Exercise Suppresses Appetite in Obesity: A Biochemical, Metabolic, and Molecular Approach

Exercise suppresses appetite in individuals with obesity irrespective of the type, duration, or intensity of the exercise. This effect is mediated through various physiological and biochemical mechanisms. Exercise influences appetite-regulatory hormones such as ghrelin and leptin, reducing hunger signals. Additionally, exercise generates metabolites and myokines, along with hepatokines, which modulate appetite suppression. Brain-derived neurotrophic factor (BDNF) is also implicated in modulating appetite. Changes in eating behaviors, gastric motility, and gastric emptying further contribute to a reduced appetite. Mental stress and body temperature alterations during exercise can also impact hunger levels. This review synthesizes current evidence and provides specific biochemical, metabolic and molecular mechanisms of how exercise and obesity affect appetite regulation. More specifically, it is extensively discussed the effect of exercise and obesity on: (1) endocrine mediators (hepatokines, metabolites, myokines, and neurotrophins); (2) physiological modulators (gastric emptying and body temperature); and (3) behavioral influences (eating patterns and visual food cues) in association with appetite regulation. Collectively, these factors highlight the complex interplay between physical activity and appetite regulation, offering insights into potential therapeutic strategies for managing obesity through exercise.