The aim of this study was to evaluate the effect of overload training on the function of peritoneal macrophages in rats, and to test the hypothesis that glutamine in vivo supplementation would partly reverse the eventual functional alterations induced by overload training in these cells. Forty male Wistar rats were randomly divided into 5 groups: control group (C), overload training group (E1), overload training and restore one week group (E2), glutamine-supplementation group (EG1), and glutamine-supplementation and restore 1-week group (EG2). All rats, except those placed on sedentary control were subjected to 11 weeks of overload training protocol. Blood hemoglobin, serum testosterone, and corticosterone of rats were measured. Moreover, the functions (chemotaxis, phagocytosis, cytokines synthesis, reactive oxygen species generation) of peritoneal macrophages were determined. Data showed that blood hemoglobin, serum testosterone, corticosterone and body weight in the overload training group decreased significantly as compared with the control group. Meanwhile, the chemotaxis capacity (decreased by 31%, p = .003), the phagocytosis capacity (decreased by 27%, p = .005), the reactive oxygen species (ROS) generation (decreased by 35%, p = .003) and the cytokines response capability of macrophages were inhibited by overload training. However, the hindering of phagocytosis and the cytokines response capability of macrophages induced by overload training could be ameliorated and reversed respectively, by dietary glutamine supplementation. These results suggest that overload training impairs the function of peritoneal macrophages, which is essential for the microbicidal actions of macrophages. This may represent a novel mechanism of immunodepression induced by overload training. Nonetheless, dietary glutamine supplementation could partly reverse the impaired macrophage function resulting from overload training.
Weihua Xiao, Peijie Chen, Jingmei Dong, Ru Wang and Beibei Luo
Jingmei Dong, Peijie Chen, Qing Liu, Ru Wang, Weihua Xiao and Yajun Zhang
To examine the excessive reactive oxygen species (ROS) mediated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and the combined effect of glutamine supplementation and diphenyleneiodonium (DPI) on the function of neutrophils induced by overtraining.
Fifty male Wistar rats were randomly divided into 5 groups: control group (C), overtraining group (E), DPI-administration group (D), glutamine-supplementation group (G), and combined DPI and glutamine group (DG). Blood was sampled from the orbital vein after rats were trained on treadmill for 11 wk. Cytokine and lipid peroxidation in blood plasma were measured by enzyme-linked immunosorbent assay. The colocalization between gp91phox and p47phox of the NADPH oxidase was detected using immunocytochemistry and confocal microscopy. The activity of NADPH oxidase was assessed by chemiluminescence. Neutrophils’ respiratory burst and phagocytosis function were measured by flow cytometry.
NADPH oxidase was activated by overtraining. Cytokine and lipid peroxidation in blood plasma and the activity of NADPH oxidase were markedly increased in Group E compared with Group C. Neutrophil function was lower in Group E than Group C. Both lower neutrophils function and higher ROS production were reversed in Group DG. The glutamine and DPI interference alone in Group D and Group G was less effective than DPI and glutamine combined in group DG.
Activation of NADPH oxidase is responsible for the production of superoxide anions, which leads to excessive ROS and is related to the decrease in neutrophil function induced by overtraining. The combined DPI administration and glutamine supplementation reversed the decreased neutrophil function after overtraining.
Chun-Chih Wang, Brandon Alderman, Chih-Han Wu, Lin Chi, Su-Ru Chen, I-Hua Chu and Yu-Kai Chang
This study aimed to determine the comparative effectiveness of aerobic vs. resistance exercise on cognitive function. In addition, salivary cortisol responses, as an indicator of arousal-related neuroendocrine responses, were assessed as a potential mechanism underlying the effects of these 2 modes of acute exercise on cognition. Forty-two young adults were recruited and performed the Stroop task after 1 session of aerobic exercise, resistance exercise, and a sedentary condition performed on separate days. Saliva samples were collected at baseline and immediately and 30 min after treatment conditions. Acute exercise, regardless of exercise modality, improved multiple aspects of cognitive function as reflected by the Stroop task. Cortisol responses were higher after both modes of acute exercise compared with the sedentary condition and were higher at baseline and 30 min afterward compared with immediately after treatment conditions. These findings suggest that acute exercise of moderate intensity facilitates cognitive function, and, although salivary cortisol is influenced by acute exercise, levels were not related to improvements in cognition.