiving the added weight. The perturbation bar was held manually, and the magnitude and direction of loading were kept consistent across all participants.

Two or three practice trials were conducted before the recording trials. In each condition, three trials were performed. Approximately 1 min of rest was provided between trials. The weight was held for 5 s, and fatigue was assessed between trials; additional rest was provided if subjective fatigue was reported. The order of conditions was randomised using the ‘rand’ function in Microsoft Excel (Microsoft, Redmond, WA, USA). The results of the trial in which the weight was placed in the center are summarised in this report.

After each experiment, the maximum voluntary contraction (MVC) of the recorded muscles was measured to normalise EMG data to 100% MVC [19]. One practice MVC trial was followed by an actual measurement, with additional trials conducted as necessary. The highest recorded activity was defined as 100% MVC. For the MA, MVC was measured by instructing the participants to clench their teeth with maximum force [20]. For the ASH, MVC was measured by having the participants resist an external force applied to the jaw to close the mouth, while the participants attempted to open it [21, 22].

2.4. Data Processing

We analysed the data using a custom‐made MATLAB program (MATLAB 2022b, MathWorks, USA). Kinematic signals from the IMUs and reflective markers were upsampled to 1000 Hz using the resampling function in MATLAB. EMG signals were downsampled to 1000 Hz, rectified, and filtered with a Butterworth bandpass filter (50–500 Hz) [23]. The filtered EMG signals were then smoothed using a moving average over a 100‐ms time window and normalised by the activity recorded during the MVC trials. Time zero (T0; at the moment of perturbation) was defined as the time when the change in vertical force measured using the force platform exceeded the baseline mean by more than two standard deviations (SDs). We computed the maximum vertical displacement of the bar from the baseline after the perturbation using the reflective marker position as the bar drop distance. The maximum COP displacement in the anteroposterior (AP) coordinate system was computed as a measure of postural stability. We calculated integrated EMG (iEMG) activity levels using normalised EMG signals from four different epochs, each lasting 150 ms, to characterise anticipatory postural adjustments (APAs) [24] and compensatory postural adjustments (CPAs) [25, 26]. The timings of the four epochs were as follows: (1) −150 ms to T0 (anticipatory postural adjustment, APA1), (2) T0 to +150 ms (compensatory postural adjustment 1, CPA1), (3) +150 ms to +300 ms (compensatory postural adjustment 2, CPA2). For each measured muscle, we classified the trials into two groups based on whether the EMG activity during APA1 to CPA2 exceeded the mean ± 2 SD of the baseline quiet standing activity. Trials with and without a significant increase in EMG activity between APA1 and CPA2 were counted as active (A) and non‐active (N) trials, respectively.

2.5. Statistical Analysis

The analysis used the mean values of each condition for each participant. All group data are presented as medians with interquartile ranges (IQR). The bar drop distance between conditions was compared using the Wilcoxon signed‐rank test. Differences in EMG activity were examined using the Friedman test, with eight groups defined by two conditions (C‐cond and U‐cond) and four epochs (Baseline, APA1, CPA1, and CPA2). When a significant difference was detected, pre‐planned contrasts [27] were performed using the Wilcoxon signed‐rank test. These contrasts included comparisons within each condition between baseline and APA1, CPA1, and CPA2, as well as comparisons between C‐cond and U‐cond within each epoch. To control for multiple comparisons, we applied the Bonferroni correction, resulting in an adjusted alpha level of 0.005 (0.05/10).

For each muscle (MA and ASH), we calculated the percentage of trials in which EMG activity exceeded the baseline quiet‐standing level and compared these percentages between conditions using the chi‐square test, with the Bonferroni correction applied (adjusted alpha = 0.001; 0.05/4). To investigate the relationship between the presence of muscle activity exceeding baseline and postural stability, we compared COP displacements between A and N trials for each muscle and condition using the Mann–Whitney U test with Bonferroni correction (adjusted alpha = 0.006; 0.05/8).

We conducted all statistical analyses using R version 4.2.2 (R Foundation for Statistical Computing, Austria) with the EZR graphical interface (Jichi Medical University, Japan). The significance level was set at 5%.

3. Results

3.1. Participants

We collected data from 15 participants. Although the minimum required sample size was 11, the formal analyses included 12 participants (seven males and five females; median [interquartile range], age: 21.00 [21.00–22.25] years; height: 166.50 [157.00–175.75] cm; body weight: 62.50 [51.50–67.00] kg; body mass index: 21.29 [20.80–22.18] kg/m2) after excluding data from three participants due to missing kinematic data.

3.2. Differences in Bar and COP Displacements Between Conditions

The vertical displacements of the bar in C‐cond and U‐cond are shown in Figure 1B. Compared with the C‐cond, the vertical displacement (median [interquartile range]) was significantly greater in the U‐cond (−27.36 [−40.12 to −15.68] mm vs. −46.03 [−53.36 to −34.75] mm, p < 0.05; Figure 1B). The COP displacement in the anterior–posterior direction (COPAP; where positive and negative values indicate forward and backward displacement, respectively) did not differ significantly between the C‐cond and U‐cond (36.10 [26.78–64.11] mm vs. 36.31 [29.02–49.49] mm; Figure 1C).

3.3. Changes in Muscle Activity Before and After Postural Perturbation

The activities of the right MA and right ASH in C‐cond and U‐cond as examples are shown in Figure 2. Furthermore, two examples of EMG activity classification are shown in Figure 3A, the MA was classified as non‐active because its activity did not exceed baseline, whereas in Figure 3B, the ASH was classified as active because its activity exceeded baseline. The maximum %MVC values (median [interquartile range]) for baseline, APA1, and CPA1–2 in each condition are summarised in Figure 4. Compared with baseline, the U‐cond showed significant increases in muscle activity in the right MA and the right ASH (APA1 and CPA1) and the left ASH (APA1 and CPA1‐2; Figure 4). Comparisons between the C‐cond and U‐cond (Figure 4, Table S1) revealed significantly greater muscle activity in the U‐cond for the left MA at baseline, and for the right ASH at baseline, APA1, and CPA1.

FIGURE 2.

FIGURE 2

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Right masseter and right anterior suprahyoid muscle activities. The results of a single subject for each C‐cond and U‐cond of three trials are shown. Blue line: C‐cond; red line: U‐cond; vertical red line and triangle: start of the external perturbations. In the right anterior suprahyoid muscle, muscle activity increased in U‐cond. C‐cond, cued condition; U‐cond, uncued condition.

FIGURE 3.

FIGURE 3

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(A) Suprahyoid muscle activity during active (A) trials. (B) Masseter muscle activity during non‐active (N) trials. EMG activity during APA1 and CPA1–2 exceeds the baseline mean ± 2 SDs in the A but not in the N trials. Muscle onset (black triangle) is defined as the point where the EMG activity surpasses or drops below the baseline mean by > 2 SDs. Time zero (T0) indicates the perturbation onset, defined as the time when the vertical force measured by the force platform exceeded baseline by more than 2 SD. iEMG levels were calculated from normalised EMG signals across four 150‐ms epochs: (1) APA1 (−150 ms to T0); (2) CPA1 (T0 to +150 ms); (3) compensatory postural adjustment 2 (CPA2; +150 ms to +300 ms). APA, anticipatory postural adjustment; CPA, compensatory postural adjustment; EMG, electromyography; iEMG, integrated EMG; SD, standard deviation.

FIGURE 4.

FIGURE 4

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Changes in muscle activity before and after postural perturbation in the C‐cond (white box) and U‐cond (grey box). Wilcoxon signed‐rank test, adjusted p < 0.05 (Bonferroni correction), *†adjusted p < 0.05. *Significant difference between the C‐cond and U‐cond within the same epochs. †Significant difference between baseline and each epoch (i.e., APA1–CPA2) within the U‐cond. The Supporting Information includes detailed presentations of the described values. APA, anticipatory postural adjustment; ASH, anterior suprahyoid muscle; gastrocnemius muscle; C‐cond, cued condition; CPA, compensatory postural adjustment; MA, masseter muscle; U‐cond, uncued condition.

3.4. Relationships Between Muscle Activity Exceeding Baseline and Postural Sway

The proportions of trials in which muscle activity exceeded baseline levels in each condition are summarised in Table 1. In the left ASH, significantly more trials in the U‐cond exhibited muscle activity exceeding baseline levels compared with the C‐cond (Table 1) (χ 2 = 8.963, adjusted p < 0.05). We also observed a trend towards increased muscle activation exceeding baseline levels in the U‐cond compared with the C‐cond.

TABLE 1.

Percentages of trials with muscle activity above baseline for each experimental condition.

Right Left
C‐cond (%) U‐cond (%) p C‐cond (%) U‐cond (%) p
MA 36.11 55.56 0.1554 36.11 52.78 0.2355
ASH 50.00 77.78 0.0263 58.33 91.67 0.0028*
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Abbreviations: ASH, anterior suprahyoid muscle; C‐cond, cued condition; MA, masseter muscle; U‐cond, uncued condition.

*

Adjusted p < 0.05; significant difference on the same side between the C‐cond and U‐cond. Chi‐square test, adjusted p < 0.05 (Bonferroni correction).

The results of the comparison of the maximum COP displacement between trials with (A: active) and without (N: non‐active) muscle activity exceeding the baseline levels are summarised in Table 2. In the C‐cond, COPAP did not differ significantly between active and non‐active trials. In the U‐cond, COPAP displacement was significantly greater in trials with muscle activity in the left MA (A: 43.02 [35.55–65.60] mm, n = 19; N: 29.57 [25.31–36.35] mm, n = 17; adjusted p < 0.05) and right ASH (A: 37.26 [31.82–55.81] mm, n = 28; N: 26.71 [22.91–30.31] mm, n = 8; adjusted p < 0.05).

TABLE 2.

Comparisons of anterior–posterior COP displacement based on active or non‐active muscle activities.

C‐cond U‐cond
A (mm) N (mm) p A (mm) N (mm) p
MA R 52.00 [27.43–66.42] 36.08 [26.74–45.40] 0.429 40.26 [32.35–64.79] 31.73 [26.56–38.81] 0.0342
L 40.67 [30.77–52.18] 28.87 [26.52–65.27] 0.347 43.02 [35.55–65.60] 29.57 [25.31–36.35] 0.0029*
ASH R 35.45 [26.06–52.14] 38.45 [27.32–65.64] 0.496 37.26 [31.82–55.81] 26.71 [22.91–30.31] 0.0046*
L 36.11 [27.29–52.00] 30.77 [26.18–68.86] 0.810 36.35 [31.26–51.18] 26.97 [26.14–28.27] 0.067
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Note: Values are provided as medians [interquartile range]. Mann–Whitney U test.

Abbreviations: A, active; ASH, anterior suprahyoid muscle; C‐cond, cued condition; COP, center‐of‐foot‐pressure; L, left; MA, masseter muscle; N, non‐active; R, right; U‐cond, uncued condition.

*

Adjusted p < 0.05, adjusted p < 0.05 (Bonferroni correction).

4. Discussion

This study investigated the relationship between jaw muscle activity and postural stability by analysing differences in jaw muscle activation and postural sway. Our results showed a significantly larger bar drop displacement in the uncued condition (U‐cond) but no significant difference in maximum anterior–posterior COP displacement between conditions. In response to perturbation, the MA and ASH muscles did not show significant activation during quiet standing in the C‐cond, whereas in the U‐cond, both muscles showed significant activation during anticipatory (APA) and compensatory (CPA1, CPA2) phases. These muscles exhibited greater activation in the U‐cond than in the C‐cond. Furthermore, COP displacement was significantly greater when increased activation occurred in the MA and ASH muscles under the U‐cond, indicating a relationship between jaw muscle activation and postural sway.

In both conditions, jaw muscle activity significantly increased from baseline, particularly during compensatory postural adjustments. We observed the condition‐specific differences in activation levels in both the anticipatory and entire compensatory phases for the ASH muscles. These findings are consistent with previous studies on sudden loads to the upper limb and jaw movements under varying perturbation predictability [28]. In jaw muscles, compensatory activity is greater under unpredictable than predictable conditions, with jaw‐opening muscles potentially displaying distinct features in response to external perturbations [28, 29]. In the present study, the difference in COP displacement between conditions suggests that compensatory postural adjustments maintained comparable stability, even when perturbations were unpredictable. Additional analysis revealed greater COP displacement when jaw muscle EMG activity was present in the U‐cond (Table 2), suggesting that jaw muscle activity contributes to postural adjustments and stabilisation of jaw position.

Jaw‐closing muscles, which contain numerous muscle spindles, show stretch reflex activation during downward mandibular movements while running [30]. Conversely, judo athletes experiencing strong postural perturbation do not show occlusal contact, although both jaw‐closing and jaw‐opening muscles are activated, particularly jaw‐opening muscles [31]. The ASH muscles lack muscle spindles; thus, their activity may reflect complex control involving muscles attached to the mandible and hyoid bone [32]. Observations of tonic and phasic stretch responses in jaw‐opening muscles suggest that proprioceptive inputs to motoneurons, possibly from spindle afferents, free nerve endings, temporomandibular joint proprioceptors, or tendon organ afferents, contribute to their regulation [33, 34, 35, 36].

In CPA1 (T0 to +150 ms), the initial compensatory response to rapid postural perturbation is primarily organised at the spinal level, as time constraints limit cortical and subcortical influence. The transcortical loop latencies in lower‐limb muscles are approximately 85–100 ms [37]. Postural responses mediated by the brainstem are also possible, as head acceleration following perturbation onset can be detected through vestibular input. The increased jaw muscle activity in the U‐cond during CPA1 and CPA2 may correspond to short‐ and middle‐latency responses involving spinal and brainstem processing [38]. In the C‐cond, prior knowledge of the perturbation reduced reactive cortical activity, whereas in the U‐cond, cortical activity may increase in response to postural error detection, leading to greater muscle activity amplitude [39]. Cerebellar gain control mechanisms, which scale early anticipatory responses during postural perturbations [40], may play a similar role during upper‐limb perturbations.

Differences in muscle activity patterns between cued and uncued conditions may relate to how the nervous system primes responses. In the C‐cond, the cerebral cortex and brainstem generate anticipatory responses based on context, with voluntary adjustments added if initial responses are inadequate [41]. In the U‐cond, increased activity may involve a startle response triggered by visual, auditory, or somatosensory stimuli. The neural circuit for somatosensory startle likely involves the nucleus reticularis pontis caudalis (nRPC), similar to the acoustic startle reflex (ASR) [42]. Temporal and MA muscle responses in whole‐body ASR may also be mediated by the nRPC [43]. Although startle responses are polysynaptic and often observed in free‐fall or loud‐sound conditions, reports on jaw‐opening muscles are lacking. Our findings suggest that a startle‐like response from somatosensory input in the U‐cond could have increased jaw muscle activity via a similar neural pathway.

Most prior studies on stomatognathic function and postural control focused on jaw‐closing muscles. While clenching can enhance stability, our results indicate that evaluating only jaw‐closing muscle activity is insufficient when assessing postural stability without clenching instructions. One possible role for the observed co‐activation of jaw‐opening and jaw‐closing muscles is ‘bracing’ in which the mandible is held in position without tooth contact, involving simultaneous contraction of both muscle groups [13, 44]. Precise measurement of jaw position is needed to clarify the role of these muscles in postural adjustments, a limitation of the present study. Future studies are needed to clarify this point by incorporating mandibular position measurements during postural adjustments.

The findings of this study have several clinical implications. First, our results demonstrated a clear functional coupling between jaw muscle activity and postural control mechanisms, suggesting that dysfunction of the jaw muscles may affect postural stability. Observations of individuals with reduced stomatognathic function could further clarify the contribution and interrelationships of jaw muscles in maintaining posture. This, in turn, may lead to applications in screening, maintenance, and training aimed at improving overall postural control. Second, our findings suggest that not only jaw‐closing muscles but also jaw‐opening muscles may play supportive roles in postural control in response to perturbation. Previous studies have reported that clenching training targeting jaw‐closing muscles can improve standing balance [45]. Furthermore, swallowing function declines in older adults along with a reduction in mouth‐opening force, which serves as an indicator of jaw‐opening muscle function, including that of the ASH muscles [46]. Based on our results, training interventions targeting oral functions through jaw‐opening muscle exercises may not only improve swallowing function but also enhance postural control in response to perturbations. Future studies should further investigate these points.

This study has several limitations. First, the bar used to apply the perturbation was held manually by an assistant, which may have caused slight deviations from a perfectly horizontal position, potentially affecting the accuracy of the perturbation. Second, we measured muscle activity using surface EMG. To minimise signal contamination, we used small electrodes (20 mm diameter) for the jaw muscles and verified distinct activation patterns for each muscle. Nonetheless, surface EMG inherently carries the risk of crosstalk from adjacent muscles, particularly in small‐volume muscles such as jaw‐opening muscles. Third, although both male and female participants were included, the lack of sufficient statistical power prevented subgroup analysis to examine potential sex differences. Future investigations should consider whether sex‐specific factors influence the outcomes observed in this study. Fourth, we did not measure jaw position and tooth contact in this study, although these factors may influence jaw muscle activity. However, we aimed to examine the relationship between jaw‐closing and jaw‐opening muscle activity and posture in each participant's resting state rather than the effects of jaw position or tooth contact on posture maintenance. Future research should incorporate these measurements to further clarify the role of jaw muscles in postural adjustments. Finally, although the experiments were conducted in a controlled laboratory environment with minimal external distractions (only the participant and three assistants present and no background noise or unrelated conversation), factors such as participant fatigue, lapses in concentration, or subtle distractions could not be entirely ruled out. These factors may have influenced muscle activity and postural responses. Future studies should consider implementing measures to monitor and control fatigue and attention fluctuations to further improve data reliability.

5. Conclusions

This study examined jaw muscle activity during cued and uncued postural perturbations. We observed significant activation of jaw‐opening muscles, particularly under unpredictable conditions. Greater COP displacement occurred when jaw muscle activation was present, suggesting their involvement in maintaining stability when postural instability increases. Our findings demonstrate that both jaw‐closing and jaw‐opening muscles, especially the ASH, are actively involved in postural control during perturbations, particularly under unpredictable conditions. Moreover, these results provide novel evidence for the contribution of jaw‐opening muscles to postural control in humans.

Author Contributions

Yosuke Tomita and Yoshitaka Suzuki designed the study. Akari Shibagaki, Yosuke Tomita, and Yoshitaka Suzuki collected and analysed the data. Akari Shibagaki, Yosuke Tomita, and Yoshitaka Suzuki wrote the manuscript. Kazuo Okura, Masamitsu Oshima, and Yoshizo Matsuka discussed experimental design and results and revised the final manuscript. Jaime Fabillar Jr. checked the manuscript. All the authors have read and agreed to the published version of the manuscript.

Conflicts of Interest

The authors declare no conflicts of interest.

Supporting information

Table S1: joor70086‐sup‐0001‐TableS1.docx.

JOOR-53-456-s001.docx (25.3KB, docx)

Acknowledgements

We thank all the study participants. This work was supported by the JST SPRING to A.S. (Grant number JPMJSP2113).

Funding: This work was supported by the JST SPRING to A.S. (Grant number JPMJSP2113).

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

Table S1: joor70086‐sup‐0001‐TableS1.docx.

JOOR-53-456-s001.docx (25.3KB, docx)

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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