Abstract
BACKGROUND Breast cancer survivors (BCS) demonstrate attenuated immune cell mobilization following acute exercise, with partial restoration following exercise training. Epinephrine (EPI) and norepinephrine (NE) are responsive to exercise-stress and directly regulate immune cell function, indicating a potential role in this restorative process. Similar attenuations in catecholaminergic signaling have been reported in BCS post-exercise; however, it is unknown whether this is maintained within a trained state. We hypothesized that compared to non-cancer controls (CON), acute exercise would induce an attenuated catecholaminergic response in untrained BCS, which would be recovered to levels similar to CON after training. AIM To compare acute exercise-induced catecholaminergic responses between BCS and CON before (PRE) and after (POST) completing a community-based exercise intervention. METHODS Thirteen BCS (age: 56 +/- 2 years, body fat: 39.7% +/- 1.3%) and 13 CON (age: 56 +/- 2 years, body fat: 41.2% +/- 1.7%) performed 45 minutes of intermittent cycling at 60% peak power output PRE and POST 16 weeks of community-based exercise training. Blood samples were collected at baseline (BASE), immediately (0 hour), and 1-hour (1 hour) post-exercise for assessment of the acute EPI and NE response. Separate linear mixed models were used for PRE and POST EPI and NE assessment. RESULTS At PRE, both BCS and CON demonstrated increases in EPI (+87.4 pg center dot mL(-1), P < 0.001) and NE (+1295 pg center dot mL(-1), P < 0.001) at 0 hour, with no group differences. At POST, group differences in NE initiation (0 hour-BASE) were not statistically significant (-544.9 pg center dot mL(-1), P = 0.115, g = 0.92), despite divergent responses between BCS (+28%, P = 0.175, g = 0.36) and CON (-13%, P = 0.377, g = 0.23). No group differences were observed for NE recovery (1 hour-0 hour) nor for EPI initiation or recovery. CONCLUSION BCS and CON present with similar exercise-induced catecholaminergic responses regardless of training, suggesting an alternative mechanism may have made a greater contribution to the training-induced immune cell revival previously observed.