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. 2021 Jan 13;10(1):146. doi: 10.3390/cells10010146

Figure 4.

Figure 4

Pharmacological activation of β2-AR receptors leads to increased mitochondrial respiration in skeletal muscle. Experimental design for pharmacological treatments in mice (a), basal mitochondrial OCR (oxygen consumption ratio) (b), maximal mitochondrial OCR induced by ADP (c), ATP-independent OCR measured in the presence of oligomycin (d), and the respiratory control ratio (e) in permeabilized fiber bundles of tibialis anterior muscle isolated from mice treated with the non-selective β-AR agonist isoproterenol (ISO—single dose—10 mg/kg, i.p. 30 min), with or without β2-AR receptor blockade with ICI 118,551 (single dose—10 mg/kg, i.p., 30 min prior to ISO treatment). Basal mitochondrial OCR (f), maximal mitochondrial OCR induced by ADP (g), ATP-independent OCR measured in the presence of oligomycin (h), and the respiratory control ratio (i) in permeabilized fiber bundles of tibialis anterior muscle isolated from mice treated with the selective β2-AR agonist formoterol (FOR-single dose—10 µg/kg, i.p., 30 min). Data are presented as mean ± SE. * p < 0.05 vs. control and ** p < 0.05 vs. ISO. n = 5/group.