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Changes in Masseteric Hemodynamics Time-related to Mental Stress
O. Hidaka*,
M. Yanagi and
K. Takada
Department of Orthodontics and Dentofacial Orthopedics, Graduate School of Dentistry, Osaka University, 1-8 Yamadaoka, Suita, Osaka, 565-0871, Japan;
Correspondence: * corresponding author, hidakao{at}dent.osaka-u.ac.jp
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ABSTRACT
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Mental stress may cause a dissociation of sympathetic outflow to different regions. However, it remains unclear how the sympathetic outflow to jaw muscles is related to other sympathetic outflow under mental stress. The objective of this study was to clarify the temporal relationship between the finger sweat expulsion elicited by mental stress and the hemodynamic and electromyographic changes in the masseter muscle. Healthy adult female volunteers participated in this study. Masseteric hemodynamic changes were closely time-related to mental stress, showing a decrease in oxygen saturation of muscle blood around the onset of mental stress. In contrast, EMG activity of jaw-closing muscles was not time-related to mental stress. These results suggest that mental stress induces hemodynamic changes that are not associated with EMG activity in the masseter muscle of healthy adult females.
Key Words: skin blood flow • sweat • intramuscular blood flow • near-infrared spectroscopy • laser-Doppler flowmetry
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INTRODUCTION
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Emotional conditions and stress situations are usually coupled with an increase in sympathetic outflow (Callister et al., 1992). The increased sympathetic outflow elicits an enhancement in muscle tone because sympathetic stimulation influences motor function by affecting muscular contraction (Passatore and Grassi, 1989; Grassi et al., 1996). Application of sympathomimetic agents also affects the functioning of skeletal muscles through changes in blood flow, muscle spindle activity, and extrafusal muscle activity (Janig, 1985). Thus, the sympathetic outflow is closely related to muscle function.
Sympathetic outflow control, however, is highly differentiated according to regions (Mellander and Johansson, 1968; Wallin and Fagius, 1988). Moreover, mental stress can cause a dissociation of sympathetic outflow to different regions (Rusch et al., 1981; Anderson et al., 1987). It remains unclear how the sympathetic outflow to jaw muscles is related to sympathetic outflow to other regions under mental stress. If jaw muscles are susceptible to mental stress, hemodynamic and/or electromyographic changes will be observed when sympathetic outflow to other regions is obvious. This is because sympathetic outflow can affect hemodynamic and electromyographic activities, both of which may be a causative factor in temporomandibular disorders (Rasmussen et al., 1977; Hubbard and Berkoff, 1993). It is therefore worth examining how electromyographic and/or hemodynamic activities of jaw muscles are susceptible to mental stress.
The objective of this study was to clarify whether the hemodynamic and electromyographic activities of the masseter muscle synchronize with finger sweating, and if so, which is susceptible to mental stress. Finger sweat expulsion was measured because it is an indicator of mental stress (Fealey, 1996) and can be recognized as an event signal.
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MATERIALS & METHODS
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Subjects
Healthy adult volunteers (ten females: mean age, 25.3 ± 0.9 yrs) with complete dentition except for third molars participated in the study. They exhibited Angle Class I molar relationships without tooth crowding or clinical signs of jaw dysfunction. Women were chosen because many more women than men develop temporomandibular disorders (Pedroni et al., 2003). Since activation of the autonomic nervous system may vary within the menstrual cycle (Asso and Braier, 1982), the experiments were performed under a standardized condition where the subjects were in the follicular phase of the menstrual cycle on the day of the experiment. All subjects participated after giving informed consent to the protocol that was reviewed and approved by the Ethics Committee of the Faculty of Dentistry.
Mental Stress Task
A Chinese character identification test requiring sensory intake behavior (Williams et al., 1975) was used. The subjects were shown an array (20 x 40) of 10 similar Chinese characters put in random order, and asked to pick out, as quickly as possible, a previously given character.
Measurements
The following signals were continuously recorded: finger sweat rate, finger skin blood flow (FSBF), jaw musculature electromyograms (EMGs), and kinetics of masseter muscle oxygenation.
Sweat rate was measured with a ventilated capsule equipped with a capacitance hygrometer (ATMO CHART SS-100II, KANDS, Kariya, Japan). A sweat capsule covering an area of 1.0 cm2 was mounted on the left index finger tip, and was ventilated with dry air at a rate of 0.3 L/min. The humidity sensor was placed 4 m away from the capsule outlet. The delay in sensing was adjusted.
FSBF was measured by means of laser-Doppler flowmetry (LDF). An LDF instrument (FLO-C1, Omegawave, Tokyo, Japan) was used with the time constant of 0.1 sec. LDF probes with an optical fiber-opening distance of 0.7 mm were attached to the skin within the sweat capsule, and enabled measurements to be made at a depth of 1.2 mm (Hirata et al., 1988).
EMG activity was recorded in the superficial masseter and anterior temporalis muscles on both sides with Beckman-type surface electrodes (NT-213U, Nihonkoden, Tokyo, Japan). The electrodes were placed 10 mm apart over the surface of the muscle, in line with the direction of action of the muscle. The indifferent electrode was secured to the right earlobe.
The kinetics of muscle oxygenation was analyzed only in the masseter muscle, with the use of a laser tissue blood oxygen monitor (BOM-L1TR, Omegawave), because placing the detector over the temporalis was difficult. This instrument uses near-infrared spectroscopy (NIRS), a non-invasive technique that involves the differential absorption properties of hemoglobin to evaluate skeletal muscle oxygenation (Mancini et al., 1994), and the validity of NIRS for measuring muscle hemodynamics has been confirmed in previous studies (Mancini et al., 1994; Delcanho et al., 1996). NIRS allows for determination of the relative tissue levels of oxygenated hemoglobin (OxyHb), deoxygenated hemoglobin (DeoxyHb), and total hemoglobin (TotalHb) based on the Beer-Lambert law. The light probe and the detector, which were covered with a rubber sheet and vinyl, were placed, 30 mm apart, over the left masseter muscle.
Experimental Protocols
All subjects came to the laboratory for orientation within a week prior to the experimental session and were introduced to the mental task. This was to ensure that all subjects were familiar with the experimental protocol.
The experiments were performed in the early evening in a noiseless room in which the ambient temperature (Ta) and humidity were controlled (Ta, 26.5 ± 0.7°C; relative humidity, 35 ± 13 %). The subjects were instructed to do the following, during which measurements were made: 3 sec of maximum voluntary contraction (MVC), 5 min of rest, 30 min of mental task, 5 min of rest, and 3 sec of MVC. At the end of the experimental periods, the subjects were asked to report their perceived stress on a scale of: 0, not stressful; 1, somewhat stressful; 2, stressful; 3, very stressful; and 4, extremely stressful.
Data Analysis
The data were digitized by means of an analog-to-digital converter (CED1401, Cambridge Electronic Design, Cambridge, UK) at 2 kHz for the EMG signals and at 200 Hz for all the other measurements. The data were analyzed with the use of Spike2 software (Cambridge Electronic Design, Cambridge, UK). The EMG data were rectified by the software and smoothed by a nine-point moving average. Data from a 20-minute period of the mental task (5–25 min) were analyzed.
Individual sweat responses were defined as a transient, pulsatile increase in sweat rate (Fig. 1 ), and thereby the onset of the response was determined as an inflection point (Sugenoya et al., 1998). A proximal time window to the onset of sweat expulsion (PWSE) was determined in the event (sweat expulsion)-triggered averages (see Fig. 2) for investigation of any change that is time-related to the onset of sweat expulsion.
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Figure 1. Raw signal recordings of sweat expulsion and FSBF from the finger, hemodynamic parameters from the left masseter muscle, and EMGs from the masseter and temporalis muscles. Dotted vertical lines ( ) indicate the onset of sweat expulsion. F-Sweat, finger sweat; FSBF, finger skin blood flow; EMG, electromyogram; L, left; R, right; Temp, temporalis muscle; Mass, masseter muscle; OxyHb, oxygenated hemoglobin; DeoxyHb, deoxygenated hemoglobin; StO2, tissue blood oxygen saturation.
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Figure 2. Changes in FSBF, hemodynamic parameters, and EMGs time-related to finger sweat expulsion. Data were obtained from an average of 27 sweeps of waveforms from the same subject, as in Fig. 1 . A temporal reference point (solid vertical line) was obtained from the onset of sweat expulsion (dotted vertical line []), but the time delay in sensing humidity (3.2 ± 0.4 sec) was corrected by a shifting of the dotted vertical line to the solid vertical line (horizontal double-headed arrow). Twenty-second sweeps of waveform data around the onset of sweat expulsions were abstracted and averaged after alignment at the temporal reference point. The gray area indicates the 10-second period with its center at the temporal reference point and defined as a proximal time window to the onset of sweat expulsion (PWSE), and vertical double-headed arrows indicate maximum trace deflections within PWSE. F-Sweat, finger sweat; FSBF, finger skin blood flow; EMG, electromyogram; L, left; R, right; Temp, temporalis muscle; Mass, masseter muscle; OxyHb, oxygenated hemoglobin; DeoxyHb, deoxygenated hemoglobin; StO2, tissue blood oxygen saturation (OxyHb/TotalHb x 100).
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We used the Wilcoxon signed-rank test to check for differences between two groups, PWSE and non-PWSE. We used Pearson’s linear correlation test to evaluate the relationship between the sweat expulsion intensity (tan  , Fig. 2) and other measurements of PWSE. Values of p less than 0.05 were considered to be significant. Statistical analysis was performed with the use of Stat View 5.0 software (SAS Institute, Cary, NC, USA).
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RESULTS
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All the subjects reported at the end of the experiment that their perceived stress scale was 2 (stressful) or 3 (very stressful).
Synchronization between sweat expulsions and FSBF decreases was observed in typical tracings of recordings, but such a clear synchronization was hard to see between sweat expulsions and other measurements (Fig. 1).
To ensure synchronization between sweat expulsions and other measurements, we obtained averaged patterns of FSBF, muscle oxygenation, and rectified EMGs in response to sweat expulsion (Fig. 2). In PWSE, downward deflections were observed in FSBF, StO2, and OxyHb, and an upward deflection in DeoxyHb. Regarding the rectified EMG, sporadic bursts were found in both PWSE and non-PWSE.
When integrated values of measurements were compared between PWSE and non-PWSE, EMGs did not show a consistent change (Fig. 3A), while each of the hemodynamic parameters showed a consistent decrease or increase (Fig. 3B). OxyHb, StO2, and FSBF were smaller in PWSE (p = 0.0069 for OxyHb, p = 0.0051 for StO2, p = 0.0469 for FSBF; Wilcoxon signed-rank test), whereas DeoxyHb was larger (p = 0.0125, Wilcoxon signed-rank test). However, no significant difference was found in the total amount of hemoglobin, TotalHb (p = 0.2026, Wilcoxon signed-rank test).
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Figure 3. Changes in the masseter muscle that are time-related to the onset of finger sweat expulsion. Each value at non-PWSE was normalized to the corresponding value at PWSE (100%). PWSE, proximal window of sweat expulsion (see Fig. 2). IEMG, integrated electromyographic activity; OxyHb, oxygenated hemoglobin; DeoxyHb, deoxygenated hemoglobin; StO2, tissue blood oxygen saturation; FSBF, finger skin blood flow.
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When signal deflections for hemodynamics were compared between PWSE and non-PWSE (Fig. 3C), FSBF showed a greater signal deflection in PWSE (p = 0.0166, Wilcoxon signed-rank test), but OxyHb, DeoxyHb, and StO2 did not.
For the values that showed significant changes between PWSE and non-PWSE, Pearson’s correlation coefficients were calculated between the sweat expulsion intensity and other measurements of PWSE. Significant correlations were scarcely found (see Table).
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DISCUSSION
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Hemodynamics Time-related to Mental Stress
FSBF showed a clear decrease that was time-related to mental sweat expulsion. This is in agreement with the findings that mental stress induces an increase in the sympathetic outflow (Delius et al., 1972). The coincidence of mental stress and FSBF change implies that the sympathetic outflow is related to mental stress.
Masseteric hemodynamics was closely time-related to mental stress. All the hemodynamic parameters except for TotalHb showed significant differences between PWSE and non-PWSE. The hemodynamic change was not secondary to the muscle contraction which decreases blood flow due to the compression or occlusion of the vasculature within the contracting muscle (Kim et al., 1999). This is because EMG activity of the masseter muscle was not time-related to mental stress. Therefore, there is a time-linkage between the sympathetic outflow regulating mental stress and that regulating vascular smooth muscle in the masseter muscle. The time-linkage is somewhat surprising, because there can be a difference between sympathetic outflows to different tissues, such as skin and skeletal muscle, and outflows to various regions within the same tissue may sometimes differ (Wallin and Fagius, 1988). Moreover, mental stress is involved in regional differences of sympathetic outflow. It has been shown that mental stress causes a dissociation of sympathetic outflow to the arm and leg, with leg muscle sympathetic nerve activity (MSNA) increasing and arm MSNA remaining unchanged (Anderson et al., 1987). Besides the sympathetic outflow of the central regulatory mechanisms, local regional factors may be involved in the sympathetic dissociation according to the region. Possible factors are the density of sympathetic innervation, the extent of smooth muscle in the vessel, and the sensitivity of the vascular smooth muscle to the sympathetic transmitter (Feigl, 1989). Such potential factors that cause regional differences in the peripheral sympathetic response would explain only a few significant correlations between the sweat expulsion intensity and the amount of hemodynamic response (Table). Although the correlation was weak, the masseteric hemodynamics showed a response that was time-related to mental stress. This would imply that the masseter muscle is sensitive to mental stimuli.
Kinetics of Peripheral Masseter Muscle Oxygenation
The most notable change that was time-related to mental stress was a decrease in StO2 around the onset of mental stress. This was caused by the opposing behaviors of OxyHb and DeoxyHb, because no significant change was found in TotalHb. Capillaries and non-muscular venules are exchange vessels, and the concentration of OxyHb is higher in arterioles than in venules, whereas the concentration of DeoxyHb is higher in venules (Renkin, 1989). NIRS monitors hemoglobin in all vessels within the tissue of interest (arteries, arterioles, capillaries, venules, and veins) (Delcanho et al., 1996). Therefore, the most straightforward explanation for the kinetics is concomitant arterial vasoconstriction and venous vasodilatation. This may be supported by regional (arteries/arterioles vs. veins/venules) variations in vasomotor tone control. The density of sympathetic innervation is greater in arterioles than in venules (Renkin, 1989). For venodilatation, myogenic control in the venule, accompanied by arterial vasoconstriction, would have overridden possible sympathetic neural control to the venule.
Another possible explanation is also related to differentiated vasomotor control. Larger arterioles can be controllers of resistance and therefore of blood flow through the tissue, whereas smaller, more distal, arterioles play a primary role in control of capillary blood flow distribution and capillary recruitment (Murrant and Sarelius, 2000). Thus, muscle oxygen extraction is determined largely by the tone of pre-capillary sphincters of terminal arterioles within skeletal muscle (Renkin and Rosell, 1962; Mellander and Johansson, 1968). Regional differences in the response to sympathetic vasoconstrictor discharge must be carefully considered in examination of the contributions of sympathetic nerves to the regulation of vascular tone. Activation of  1- and 2-adrenergic receptors will cause vasoconstriction (McGillivray Anderson and Faber, 1991; Leech and Faber, 1996), while activation of β2-adrenergic receptors would cause vasodilation (Lundvall and Hillman, 1978; Hillman and Lundvall, 1981). If it is assumed that the smaller arteriole relaxation is concomitant with the larger arteriole contraction, the chance of converting OxyHb to DeoxyHb in the exchange vessel may increase, because the blood volume in the exchange vessel is increased.
This is the first confirmation of masseteric hemodynamic changes that are time-related to mental stress. When one considers that masseteric EMG activity was not time-related to mental stress, the hemodynamic changes might play a greater role in the etiology of jaw muscle dysfunction associated with mental stress. However, further study is needed to clarify the physiological significance of the hemodynamic behavior.
EMG Activity
EMG activity of the masseter and temporalis muscles was not time-related to mental stress. The failure to find EMG activity time-related to mental stress does not necessarily mean that EMG activity is insensitive to sympathetic nervous activity. Post-ganglionic sympathetic neurons innervating jaw muscles potentially release both noradrenaline and its co-transmitter, neuropeptide Y (NPY) (Lundberg et al., 1983), which induce a long-lasting, dose-dependent increase in twitch tension by acting directly on skeletal muscle fibers (Grassi et al., 1996). Thus, it seems that in the muscular district, the adrenergic-peptidergic co-operation is not limited to vascular smooth muscle but is also effective in skeletal muscle fibers. Furthermore, the sympathetic system may modulate muscle spindle afferent activity. It has been proposed that the sympathetic influence on spindle information would be most likely tonic, and the sympathetic system could participate reflexly in modifying muscle tone (Grassi et al., 1996). On the other hand, sympathetic activation would exert a powerful depressant action on jaw jerk and tonic vibration reflexes (Grassi et al., 1996). This indicates a reduction of spindle sensitivity to change in muscle length and would affect chewing function (Hidaka et al., 1999). EMG activity is thus regulated in a complicated manner, which could mask the effect of sympathetic outflow coincident with mental stress. This seems to be a likely explanation for non-existence of concomitant EMG activity.
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ACKNOWLEDGMENTS
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We thank Dr. S. Kashima (Omegawave) for his advice. The research was supported by grants from the Japan Society for the Promotion of Science (Nos. 12470459 and 15390632).
Received for publication November 22, 2002.
Revision received October 20, 2003.
Accepted for publication December 3, 2003.
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Journal of Dental Research, Vol. 83, No. 2,
185-190 (2004)
DOI: 10.1177/154405910408300220
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ABSTRACT
INTRODUCTION