# Exercise Suppresses Appetite in Obesity: A Biochemical, Metabolic, and Molecular Approach
## 6 Exercise and Gastric Motility and Emptying  
Exercise also modulates gastric motility associated with gastric emptying and has been suggested as a rate-limiting step in the transfer of nutritional substances to the small intestine to temporarily inhibit appetite and the desire to eat [496; 497] (Figure 6). Food entering the small intestine causes gastric distention, the stimulation of intestinal mechano- and chemo-receptors, and the release of several gut peptides [498; 499]. The influence of gastric distention on appetite is mediated by stimulating stretch and tension mechanoreceptors, which then signal the brain [500; 501]. Researches have established a direct relationship between satiety perception and gastric distension [502; 503] and an inverse correlation between gastric volume and food intake [504]. Hence, an accelerated rate of gastric emptying abates gastric distention associated with overeating, while slower gastric emptying is associated with gastric distention, the feeling of fullness, and reduced food intake [503; 505]. Additionally, a delay in gastric emptying into the small intestine is commensurate with mitigating the effects of intestinal appetite peptides [506]. Exercise improves gastrointestinal function, including the gastric emptying rate and gut motility [507; 508; 509]. Chronic exercise-mediated faster emptying is accompanied with an increased desire to consume food [508] and increased meal frequency by reduced gastric distention and fullness, which are compensatory mechanisms to meet expenditure energy during exercise [510]. These effects on the gastrointestinal tract are dependent on exercise intensity and duration, the food volume, and the amount of food consumed before exercise [511; 512; 513; 514]. In this context, it has been indicated that faster gastric emptying, as an adaptation to exercise training, only emerges in individuals who have trained for a long period of time, at least 6 months [509]. Consistently, a 4-week exercise protocol that combined high-intensity and continuous exercise failed to increase gastric emptying in men with overweight/obesity [515]. According to precedent reports, the intensity of exercise has an important role in gastric motility, or rather, the gastric emptying rate, such that it is accelerated during low-intensity exercises and delayed during high-intensity exercises [516; 517]. Low-intensity exercise accelerates gastric emptying (characterized by expelling looser stool) compared to moderate or high-intensity exercise [516]. Diminished gastric motility mediated by high-intensity exercise reduces appetite [37; 517], partly due to increased lactate concentrations and sympathetic stimulation during these exercise types (Figure 6). An increased lactate concentration promotes CO\({}_{2}\) production to cause the bicarbonate-mediated buffering of H+ ions [518]; CO\({}_{2}\) incurs intestine distention and alters gastric motility [519]. In addition to the enteric nervous system controlling the gastrointestinal function, the extrinsic innervation of the gastrointestinal tract by sympathetic and parasympathetic nerves also regulates, modulates, and coordinates gastrointestinal function [520]. The sympathetic innervation of the gastrointestinal tract originates from the intermediolateral column of the thoracolumbar spinal cord [521] and provides an inhibitory input to the smooth muscle of the gastrointestinal tract, resulting in tonic inhibitory effects on mucosal secretion and reduced gastrointestinal blood flow by causing vasoconstriction. The modulation of gastrointestinal motility primarily occurs by the modulation of the presynaptic release of neurotransmitters. However, parasympathetic nerves also provide both inhibitory and excitatory inputs to the stomach and small intestine, allowing for the precise control of gastrointestinal function. Extrinsic parasympathetic inputs to the stomach and gastrointestinal tract are supplied by the vagus nerve and efferent cell bodies, which are located in the dorsal motor nucleus (DMV) in the hindbrain [522; 523; 524].