Are the relationships between early activation of lymphocytes and cortisol or testosterone influenced by intensified cycling training in men?

The effects of exercise training on lymphocyte responses, as well as changes in circulating endocrine parameters at rest, were investigated. Seven male cyclists participated in a 4 week high-intensity (HI) cycling training intervention. Training improved performance significantly (peak power output (PPO): 1.4%, p < 0.05; 5 km time trial: 3.8%, p < 0.01; 40 km time trial: 0.4%, p < 0.05). Resting hormone concentrations (testosterone, sex hormone binding globulin (SHBG), cortisol, corticosteroid-binding globulin (CBG), and dehydroepiandrosterone-sulphate (DHEA-S)) were unchanged, with the exception of a 20% decrease in testosterone post-HI training (p < 0.067). Subjects' CD3(+) cell counts decreased by 15% (p < 0.05), owing to significantly decreased CD4(+) cell counts and slightly lower CD8(+) and natural killer (NK) cell counts. Spontaneous in vitro CD69 expression increased in CD4(+) cells (mean +/- SD, pre: 12 +/- 6 cells.mu L-1; post: 35 +/- 37 cells.mu L-1; p < 0.05), but not in CD8(+) cells (pre: 20 +/- 29 cells.mu L-1; post: 33 +/- 16 cells.mu L-1). Mitogen-induced CD69 expression decreased in both CD4(+)cells-gL-1). Mitogen-induced CD69 expression decreased in both CD4+ (pre: 1570 1258 cells-pL-1; post: 596 +/- 597 (pre: 1570 +/- 1258 cells-pL-1; post: 596 +/- 597 cells.mu L-1; p < 0.05) and CD8(+) lymphocytes (pre: 676 +/- 434 cells.mu L-1; post: 412 +/- 235 cells.mu L-1; p < 0.05). Testosterone correlated positively with several immune parameters at baseline, whereas cortisol correlated negatively with parameters of the innate immune system post-HI training. We conclude that the stress of unaccustomed exercise is evident in resting lymphocytes, but not in resting endocrine parameters. However, correlations between testosterone and cortisol and immune parameters suggest that these 2 hormones play a role in modulating immune status. Our results indicate the importance of assessing both spontaneous and mitogen-induced aspects of immune-cell activation.