Although dietary fiber treatment alters the gut microbiota and its metabolite production, it is unclear whether or not exercise habits can have a supplemental effect on changes in gut microbiota in dietary fiber-treated mice. To clarify the supplemental effect of voluntary exercise on gut microbiota in partially hydrolyzed guar gum (PHGG), which is a soluble dietary fiber, treated mice under high-fat diet (HFD) feeding, 4-week-old male C57BL/6J mice (n = 80) were randomly divided into two dietary groups: the control-diet (CD) and HFD. Then, each dietary group was treated with or without PHGG, and with or without wheel running. After the experimental period, measurement of maximal oxygen consumption, a glucose tolerance test and fecal materials collection for analysis of gut microbiota were carried out. Voluntary exercise load in PHGG treatment under HFD feeding showed the supplemental effect of exercise on obesity (p < 0.01) and glucose tolerance (p < 0.01). Additionally, in both CD and HFD groups, voluntary exercise accelerated the decrease in the Firmicutes/Bacteroidetes ratio in mice fed with PHGG (p < 0.01). These findings suggest that voluntary exercise might activate the prevention of obesity and insulin resistance more via change in gut microbiota in mice administrated with PHGG.

Our previous study showed that lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF)-α production is inhibited by acute exhaustive exercise in mice, leading to transient immunodepression after exercise. Sparassis crispa (SC), an edible mushroom, has immunopotentiative properties. This study aimed to clarify the effects of SC intake on reduced LPS-induced TNF-α production upon exhaustive exercise in mice. Male C3H/HeN mice were randomly divided into three groups: normal chow intake + resting sedentary, normal chow intake + acute exhaustive treadmill running exercise, and SC intake (chow containing 5% SC powder for 8 weeks) + the exhaustive exercise groups. Each group was injected with LPS immediately after the exhaustive exercise or rest. Plasma and tissue TNF-α levels were significantly decreased by exhaustive exercise. However, this reduction of the TNF-α level was partially attenuated in the plasma and small intestine by SC intake. Although levels of TLR4 and MyD88 protein expression were significantly decreased in tissues by exhaustive exercise, the reduction of TLR4 and MyD88 levels in the small intestine was partially attenuated by SC intake. These results suggest that SC intake attenuates exhaustive exercise-induced reduction of TNF-α production via the retention of TLR4 and MyD88 expression in the small intestine.

Macrophages migrate and invade into damaged muscle rapidly and are important for muscle repair and subsequent regeneration. The exact cellular and biological events that cause macrophage migration toward injured muscle are not completely understood. In this study, the effect of macrophage differentiation on the chemotactic capability to invade local damaged muscle was investigated using an in vitro model of muscle injury. We used C2C12 cell myoblasts and J774 cell macrophages, and the “killed-C2C12” cells were combined with live C2C12 cells as a partially damaged muscle model. The cultured J774 cells, with or without lipopolysaccharide (LPS), were treated with Ly294002 (Ly), which is an inhibitor of phosphoinositide 3-kinase (PI3K). In order to evaluate the polarization effect of LPS stimulation on J774 cells, expression of cell surface Toll-like receptor 4 (TLR4), CD11c and CCR2, and expression of F-actin intensity, were analyzed by flow cytometry. The real-time horizontal chemotaxis assay of J774 cells was tested using the TAXIScan device. The expressions of TLR4, CD11c, and F-actin intensity in LPS-treated cells were significantly higher than those in Ctrl cells. In LPS-treated cells, the chemotactic activity toward damaged muscle cells completely disappeared. Moreover, the reduced chemotaxis depended far more on directionality than velocity. However, Ly treatment reversed the reduced chemotactic activity of the LPS-treated cells. In addition, cell-adhesion and F-actin intensity, but not CCR2 expression, in LPS-treated cells, was significantly reduced by Ly treatment. Taken together, our results suggest that the PI3K/Akt activation state drives migration behavior towards damaged muscle cells.

Background: Cactus contains dietary fiber and minerals and is expected to have preventive effects against diabetes, arteriosclerosis, and other diseases. Additionally, cactus intake induces the production of short-chain fatty acids derived from the gut microbiota, which might influence immune functions. In this study, we examined the effects of a cactus (Nopalea cochenillifera: NC)-supplemented diet on lipopolysaccharide (LPS)-induced immune responses and intestinal barrier function. Methods: Male C3H/HeN mice were randomly divided into three groups—no fiber (NF), cellulose-containing fiber (Cellu), and cactus-added (NC) diets—for 6 weeks. The TNF-α and IL-10 responses to LPS, antibody titers, and intestinal barrier function, as well as the fecal microbiota, were analyzed. Results: The plasma TNF-α but not the IL-10 concentrations were significantly higher in the NC group than in the NF and Cellu groups. Furthermore, the plasma IgG antibody titers were significantly higher in the NC group than in the other groups. The NC group showed higher mucin content and IgA antibody titers in their feces compared with the Cellu group. The succinate and lactate contents, which induce a reduction in TNF-α secretion by macrophages, in the cecum of the NC group were significantly lower than those in the Cellu and NF groups. In contrast, the butyrate content was significantly higher in the cecum of the NC group compared to that of the Cellu group, with a significantly higher relative abundance of butyrate-producing bacteria. Conclusions: Taken together, we found that cactus intake regulates innate and adaptive immune function via the gut microbiota in mice. Therefore, cactus supplementation might serve as a strategy to develop novel functional foods with dietary fiber.

In understanding the relationship between exercise and immunity, the “open window theory” is a well-known theory stating that immediately after high intensity exercise, temporary immunosuppression occurs, which increases the risk of infections such as upper respiratory tract infections. Why does such a phenomenon occur? Does immunosuppression after severe exercise have physiological significance? In this paper, we propose a theory of super homeostasis. In other words, we verify that the open window theory is an important biological reaction when trying to understand the reason why we do exercise, more than it is the indispensable physiological response to the whole body.