A significant proportion of the mortality and morbidity of severe burns is attributable to the ensuing hypermetabolic response that typically lasts for at least 9-12 months post-injury. This is associated with impaired wound healing, increased infection risks, erosion of lean body mass, hampered rehabilitation and delayed reintegration of burn survivors into society. The endocrine status is markedly altered during this period with an initial and then sustained increase in proinflammatory 'stress' hormones such as cortisol and other glucocorticoids, and catecholamines including epinephrine and norepinephrine by the adrenal medulla and cortex. These hormones exert catabolic effects leading to muscle wasting, the intensity of which depends upon the percentage of total body surface area (TBSA) involved, as well as the time elapsed since initial injury. Pharmacological and non-pharmacological strategies may be used to reverse the catabolic effect of thermal injury. Of these, β-adrenergic blockade with propranolol has been the most efficacious anti-catabolic therapy in the treatment of burns. The underlying mechanism of action of propranolol is still unclear, however its effect appears to occur due to an increased protein synthesis in the face of a persistent protein breakdown and reduced peripheral lipolysis. This article aims to review the current understanding of catecholamines in postburn muscle wasting and focuses on the clinical and metabolic effects of β-blockade in severe burns.