Relations between anhedonia and physical activity.

There is an extensive body of literature documenting an inverse association between level of depressive symptoms and physical activity (PA). Although some investigations have not found evidence of this association,1 results from observational studies are typically consistent with a multidirectional relationship between depressive symptoms and PA.2,3 That is, higher level of depressive symptoms prospectively predicts lower PA over time,2,3 lower PA increases risk of future depressive symptoms,2–7 and depression and low PA are concurrently associated with one another.5,8 This association exists over and above other potentially confounding factors2,3 and appears to extend across (1) subclinical depressive symptoms and major depression;3 (2) various levels of PA frequency, intensity, and duration;9 and (3) a variety of different age-groups.2,3,10 Despite consistent evidence that the association between depressive symptoms and lower PA exists, the mechanisms underlying this relation are not entirely clear. This is an important gap in the literature because clarification of the nature and mechanisms of the depression-PA association could advance theoretical models of health behavior and shed light on intervention targets for people with emotional disturbance who are not physically active.7 The heterogeneity of depressive symptoms may be an important barrier that has often been overlooked in prior PA research. Most extant studies regard depression as a unitary homogenous phenotype that can be identified by computing the combined overall severity across all depressive symptoms. However, depression may be more accurately characterized as a complex set of numerous intermediate phenotypes that only loosely cluster together with one another.11 It has therefore been proposed that by partitioning depression into more narrow classifications based on key individual features (eg, depressed mood, anhedonia, appetite changes, psychomotor disturbance, stress sensitivity), phenotypic markers representing more direct expressions of underlying mechanisms might be isolated.11 Indeed, different symptoms in depression may have unique psychosocial and biological determinants.12,13 Therefore, investigating the role of intermediate depressive phenotypes in PA may yield more meaningful insights into the relation between depressive symptoms and low PA. Anhedonia—the inability to experience pleasure in response to rewarding stimuli—is a unique depressive phenotype11 that may be useful for PA research. Though levels of anhedonia can fluctuate over time in some circumstances (eg, onset to offset of depressive episodes), anhedonia is typically stable.18 Anhedonia lies on a continuum; varies widely in the population; is psychometrically distinct from other constructs such as affective flattening, sadness, and amotivation; and is unique from but correlated with level of overall depressive symptomatology.18–20 Anhedonia’s neuropathology putatively involves attenuated mesolimbic and nigrostriatal activity and reduced sensitivity to the effects of nondrug rewards on phasic mesolimbic dopamine release.21,22 Of note, anhedonia associates with increased risk of cardiac events,14,15 cigarette smoking,16 and illicit drug use.17 Given its role in heart disease and health behaviors, anhedonia may also relate with PA. Anhedonia may be inversely associated PA for several reasons. PA has been shown to acutely enhance dopaminergic activity within the striatum.23,24 Given that treatments which enhance dopamine raise responsiveness to rewards,25,26 it is possible that PA may acutely counteract anhedonia. It is also possible that anhedonia may diminish motivation to engage in PA. Because people with high anhedonia experience deficient levels of pleasure from most nonpharmacological rewards,27 they may find PA to be less pleasurable, which could in turn reduce desire to engage in PA.28 Thus, the inverse relation between anhedonia and PA may be mediated by lower levels of PA’s subjective rewarding effects. However, to our knowledge, there are no extant studies on the relation between anhedonia and PA in humans. This article reports results from a preliminary investigation of the association between anhedonia and PA using a cross-sectional correlational design in a sample of college students. Using this sample allows us to understand the link between anhedonia and PA during a high-risk period for affective turmoil, as age of first depressive episode for many individuals occurs during young adulthood.29 Furthermore, young adulthood is typically a period in which PA declines.30 In addition, we examine several PA outcomes (eg, frequency, duration, intensity) separate from one another in this initial study, given that the relation between mood disturbance and PA may vary across different doses of PA.9 The primary aims were: (1) to examine the relation between anhedonia and frequency, duration, and intensity of PA; and (2) to investigate whether the subjective rewarding effects of PA mediate the relationship between anhedonia and low PA.