Also, in our study, we utilized resistance-trained athletes who performed exercises designed to be similar to that used in more typical athletic regimens and recruit and activate a large amount of muscle tissue. after RE (randomized, double blind design). Saliva and venous blood were collected pre-, post- and 90 min post-exercise. Results No change occurred in s-IgA from rest relative to osmolality or as a secretion rate (p 0.05). IL-2 levels were unchanged by exercise in both trials (time effect p = 0.342). IL-5 was significantly (time effect p = 0.04) decreased between rest (1.55 0.07 pg?ml-1) and 90 min post-exercise (0.96 0 .11 pg?ml-1), with no difference between treatments (group x time effect p = 0.610). There was no time-by-treatment conversation (p 0.05) observed between CHO and P treatments for s-IgA or IL-5. Conclusion IL-5 decreases after RE, but s-IgA and IL-2 levels remain stable. CHO ingestion prior to-, during or following RE did not appear to alter salivary immune responses. = 10)= 0.821; Table? 2). No changes in IgA levels from resting values were found when considered relative to osmolality (time effect p = 0.747) or as a secretion rate (time effect p = 0.792). Table 2 Salivary immunoglobulin A responses to resistance exercise with carbohydrate ingestion or placebo (n=10) thead valign=”top” th align=”left” rowspan=”1″ colspan=”1″ Variable /th th align=”center” rowspan=”1″ colspan=”1″ Condition /th th align=”center” rowspan=”1″ colspan=”1″ Pre /th th align=”center” rowspan=”1″ colspan=”1″ Post /th th align=”center” rowspan=”1″ colspan=”1″ 60min Recovery /th /thead S-IgA secretion PLC hr / PLC hr / 208.3 123.5 hr / 223.7 299.6 hr / 211.2 148.0 hr / rate (gmin-1) hr / CHO hr / 193.7 92.9 hr / 189.3 230.4 hr / 270.0 386.1 hr / S-IgA:osmolality hr / PLC hr / 8.60 5.33 hr AZ191 / 13.33 7.42 hr / 10.79 7.84 hr / (gkg-1)CHO11.00 8.689.23 7.6010.44 8.00 Open in a separate window Interleukin 2 and interleukin 5 responses Resting IL-2 was significantly higher in CHO than in P (p = 0.028; Table? 3). Therefore, resting IL-2 measures were entered as a covariate in a 2×2 (treatments x time) repeated measures ANCOVA. Using this comparison, IL-2 was unchanged after RE (time effect p = 0.359). There were no differences between CHO or P in IL-5 (treatment x time conversation p = 0.610). IL-5 was significantly decreased after RE (time effect p = 0.040). Specifically, IL-5 was significantly (?37%) lower than resting levels at 90 min post (p = 0.008). Table 3 Interleukin-2 and interleukin-5 response to resistance exercise with carbohydrate ingestion or placebo (n=7) thead valign=”top” th align=”left” rowspan=”1″ colspan=”1″ Variable /th th align=”center” rowspan=”1″ colspan=”1″ Condition /th th align=”center” rowspan=”1″ colspan=”1″ Pre /th th align=”center” rowspan=”1″ colspan=”1″ Post /th th align=”center” rowspan=”1″ colspan=”1″ 60min Recovery /th /thead Interleukin 2 hr / PLC hr / 4.62 6.42* hr / 6.14 12.32 hr / 20.88 29.63 hr / AZ191 (pgml-1) hr / CHO hr / 64.04 54.52* hr / 36.89 18.82 hr / 11.63 9.90 hr / Interleukin 5 hr / PLC hr / 1.73 0.61 hr / 1.07 0.38 hr / 0.60 0.70 hr / (pgml-1)CHO1.67 0.321.43 0.301.09 0.47 Open in a separate window *indicates p 0.01 difference between conditions. Discussion Despite the tremendous growth of investigations regarding the impact of endurance exercise on immune parameters, still less is known about the effects of resistance exercise. Several investigations suggest that reduced levels of S-IgA are associated with an increased risk of URTI during periods of heavy training, and it has been suggested that CHO supplementation may influence immune indices in response to heavy exertion. The purpose of this investigation was to determine whether carbohydrate ingestion prior to-, during and following RE would alter the immune response to RE. Ours was the first study to examine AZ191 s-IgA and cytokine responses using paired-exercises, which lasted over 30 min, shown to elicit a greater stress and immune response . We hypothesized that CHO ingestion would result in a lesser Mouse monoclonal antibody to p53. This gene encodes tumor protein p53, which responds to diverse cellular stresses to regulatetarget genes that induce cell cycle arrest, apoptosis, senescence, DNA repair, or changes inmetabolism. p53 protein is expressed at low level in normal cells and at a high level in a varietyof transformed cell lines, where its believed to contribute to transformation and malignancy. p53is a DNA-binding protein containing transcription activation, DNA-binding, and oligomerizationdomains. It is postulated to bind to a p53-binding site and activate expression of downstreamgenes that inhibit growth and/or invasion, and thus function as a tumor suppressor. Mutants ofp53 that frequently occur in a number of different human cancers fail to bind the consensus DNAbinding site, and hence cause the loss of tumor suppressor activity. Alterations of this geneoccur not only as somatic mutations in human malignancies, but also as germline mutations insome cancer-prone families with Li-Fraumeni syndrome. Multiple p53 variants due to alternativepromoters and multiple alternative splicing have been found. These variants encode distinctisoforms, which can regulate p53 transcriptional activity. [provided by RefSeq, Jul 2008] perturbation in s-IgA and circulating cytokines from resting values as compared to placebo. The major findings of this study were: 1) resistance exercise did not result in measureable changes in s-IgA or IL-2 responses; 2) a significant reduction in IL-5 responses were observed; 3) contrary to our hypothesis, CHO supplementation prior to-, during, and following RE had no effect on immune responses. These findings help to clarify what has been previously unknown in this area. The central premise behind our hypothesis was that carbohydrate ingestion would blunt the rise of epinephrine and norepinephrine during RE, and thus alter s-IgA and circulating cytokines measured as compared to control. Some previous studies  of carbohydrate ingestion during exercise have found significant reductions in epinephrine and norepinephrine while others have found no effect . Thus the impact of carbohydrate ingestion around the catecholamine response to exercise appears to be variable. This variability may be explained in part by training status, with less-conditioned subjects more likely to experience a difference in the catecholamine response to exercise after carbohydrate ingestion . Subjects in the present study were highly trained, RE athletes and as such.
Also, in our study, we utilized resistance-trained athletes who performed exercises designed to be similar to that used in more typical athletic regimens and recruit and activate a large amount of muscle tissue
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