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Psychosomatic Medicine 68:224-230 (2006)
© 2006 American Psychosomatic Society

ORIGINAL ARTICLES

Depressive Mood Symptoms and Fatigue After Exercise Withdrawal: The Potential Role of Decreased Fitness

Ali A. Berlin, MS, Willem J. Kop, PhD and Patricia A. Deuster, PhD

From the Uniformed Services University of the Health Sciences, Bethesda, Maryland.

Address correspondence and reprint requests to Ali A. Berlin, MS, Department of Medical and Clinical Psychology, 4301 Jones Bridge Road, Bethesda, MD 20814. E-mail: aberlin{at}usuhs.mil


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Objective: Depressive symptomatology is more prevalent among sedentary than physically active individuals. The present prospective study examines whether withdrawal of regular aerobic activity provokes depressive mood symptoms and fatigue, and to what extent reductions in fitness levels contribute to the development of these symptoms.

Methods: Forty participants (mean age of 31.3 ± 7.5 years, 55% women) who exercised regularly (≥30 minutes aerobic exercise ≥3 times/week) were randomized to aerobic exercise withdrawal (n = 20) or to continue regular exercise (n = 20) for 2 weeks. Protocol adherence was documented using ambulatory actigraphy. Negative mood was measured with the Profile of Mood States (POMS), depressive symptoms with the Beck Depression Inventory–II (somatic and cognitive–affective components), and fatigue with the Multidimensional Fatigue Inventory (MFI). Fitness levels were documented by cycle ergometry testing.

Results: Fatigue and somatic depressive symptoms emerged after 1 week of exercise withdrawal (p = .05) and subsequently predicted the development of cognitive–affective depressive symptoms at 2 weeks (ß = 0.62; p = .046). Exercise withdrawal also resulted in increased negative mood (POMS; p ≤ .01), and this increase was correlated with decreases in fitness level (r = –0.36, p = .03). Decreased fitness was related to increased POMS fatigue (p = .003) when statistically adjusting for baseline fitness levels and group condition.

Conclusion: Depressed mood and fatigue are commonly observed in individuals deprived of usual exercise activities, and the increase in fatigue may be partially mediated by reduced fitness levels. These findings may explain mood changes in response to short-term exercise withdrawal such as injuries and recovery from medical procedures that do not require full bedrest.

Key Words: depression • exercise deprivation • fatigue • mood • physical activity

Abbreviations: BDI-II = Beck Depression Inventory–II; BMI = body mass index; HR = heart rate; MET = metabolic equivalent of task; MFI = Multidimensional Fatigue Inventory; POMS = Profile of Mood States; TMD = total mood disturbance; VO2max = maximum volume of oxygen that can be used per minute; index of maximal aerobic power.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Depressivesymptoms occur more frequently in sedentary compared with physically active individuals (1–4). Transient periods of reduced physical activity (e.g., as a consequence of injury) also result in depressive symptomatology and fatigue (5–9). The relationship between low physical activity and depressive symptoms may be mediated in part by physiological changes after reduced exercise levels, including decreased fitness levels (maximum volume of oxygen that can be used per minute [VO2max]), and biological changes (e.g., increased markers of inflammation and coagulation) (10,11). Depressive mood symptoms are also consistently documented after cessation of regular exercise training, with low energy, fatigue, tension, confusion, decreased self-esteem, insomnia, and irritability as the most common symptoms (6,9,12–15). However, the naturalistic settings of these investigations pose limitations to the conclusions that can be drawn because of the possible effects of confounding variables (e.g., initial physical activity level and weight changes). These limitations can be circumvented by using voluntary exercise-withdrawal research designs (reduction of regular exercise under experimental control), which enable systematic investigation of the relationship between exercise and depressive symptoms (6).

Sedentary individuals have lower fitness levels (i.e., maximal aerobic power assessed by VO2max) compared with physically active individuals (16). Reductions in activity levels can also lower VO2max. For example, manipulation of activity by imposing bedrest reduces VO2max levels by 11% to 17%, depending on the initial fitness level, duration of confinement, and participants’ health status (10,17–19). However, the role of fitness in the relationship between low physical activity levels and depressive symptomatology has not been systematically investigated.

The present study examines the hypothesis that exercise withdrawal results in depressive mood symptoms, and that somatic depressive symptoms (e.g., fatigue and sleep problems) will develop before subsequent cognitive–affective depressive symptoms (8). It is further hypothesized that the extent of fitness reduction after exercise withdrawal will predict the magnitude of depressive symptoms using a controlled longitudinal experimental design.


   METHODS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Participants
Participants (n = 40, age 31.3 ± 7.5, 55% women) were recruited through newspaper and local advertisements. Participants were eligible if they engaged in aerobic exercise for at least 30 consecutive minutes a day for at least 3 days per week over the past 6 months (20). Exclusion criteria were: 1) age <18 or >45 years; 2) use of antiinflammatory or anticoagulant medications other than aspirin; 3) history of cardiovascular disease; 4) hypertension (blood pressure >140/90 mm Hg); 5) obesity (body mass index (BMI) >30 kg/m2); and 6) currently under treatment for psychiatric or psychological disorder. Participants were randomized, independent of baseline psychological measures, to either stop (n = 20) or to continue (n = 20) regular aerobic exercise activities. The duration of the study was set at 2 weeks to optimize evaluation of mood changes after exercise withdrawal (8). Recruitment for this study began in the summer of 2004 and all participants completed the protocol by early fall of 2004.

Procedures
The research was approved by the Institutional Review Board of the Uniformed Services University of the Health Sciences and all participants provided written informed consent. In the informed consent document, participants were informed that the study was designed to examine "the effects of exercise withdrawal on physical function and mood." Psychological assessments and exercise testing were performed during each of three laboratory visits: baseline, 7 days into the protocol (week 1), and 14 days into the protocol (week 2). Psychological questionnaires were completed after an initial 10-minute rest period. A bicycle ergometry fitness test was performed at the end of each of the three study visits. To evaluate protocol adherence, all participants were equipped with an ambulatory activity monitor during the course of the study (Actiwatch; Mini-Mitter Co., Bend, OR).

Instruments
Psychological Measures
The Profile of Mood States (POMS) was used as an index of negative mood (21) and depressive symptoms were assessed using the Beck Depression Inventory–II (BDI-II) (22). The POMS is commonly used in the exercise psychology literature (23) and the total mood disturbance score (POMSTMD) was calculated by summation of the five negative affect scales (fatigue, depression, tension, anger, confusion) and subtraction of the vigor scale (21). The "past week" instruction set was used for the POMS and BDI-II to match the timing schedule of the weekly study visits (21). The BDI-II was used to assess depressive symptoms (22). BDI-II score can be divided into somatic (e.g., loss of energy, sleep problems, changes in appetite, poor concentration, and fatigue) and cognitive–affective (e.g., sadness, sense of failure, loss of pleasure, guilt, punishment, self-dislike, self-criticalness, suicidal thoughts, crying, agitation, loss of interest, indecisiveness, worthlessness, and irritability) symptoms based on prior factor-analyses of interitem correlations (24,25).

Fatigue assessments were based on the Multidimensional Fatigue Inventory (MFI) (26). The MFI consists of 20 items and has good internal consistency (Cronbach’s {alpha} = 0.84) (26).

Initial Activity Level
The Aerobics Center Longitudinal Study Physical Activity Questionnaire (27) was used to assess initial physical activity levels to establish whether participants were at equivalent physical activity levels at the time of study enrollment. The questionnaire evaluates leisure time exercise participation (including intensity of activities) over the previous 6 months. Reported exercise participation per week was converted to energy expenditure (kcal) estimates by using established metabolic equivalent of task (MET) values for each activity (28).

Physical Fitness During Ergometry Exercise Testing
Progressive bicycle ergometry exercise with increasing workloads was used to document physical fitness at each of the three study visits (Monark Ergomedic 828E Ergometer, Vansbro, Sweden). Participants underwent submaximal exercise testing on a stationary bicycle by pedaling for 2 minutes at four increasing power outputs at 60 revolutions per minute. The starting power was 30 W for women and 60 W for men and increased by 30 W per stage as described previously (29). The test was discontinued when 85% of age-based maximum heart rate (HR: 0.85 x [220-age]) was reached or 8 minutes of exercise were completed. Thus, the maximal power output attained by each participant was below maximal exercise capacity (29).

Heart rates at the end of each stage were used to determine the slope of the heart rate as a function of power output line, and VO2max was then estimated from extrapolating the line to estimated maximal heart rate (220-age) (30). The estimation of VO2max used the established relationship between watts and oxygen uptake and the linear relation between heart rate and oxygen uptake (30). Normal VO2max values range from 20.0 to 65.0 mL/kg per minute (31). Estimated VO2max has a strong correlation with directly measured VO2max (r’s range from 0.70 to 0.85) (29).

Ambulatory Monitoring
To document protocol adherence, ambulatory physical activity levels were assessed using an actigraph accelerometer (Actiwatch; Mini-Mitter Co.) throughout the duration of the study (14 days). Participants in the exercise-withdrawal group were given instructions not to engage in their usual aerobic exercise activities and were informed that the actigraph accelerometer enabled the investigators to verify protocol adherence. The actigraph is a wristwatch-sized (37 x 29 x 9 mm), lightweight (17 g) device that has been validated previously to assess whole-body movements during daily life activities (32,33). Actigraph signals are based on a piezoelectric sensor that generates a voltage when the device undergoes a change in acceleration (34). Care was taken for proper placement of the actigraph using a standardized mounting and positioning protocol on the participant’s nondominant wrist (32,34).

Activity counts were summed over 5-minute epochs and recorded continuously (24 hours per day). Peak activity levels were defined as the highest 5-minute period during the entire 2-week observation period. Average activity values were calculated as the average of all 5-minute epochs over the course of the study (34). Based on previous research, it was hypothesized that a between-groups difference on peak activity would occur over the exercise-withdrawal period (34).

Statistical Analyses
Data are presented as means ± standard deviations or percentages as appropriate. To compare the exercise-withdrawal group with the control group, 2 x 3 mixed-model analyses of variance (ANOVAs) were conducted, in which the experimentally induced exercise-withdrawn group was compared with the group continuing exercise (two-level between-subjects factor) and assessments over the three study visits were included as a three-level within-subjects factor. Significant main and interaction effects were further examined using independent and paired t-tests.

To evaluate the predictor of depressive symptoms at the end of 2 weeks of exercise withdrawal, hierarchical regression analysis examined cognitive–affective symptoms at week 2 as the dependent variable and included somatic symptoms at week 1 as the primary predictor variable; potentially confounding factors were adjusted for (group condition, baseline cognitive–affective symptoms, baseline somatic symptoms, and cognitive–affective symptoms at week 1).

To examine the relationship between changes in fitness and the development of depressive mood symptoms and fatigue, estimated VO2max values at week 2 were subtracted from estimated VO2max values at baseline, and the scores on questionnaires (POMS, BDI-II, and MFI) at week 2 were subtracted from the scores at baseline. These change scores were then correlated to determine if there was a statistically significant relationship between changes in fitness and changes in depressive mood. If a significant association was found, then additional multivariate regression analyses were performed, adjusting for baseline fitness level and group status.

Subgroup analyses were performed on the participants in the exercise-withdrawal condition. The group was split into participants with decreased fitness over the 2-week experimental manipulation and those participants without decreased fitness. The fitness level (VO2max) at week 2 was subtracted from the fitness level at baseline. If this subtraction resulted in a positive number (a decrease in VO2max), the participant was allocated to the "fitness decreased" group, and if change was zero or negative, then the participant was allocated to the "fitness increased/unchanged" group.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
DISCUSSION
 NOTES
 REFERENCES
 
Participant Characteristics and Manipulation Check
The exercise-withdrawal and control groups were comparable with respect to age, gender, initial activity level, fitness, depressive mood symptoms, and fatigue at baseline (Table 1). To establish whether the experimental group adhered to the exercise-withdrawal protocol, ambulatory actigraphy data were examined for peak and average activity levels (34). The exercise-withdrawal group engaged in significantly less peak activity levels (12,794 ± 7778 activity counts) than the experimental group (18,300 ± 6214 activity counts; p = .02), which confirmed adherence to the exercise-withdrawal procedure. Consistent with prior studies (34), no statistically significant differences were observed between the experimental and control groups on average daily activity levels, although a trend in the expected direction was observed (976 ± 249 versus 1138 ± 285 activity counts/day, respectively; p = .07). Thus, the experimental group engaged in less high-intensity activity levels than the control group.


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  		TABLE 1. Participant Characteristics

 

Exercise Withdrawal and Depressive Mood Changes
Exercise withdrawal resulted in significantly higher negative mood compared with the control condition (Fig. 1). A significant interaction between group status and time on POMSTMD (Finteraction[2,68] = 6.07; p = .004) was observed. Analyses of simple effects revealed that the withdrawal group displayed higher negative mood scores (POMSTMD) than the control group at week 2 (p = .03). A significant increase in negative mood (POMSTMD) in the experimental group (F[1,18] = 4.57; p = .04) was observed, whereas the control group showed a trend for a decrease in negative mood (F[1,18] = 3.64; p = .07). The POMS subscales accounting for the effects of 2-week exercise withdrawal were: fatigue (7.50 ± 6.36 versus 2.5 ± 3.6; p = .01), tension (7.63 ± 5.46 versus 4.50 ± 4.51; p = .04), and vigor (13.28 ± 8.44 versus 19.11 ± 5.44; p = .04; exercise withdrawal versus control, respectively).


Figure 18
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  		Figure 1. Increased Profile of Mood States total mood disturbance during exercise withdrawal versus. control participants. Error bars represent standard errors of the mean (SEM). *p < .05 exercise-withdrawn versus controls.

 

Depressive mood as documented by the BDI-II revealed consistent results. A significant group by time interaction for BDI-II scores (Finteraction[2,68] = 7.48; p = .001) was observed. Analyses of simple effects revealed that the withdrawal group displayed higher BDI-II scores as compared with controls at week 2 (4.72 ± 3.30 versus 1.44 ± 2.59; p = .01). A significant increase in depressive mood (BDI-II) in the experimental group (F[1,17] = 5.22; p = .04) was observed, whereas the control group showed a decrease in depressive mood (F[1,17] = 5.01; p = .04).

Trajectory of Fatigue and Depressive Mood Changes During Exercise Withdrawal
Examination of specific increases in depressive mood symptoms during exercise withdrawal indicated that somatic depressive symptoms developed before cognitive–affective depressive symptoms (Fig. 2). Significant group differences in somatic symptoms occurred at week 1 (p = .05) and week 2 (p = .01), whereas cognitive–affective depressive symptoms were significant between the groups only at week 2 (p = .02) and not at week 1 (p = .44). These findings suggest that somatic symptoms occur earlier after exercise withdrawal (after 1 week) than cognitive–affective symptoms (after 2 weeks; Fig. 2).


Figure 28
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  		Figure 2. Differential response of somatic (A) and cognitive–affective (B) depressive symptoms in response to exercise withdrawal. Error bars represent standard error of mean. *p < .05 exercise-withdrawn versus controls.

 

These data were consistent with results obtained from the fatigue inventory (MFI). A significant interaction between group status and time was observed for the MFI (Finteraction[2,72] = 8.25; p = .001). For the MFI, groups were not significantly different at baseline (p = .95) but were significantly different at week 1 (45.37 ± 11.70 versus 38.26 ± 10.50; p = .05; exercise withdrawal versus control) and continued to be significant at week 2 (48.40 ± 14.53 versus 37.90 ± 10.10; p = .01).

To further evaluate the progression of depressive symptoms, hierarchical regression analysis was performed examining the BDI-II-based somatic and cognitive–affective subscales (Fig. 2). Somatic symptoms at week 1 were predictive of cognitive–affective symptoms at week 2 (R2 change = 0.09; ß = 0.62; p = .046) while adjusting for potentially confounding variables (group condition, baseline somatic symptoms, baseline cognitive–affective symptoms, and cognitive– affective symptoms at week 1). Therefore, in the progression of mood-related symptoms, somatic symptoms develop first and subsequently predict cognitive–affective symptoms.

Fitness and the Development of Depressive Mood
As shown in Table 2, the exercise-withdrawal group displayed no significant change in estimated VO2max or fitness levels over the 2 weeks (p = .59), whereas the control group displayed a modest increase in VO2max (p = .05; pinteraction = .11). All of the further analyses involving fitness were conducted for exploratory purposes, because the change in fitness measured is within the expected error range of repeated bicycle ergometry exercise tests (8% to 12% error in estimated VO2max) (35).


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  		TABLE 2. Fitness Results Before and After 2 Weeks of Exercise Withdrawal (Standard Deviation)

 

The magnitude of reduction in fitness level, in the experimental group, was associated with increases in negative mood as assessed by the POMSTMD score (r = –0.36, p = .03). Changes in fatigue and vigor scores from the POMS subscales accounted for these associations with changes in VO2max (r = –0.37; p = .02 and r = 0.39; p = .02, respectively). Changes in fatigue as measured by the MFI were also related to changes in fitness (r = –0.32; p = .05). The BDI-II as well as its somatic and cognitive–affective components were not significantly correlated with changes in VO2max (r’s = –0.11, –0.10, and –0.03, respectively; p’s > .2).

Baseline VO2max levels were negatively related to the reduction in fitness over 2 weeks (r = –0.58, p = .01) in the experimental group such that those with highest baseline fitness values had the greatest reductions in fitness. In contrast, no relationship was found between baseline fitness levels and changes in fitness among controls (r = –0.08, p = .74). Accordingly, statistical analyses were adjusted for baseline fitness levels. Baseline VO2max levels were not related to changes in depressive symptoms (POMSTMD, BDI-II, and MFI) in either the experimental or control groups (r’s < 0.30; p’s > .20).

A subgroup of exercise-withdrawn participants (n = 10) displaying a reduction of fitness level (from 46.7 ± 9.2 to 43.1 ± 8.2 mL/kg per minute; p = .02) during exercise withdrawal developed more depressive mood than participants who did not decrease in fitness (Fig. 3). Specifically, participants who displayed decreased fitness had higher POMSTMD scores than those whose fitness did not decrease ({Delta} = 24.98 ± 30.83 versus {Delta} = 2.68 ± 20.39; p = .04). Increases in fatigue ({Delta} = 4.89 ± 5.80 versus {Delta} = 0.22 ± 5.85; p = .04) and decreases in vigor ({Delta} = –8.78 ± 3.19 versus {Delta} = –3.10 ± 7.22; p < .01) were observed among participants displaying reduced fitness. A similar pattern was found for depressive symptoms assessed by the BDI-II ({Delta} = 2.20 ± 2.44 versus {Delta} = 1.13 ± 4.02; p = .02). Although the MFI revealed the same pattern of results as the POMSTMD and BDI-II, the comparison did not reach statistical significance ({Delta} = 12.90 ± 9.85 versus {Delta} = 5.00 ± 15.15; p = .19).


Figure 38
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  		Figure 3. Increased Profile of Mood States total mood disturbance during exercise withdrawal in participants with decreased fitness level (VO2max) (n = 10) compared with participants with increased or unchanged fitness level (n = 10). Error bars represent standard errors of the mean (SEM). *p < .05 decreased fitness versus increased/unchanged fitness.

 

Multiple regression analyses were conducted to examine which depressive and fatigue symptoms were related to changes in fitness level when adjusting for potentially confounding factors (group condition and initial fitness level). The POMS fatigue subscale was the only measure that remained significantly associated with decreased fitness after adjusting for baseline fitness and experimental versus control group status (R2 change = 0.19; ß = 0.48; p = .003).


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
NOTES
 REFERENCES
 
This investigation documents that aerobic exercise withdrawal results in depressive mood symptoms, fatigue, and a loss of vigor. The present investigation also demonstrates that somatic depressive symptoms (e.g., fatigue) precede the onset of subsequent cognitive–affective symptoms (e.g., sadness). The fatigue symptoms after exercise withdrawal may in part reflect reductions in physical fitness among individuals with reduced activity levels.

Prior research indicates that depressive symptoms develop in reaction to the cessation of exercise (5–9). The observation that somatic depressive symptoms precede cognitive–affective symptoms is consistent with a report by Morris et al. (8). In addition, the current findings add to this literature that somatic symptoms predict the magnitude of subsequent cognitive–affective symptoms independent of initial depressive symptoms and other potential confounding factors. This trajectory of depressive symptom development may be explained by the potentially lower thresholds for reporting somatic symptoms compared with cognitive–affective symptoms. An alternative explanation is that somatic symptoms may reflect early onset biological consequences of exercise withdrawal, thereby promoting the likelihood of developing a broader range of depressive symptoms. The early onset of somatic symptoms may have important clinical implications, because individuals who are vulnerable to develop depression in response to reduced exercise may be identified by evaluating initial display of somatic symptoms.

This study indicates that individual differences exist in the likelihood of developing reduced fitness and depressive symptoms under conditions of exercise withdrawal. The overall reduction in fitness levels among the exercise-withdrawn participants (i.e., VO2max or total exercise time) were not statistically significant, which is consistent with other observations (e.g., a 6-week exercise-withdrawal period failed to elicit significant mean changes in VO2max [36]). The magnitude of fitness reduction in VO2max was not related to protocol adherence as documented by ambulatory activity monitoring (r = 0.23; p = .25). We found that higher initial fitness levels were correlated with a greater reduction in fitness during exercise withdrawal (r = –0.58; p = .01). Importantly, participants with reductions in VO2max displayed significantly more depressive symptoms compared with those who did not develop decreased fitness (Fig. 3), suggesting that even small reductions in fitness may be involved in the development of depressive symptoms after exercise withdrawal. However, most participants had changes in fitness that fell within the estimated error range of the VO2max values, and after controlling for potential confounding variables, changes in fitness were only related to the symptom of fatigue.

Study Limitations
Exercise withdrawal was limited to discontinuation of high-level aerobic activities only rather than all physical activity. This moderate reduction in overall activity levels may have attenuated the results related to depressive mood induction and the magnitude of decreases in fitness. Previous research showing a reduction in VO2max used more extreme-withdrawal paradigms such as bedrest (18,19). The measures used to quantify fitness levels in the present study may not have been sensitive enough to optimally detect subtle changes in fitness that occur with removal of peak activity levels only. Other measures such as direct assessments of expired oxygen may be preferable to document such subtle fitness changes. Despite these limitations in the assessment of fitness levels, significant relationships between changes in fitness and mood and fatigue were observed in the present study.

A second potential limitation is that 2 weeks of exercise withdrawal may not be associated with the same biological and behavioral concomitants as in long-term reduced exercise levels among sedentary individuals. Sedentary individuals also tend to be more obese than physically active individuals (37). Our sample was in the normal range of BMI, and BMI did not change significantly during exercise withdrawal. Thus, although experimental control of exercise levels and ambulatory assessments of protocol compliance are strengths of the present investigation, the results may not be generalizable to other populations such as sedentary individuals or individuals exposed to complete withdrawal of physical activity (e.g., confinement to bedrest).

The participants were informed that the study examined changes in mood in response to exercise withdrawal as part of the consent process. The explanation of the study aims may have predisposed participants to report depressive symptoms in the experimental group and to not report depressive symptoms in the control group, particularly because participants were not blind to the experimental manipulation. In addition, the discontinuation of exercise involves withdrawal of a possibly pleasurable activity. The results of the study could therefore reflect consequences of being deprived of a pleasurable activity rather than specifically relate to exercise withdrawal per se. However, the subgroup of participants who developed decreased fitness (which is not based on self-report) experienced significantly greater increases in negative mood, thus suggesting validity of the exercise-withdrawal paradigm.

Clinical Implications
Exercise withdrawal results in increased depressive symptomatology in healthy, nondepressed individuals. The paradigm used in the present study may be relevant to the understanding of mood changes observed in response to involuntary withdrawal of exercise such as with injuries and other circumstances of prolonged immobility (i.e., space travel and deployment in submarines). The observed increases in depressive symptomatology remained in the subsyndromal range of depression scores and none of the participants developed major depressive disorder in response to 2 weeks of exercise withdrawal. Therefore, the current findings may not generalize to the development of full depressive episodes in response to extreme forms of exercise withdrawal. Additional longitudinal studies that use sustained and more intense exercise-withdrawal paradigms are needed to further examine the relationship between reduced exercise and depression.

This study may be the first step to identify potential risk-stratification measures for populations exposed to exercise withdrawal. In the current investigation, both decreases in fitness level and the emergence of initial somatic symptomatology are candidates for risk stratification, but more research is needed before this information can be applied in clinical settings. Recent evidence suggests that vulnerability factors for negative mood after exercise withdrawal also include autonomic nervous system measures (lower vagal tone), low-grade inflammatory measures, and lower cortisol levels (38). These factors may therefore be important to determine in cases in which reduction of habitual exercise levels can be anticipated and planned (e.g., postsurgical bedrest, space travel). Monitoring of somatic symptoms may also be used to initiate preventive pharmacological or behavioral interventions in individuals exposed to confinement and other circumstances of reduced exercise levels. Future research is required to document whether such interventions can reduce the risk of depressive symptoms in response to exercise withdrawal.

We thank Micah Stretch and Rachel Hoult for their help in conducting the experiments and data collection.


   NOTES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
REFERENCES
 
The opinions and assertions expressed here are those of the authors and are not to be construed as reflecting the views of the USUHS or the U.S. Department of Defense.

This work was supported in part by a grant from the Charles E. Dana Foundation and from the NIH (HL58638 and T32 HL69751).

DOI:10.1097/01.psy.0000204628.73273.23


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 

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