Blocking Peripheral Beta‐Adrenergic Receptors Reduces Induction of Skeletal Muscle Thermogenesis

Obesity is a worldwide trend that is cause for concern due to its detrimental effects on numerous health factors and increased risk of mortality. The propensity for obesity, although influenced by diet, is also worsened by sedentary lifestyle. Indeed, individuals' daily activity levels and activity energy expenditure predict weight gain and obesity. Increased energy expenditure, whether deliberate or spontaneous, is associated with leanness and reduced risk for obesity. With respect to increasing energy expenditure through thermogenesis, previous investigation has focused largely on browning of white adipose and brown adipose tissue thermogenesis, with much less attention paid to mechanisms mediating thermogenesis in skeletal muscle. Here, we investigated the effects of contextually induced muscle thermogenesis in rats through exposure to predator odor in rats. We hypothesize that thermogenesis in skeletal muscle is mediated by the sympathetic nervous system (SNS), specifically through activation of muscle β‐adrenergic receptors. To test this, we examined the effects of nadolol, a peripherally acting β‐adrenergic antagonist, on predator odor‐induced thermogenesis. IPTT‐300 transponders from Bio Medic Data Systems were surgically implanted in the left and right gastrocnemius muscles of male rats (N=13). Rats were exposed to each of four conditions (2×2): nadolol or saline vehicle, each with and without predator odor (1.5″×2″ towel with ferret odor) or control stimulus; muscle temperatures were measured over 120 minutes. Predator odor significantly induced muscle thermogenesis in vehicle‐treated animals. The mixed β‐adrenergic antagonist nadolol significantly reduced predator odor‐induced thermogenesis. This demonstrates that predator odor‐induced skeletal muscle thermogenesis is mediated, at least in part, by β‐adrenergic receptor activation, likely stemming from sympathetic nerve activation. Our previous work has demonstrated that this thermogenic induction is accompanied by enhanced energy expenditure. With the focus on muscle, rather than adipose thermogenesis, we establish a pathway that expands the understanding of energy balance, its mechanisms, and possible treatments. Going forward, induction of muscle thermogenesis may be applied to the treatment of obesity. Support or Funding Information NIH NIDDK R15‐DK‐097644 and R15‐DK‐108668 to CMN This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .