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Psychosomatic Medicine:
doi: 10.1097/PSY.0b013e3182223b28
Original Article

The Interplay Between Physical Activity and Anxiety Sensitivity in Fearful Responding to Carbon Dioxide Challenge

Smits, Jasper A.J. PhD; Tart, Candyce D. MA; Rosenfield, David PhD; Zvolensky, Michael J. PhD

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Author Information

From the Department of Psychology (J.A.J.S., C.D.T., D.R.), Southern Methodist University, Dallas, Texas; and Department of Psychology (M.J.Z.), University of Vermont, Burlington, Vermont.

Address correspondence and reprint requests to Jasper A.J. Smits, PhD, Department of Psychology, Southern Methodist University, Dedman College, PO Box 750442, Dallas, TX 75275. E-mail: jsmits@smu.edu

J.A.J.S. is supported by the National Institutes of Health Grants R01MH075889 and R01DA027533 and has received royalties from Oxford University Press. M.J.Z. is supported by the National Institutes of Health Grants R01DA027533 and R01MH076629.

All authors declare that they have no conflicts of interest.

Received for publication September 2, 2010; revision received March 17, 2011.

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Abstract

Objective: Physical activity may confer protective effects in the development of anxiety and its disorders. These effects may be particularly strong among individuals who have elevated levels of anxiety sensitivity (AS; i.e., the fear of somatic arousal), an established cognitive-based risk factor for anxiety and its disorders. The present study performed a laboratory test of the interplay between physical activity and AS.

Methods: The participants were adults free of Axis I psychopathology (n = 145) who completed measures of physical activity and AS before undergoing a recurrent 20% carbon dioxide-enriched air (CO2) challenge.

Results: Consistent with the hypothesis, physical activity was significantly related to CO2 challenge reactivity among persons with elevated levels of AS, at high levels of physical activity (p <.001) but not at low levels of physical activity (p =.90). Also consistent with hypothesis, irrespective of the level of physical activity, physical activity did not relate significantly to CO2 challenge reactivity among persons with normative levels of AS (p =.28).

Conclusions: These findings provide novel empirical insight into the role that physical activity may play in terms of resiliency for the development of anxiety disorders. Specifically, the protective effects of physical activity may only be evident at higher doses and among persons who are at increased risk of developing anxiety disorders because they have elevated AS.

OR = odds ratio; AS = anxiety sensitivity; CO2 = carbon dioxide; SCID-NP = Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition-Non-patient Edition; EHS = Exercise Health Survey; ASI = Anxiety Sensitivity Index; SUDS = Subjective Units of Distress Scale; MLM = multilevel mixed-effects regression analysis; PA = physical activity

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INTRODUCTION

Growing evidence suggests that regular physical activity (PA) is a possible protective factor in terms of the development of anxiety and its disorders. For example, Goodwin (1) observed that regular PA predicted lower prevalence of panic attacks (odds ratio [OR] = 0.73), social phobia (OR = 0.65), specific phobia (OR = 0.78), and agoraphobia (OR = 0.64), among a representative adult sample in the United States. These effects were evident after controlling for demographic variables and co-occurring physical and mental health conditions. In this same study, there was also evidence for a dose-response relationship between PA and mental health problems, such that the lowest prevalence rates of anxiety disorders were observed among persons who exercised regularly, followed by those who exercised occasionally, rarely, and never, respectively (1). A recent prospective study has further found that PA is associated with a reduced incidence of anxiety disorders (2). Specifically, using a representative sample (N = 2548) of adolescent and young adults (ages 14-24 years) from Munich, Germany, Ströhle and colleagues (2) found that the incidence of any anxiety disorder during a 4-year follow-up was significantly lower among persons who reported engaging in regular PA versus those who reported no PA (OR = 0.52).

Extant work on the role of PA in the development of anxiety and its disorders has primarily focused on establishing the general overall effects of PA (1,2). With any observed main effects, there is evidence of individual variability, which prompts research on identifying moderators. Determining whether the putative protective effects of PA with respect to anxiety vulnerability are equally applicable to all persons or whether these effects are relevant to only a subset of the population has important implications for prevention. Accordingly, there is a need to empirically explore the interplay between PA and the established risk factors for anxiety disorders.

Perhaps one of the most well-known cognitive-based risk factors for anxiety disorders is anxiety sensitivity (AS) (3). AS is defined as the extent to which individuals believe that anxiety and anxiety-related bodily sensations (i.e., somatic arousal) have harmful consequences (4,5). AS is distinct from the temperament variables of trait anxiety (6) and negative affectivity (7); it reflects beliefs about internal sensations as opposed to frequency of (negative) mood symptoms. Laboratory (8-11) and prospective (12-16) studies consistently indicate that AS increases the risk for more intense anxiety symptoms and anxiety psychopathology.

Building on previous work (1,2), in the present study we sought to perform a test of the potential interplay between regular PA and AS with respect to anxiety vulnerability. We theorized that PA would interact with AS to significantly decrease vulnerability in anxiety-based emotional reactivity to bodily perturbation. This hypothesis was guided by extant work suggesting that the apparent protective effects of regular PA on the development of anxiety and its disorders may be centered on reduced reactivity to anxiety-provoking stimuli (17). Indeed, a series of recent studies have shown that an acute bout of exercise reduces fearful responding to panicogenic agents such as carbon dioxide-enriched air (CO2) (18,19) and cholecystokinin tetrapeptide (20,21). More importantly, the results from both animal and human studies converge to indicate that regular PA reduces physiological and psychological reactivity to psychological stressors (17,22-26). Accordingly, because it is associated with reduced reactivity to stressors, regular PA may buffer the effects of bodily perturbation on anxiety for persons who are prone to respond to such stressors with anxiety (i.e., persons with elevated levels of AS) but not for those who do not tend to respond to such stressors with anxiety (i.e., persons with nonelevated levels AS). In addition, there is some work to suggest that the buffering effects of PA on responses to bodily perturbation among individuals with elevated AS may vary across levels of PA. Indeed, Dishman and colleagues (27) reported that substantial reductions in trait anxiety become only evident when persons reach a certain "threshold" of PA (i.e., 4 to 5 months of exercise training). This observation coupled with the finding that reduced stress reactivity has been linked to regular PA may suggest that the PA-buffering effects for individuals with elevated AS may only be evident among individuals who engage in PA frequently.

We used a CO2 challenge laboratory paradigm in testing the present research questions. Inhalation of CO2-enriched air is an ideal paradigm for the current test because it induces the somatic arousal characteristic of panic attacks (27) and CO2 challenge reactivity has been found to significantly prospectively predict the onset of spontaneous panic attacks in the future (28,29). In the current study, the participants were young adults free of both Axis I psychopathology and history of panic attacks who reported various levels of regular PA. Nonclinical healthy persons were sampled to rule out the possibility that any observed differences would be attributable to preexisting psychological or health problems (30). We hypothesized that CO2 challenge reactivity would vary as a function of the interaction between PA and AS. Specifically, we expected no relationship between PA and CO2 challenge reactivity among individuals with low or normative levels of AS. Furthermore, we expected that, among individuals with elevated levels of AS, the relationship between PA and CO2 challenge reactivity would be significant but discontinuous, such that greater PA would be related to lower CO2 reactivity only for PA levels above a certain threshold.

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METHODS

Participants

The participants were 145 adults (83 females) between the ages of 18 and 59 years (mean [M] = 21.6 [standard deviation {SD} = 7.43] years) from the University of Vermont and the greater Burlington, Vermont community. The individuals were recruited through newspaper and other local advertisements posted in university and nonuniversity settings. The racial distribution of the sample generally reflected that of the local population (31): 93.1% (n = 135) white, 2.8% (n = 4) African American, 1.4% (n = 2) Hispanic, 1.4% (n = 2) Asian, 0.7% (n = 1) "other," and 0.7% (n = 1) did not specify race. The marital status for the vast majority of the sample was single (n = 141, 97.2%), and on average, the participants had completed 13.2 (SD = 1.80) years of education.

The participants were excluded for a history of Axis I psychiatric disorders, including nonclinical panic attacks, based on their responses to the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Non-patient version (SCID-NP) (32). Interrater reliability for the SCID-NP for Axis I diagnoses and subclinical panic attack history has been high in our group (33). The participants were also excluded from participation if they reported a) current suicidal or homicidal ideation, b) current use of psychotropic medication, c) pregnancy, d) current serious medical conditions (e.g., cancer), e) serious breathing difficulties or respiratory-based illness (e.g., asthma, emphysema), or f) limited mental competency or inability to give informed, written consent. As in past work (33), these additional exclusionary criteria were assessed within the context of the structured interview as an additional supplemental set of (standardized) interview-based medical screening questions. Finally, we excluded from our investigation participants who reported no PA. This exclusion criterion was used for three reasons. First, the present study was an investigation of the influence of the amount of PA and not the occurrence of PA. Second, those who never engage in PA tend to differ from those who do on numerous psychological and or physical health dimensions (27), which would make the interpretation of the effects of PA difficult. Third, from a statistical perspective, calculating unbiased estimates of causal effects requires that the distributions of the effects must be completely overlapping (34). It is unlikely that the distributions of the effects of persons who report no PA and those who do engage in regular PA will be completely overlapping.

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Procedures

A detailed description of the procedures has been provided elsewhere (35).1 In short, interested participants responding to community-based advertisements for a laboratory study of anxiety were screened by a trained research assistant using the SCID-NP and scheduled by telephone for an individual laboratory appointment. Eligible participants completed a self-report questionnaire packet before beginning the laboratory component of the study. The participants were instructed not to consume caffeine or engage in strenuous PA for 3 hours before their scheduled laboratory visit. During the laboratory component of the study, the participants sat at a desk supporting a computer, which was programmed to administer the CO2 administrations. After completing physiological hookup and listening to experimental instructions, the participants were fitted with a positive-pressure continuous positive airway pressure mask. The experimenter observed the participants from an adjacent control room containing a computer-operated apparatus designed to automatically provide the participants with either room air or a mixture of 20% CO2-enriched room air. The apparatus (36) assured that all participants received six CO2 inhalation trials and 18 room air inhalation trials each lasting 90 seconds. Furthermore, all participants received the same trial order with CO2 administrations occurring on Trials 3, 6, 9, 14, 19, and 22. Lastly, because the original study (35) examined whether CO2 challenge reactivity would vary as a function of the predictability of the biologic stressor, each inhalation trial began with an instruction informing the participant of the trial type (room air or 20% CO2).2 Thus, the participants received a total of 24 trials, of which six were CO2 inhalations (three predictable and three unpredictable) and 18 were room air inhalations (nine predictable and nine unpredictable). After the laboratory component of the study, the participants were debriefed and paid $30 for their participation. All procedures were approved by the University of Vermont Institutional Review Board. The data were collected between September 2003 and August 2008.

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Measures
Physical Activity

The Exercise Health Survey (M.J.Z., unpublished data, 2002) is a self-report measure that includes questions pertaining to the weekly amount of time spent in PA and is comparable to that used in the previous work documenting PA-anxiety relations (1,2,37) as well as measures of PA used in large-scale epidemiological studies relating regular PA to morbidity and mortality (38-40). Specifically, the measure lists a variety of types of moderate- and vigorous-intensity activities and asks participants how many days per week on average they engage in these or other activities, and the duration of their exercise sessions per occasion. Using this information, we calculated the average minutes per week of PA.

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Anxiety Sensitivity

The Anxiety Sensitivity Index (ASI) is a 16-item questionnaire on which respondents indicate on a 5-point Likert-type scale (0 = very little to 4 = very much) the degree to which they fear anxiety symptoms and their negative consequences (41). The ASI is widely used and has demonstrated good psychometric properties (42). A large body of work suggests that AS is an important cognitive-based predictor of emotional response to biologic challenge (8,11,43) and AS has been shown to affect estimations of cardiovascular fitness obtained by cycle ergometer testing (44). In the present investigation, we used the total ASI score because it represents the global-order AS factor and therefore takes into consideration the different types of fears, including fears of anxiety-related somatic, cognitive, and social cues.

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Challenge Measures

The participants were asked to provide ratings of their current level of anxiety at baseline and at the end of each inhalation trial using an 11-point Likert-type rating scale, similar to those used in the past work (e.g., Subjective Units of Distress Scale [SUDS]) (45), ranging from 0 (no anxiety) to 10 (extreme anxiety). Specifically, the participants provided a SUDS rating at the end of each of the 24 trials (regardless of whether CO2 was delivered during that trial).

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DATA ANALYSIS

To test whether AS moderated the effect of PA on CO2 challenge reactivity, we used a multilevel, within-subjects, multilevel mixed-effects regression analysis (MLM) using the program Hierarchical Linear and Nonlinear Modeling version 6.06 (46). MLM was selected because of its flexibility in modeling complex relationships, its lack of restrictive assumptions, and its ability to include all of the observations of all subjects regardless of missing data. In addition, Hierarchical Linear and Nonlinear Modeling 6.06 provides significance tests using "robust" standard errors (SEs), which are robust to violations of multivariate normality. The Level 1 portion of the MLM analysis modeled the outcomes (SUDS) from each inhalation trial as a function of inhalation type (room air = 0, CO2 = 1). Also, because previous findings with this sample (35) indicated that predictability was a significant determinant of SUDS, we included predictability (predictable = 0, unpredictable = 1) as a covariate. As such, the Level 1 portion of the MLM model was

Given this coding of the Level 1 predictors, β0j represented the average SUDS ratings for the predictable room air trials, β1j represented the mean difference between SUDS reported for CO2 versus room air inhalations (herein referred to as "CO2 challenge reactivity"), and β2j is the mean difference between the predictable and unpredictable trials.

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The Level 2 portion of the MLM model allowed us to examine whether individual characteristics, such as PA and AS, predicted differences in mean SUDS ratings for the room air trials (β0j) and for CO2 challenge reactivity (β1j). As noted previously, we included predictability in the Level 1 model because predictability was significantly associated with SUDS for room air trials (35). Because we had no hypotheses regard ing the effect of predictability on CO2 challenge reactivity, we included it in the model to account for variance related to predictability, but we did not include any Level 2 predictors for it.

Level 2 predictors of β0j and β1j included PA and AS. To test for discontinuous relations between PA and CO2 challenge reactivity, we followed guidelines put forth by Singer and Willett (47). Specifically, we added an additional term to allow the relationship between PA and CO2 challenge reactivity to change at 1 SD above the mean of PA (the threshold). We selected this threshold of 1 SD above the mean following a common practice when investigating interactions (48). The PA "slope difference" term was coded 0 for PA below threshold and coded with the amount by which the participant's PA exceeded the threshold for those with PA levels more than 1 SD above the mean (i.e., if PA was 1.55, the slope difference term would be coded 1.55−1 = 0.55) (47). Because we expected a slope difference only for those with high AS, we included a term for the interaction between AS and the slope difference (i.e., AS by PA slope difference). Although we did not expect that AS would moderate the relationship between PA and CO2 challenge reactivity among individuals below the PA threshold, we included the AS by PA interaction in our initial model to examine this possibility. Furthermore, we included sex (0 = male, 1 = female) as a covariate because females tend to report both higher AS (42) and lower levels of PA than males (49). Finally, because the age of our participants varied, we included age (log transformed to reduce skewness) as an additional covariate in the model. All predictors were converted to z scores to enhance the interpretation of the findings. Accordingly, the Level 2 equations were:

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RESULTS

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Preliminary Analysis

On average, participants were relatively active (MPA = 148.28 [SD = 77.98]) and had AS levels similar to those observed in other community samples (MAS = 15.88 [SD = 9.44]) (3). As expected, females reported higher AS levels than males (17.42 versus 15.88; F[1,141] = 5.43, p <.05), and males reported more weekly minutes of PA than females (169.28 versus 132.60; F[1,143] = 8.25, p <.01).

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Hypothesis Testing

Because our hypotheses were centered on CO2 challenge reactivity, we will focus on the results of the second set of Level 2 equations (i.e., predictors of β1j). Initial analyses indicated that neither sex nor the interaction of AS and PA for PA below the "threshold" were significant (p =.59 and p =.65, respectively), so they were dropped from the model, and the analysis was recomputed. In this final model, age was marginally related to CO2 challenge reactivity (b = −0.38, SEb = 0.21, t125 = −1.77, p =.08); we retained this term in the model to be conservative. As predicted, CO2 challenge reactivity varied as a function of AS (b = 0.35, SEb = 0.17, t125 = 2.05, p <.05) but not as a function of PA (b = −0.03, SEb = 0.23, t125 = −0.12, p =.90) among persons whose PA was below the threshold (Fig. 1). Furthermore, consistent with hypothesis, there was a significant interaction between AS and the PA slope difference (b = −0.54, SEb = 0.24, t125 = 2.27, p <.05), indicating that the relationship between PA and CO2 challenge reactivity changed at 1SD above the mean of PA, and that change depended on the level of AS. Following the guidelines put forth by Aiken and West (48), we examined the change in the relationship between PA and CO2 challenge reactivity for participants with high and normative levels of AS. We used a score of 1 SD above the mean AS score (25.32) to represent high levels of AS (50), and we used the mean AS score in the sample (15.88) to represent normative levels (50). The results are presented in Figure 1. Consistent with hypothesis, among individuals with high levels of AS, there was a significant discontinuity in the relationship between PA and CO2 challenge reactivity when PA exceeded 1 SD above the mean (bΔ = −0.87, SEb = 0.35, t125 = 2.47, p =.01). Specifically, below the threshold, there was no relationship between PA and CO2 challenge reactivity (b = −0.03, SEb = 0.23, t125 = −0.12, p =.90), but above the 1 SD threshold, the relationship was significant (b = −0.90, SEb = 0.21, t125 = 4.25, p <.001; Fig. 1). In addition, consistent with hypothesis, among individuals with normative levels of AS, there was no discontinuity in the relationship between PA and CO2 challenge reactivity (bΔ = −0.34, SEb = 0.34, t125 = 1.08, p =.28). Specifically, the relationship between PA and CO2 challenge reactivity was not significant either below (b = −0.03, SEb = 0.23, t125 = −0.12, p =.90) or above the threshold (b = −0.35, SEb = 0.21, t125 = 1.70, p =.09; Fig. 1). The proportion of the total between-subjects variance of CO2 challenge reactivity accounted for by this model was 9.3%.

Figure 1
Figure 1
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In supplementary analyses, we investigated other lower potential thresholds (as low as the average level of PA). The results indicated that, as we lowered the threshold, the relationship between PA and CO2 challenge reactivity remained significant among individuals with high AS. However, the strength of this relationship generally decreased in magnitude as the threshold decreased. Thus, in this data set, we could not identify a clear cut off, over which there was a definite relationship between PA and CO2 challenge reactivity and under which such a relationship did not exist. Therefore, we can only conclude that PA is related to reduced CO2 challenge reactivity for high-AS individuals when PA levels are high. Future research should examine whether this relationship abruptly changes from nonsignificant to significant at a certain threshold.

Lastly, we examined the possibility that the moderating effects of AS were accounted for by one of the ASI subscales (ASI-physical, ASI-social, or ASI-mental) (42). Specifically, we reran the analysis three times, each time substituting the one of the ASI subscale scores for the ASI total score. The results of each of these three models mirrored those of the model with the ASI total score (i.e., significant and nonsignificant terms remained significant and nonsignificant, respectively). These findings suggest that the relationship between AS and PA does not seem to be specific to, or accounted for, by any particular ASI subscale.

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DISCUSSION

In the present study, we sought to examine the hypothesis that AS would moderate the relationship between PA and emotional reactivity to bodily perturbation. We found evidence consistent with this hypothesis. Specifically, we did not observe a significant effect of PA on CO2 challenge reactivity for individuals with nonelevated levels of AS. However, consistent with hypothesis, for individuals with elevated levels of AS, higher levels of PA were related to significantly lower CO2 challenge reactivity, but only among those who reported high levels of PA.

The finding that AS moderates the relationship between regular PA and CO2 challenge reactivity suggests that the apparent protective effects of regular PA with respect to anxiety vulnerability (1,2) may be particularly applicable to persons who have elevated AS. The interplay between AS and PA observed in the present study also provides novel empirical insight into the potential effect of regular PA on modulating risk conferred by AS in the development of anxiety disorders. Indeed, our results indicate that, for people with high levels of PA, those with high levels of AS show no greater CO2 challenge reactivity than those with normal levels of AS. Accordingly, because CO2 challenge reactivity is a predictor of future panic attacks (28,29), these findings suggest that high levels of PA may reduce the risk of panic attacks and other anxiety-related problems among those with high levels of AS. Future studies should examine whether regular PA indeed reduces the risk for panic attacks among persons high in AS using prospective designs and time sampling approaches (e.g., ecological momentary assessment protocols).

The observation that PA interacts with AS to predict CO2 challenge reactivity also may help explain the relative predictive power of AS in any given study. That is, because the effects of AS on fear reactivity to CO2 challenge can vary from small to large (4,51), it is possible that PA may serve as a qualifying, but often unrecognized, factor in understanding such variability. These data therefore highlight the potential importance of documenting PA and understanding its contribution to the expression of anxious and fearful responding to bodily sensations.

Although the present data provide evidence that high levels of PA were related to significantly lower CO2 challenge reactivity among persons with elevated levels of AS, but not among individuals with normative levels of AS, the exact mechanisms underlying such effects remain unclear. There are a number of non-mutually exclusive possibilities that may warrant further scientific attention. One possibility is that higher levels of PA may facilitate corrective fear learning for those high in AS. It also may be possible that high levels of PA promotes more adaptive regulation of affect and thereby modulates fear responsivity. A final possibility is that high levels of PA for those high in AS may alter brain circuits that mediate fear responsivity. Clearly, elucidating the mechanisms linking the risk and protective factors to clinical conditions will facilitate theoretical refinement of models of disorder development and aid in tailoring preventative work on specific conditions.

If replicated and extended, the present laboratory results, in conjunction with earlier field-based work (1,2), provide guidance for anxiety disorder prevention program development. Initial work in this area has focused on the evaluation of cognitive-behavioral programs designed to target AS (52-54). Numerous scholars have suggested that such prevention programs may benefit from the inclusion of health-oriented tactics to modify AS and related anxiety risk processes (55,56). PA promotion may represent one such tactic. The present study findings indicate that adding a PA component to cognitive (e.g., cognitive restructuring) and behavioral (e.g., interoceptive exposure) strategies may offer a more powerful means to reduce the risk for anxiety disorder development. PA programs may also be useful as stand-alone interventions in reducing the deleterious effects of AS. PA programs (either alone or in tandem with other interventions) may be especially efficacious because exercise has also been shown to reduce AS levels (57-59). Thus, incorporating PA into prevention programs targeting AS may be particularly potent because it buffers some of the negative consequences of AS (hyperreactivity), as demonstrated in the present study, and it can reduce overall levels of AS. Lastly, because PA also has established physical health benefits, it would likely bolster global-based improvement in multiple domains of life functioning.

The present study has several limitations, some of which provide suggestions for future research. First, the sample was limited in that it was composed primarily of a relatively homogenous group of young adults. To increase the generalizability of these findings, it will be important for researchers to draw from populations other than those used in the present study. Second, although the present investigation examined the interplay between regular PA and AS, AS represents only one exemplar risk factor for anxiety psychopathology. Thus, exploration of the role of PA in mitigating the effects of other risk factors for anxiety disorders may inform the relative degree of specificity of the observed findings from a vulnerability-resilience perspective. Finally, the present study was focused on a laboratory model of fear responding. Laboratory findings may not fully generalize to naturally occurring fear behavior (60). Similarly, it is not possible to rule out spuriousness in these types of investigations. PA and symptoms of anxiety and depression may be influenced by common factors (61). Accordingly, scientific attention should be given to the potential influence of other risk factors on the observed relationships, including genetic risk factors (62).

Overall, the present investigation adds uniquely to the extant empirical literature on the role of PA in modifying risk for anxious and fearful responding to bodily sensations. The results suggest that those with elevated levels of AS and high levels of PA showed significantly reduced CO2 challenge reactivity relative to those with elevated levels of AS and low levels of PA. These laboratory findings highlight the potential promise of PA as a protective factor for the expression of fear reactivity to somatic perturbation.

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This study is based on an investigation from which other results have previously been reported (35). None of the predictors of outcome in the present study was investigated in the prior report. Cited Here...

For unpredictable trials, the instruction "Unpredictable Trial: You will NOT be told whether or not you will receive CO2 on this trial" appeared on the computer screen. For predictable trials, either the instruction "Predictable Trial: You will receive CO2 on this trial" or "Predictable Trial: You will not receive CO2 on this trial" appeared on the screen, depending on whether or not it would be a CO2 trial. The participants were never misinformed. As reported by Yartz and colleagues (35), the results indicated that equivalent levels of anxiety were experienced during predictable and unpredictable administrations of 20% CO2-enriched air. However, because predictability was significantly associated with anxiety for room-air trials, this variable was included as a covariate in the present analysis. Cited Here...

Keywords:

physical activity; exercise; anxiety; anxiety sensitivity; biologic challenge

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