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Homeothermic mammals including humans produce heat (also termed thermogenesis) inside their body to maintain constant body temperature. It has been shown that thermogenesis is elevated by several external factors; prominent being cold, diet, and physical exercise. This modulation ability is termed as “Adaptive Thermogenesis (AT).” Intake of high calorie diet was also shown to increase thermogenesis in laboratory animals, a phenomenon termed as diet-induced thermogenesis (DIT) (1). Research on finding out the mechanisms of DIT intensified in the recent years, as obesity and associated metabolic disorder increased rapidly all over the world. It is hoped that mechanisms of AT can be targeted to increase energy expenditure and provide protection against metabolic diseases including obesity. Brown adipose tissue (BAT) and skeletal muscle have emerged as the two major sites of AT. Major heat producer in BAT is a protein called uncoupling protein (UCP) 1 that dissipates proton gradient in mitochondria and thereby resulting in heat production (2). Few additional thermogenic mechanisms have also been reported in BAT such as futile TG lipolysis/esterification, creatine/phosphocreatine cycling, and ATP-dependent Ca2+-cycling (3–5). The understanding of mechanisms of AT in the skeletal muscle has been slow and forms the major focus of this review.

Non and Epigenetic Mechanisms in Regulation of Adaptive Thermogenesis in Skeletal Muscle