The impact of catecholamines on skeletal muscle following massive burns: Friend or foe?

• Published in: Burns 2021-06, Vol.47 (4), p.756-764
• Main Authors: Blears, Elizabeth, Ross, Evan, Ogunbileje, John O., Porter, Craig, Murton, Andrew J.
• Format: Article
• Language: English
• Subjects: Beta-adrenergic signaling; Burns; Hypermetabolism; Lipolysis; Muscle cachexia; Muscle protein turnover
• ISSN: 0305-4179; 1879-1409
• DOI: 10.1016/j.burns.2021.01.009

•Burns-induced catecholamine surge contributes to hypermetabolism and muscle cachexia.•β-Blockade appears beneficial at reducing hypermetabolism and muscle catabolism.•In contrast, in healthy individuals, β2-agonists induce muscle hypertrophy.•Benefits of β-blockade on muscle protein turnover appear due to preventing lipolysis.•Use of β1-antagonists while inhibiting lipolysis may aid muscle recovery after burns. Profound skeletal muscle wasting in the setting of total body hypermetabolism is a defining characteristic of massive burns, compromising the patient’s recovery and necessitating a protracted period of rehabilitation. In recent years, the prolonged use of the non-selective beta-blocker, propranolol, has gained prominence as an effective tool to assist with suppressing epinephrine-dependent burn-induced hypermetabolism and by extension, blunting muscle catabolism. However, synthetic β-adrenergic agonists, such as clenbuterol, are widely associated with the promotion of muscle growth in both animals and humans. Moreover, experimental adrenodemedullation is known to result in muscle catabolism. Therefore, the blunting of muscle β-adrenergic signaling via the use of propranolol would be expected to negatively impair muscle protein homeostasis. This review explores these paradoxical observations and identifies the manner by which propranolol is thought to exert its anti-catabolic effects in burn patients. Moreover, we identify potential avenues by which the use of beta-blocker therapy in the treatment of massive burns could potentially be further refined to promote the recovery of muscle mass in these critically ill patients while continuing to ameliorate total body hypermetabolism.