Pharmacological activation of β2-AR receptors leads to increased mitochondrial function and ATP production in C2C12 myotubes. Experimental design for pharmacological treatments in C2C12 myotubes (a), basal mitochondrial OCR (oxygen consumption ratio) (b), maximal mitochondrial OCR induced by FCCP (c), ATP-independent OCR measured in the presence of oligomycin (d), and ATP production (e) in C2C12 myotubes acutely exposed to the non-selective β-AR agonist isoproterenol (ISO—1 µM for 30 min), with or without β2-AR receptor blockade with ICI 118,551 (300 nM, 30 min prior to ISO treatment). ATP production (f) in C2C12 myotubes acutely exposed to the selective β2-AR agonist formoterol (10 µM for 30 min). Data are presented as mean ± SE. * p < 0.05 vs. control and ** p < 0.05 vs. ISO. n = 8/group.