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

We used beta -adrenergic receptor stimulation and blockade as a tool to stu dy substrate metabolism during exercise. Eight moderately trained subjects cycled for 60 min at 45% of (V) over dot o(2peak) 1) during a control trial (CON); 2) while epinephrine was intravenously infused at 0.015 mug . kg(-1 ) . min(-1) (beta -STIM); 3) after ingesting 80 mg of propranolol (beta -BL OCK); and 4) combining beta -BLOCK with intravenous infusion of Intralipid- heparin to restore plasma fatty acid (FFA) levels (beta -BLOCK+LIPID). beta -BLOCK suppressed lipolysis (i.e., glycerol rate of appearance) and fat ox idation while elevating carbohydrate oxidation above CON (135 +/- 11 vs. 11 3 +/- 10 mu mol . kg(-1) . min(-1); P < 0.05) primarily by increasing rate of disappearance (Rd) of glucose (36 +/- 2 vs. 22 +/- 2 <mu>mol . kg(-1) . min(-1); P < 0.05). Plasma FFA restoration (<beta>-BLOCK+LIPID) attenuated the increase in R-d glucose by more than one-half (28 +/- 3 mu mol . 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 ot her hand, <beta>-STIM markedly increased glycogen oxidation and reduced glu cose clearance and fat oxidation despite elevating plasma FFA. Therefore, r educed plasma FFA availability with beta -BLOCK increased R-d glucose, wher eas beta -STIM increased glycogen oxidation, which reduced fat oxidation an d glucose clearance. In summary, compared with control exercise at 45% (V) over dot o(2 peak) (CON), both beta -BLOCK and beta -STIM reduced fat and i ncreased carbohydrate oxidation, albeit through different mechanisms.