Table 1.
Exercise-induced changes in white blood cell and CD4+ lymphocytes.
Figure 1.
Th17 levels increase in response to strenuous endurance exercise.
(A) Mean values of unstimulated Th17 cells, in response to endurance exercise. (B) Representative Th17 cell levels, as detected by flow cytometry: Upper panel: unstimulated Th17 cells (pre-stimulation with PMA was not used prior to detection of IL-17). Lower panel: levels of PMA-stimulated Th17 cells Pre = pre-exercise, Post = post-exercise, Recovery = 10 days post-exercise. * = statistically significant differences (p<0.05).
Figure 2.
Sustained decrease in Tregs and FOXP3 levels in response to endurance exercise.
Percent change in of CD4+CD25+FoxP3+ (Tregs), from the total CD4+ lymphocytes (A) and mean fluorescence intensity (MFI) of FOXP3 within the Tregs (B) in response to endurance exercise, as analyzed by flow cytometry. (C) Representative Tregs levels, as detected by flow cytometry. Pre = pre- exercise, Post = post- exercise, Recovery = 10 days post-exercise. ** = statistically significant differences (p<0.01).
Figure 3.
Endurance exercise induced changes in cytokine levels.
Shown are changes in serum levels of cortisol, IL-6, IL-10 and TGFβ (ELISA) in response to endurance exercise. Pre = pre- exercise, Post = post- exercise, Recovery = 10 days post-exercise. * = statistically significant differences (p<0.05).
Figure 4.
Post-race serum can induce a decrease in Tregs levels in vitro.
Shown are changes in controls' PBMNC that were incubated for 4 hours with athletes' pre-race (pre) and post-race (post) serum. Athletes post-race serum induced a significant decrease in controls Tregs levels (mean percent of Tregs 3±1.93% and 1.9±1.6% in pre- and post-race serum, respectively; p = 0.009 Student t test).
Figure 5.
A model of homeostatic balance between Tregs and Th17 under endurance exercise.
Endurance exercise induced a significant increase in Th17 cells and a sustained decline in peripheral blood Tregs population. These alterations in CD4+ T cell sub-populations may be attributed to changes in TGFβ, IL-6 and IL-2 serum levels.