# Exercise Suppresses Appetite in Obesity: A Biochemical, Metabolic, and Molecular Approach
## 1 Introduction  
Obesity levels have increased exponentially, making it a global epidemic; obesity increases the risk of developing comorbidities, including type 2 diabetes mellitus, cardiovascular diseases, hypertension, and liver and endometrial cancers [1,2]. Obesity is a consequence of long-term changes in energy balance in which energy intake exceeds energy expenditure [3], where a mismatch of lower than 0.5% in caloric intake over caloric expenditure can result in weight gain [4]. This imbalance between energy intake and expenditure likely results from disrupted mechanisms regulating appetite and eating behaviors [5]. Appetite is influenced by a multiplicity of physiological, psychological, and environmental factors that are integrated in the brain to impact eating behaviors [6,7]. Signals from the hypothalamus normally regulate appetite and energy intake; the hypothalamus and, in particular, the arcuate nucleus (ARC), receive and processes neuronal, metabolic, and endocrine signals from various tissues and organs to establish energy homeostasis by maintaining energy intake and expenditure [8]. For further discussion concerning the neuroanatomy and physiological function of ARC, refer to relevant studies in the literature [9, 10, 11, 12, 13, 14]. Briefly, the brainstem receives vagal efferent neurons from the gastrointestinal tract and acts as a platform for amalgamating endocrine and neuronal signals [15]. Although most peripheral signals influencing the appetite control system originate from the gastrointestinal tract, other organs, such as adipose tissue, metabolites [16,17], and even external stimuli from food and the external environment, such as restraint, disinhibition, and hedonic sensation [18,19], also regulate appetite and energy intake. Exercise influences and alters these appetitive signals [20,21] and is considered a therapeutic treatment and an adjunct intervention against obesity and its negative health consequences [22]. Physical activity and exercise reduce obesity by regulating mean body weight and adipose tissue function [23]. Increased energy expenditure induced by exercise creates a negative energy balance without changes in compensatory energy intake following acute and chronic exercise [24,25]. Physical activity is a mechanical and a metabolic stress that instigates some time-dependent processes to produce morphological and functional changes, leading to either acute and chronic adaptations according to the exercise type, intensity, and duration [26]. Endurance or aerobic training causes a transition of muscle fiber type from IIb to more oxidative types IIa and I, which are characterized by increases in mitochondrial size and number, an improved capillary network surrounding each fiber type, and elevated levels of carnitine palmitoyl transferase. These adaptive changes stimulate the \(\beta\)-oxidation of fat and cause increases in energy expenditure [27, 28, 29]. On the other hand, resistance/strength training leads to increased muscle size, which promotes protein synthesis, and increases in the resting metabolic rate, resulting in weight loss [30,31]. Influencing energy intake and appetite regulation is another mechanism through which acute and chronic exercise partly alters energy balance and body weight [32, 33, 34]. Acute exercise on a treadmill at 60% VO\({}_{\text{2 peak}}\) for 60 min reduces appetite and energy intake in individuals with obesity [35]. Some of these exercise effects cause fluctuations in the concentrations of appetite-regulatory hormones, such as peptide YY (PYY), ghrelin, glucagon-like peptide (GLP), among others [21,36]. Chronic [32,37] and acute [32] exercise changes subjective and homeostatic influences of appetite to cause a sensation of postprandial fullness. Chronic exercise modulates the sensitivity of appetite control by moderating eating or eating behaviors, amending the responses to hunger signals, postprandial satiety signals, and modulating hedonic responses [38, 39, 40].