خستگی، خلق و خو و واکنش پذیری قلبی حیاتی در استرس ناشی از کار
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|39030||2004||15 صفحه PDF||سفارش دهید||6482 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Biological Psychology, Volume 65, Issue 2, January 2004, Pages 121–135
Abstract The associations between vital exhaustion (long-term stress), temperament, and cardiac reactivity were studied during an experimentally induced stress in a sample of 76 healthy subjects. Vital exhaustion was assessed with the Maastricht Questionnaire(MQ), and temperament with Cloninger’s Temperament and Character Inventory (TCI). Cardiac reactivity was measured in terms of heart rate, respiratory sinus arrhythmia, and pre-ejection period. They were continuously measured during three stressors, i.e. mental arithmetic, reaction time, and giving speech. Results showed that vital exhaustion (long-term stress) was first of all associated with parasympathetic withdrawal. In addition, among exhausted persons the initial parasympathetic tone had no effect on task-induced parasympathetic reactivity, whereas in non-exhausted subjects parasympathetic reactivity was greatest when initial parasympathetic tone was high. Vital exhaustion interacted with temperament and gender: exhausted, persistent women expressed the highest level of physiological stress reactivity. Findings suggest that background stress may diminish one’s capacity to cope with acute stress.
Introduction Vital exhaustion, a state of an unusual fatigue, a loss of mental and physical energy, and an increased irritability, is labeled a risk indicator of coronary heart disease. Epidemiological studies have demonstrated its presence both before (Appels and Mulder, 1988) and after (Mendes de Leon et al., 1996) the occurrence of myocardial infarction. In addition, exhaustion is a common condition after stroke (Ingles et al., 1999). Finally, exhaustion is seen to be of importance for rehabilitation, exhaustion-related implications for rehabilitation expressed in the form: “I want to, but I can’t” (Appels, 2001). Pathophysiological aspects of the relationship between infarction or stroke and vital exhaustion can only be speculated about. Stress might be among key concepts. Vital exhaustion is seen as an indicator of long-term mental stress (Ingles et al., 1999), and it has also been shown to be related to insulin resistance syndrome (IRS) through the pituitary hypothalamic adrenocortical (HPA) axis (Keltikangas-Järvinen et al., 1996) which is a physiological indicator of long-lasting stress (Palkovits, 1987). IRS (i.e. hyperinsulinemia, hypertension, hypertriglyceridemia, a decreased plasma concentration of high-density lipoprotein (HDL), and abdominal obesity) in turn, is a risk factor both for stroke and coronary heart disease (Pyorala et al., 2000). As far as we know, there is no study investigating the association between vital exhaustion and physiological reactivity under short-term stress. This study was undertaken with this purpose. The first aim was to determine whether there is an association between vital exhaustion (i.e. chronic stress) and cardiac autonomic reactivity in task-induced stress (in acute stress). It was hypothesized that long-term mental stress impaires one’s physiological coping with acute stress. Previously we have found that vital exhaustion is associated with a certain temperament, that is, with a tendency to be fearful and worried even in supportive circumstances, and to be inhibited even by minor risks (Keltikangas-Järvinen, 2000). Subsequently, the second question was whether temperament plays a role in stress-related cardiac reactivity among exhausted people. Temperament refers to individual differences in mental and physiological reactivity that are attributable to individual differences in neural function (for a review, see Bates and Wachs, 1994). It is inherited, at least to some extent, and very stable over time and situations. Temperament may play an important role in moderating stress, i.e. in environmental interpretations, in coping with stress, and in consequences of stress. In other words, an inherited temperament might help to explain why the same daily troubles constitute a positive challenge to one person, but distress to another, and especially why the same daily distress has such widely varying somatic endpoints in different persons. Cloninger’s (1987) theory on temperament has recently received attention in epidemiological studies (Keltikangas-Järvinen et al., 1999). Cloninger’s formulation of temperament was inferred from genetic studies of personality and neurobiological studies of the functional organization of brain networks. According to this model, temperament consists of four dimensions, which are moderately heritable and related to the brain systems, that is, the amygdala, hypothalamus, striatum, and other parts of the limbic system. Temperament is involved in individual differences in response to environmental stimuli such as novelty, danger or punishment, and reward. The four neurobiologically-based temperament dimensions are Reward dependence (RD), Harm avoidance (HA), novelty seeking (NS), and persistence (P). RD is associated with individual variation in norepinephrine levels, and refers to a tendency to respond intensely to signals of reward, in particular to social approval and succor. People with high RD tend to maintain behaviors that have previously been socially rewarded. They seek social support, attachments, and praise from others. HA is associated with individual variation in serotonin levels. It refers to a tendency to intensely respond to aversive stimuli, novelty, and nonreward, leading to inhibition of behaviors and social withdrawal. NS, associated with variation in dopamine levels, is a tendency to react with excitement to novelty and to actively avoid monotony and frustration. P, originally a component of reward dependence, reflects a tendency towards perfectionism and perseverance despite frustration and fatigue. Our previous study discovered a relationship between P, RD, and insulin resistance syndrome (Keltikangas-Järvinen et al., 1999). A well-documented association between environmental stress and IRS suggests that we should see IRS as an indicator of chronic stress. Our finding has prompted us to ask whether the same temperament dimensions play a role in physiological response to acute stress, as well. Given that vital exhaustion is shown to be associated both with temperament and long-term stress, the second aim of this study was to determine whether vital exhaustion is associated with task-induced cardiac stress reactions, and whether temperament modifies this association. Gender differences were also highlighted, because our above-mentioned previous study had indicated that the role of temperamental factors was dependent on gender: the same factors, that were risk markers among men were neutral, or even protective, among women, and vice versa. Finally, the role of a type of a stressor was studied by using a series of different stimuli. One essential consideration in temperament theories is that the magnitude of stress varies according to the relevance of the stressor to the particular temperament.
نتیجه گیری انگلیسی
Results Table 1 shows the mean values for the VE and Cloninger’s temperament variables. Women scored higher than men on VE and HA; other significant gender differences did not exist. The mean vital exhaustion score was 9.0 (S.D.=7.3) when the five-point Likert scale used to measure vital exhaustion in this study was adjusted to correspond to the original scale of Maastrich Questionnaire (1=0, 2=0, 3=1, 4=2, 5=2). Our study included 14 subjects (18.4%) with MQ scores ≥14, a cutoff score used by Appels et al., 1997 to denote vitally exhausted. The results for cardiac activity are summarized in Table 2. Table 1. Mean values for the vital exhaustion and temperament variables in men and women Variable Men (n=35) Women (n=41) Mean S.D. Mean S.D. t (74) VE 41.1 12.9 46.6 11.0 −2.02* VEa 7.7 7.8 10.1 6.8 −1.49 NS 126.9 18.4 120.0 14.1 1.87 HA 83.0 18.2 93.3 17.6 −2.52* RD 76.8 9.6 81.2 10.3 −1.92 P 26.1 4.6 25.4 4.0 0.68 Note: VE, vital exhaustion; NS, novelty seeking; HA, harm avoidance; RD, reward dependence; and P, persistance. a Results considering vital exhaustion when the five-point Likert scale used to measure vital exhaustion in this study was adjusted to correspond to the original scale of Maastrich Questionnaire (1=0, 2=0, 3=1, 4=2, 5=2). * P<0.05. Table options Table 2. Means (and standard deviations) of cardiac activity during different phases of the experiment among women and men Phase Base 1 Math RT Speech Base 6 Men HR (beats per minute) 70.2 (10.5) 83.6 (15.1) 72.1 (13.7) 93.4 (19.3) 71.2 (13.0) ΔHR (beats per minute) 13.5 (12.5) 2.0 (8.1) 22.5 (15.1) RSA (log ms2) 2.84 (0.21) 2.62 (0.28) 2.88 (0.21) 2.74 (0.34) 2.85 (0.29) ΔRSA (log ms2) −0.23 (0.25) 0.02 (0.18) −0.11 (0.37) PEP (ms) 95.3 (13.1) 79.0 (19.7) 85.2 (18.8) 75.6 (17.3) 99.3 (12.2) ΔPEP (ms) −15.4 (16.3) −9.2 (14.8) −18.6 (14.6) Women HR (beats per minute) 73.0 (8.4) 88.6 (17.8) 77.3 (12.8) 106.2 (16.0) 72.2 (10.7) ΔHR (beats per minute) 5.2 (12.4) 4.2 (7.4) 32.2 (14.3) RSA (log ms2) 2.83 (0.25) 2.65 (0.30) 2.85 (0.21) 2.56 (0.30) 2.81 (0.25) ΔRSA (log ms2) −0.23 (0.26) −0.01 (0.13) −0.29 (0.30) PEP (ms) 95.0 (9.5) 79.2 (14.3) 82.9 (12.4) 71.9 (15.6) 97.8 (9.8) ΔPEP (ms) −15.7 (13.4) −13.0 (11.0) −24.5 (14.2) Note: HR, heart rate; RSA, respiratory sinus arrhythmia; and PEP, pre-ejection period. Table options Correlation between VE and HA was significant, r=0.54, P<0.001, while the correlations of VE with RD, NS, and P were nonsignificant (rs=−0.16, −0.16, and −0.05, respectively). 3.1. Effects of age, gender, and baseline level on cardiac baseline levels and reactivity Task × Age interaction, F(2,51,ε=0.88)=3.64, P=0.035, η2=0.06 modified the main effect of Age, F(1,52)=6.44, P=0.014, η2=0.11 when predicting ΔRSA. Contrasts indicated that during math, age was associated with higher RSA reactivity. In addition, Age had a significant main effect when predicting RSA levels during B1, F(1,67)=4.26, P=0.043, η2=0.06, and during B6, F(1,60)=7.02, P=0.010, η2=0.11, indicating that older subjects had lower RSA magnitudes during baselines than younger subjects. There was also a significant Task×Age interaction for ΔPEP, F(1,58)=4.58, P=0.012, η2=0.07. Contrasts indicated that during RT and speech younger subjects expressed higher PEP reactivity than older, whereas during math the reverse was true. In addition, Age had a significant main effect for baseline PEP during B6, F(1,61)=5.60, P=0.021, η2=0.08, that is, age was associated with higher last baseline levels of PEP. Task × Gender interaction, F(2,56,ε=0.73)=5.05, P=0.016, η2=0.08 modified the main effect of Gender, F(1,57)=5.20, P=0.026, η2=0.08 when predicting ΔHR. Contrasts indicated that women showed greater HR reactivity than men, and especially during speech. There was a significant main effect for B1 for ΔRSA, F(1,52)=30.75, P<0.001, η2=0.37, and ΔPEP, F(1,59)=4.65, P=0.035, η2=0.07, indicating that the higher initial baseline levels of RSA and PEP were associated with higher reactivity. 3.2. Effects of VE and its interactions with temperament variables on cardiac baseline levels and reactivity 3.2.1. Baseline levels VE and its interactions with temperament were nonsignificant when predicting initial baseline levels of HR, RSA, and PEP. 3.2.2. Heart rate reactivity VE main effect was nonsignificant when predicting ΔHR. When interactions with temperament variables were included, there was a significant Task × Gender × VE × P interaction, F(2,50,ε=0.76)=8.05, P=0.001, η2=0.14. Contrasts indicated that during speech, women with high VE and high P exhibited the highest HR reactivity, whereas women with high P and low VE exhibited the lowest HR reactivity ( Fig. 1a). There were no significant differences among men. Mean delta heart rate (HR), respiratory sinus arrhythmia (RSA), and pre-ejection ... Fig. 1. Mean delta heart rate (HR), respiratory sinus arrhythmia (RSA), and pre-ejection period (PEP) during the tasks in different vital exhaustion and persistance groups. Figure options 3.2.3. Respiratory sinus arrhythmia reactivity B1 × VE interaction, F(1,52)=11.08, P=0.002, η2=0.18 modified the main effect of VE, F(1,52)=11.38, P=0.001, η2=0.18, when predicting ΔRSA. VE was associated with higher RSA reactivity, but highest reactivity was among low VE subjects with high initial baseline RSA. That is, among high VE subjects, initial baseline level had no effect on RSA reactivity, whereas among low VE subjects, RSA reactivity was highest when initial baseline level was high ( Fig. 2). Mean delta respiratory sinus arrhythmia (RSA) during the tasks (math, reaction ... Fig. 2. Mean delta respiratory sinus arrhythmia (RSA) during the tasks (math, reaction time, and speech) in subjects with high/low vital exhaustion and high/median/low initial baseline RSA value. Error bars show mean ± S.E.M. Figure options When interactions with VE and temperament variables were included, there was also a significant Task × Gender × VE × P interaction, F(2,50,ε=0.82)=5.25, P=0.011, η2=0.09. Contrasts indicated that women with high P and high VE had the highest RSA reactivity during speech, whereas women with high P and low VE had the lowest RSA reactivity during speech ( Fig. 1b). There were no significant differences among men. 3.2.4. Pre-ejection period reactivity VE main effect was nonsignificant when predicting ΔPEP. When interactions with VE and temperament variables were included, there was a significant Task × VE × P interaction, F(2,52)=3.48, P=0.034, η2=0.06. Contrasts indicated that High P/low VE and low P/high VE subjects had greater sEP reactivity than low P/low VE and high P/high VE subjects during RT and speech tasks ( Fig. 1c).