Heat stress (HS) is a major obstacle to poultry production. In the US alone, annual loss due to HS is estimated to be about $ 2.3 billion. Broilers raised under HS conditions reduce their feed intake, resulting in low energy levels and nutrients including glucose. The mechanistic target of rapamycin (mTOR) acts as an energy sensor, therefore, the putative reduction in energy generation by chickens reared under HS deactivates mTOR and its downstream effects. The primary objective of this study was to examine the effects of glucose supplementation on mRNA expression of genes associated with protein biosynthesis and apoptosis in the pectoralis major of chickens that were raised either in a thermoneutral (TN) or HS environment. Dysregulation of the mTOR signaling pathway alters protein biosynthesis and apoptosis in HS birds. Moderating the levels of glucose could restore regular mTOR signaling and improve protein biosynthesis while inhibiting catabolic activities and apoptosis.