Volume 29, Issue 10 (12-2022)                   RJMS 2022, 29(10): 211-221 | Back to browse issues page

Research code: IR.IAU.K.REC.1400.21
Ethics code: IR.IAU.K.REC.1400.21
Clinical trials code: IR.IAU.K.REC.1400.21

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Sabaei Y, Sarshin A, Rahimi A, Feizolahi F. The Effect of Caffeine Supplementation and Exhausting Exercise on Inflammatory Factors in Hot Environments. RJMS 2022; 29 (10) :211-221
URL: http://rjms.iums.ac.ir/article-1-7368-en.html
Clinical Care and Health promotion Research Center, Karaj branch, Islamic Azad University, Karaj, Iran , Amsarshin@gmail.com
Abstract:   (907 Views)
Background & Aims: The immune system is affected by a variety of physiological and psychological pressures (1). Exercise has been shown to impair immune system function, which appears to depend on the intensity and duration of exercise and the secretion of stress hormones (2). Exercise in a high temperature environment has a synergistic effect on stress responses to exercise (3, 4). Acute stress (e.g., cortisol) and inflammatory responses (e.g., cytokines) after exercise at warm temperatures are greater than those seen at lower temperature conditions (5). Heat stress caused by high ambient temperatures can affect physical function; Tolerance to exercise in hot environments is lower than cold environments (6). There have been numerous reports of increased plasma cortisol responses (9, 10) and production of cytokines (4, 11) seeking to limit fluid intake during acute exercise. Recently, Costello et al. (2018) showed that acute exercise in a warm environment increases the levels of interleukin-6 (IL6) and plasma cortisol only in conditions of fluid restriction (12). Ignoring the increase in physical and psychological stress experienced while exercising in conditions of ambient heat and dehydration combined with improper recycling can increase the risk of various diseases (4, 13) and impair athletic performance (14). Caffeine is one of the most common dietary supplements in the world, which has been used as a factor to increase physical-mental functions and delay fatigue in athletes (15). Also, caffeine, with its energizing and anti-inflammatory properties, in addition to increasing athletic performance, can reduce the inflammatory responses caused by strenuous exercise (16, 17). In this regard, Fedor (2010) examined the acute use of two doses of 4 and 7 mg / kg body weight of caffeine and showed that only higher doses of caffeine can prevent proinflammatory cytokines caused by moderate-intensity endurance training (18). Jafari et al. (2014) showed that acute consumption of 6 and 9 mg / kg body weight of caffeine inhibits the increased response of serum tumor necrosis factor (TNFα) following a period of debilitating resistance activity (19). However, the lack of effect of acute caffeine consumption on the response to inflammatory markers following exercise has also been reported in some studies (20, 21).
consumption to possibly modulate the response to inflammatory parameters caused by exercise in conditions of ambient heat and dehydration has not been studied. Research findings also indicate a discrepancy between the results regarding acute caffeine consumption and the response to inflammatory markers following exercise; Considering the important role of caffeine supplementation along with exercise on physical function as well as reducing inflammation, it seems that the study of the effects of exercise and caffeine supplementation on inflammatory markers is of great importance, but according to studies, the findings are very limited in this regard. Therefore, the aim of this study was to investigate the effect of caffeine supplementation and exhausting exercise on inflammatory factors in hot environments.
Methods: In this experimental study, 30 male athletes with an average age of 26.6 ± 3.9 years in dehydrated conditions were selected in an accessible and targeted manner and divided into three groups of caffeine consumption (number = 10 people), placebo group (number = 10 people) and the control group (number = 10 people) were divided. Caffeine group consumed 6 mg / kg body weight of caffeine. 60 minutes later, the subjects performed a series of increasingly exhausting aerobic exercise. Data were analyzed using analysis of variance with repeated measures, One-way ANOVA and Tukey post hoc test at the P<0.05.
Results: The results showed that immediately after exercise, the levels of IL1B, TNFα and IL6 were significantly higher than the control group (p≥0.001). The caffeine group experienced a greater increase in IL6 (p≥0.001) and IL1B (p≥0.05) and a smaller increase in TNFα compared to the sham group (p≥0.001). Also, hs-CRP levels were significantly higher than baseline in the exercise group (p≥0.001).
Conclusion: The results of this study indicate that maximal aerobic function increased following caffeine consumption. The findings of this study were consistent with the results of Previous research (26-28). In this study, we used the Bruce treadmill test, while in the study, the 20-meter shuttle test was used as the maximum aerobic test. In addition, the high ambient temperature and dehydration conditions present in the present study could be another reason for the differences in the present results with the study of Lamina and Musa (29). The results showed that acute exercise significantly increased plasma IL1β, IL6, TNFα and hs-CRP levels in caffeine and sham groups. Consistent with these findings, increased blood levels of inflammatory agents following acute exercise have been reported in many studies (27, 30). Consistent with the results of the present study, previous studies have shown that caffeine consumption increased the IL6 response after maximal aerobic activity (34, 35). One of the reasons for this observation is that more cytokine secretion through caffeine consumption is associated with higher power output and greater metabolic stress (further increase in adrenaline and plasma lactate after exercise) (34, 35). Therefore, it seems that caffeine consumption may not have a direct effect on IL6, but rather increases the IL-6 response by increasing potency and consequently the need for higher metabolism.
One of the important findings of the present study was that acute caffeine consumption did not affect basal inflammatory factors, because there was no difference between the mean levels of basal inflammatory factors in the study groups. This observation is consistent with the results of studies by Arsenault et al. (36) and Kempf et al. (37), but with the results of studies by Fletcher and Bishop (38) and Jafari et al. (19) that increase basal levels of inflammatory markers in response to Acute caffeine consumption has been reported to be inconsistent. One possible reason for this discrepancy may be related to the conditions of the subjects; The subjects in the present study were in dehydrated conditions and at ambient temperature, which may have increased the basal levels of inflammatory markers by increasing the secretion of stress hormones and, therefore, reduced the effect of caffeine on these factors. Because the secretion of stress hormones (epinephrine and cortisol) has been cited as one of the basic mechanisms for increasing basal levels of inflammatory markers due to caffeine consumption (38, 39).
 In the present study, acute caffeine consumption further increased plasma IL6 levels in response to exercise. Consistent with this finding, some previous studies in this field have reported higher increases in plasma IL6 levels following exercise in subjects who consumed caffeine (35, 40). This higher increase in IL6 levels following caffeine supplementation is mainly attributed to a decrease in IL6 clearance by the liver, which occurs due to decreased visceral blood flow due to increased adrenaline (30). Another finding of the present study was that acute caffeine consumption reduced the rate of exercise-induced increase in TNFα. Horrigan et al. (2004) showed that caffeine consumption suppresses the production of proinflammatory cytokine TNFα in human blood and this effect is mediated by modulating the cyclic AMP / protein kinase A signaling pathway (41). Caffeine and its metabolite, theophylline, have also been shown to directly activate the enzyme histodoniestylase, which also distills central histone and reduces the transcription of inflammatory genes (17). In the present study, elevated IL1β and TNFα levels returned to baseline levels during blood sampling 24 hours after exercise in subjects experiencing caffeine supplementation, but remained elevated in the sham group. There were some limitations in the present study, such as the lack of measurement of other inflammatory factors. Examining the effect of different doses of caffeine supplementation after exercise can also help to better explain and interpret the results. This is a research weakness suggested by future studies to measure these post-exercise indicators along with caffeine consumption in athletes. It seems that the maximal exercise in hot environments and dehydration status increases the release of inflammatory markers that appear to be moderated by caffeine consumption. Also, caffeine use is associated with faster recovery of inflammatory status.
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Type of Study: Research | Subject: Exercise Physiology

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