Key pointsr Aerobic exercise, such as running, enhances adult hippocampal neurogenesis (AHN) in rodents. r Little is known about the effects of high-intensity interval training (HIT) or of purely anaerobic resistance training on AHN.r Here, compared with a sedentary lifestyle, we report a very modest effect of HIT and no effect of resistance training on AHN in adult male rats.r We found the most AHN in rats that were selectively bred for an innately high response to aerobic exercise that also run voluntarily and increase maximal running capacity.r Our results confirm that sustained aerobic exercise is key in improving AHN.Abstract Aerobic exercise, such as running, has positive effects on brain structure and function, such as adult hippocampal neurogenesis (AHN) and learning. Whether high-intensity interval training (HIT), referring to alternating short bouts of very intense anaerobic exercise with recovery periods, or anaerobic resistance training (RT) has similar effects on AHN is unclear. In addition, individual genetic variation in the overall response to physical exercise is likely to play a part in the effects of exercise on AHN but is less well studied. Recently, we developed polygenic rat models that gain differentially for running capacity in response to aerobic treadmill training. Here, we subjected these low-response trainer (LRT) and high-response trainer (HRT) adult male rats to various forms of physical exercise for 6-8 weeks and examined the effects on AHN. Compared with sedentary animals, the highest number of doublecortin-positive hippocampal cells was observed in HRT rats that ran voluntarily on a running wheel, whereas HIT on the treadmill had a smaller, statistically non-significant effect on AHN. Adult hippocampal neurogenesis was elevated in both LRT and HRT rats that underwent endurance training on a treadmill compared with those that performed RT by climbing a vertical ladder with weights, despite their significant gain in strength. Furthermore, RT had no effect on proliferation (Ki67), maturation (doublecortin) or survival (bromodeoxyuridine) of new adult-born hippocampal neurons in adult male Sprague-Dawley rats. Our results suggest that physical exercise promotes AHN most effectively if the exercise is aerobic and sustained, especially when accompanied by a heightened genetic predisposition for response to physical exercise. Abbreviations AHN, adult hippocampal neurogenesis; BDNF, brain-derived neurotrophic factor; BrdU, bromodeoxyuridine; HIT, high-intensity interval training; HRT, high-response trainer; LRT, low-response trainer; RW, running wheel; Sed, sedentary; TBS, Tris-buffered saline;V O2 max , maximal oxygen uptake.

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Understanding the importance of the gut microbiota (GM) in non-alcoholic fatty liver disease (NAFLD) has raised the hope for therapeutic microbes. We have shown that high hepatic fat content associated with low abundance of Faecalibacterium prausnitzii in humans and, further, the administration of F. prausnitzii prevented NAFLD in mice. Here, we aimed at targeting F. prausnitzii by prebiotic xylo-oligosaccharides (XOS) to treat NAFLD. First, the effect of XOS on F. prausnitzii growth was assessed in vitro. Then, XOS was supplemented or not with high (HFD, 60% of energy from fat) or low (LFD) fat diet for 12 weeks in Wistar rats (n = 10/group). XOS increased F. prausnitzii growth, having only a minor impact on the GM composition. When supplemented with HFD, XOS ameliorated hepatic steatosis. The underlying mechanisms involved enhanced hepatic β-oxidation and mitochondrial respiration. Nuclear magnetic resonance (1H-NMR) analysis of cecal metabolites showed that, compared to the HFD, the LFD group had a healthier cecal short-chain fatty acid profile and on the HFD, XOS reduced cecal isovalerate and tyrosine, metabolites previously linked to NAFLD. Cecal branched-chain fatty acids associated positively and butyrate negatively with hepatic triglycerides. In conclusion, XOS supplementation can ameliorate NAFLD by improving hepatic oxidative metabolism and affecting GM.

50ml/wk and undertook 6-wks resistance-exercise (RE; 6×8 repetitions, 75%-1RM 37 3/wk) with BWE monitored by saliva sampling and muscle biopsies (for determination 38 of RNA synthesis) 0-3-6-wks. Ribose mole percent excess (r-MPE) from purine 39 nucleotides was analyzed via GC-MS/MS. Proliferating C2C12 cells r-MPE exhibited a 40 rise-to-plateau while IGF-1 increased myotube RNA from 76±3ng/ul to 123±3ng/ul and 41 r-MPE by 0.39±0.1% (both P<0.01). After 3-wks, rat quadriceps r-MPE had increased 42 to 0.25±0.01% (P<0.01) and was greater with running-exercise (0.36±0.02%; P<0.01)). 43Human muscle r-MPE increased to 0.06±0.01% and 0.13±0.02% at 3/6-wks 44 respectively equating to synthesis rates of ~0.8%/d, increasing with RE to 1.7±0.3%/d 45 (P<0.01) and 1.2±0.1%/d (P<0.05) at 3/6-wks, respectively. Therefore, we have 46 developed and physiologically validated a novel technique to explore ribosomal 47 biogenesis in a multi-modal fashion.