Collectively, the available data strongly support that, in addition to other well-known internal and external factors, exercise appears to be an environmental factor that can determine changes in the qualitative and quantitative gut microbial composition with possible benefits for the host. In fact, stable and enriched microflora diversity is indispensable to the homeostasis and normal gut physiology contributing also to suitable signaling along the brain-gut axis and to the healthy status of the individual. Exercise is able to enrich the microflora diversity; to improve the Bacteroidetes-Firmicutes ratio which could potentially contribute to reducing weight, obesity-associated pathologies, and gastrointestinal disorders; to stimulate the proliferation of bacteria which can modulate mucosal immunity and improve barrier functions, resulting in reduction in the incidence of obesity and metabolic diseases; and to stimulate bacteria capable of producing substances that protect against gastrointestinal disorders and colon cancer (such as, SCFAs). Therefore the exercise can be used as a treatment to maintain the balance of the microflora or to rebalance his eventual dysbiosis, thus obtaining an improvement of the health status. Nevertheless further studies are needed to fully understand the mechanisms that determine changes in the composition and functions of the microflora caused by exercise and all their related effects. In addition exercise-altered microbiota could be used to look for new approaches in the treatment of metabolic and inflammatory diseases in which it is well known that the microbiota plays an important role.
Metabolism of propanoate begins with its conversion to propionyl coenzyme A (propionyl-CoA), the usual first step in the metabolism of carboxylic acids. Since propanoic acid has three carbons, propionyl-CoA can directly enter neither beta oxidation nor the citric acid cycles. In most vertebrates, propionyl-CoA is carboxylated to D-methylmalonyl-CoA, which is isomerised to L-methylmalonyl-CoA. A vitamin B 12 -dependent enzyme catalyzes rearrangement of L-methylmalonyl-CoA to succinyl-CoA, which is an intermediate of the citric acid cycle and can be readily incorporated there.