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While a low degree of energy compensation is typically reported over the 24 h following a session of exercise, the prolonged impact of a bout of exercise on energy intake remains unclear. To overcome the challenge associated with accurately measuring energy intake in a free‐living environment, this study employed the use of a meal replacement beverage to assess the 3 day impact of an exercise session on energy intake. In a randomized, crossover study, 14 participants (8 male, 6 female) completed two trials: (1) EX: 75 min exercise on a motorized treadmill (75% VO2peak); and (2) SED: 75 min sedentary control session. Each condition was followed by 3 days of exclusive ad libitum consumption of a meal replacement beverage. Appetite‐regulating hormones, subjective appetite, energy intake, and energy expenditure were assessed. Exercise transiently suppressed the orexigenic hormone acyl‐ghrelin (p < 0.05) and elevated the appetite‐supressing hepatokine GDF‐15 (p < 0.05). Despite these acute changes, overall perceived appetite was elevated over the 3 day assessment period with exercise (p < 0.05). No increase in energy intake or change in postexercise physical activity patterns were observed. One acute session of moderate to vigorous exercise is unlikely to affect short‐term, three‐day energy balance in healthy individuals. [ABSTRACT FROM AUTHOR]

BackgroundGastrointestinal dysfunction and gut microbial composition disturbances have been widely reported in autism spectrum disorder (ASD). This study examines whether gut microbiome disturbances are present in the BTBR(T + tf/j) (BTBR) mouse model of ASD and if the ketogenic diet, a diet previously shown to elicit therapeutic benefit in this mouse model, is capable of altering the profile.FindingsJuvenile male C57BL/6 (B6) and BTBR mice were fed a standard chow (CH, 13 % kcal fat) or ketogenic diet (KD, 75 % kcal fat) for 10-14 days. Following diets, fecal and cecal samples were collected for analysis. Main findings are as follows: (1) gut microbiota compositions of cecal and fecal samples were altered in BTBR compared to control mice, indicating that this model may be of utility in understanding gut-brain interactions in ASD; (2) KD consumption caused an anti-microbial-like effect by significantly decreasing total host bacterial abundance in cecal and fecal matter; (3) specific to BTBR animals, the KD counteracted the common ASD phenotype of a low Firmicutes to Bacteroidetes ratio in both sample types; and (4) the KD reversed elevated Akkermansia muciniphila content in the cecal and fecal matter of BTBR animals.ConclusionsResults indicate that consumption of a KD likely triggers reductions in total gut microbial counts and compositional remodeling in the BTBR mouse. These findings may explain, in part, the ability of a KD to mitigate some of the neurological symptoms associated with ASD in an animal model.

[beta]-Guanadino-propionic acid ([beta]-GPA) feeding leads to reductions in skeletal muscle phosphagen concentrations and has been used as a tool with which to study the effects of energy charge on skeletal muscle metabolism. Supplementing standard rodent diets with [beta]-GPA leads to increases in mitochondrial enzyme content in fast but not slow-twitch muscles from male rats. Given this apparent discrepancy between muscle types we used [beta]-GPA feeding as a model to study signaling pathways involved in mitochondrial biogenesis. We hypothesized that [beta]-GPA feeding would result in a preferential activation of p38 MAPK and AMPK signaling and reductions in RIP140 protein content in triceps but not soleus muscle. Despite similar reductions in high-energy phosphate concentrations, 6 wk of [beta]-GPA feeding led to increases in mitochondrial proteins in triceps but not soleus muscles. Differences in the response of mitochondrial proteins to [beta]-GPA feeding did not seem to be related to a differential activation of p38 MAPK and AMPK signaling pathways or discrepancies in the induction of PPAR[gamma] coactivator (PGC)-1[alpha] and -1[beta]. The protein content and expression of the nuclear corepressor RIP140 was reduced in triceps but not soleus muscle. Collectively our results indicate that chronic reductions in high-energy phosphates lead to the activation of p38 MAPK and AMPK signaling and increases in the expression of PGC-1[alpha] and -1[beta] in both soleus and triceps muscles. The lack of an effect of [beta]-GPA feeding on mitochondrial proteins in the soleus muscles could be related to a fiber type-specific effect of [beta]-GPA on RIP140 protein content. [beta]-guanadinopropionic acid; peroxisome proliferator-activated receptor-[gamma] coactivator-l[alpha]; skeletal muscle; rat; kinase; RIP140

Objective Prebiotics and probiotics may be able to modify an obesity-associated gut microbiota. The aim of this study was to examine the individual and combined effects of the prebiotic oligofructose (OFS) and the probiotic Bifidobacterium animalis subsp. lactis BB-12 (BB-12) on gut microbiota and host metabolism in obese rats. Methods Adult male, diet-induced obese Sprague Dawley rats were randomized to: (1) Control (C); (2) 10% OFS; (3) BB-12; (4) OFS + BB-12 for 8 weeks ( n = 9-10 rats/group). Body composition, glycemia, gut permeability, satiety hormones, cytokines, and gut microbiota were examined. Results Prebiotic, but not probiotic reduced energy intake, weight gain, and fat mass ( P < 0.01). OFS, BB-12, and the combined OFS + BB-12 improved glycemia ( P < 0.05). Individually, OFS and BB-12 reduced insulin levels ( P < 0.05). Portal GLP-1 was increased with OFS, whereas probiotic increased GLP-2 ( P < 0.05). There was a marked increase in bifidobacteria and lactobacilli ( P < 0.01) with OFS that was not observed with probiotic alone. Conclusions The impact of prebiotic intake on body composition and gut microbiota was of greater magnitude than the probiotic BB-12. Despite this, an improvement in glucose AUC with both prebiotic or probiotic demonstrates the beneficial role of each of these 'biotic' agents in glycemic control. [ABSTRACT FROM AUTHOR]