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Abstract

Acute exercise mobilizes lymphocytes and monocytes into circulation and alters cortisol, but it is not known whether psychological states before exercise shape immune responses in adults, or whether cortisol mediates any associations between mood and immune mobilization. PURPOSE: To test whether baseline affect and total mood disturbance (TMD) predict lymphocyte/monocyte mobilization and 1-h recovery after aerobic training (AT) and resistance training (RT), whether they predict cortisol responses, and whether cortisol mediates mood–immune links. METHODS: This is a secondary analysis of data from a randomized, complete crossover study in which adults completed both an AT and a RT session. Composite affect (Positive Affect - Negative Affect; PANAS) and TMD (POMS) were assessed. Flow cytometry was used to obtain circulating lymphocyte and monocyte counts and subset typing before, immediately after, and 1 hour post, and Serum cortisol was at the same time points using a commercially available ELISA kit. Linear regression models tested whether composite affect and TMD predicted immune mobilization (post-exercise – pre-exercise) and recovery (1hPost-exercise – post-exercise) within AT and RT, whether these psychological variables predicted serum cortisol during mobilization and recovery, and whether cortisol predicted immune outcomes. Casual mediation models examined whether serum cortisol concentration mediated associations between mood and immune responses. RESULTS: Higher composite affect was associated with lower lymphocyte mobilization (β ≈ −18.1, p = 0.006, 95% CI −30.7 to −5.5) and greater lymphocyte recovery (β ≈ 18.8, p = 0.048, 95% CI 0.2 to 37.5), but not monocyte responses. TMD was not related to lymphocyte or monocyte mobilization or recovery. Neither composite affect nor TMD predicted serum cortisol during mobilization or recovery. In contrast, greater cortisol mobilization was positively associated with lymphocyte mobilization (β ≈ 2.96, p = 0.043, 95% CI 0.10 to 5.82), whereas associations with lymphocyte recovery and monocyte outcomes were not significant. Cortisol did not mediate the effect of composite affect on lymphocyte mobilization; the direct effect remained significant (ADE ≈ −27.3, β ≈ .03). CONCLUSION: In this sample of adults, more positive composite affect was linked to a blunted increase in lymphocytes but faster recovery, whereas TMD had no significant associations with immune or cortisol responses. Serum cortisol was positively related to lymphocyte mobilization and did not mediate relationships between affect and immune responses. These findings support that composite affect may shape the magnitude and recovery of lymphocyte responses to acute exercise through mechanisms other than cortisol.

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