ALTITUDE AND BETA-BLOCKADE AUGMENT GLUCOSE-UTILIZATION DURING SUBMAXIMAL EXERCISE

To test the hypothesis that altitude exposure increases glucose utiliz ation and that this increment is mediated by a beta-adrenergic mechani sm, the effects of hypobaric hypoxia and beta-blockade on glucose rate s of appearance (Ra) disappearance (Rd), oxidation (Rox), and leg upta ke [G over dot = 2(arteriovenous glucose difference)(1 - leg blood flo w)] were measured during rest and a given submaximal exercise task. We studied six healthy beta-blocked (beta) men [26.7 +/- 1.2 (SE) yr, 74 .0 +/- 6.6 kg] and five matched controls (C; 26 +/- 1.2 yr, 69.3 +/- 2 .6 kg) in energy and nitrogen balance during rest and leg cycle-ergome ter exercise at sea level, on acute altitude exposure to 4,300 m (baro metric pressure = 463 Torr), and after 3 wk of habituation. Subjects r eceived a primed continuous infusion of [6,6-H-2]- and [1-C-13]glucose , rested for greater than or equal to 90 min, and then immediately exe rcised for 45 min at 89 W, which elicited 49% of sea-level peak O-2 co nsumption (V over dot O-2peak; 65% of altitude V over dot O-2peak). At sea level, resting Ra was 1.47 +/- 0.19 and 1.66 +/- 0.16 mg . kg(-1) . min(-1) for C and beta, respectively, and increased to 3.04 +/- 0.25 and 3.56 +/- 0.27 mg . kg(-1). min(-1), respectively, during exercise . Thus glucose Ra was significantly increased by beta-blockade during rest and exercise at sea level. At sea level, beta-blockade increased leg G over dot, which accounted for 49 and 69% of glucose disposal dur ing exercise in C and beta, respectively. On acute altitude exposure, glucose Ra rose significantly during rest and exercise relative to sea level, whereas blockade continued to augment this increment. During e xercise on acute exposure, G over dot increased more than at sea level and accounted for a greater percentage (80 and 97%, respectively) of Rd in C and beta during exercise. Similarly, Rox values, particularly during exercise, were increased significantly at altitude relative to sea level, and beta-blockade potentiated this effect. During a given s ubmaximal exercise task after acclimatization, glucose Ra, Rox, and G over dot were increased relative to sea level, but these increments we re less than those in response to exercise measured on acute exposure. We conclude that altitude exposure increases glucose use during rest and a given submaximal exercise bout and beta-blockade exaggerates the response.