LONG-TERM INTENSIVE TRAINING REDUCES IMMUNE RESPONSE CAPABILITIES EARLY IN THE TRAINING SEASON
Teixeira, A. M., Rama, L., Morgado, J. M., Azevedo, S., Matos, A., Henriques, A., Rosada, F., & Alves, F. (2009). Cytokine production by monocytes, but not neutrophils, is hampered by long-term intensive training in elite swimmers. A paper presented at the 14th Annual Congress of the European College of Sport Science, Oslo, Norway, June 24-27.
This study investigated the influence of long-term intensive training over the functional features of innate immune cells from high-competitive level swimmers (N = 18), particularly concerning the production of inflammatory mediators. A single group repeated measures design was used in the study. Blood samples were collected after 36 hours of rest from training/exercise at four times during a training season: 1) after an off-training period of 5-6 weeks at the beginning of the winter season; 2) after seven weeks of training; 3) at the 25th week, and 4) at the 29th week of training. Measures were taken of IL-1beta, IL-6, IL-12, TNF-alpha, and MIP-1beta produced by neutrophils and monocytes with or without stimulation. Blood samples were incubated in the presence or the absence of LPS and IFN-y and the frequency of cytokine producing cells and the amount of each cytokine produced by cell were evaluated by flow cytometry. Monocytes were identified by the expression of CD33, CD14, HLA-DR, and by their FSC and SSC characteristics. Neutrophils were identified by their particular FSC and SSC characteristics and the absence of HLA-DR.
The frequency and absolute numbers of neutrophils and monocytes did not change significantly during the season with the exception of a decrease in the absolute numbers of monocytes in the first seven weeks of training. Without stimulation, no significant frequencies of cytokine producing cells were observed during the season with the exception of MIP-1beta. Six hours of stimulation with LPS and IFN-y did not induce cytokine expression by neutrophils. The number of cytokine producing monocytes significantly decreased during the season. Additionally the amount of IL-1beta, TNF-alpha, and MIP-1beta produced by these cells in response to stimulation also decreased during the training season. The differences were most noticeable between the pre-training and seventh-week blood collections, corresponding to the initial increment of training volume. There was a non-significant decrease in IL-6 and IL-12 in the first seven weeks of training.
Implication. Long-term intensive training may affect the ability of monocytes to produce important cytokines involved in immune function responses reducing the cells' capacity to respond to acute health challenges. These effects occur early in the training season and then appear to remain stable but lowered.
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