ABSTRACT
Introduction: Fat-free mass, of which skeletal muscle is amajor component, correlates positively with energy intake at energy balance. This is due to the effects of metabolically active tissue on energy expenditure which in itself appears to signal to the brain adrive to eat to ensure cellular energy homeostasis. The mechanisms responsible for this drive to eat are unknown but are likely to be related to energy utilization. Here muscle imparts an indirect influence on hunger. The drive to eat is also enhanced after muscle loss secondary to intentional weight loss. The evidence suggests loss of both fat mass and skeletal muscle mass directly influences the trajectory and magnitude of weight regain highlighting their potential role in long-termappetite control. The mechanisms responsible for the potential direct drive to eat stemming from muscle loss are unknown. Areas covered: The literature pertaining to muscle and appetite at energy balance and after weight loss was examined. Aliterature search was conducted to identify studies related to appetite, muscle, exercise, and weight loss. Expert opinion: Understanding the mechanisms which link energy expenditure and muscle loss to hunger has the potential to positively impact both the prevention and the treatment of obesity.
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Article highlights
The relationship between muscle and appetite is an unexplored area
The association between muscle and food intake at energy balance is likely due to energy expenditure as opposed to a muscle-specific signal
The potential association between muscle loss secondary to weight loss and hunger may be due to a specific signal upregulated by the muscle itself
An understanding of how muscle potentially talks to the brain to influence appetite may significantly impact both the prevention and treatment of obesity
Research is needed to understand how muscle and other organs which are reduced in mass with weight loss may increase hunger
Declaration of interest
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.