Roberts A C, Reeves J T, Butterfield G E, Mazzeo R S, Sutton J R, Wolfel E E, Brooks G A
University of California, Berkeley 94720, USA.
J Appl Physiol (1985). 1996 Feb;80(2):605-15. doi: 10.1152/jappl.1996.80.2.605.
To test the hypothesis that altitude exposure increases glucose utilization and that this increment is mediated by a beta-adrenergic mechanism, the effects of hypobaric hypoxia and beta-blockade on glucose rates of appearance (Ra), disappearance (Rd), oxidation (Rox), and leg uptake [G = 2(arteriovenous glucose difference)(1 - leg blood flow)] 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-ergometer exercise at sea level, on acute altitude exposure to 4,300 m (barometric pressure = 463 Torr), and after 3 wk of habituation. Subjects received a primed continuous infusion of [6,6-2H]- and [1-13C]glucose, rested for > or = 90 min, and then immediately exercised for 45 min at 89 W, which elicited 49% of sea-level peak O2 consumption (VO2peak; 65% of altitude VO2peak). At sea level, resting Ra was 1.47 +/- 0.19 and 1.66 +/- 0.16 mg x kg-1 x min-1 for C and beta, respectively, and increased to 3.04 +/- 0.25 and 3.56 +/- 0.27 mg x kg-1 x 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, which accounted for 49 and 69% of glucose disposal during 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 exercise on acute exposure, G 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 submaximal exercise task after acclimatization, glucose Ra, Rox, and G were increased relative to sea level, but these increments were 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.
为了验证海拔暴露会增加葡萄糖利用率且这种增加是由β-肾上腺素能机制介导的这一假设，我们测量了在休息和给定的次最大运动任务期间，低压缺氧和β-受体阻滞剂对葡萄糖的出现率（Ra）、消失率（Rd）、氧化率（Rox）以及腿部摄取量[G = 2（动静脉葡萄糖差值）（1 - 腿部血流量）]的影响。我们研究了6名健康的服用β-受体阻滞剂（β）的男性[26.7±1.2（标准误）岁，74.0±6.6千克]和5名匹配的对照组（C；26±1.2岁，69.3±2.6千克），他们在海平面休息和进行腿部蹬车运动时、急性暴露于4300米海拔（气压 = 463托）时以及适应3周后处于能量和氮平衡状态。受试者接受[6,6-2H]-和[1-13C]葡萄糖的首剂持续输注，休息≥90分钟，然后立即以89瓦的功率运动45分钟，这引发了海平面峰值耗氧量（VO2peak）的49%（海拔VO2peak的65%）。在海平面时，C组和β组休息时的Ra分别为1.47±0.19和1.66±0.16毫克·千克-1·分钟-1，运动时分别增加到3.04±0.25和3.56±0.27毫克·千克-1·分钟-1。因此，在海平面休息和运动期间，β-受体阻滞剂显著增加了葡萄糖的Ra。在海平面时，β-受体阻滞剂增加了腿部的G，在C组和β组运动期间，G分别占葡萄糖处置量的49%和69%。急性暴露于海拔时，相对于海平面，休息和运动期间葡萄糖的Ra显著升高，而阻滞剂继续增强这种升高。在急性暴露运动期间，G的增加幅度大于海平面时，且在C组和β组运动期间分别占Rd的更大比例（分别为80%和97%）。同样，Rox值，尤其是在运动期间，相对于海平面在海拔时显著增加，β-受体阻滞剂增强了这种效应。在适应后进行给定的次最大运动任务期间，葡萄糖的Ra、Rox和G相对于海平面增加，但这些增加幅度小于急性暴露时运动测量的增加幅度。我们得出结论，海拔暴露会增加休息和给定次最大运动期间的葡萄糖利用，且β-受体阻滞剂会夸大这种反应。
