Voluntary training in mice and submandibular lymphocyte response to acute exercise.
ABSTRACT Submandibular lymph nodes (SLN) are important for immune responses to antigens in the eye and oral mucosa. Athletes and exercise participants may be at increased risk of ocular, oral, and upper respiratory tract infections.
This study was conducted to examine the effects of voluntary training on the distribution, number, and apoptotic status of SLN lymphocytes in response to an acute bout of strenuous exercise.
Female C57BL/6 mice were assigned to voluntary wheel-running (WR) exercise (N=20) or were sedentary (N=10) for 16 wk. SLN lymphocytes were examined immediately (EX+Imm) or 24 h (EX+24 h) following strenuous treadmill exercise, or exposure to treadmill conditions without running (NonEX). Intracellular glutathione (GSH), mitochondrial membrane potential (MMP), cell viability (propidium iodide uptake, PI), surface phosphatidylserine (Annexin V), T-lymphocyte (CD3, CD4, CD8), and B-lymphocyte (CD19) phenotype distribution and number were assessed.
The WR mice had a higher number and percent CD8 SLN lymphocytes, higher MMP, and lower Annexin V/PI SLN lymphocytes than controls. Regardless of training status, an acute bout of strenuous exercise decreased the total and phenotype specific (CD3, CD4, CD8) number of cells, MMP, and GSH levels immediately after exercise.
WR in mice improved some aspects of cell viability in SLN lymphocytes compared with controls, but did not prevent the transient cell loss after acute treadmill exercise. Given the depletion in intracellular GSH levels, oxidative stress may account for the decline in SLN lymphocyte numbers following acute exercise. Loss of SLN lymphocytes may have consequences for ocular, oral, and upper respiratory tract health in some exercise participants and athletes during periods of overtraining.
SourceAvailable from: Ioannis S Vrabas[Show abstract] [Hide abstract]
ABSTRACT: The central aim of this review is to address the highly multidisciplinary topic of redox biology as related to exercise using an integrative and comparative approach rather than focusing on blood, skeletal muscle or humans. An attempt is also made to re-define 'oxidative stress' as well as to introduce the term 'alterations in redox homeostasis' to describe changes in redox homeostasis indicating oxidative stress, reductive stress or both. The literature analysis shows that the effects of non-muscle-damaging exercise and muscle-damaging exercise on redox homeostasis are completely different. Non-muscle-damaging exercise induces alterations in redox homeostasis that last a few hours post exercise, whereas muscle-damaging exercise causes alterations in redox homeostasis that may persist for and/or appear several days post exercise. Both exhaustive maximal exercise lasting only 30 s and isometric exercise lasting 1-3 min (the latter activating in addition a small muscle mass) induce systemic oxidative stress. With the necessary modifications, exercise is capable of inducing redox homeostasis alterations in all fluids, cells, tissues and organs studied so far, irrespective of strains and species. More importantly, 'exercise-induced oxidative stress' is not an 'oddity' associated with a particular type of exercise, tissue or species. Rather, oxidative stress constitutes a ubiquitous fundamental biological response to the alteration of redox homeostasis imposed by exercise. The hormesis concept could provide an interpretative framework to reconcile differences that emerge among studies in the field of exercise redox biology. Integrative and comparative approaches can help determine the interactions of key redox responses at multiple levels of biological organization.Journal of Experimental Biology 05/2012; 215(Pt 10):1615-25. DOI:10.1242/jeb.067470 · 3.00 Impact Factor
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ABSTRACT: Intestinal homeostasis effectors, secretory IgA (SIgA) and polymeric immunoglobulin receptor (pIgR), have been evaluated in proximal and distal small intestine with moderate-exercise training but not with strenuous exercise or a combination of these two protocols. Therefore, two groups of mice (n=6-8) were submitted to strenuous exercise, one with and one without previous training. The control group had no exercise protocol. Assessment was made of intestinal SIgA and plasma adrenal hormones (by immunoenzymatic assay), alpha-chain and pIgR proteins in intestinal mucosa (by Western blot), lamina propria IgA plasma-cells (by cytofluorometry), mRNA expression (by real-time PCR) for pIgR, alpha- and J-chains in liver and intestinal mucosa, and pro- and anti-inflammatory cytokines in mucosa samples. Compared to other exercise protocols, training plus strenuous exercise elicited: (1) higher levels of SIgA and pIgR in the proximal intestine (probably by hepatobiliary contribution); (2) higher levels of SIgA in the distal segment; (3) lower mRNA expression of some SIgA- and most pro-inflammatory pIgR-producing cytokines. SIgA and pIgR in both segments were derived from an existing pool of their corresponding producing cells. The apparent decreased translation of mRNA transcripts underlies lower levels of SIgA and pIgR in distal than proximal small intestine. There was no significant difference in the relatively high adrenal hormone levels found in both exercised groups. Further study is required about the effects of training plus strenuous exercise on pool-derived SIgA levels and mRNA expression of pro-inflammatory pIgR-producing cytokines. These results could have important implications for intestinal disorders involving inflammation and infection.Brain Behavior and Immunity 08/2012; 26(8):1300-9. DOI:10.1016/j.bbi.2012.07.018 · 6.13 Impact Factor
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ABSTRACT: The underlying mechanisms of adaptation from staying physically active are not completely revealed. This study examined the effects of 8 and 20 weeks of habitual voluntary exercise on the susceptibility of lymphocytes to oxidant-induced DNA damage, antioxidant enzyme activities in cardiac and skeletal muscles, and circulatory antioxidant profile. Forty young adult rats were randomly assigned to sedentary control and exercise groups for an experimental period of 8 or 20 weeks. Animals assigned to exercise groups were subjected to 24 h daily free access to an in-cage running wheel with circumference of 1.19 m. A magnetic digital counter was attached to the running wheel to record daily exercise distance run by the animals. Control rats were housed in cages without a running wheel, located next to the exercised animals. Body weight and food intake were recorded weekly. After the experimental periods of 8 and 20 weeks, blood, left ventricle, soleus and plantaris muscles were collected for analysis. No significant difference was found in plasma total antioxidant capacity between exercised and control animals in the 8 and 20 week groups according to our ferric reducing/antioxidant power (FRAP) analysis. However, modified FRAP for ascorbic acid (FRASC) analysis indicated that plasma ascorbic acid content was significantly increased by 46 and 34% in 8 and 20 week exercise groups, respectively, when compared with the corresponding control groups. Superoxide dismutase (SOD) activity was significantly elevated by 39% in erythrocytes of animals exercised for 8 weeks relative to control animals. In the 20 week exercise group, Glutathione peroxidase (GPx) activity in ventricle and plantaris was significantly upregulated by 477 and 290%, respectively, relative to control values. As demonstrated by comet assay, the oxidant-induced DNA damage was significantly reduced by 21 and 45% in lymphocytes of animals exercised for 8 and 20 weeks, respectively, when compared with the corresponding control lymphocytes. Our qRT-PCR analysis showed that the transcript expression of SOD2 was significantly elevated by 939% in lymphocytes of animals exercised for 8 weeks relative to control animals. Increased expressions of SOD2 (by 19%), catalase (25%), APEX nuclease (multifunctional DNA repair enzyme) 1 (APEX1; 46%), Protein kinase, DNA-activated, catalytic polypeptide (Prkdc; 9%) and O-6-methylguanine-DNA methyltransferase (Mgmt; 26%) were found in lymphocytes of animals exercised for 20 weeks relative to control rats. These results demonstrate that habitual exercise confers increased resistance of lymphocytes to oxidant-induced DNA damage, and this protective effect is possibly attributed to the regular exercise-induced elevated expression of antioxidant and DNA repairing enzymes.Experimental physiology 05/2011; 96(9):889-906. DOI:10.1113/expphysiol.2011.058396 · 2.87 Impact Factor