Effects of β-adrenergic receptor stimulation and blockade on substrate metabolism during submaximal exercise

Abstract

We used β-adrenergic receptor stimulation and blockade as a tool to study substrate metabolism during exercise. Eight moderately trained subjects cycled for 60 min at 45% of V˙o 2 peak 1) during a control trial (CON); 2) while epinephrine was intravenously infused at 0.015 μg · kg−1 · min−1(β-STIM); 3) after ingesting 80 mg of propranolol (β-BLOCK); and 4) combining β-BLOCK with intravenous infusion of Intralipid-heparin to restore plasma fatty acid (FFA) levels (β-BLOCK+LIPID). β-BLOCK suppressed lipolysis (i.e., glycerol rate of appearance) and fat oxidation while elevating carbohydrate oxidation above CON (135 ± 11 vs. 113 ± 10 μmol · kg−1 · min−1; P < 0.05) primarily by increasing rate of disappearance (Rd) of glucose (36 ± 2 vs. 22 ± 2 μmol · kg−1 · min−1; P < 0.05). Plasma FFA restoration (β-BLOCK+LIPID) attenuated the increase in Rd glucose by more than one-half (28 ± 3 μmol · kg−1 · min−1; P < 0.05), suggesting that part of the compensatory increase in muscle glucose uptake is due to reduced energy from fatty acids. On the other hand, β-STIM markedly increased glycogen oxidation and reduced glucose clearance and fat oxidation despite elevating plasma FFA. Therefore, reduced plasma FFA availability with β-BLOCK increased Rd glucose, whereas β-STIM increased glycogen oxidation, which reduced fat oxidation and glucose clearance. In summary, compared with control exercise at 45%V˙o 2 peak (CON), both β-BLOCK and β-STIM reduced fat and increased carbohydrate oxidation, albeit through different mechanisms.