Among athletes, nutrition plays a key role, supporting training, performance, and post-exercise recovery. Research has primarily focused on the effects of diet in support of an athletic physique; however, the role played by intestinal microbiota has been much neglected. Emerging evidence has shown an association between the intestinal microbiota composition and physical activity, suggesting that modifications in the gut microbiota composition may contribute to physical performance of the host. Probiotics represent a potential means for beneficially influencing the gut microbiota composition/function but can also impact the overall health of the host. In this review, we provide an overview of the existing studies that have examined the reciprocal interactions between physical activity and gut microbiota. We further evaluate the clinical evidence that supports the effects of probiotics on physical performance, post-exercise recovery, and cognitive outcomes among athletes. In addition, we discuss the mechanisms of action through which probiotics affect exercise outcomes. In summary, beneficial microbes, including probiotics, may promote health in athletes and enhance physical performance and exercise capacity. Furthermore, high-quality clinical studies, with adequate power, remain necessary to uncover the roles that are played by gut microbiota populations and probiotics in physical performance and the modes of action behind their potential benefits.

Berries contain a number of compounds that are proposed to have anticarcinogenic properties. We studied the effects and molecular mechanisms of wild berries with different phenolic profiles on intestinal tumorigenesis in multiple intestinal neoplasia/+ mice. The mice were fed a high-fat AIN93-G diet (Con) or AIN93-G diets containing 10% (w:w) freeze-dried bilberry, lingonberry (LB), or cloudberry (CB) for 10 wk. All 3 berries significantly inhibited the formation of intestinal adenomas as indicated by a 15-30% reduction in tumor number (P < 0.05). CB and LB also reduced tumor burden by over 60% (P < 0.05). Compared to Con, CB and LB resulted in a larger (P < 0.05) proportion of small adenomas (43, 69, and 64%, respectively) and a smaller proportion of large adenomas (56, 29, and 33%, respectively). Beta-catenin and cyclin D1 in the small and large adenomas and in the normal-appearing mucosa were measured by Western blotting and immunohistochemistry. CB resulted in decreased levels of nuclear beta-catenin and cyclin D1 and LB in the level of cyclin D1 in the large adenomas (P < 0.05). Early changes in gene expression in the normal-appearing mucosa were analyzed by Affymetrix microarrays, which revealed changes in genes implicated in colon carcinogenesis, including the decreased expression of the adenosine deaminase, ecto-5'-nucleotidase, and prostaglandin E2 receptor subtype EP4. Our results indicate that berries are potentially a rich source of chemopreventive components.

Estrogen receptors (ERs) [ERalpha (Esr1) and ERbeta (Esr2)] are expressed in the human colon, but during the multistep process of colorectal carcinogenesis, expression of both ERalpha and ERbeta is lost, suggesting that loss of ER function might promote colorectal carcinogenesis. Through crosses between an ERalpha knockout and Apc(Min) mouse strains, we demonstrate that ERalpha deficiency is associated with a significant increase in intestinal tumor multiplicity, size and burden in Apc(Min/+) mice. Within the normal intestinal epithelium of Apc(Min/+) mice, ERalpha deficiency is associated with an accumulation of nuclear beta-catenin, an indicator of activation of the Wnt-beta-catenin-signaling pathway, which is known to play a critical role in intestinal cancers. Consistent with the hypothesis that ERalpha deficiency is associated with activation of Wnt-beta-catenin signaling, ERalpha deficiency in the intestinal epithelium of Apc(Min/+) mice also correlated with increased expression of Wnt-beta-catenin target genes. Through crosses between an ERbeta knockout and Apc(Min) mouse strains, we observed some evidence that ERbeta deficiency is associated with an increased incidence of colon tumors in Apc(Min/+) mice. This effect of ERbeta deficiency does not involve modulation of Wnt-beta-catenin signaling. Our studies suggest that ERalpha and ERbeta signaling modulate colorectal carcinogenesis, and ERalpha does so, at least in part, by regulating the activity of the Wnt-beta-catenin pathway.

Dietary plant sterols reduce the absorption of cholesterol and therefore increase intraluminal cholesterol concentration. We examined how plant sterol esters from functional foods affect intestinal tumorigenesis in tumor-prone adenomatous polyposis coli (Apc)(Min) mice. Feeding plant sterols at 0.8% increased the number of intestinal adenomas, and the effect was significant in female mice. The concentration of mucosal free sitosterol increased by eightfold in plant sterol males and by threefold in plant sterol females when compared with respective controls. The concentration of mucosal free cholesterol was significantly lower in plant sterol males than in control males, and the decrease in free cholesterol was accompanied with a significant increase in nuclear sterol regulatory element binding protein-2. No difference was found in the levels of β-catenin, cyclin D1, epidermal growth factor receptor, extracellular signal-regulated kinase 1/2, or caveolin-1 in either gender after plant sterol feeding. Among all measured parameters, higher levels of estrogen receptor β and free cholesterol in the mucosa were among the strongest predictors of increased intestinal tumorigenesis. In addition, gene expression data showed significant enrichment of up-regulated genes of cell cycle control and cholesterol biosynthesis in plant sterol females. The results indicate that high intake of plant sterols accelerates intestinal tumorigenesis in female Apc (Min)mice; however, the mechanism behind the adverse effect remains to be discovered.

Background Probiotics may alleviate lactose maldigestion. Objectives The objective was to select a probiotic with high lactase activity and compare it with lactase and placebo in clinical trials. Methods Bacterial cultures were screened for lactase activity in a model of the upper gastrointestinal tract. Bifidobacterium lactis Bi-07 (Bi-07) counts were adjusted in subsequent experiments to correspond to 4500 Food Chemical Codex (FCC) units of lactase, the amount in the European Food Safety Authority (EFSA)-approved health claim. Two crossover clinical trials, Booster Alpha and Booster Omega, were performed in participants with lactose intolerance, where 2 × 1012 colony forming units (CFU) Bi-07, 4662 FCC lactase, or placebo was consumed simultaneously with a lactose challenge, with 1-week washouts between challenges. The trial designs were identical except for the source of lactose. Breath hydrogen concentration (BHC) was measured to assess the effect of the investigational products on lactose digestion, for which incremental area under the curve (iAUC) was the primary outcome. Peak BHC, cumulative BHC, and gastrointestinal symptoms were secondary outcomes. Results Bi-07 was superior to placebo in reducing BHC (iAUC, parts per million (ppm)∙h) in both trials (Booster Alpha: geometric least square mean ratio 0.462 [95% confidence interval (CI):0.249, 0.859], P = 0.016; Booster Omega: 0.227 [95% CI:0.095, 0.543], P = 0.001). Lactase was superior to placebo in Booster Alpha (0.190 [95% CI:0.102, 0.365], P &lt; 0.001) but not Booster Omega (0.493 [95% CI:0.210, 1.156], P = 0.102). Noninferiority of Bi-07 versus lactase was observed in Booster Omega (0.460 [95% CI:0.193, 1.096], P = 0.079, CI upper limit &lt; 1.25 noninferiority margin). Odds of abdominal pain (vs placebo: 0.32, P = 0.036) and flatulence (vs placebo: 0.25, P = 0.007) were lower with lactase in Booster Alpha. Increased odds of nausea were seen with Bi-07 (vs placebo: 4.0, P = 0.005) in Booster Omega. Conclusions Bi-07 has high lactase activity, and in 2 clinical trials, it supported lactose digestion in individuals with lactose intolerance. The clinical trials have been registered at Clinicaltrials.gov with the following identifiers: Booster Alpha: NCT03659747 (https://clinicaltrials.gov/ct2/show/NCT03659747?term=NCT03659747&draw=2&rank=1) Booster Omega: NCT03814668 (https://clinicaltrials.gov/ct2/show/NCT03814668?cond=NCT03814668&draw=2&rank=1)