Brooks G A, Wolfel E E, Groves B M, Bender P R, Butterfield G E, Cymerman A, Mazzeo R S, Sutton J R, Wolfe R R, Reeves J T
University of Colorado, Denver 80262.
J Appl Physiol (1985). 1992 Jun;72(6):2435-45. doi: 10.1152/jappl.1992.72.6.2435.
We hypothesized that the increased blood glucose disappearance (Rd) observed during exercise and after acclimatization to high altitude (4,300 m) could be attributed to net glucose uptake (G) by the legs and that the increased arterial lactate concentration and rate of appearance (Ra) on arrival at altitude and subsequent decrease with acclimatization were caused by changes in net muscle lactate release (L). To evaluate these hypotheses, seven healthy males [23 +/- 2 (SE) yr, 72.2 +/- 1.6 kg], on a controlled diet were studied in the postabsorptive condition at sea level, on acute exposure to 4,300 m, and after 3 wk of acclimatization to 4,300 m. Subjects received a primed-continuous infusion of [6,6-D2]glucose (Brooks et al., J. Appl. Physiol. 70: 919-927, 1991) and [3-13C]lactate (Brooks et al., J. Appl. Physiol. 71:333-341, 1991) and rested for a minimum of 90 min, followed immediately by 45 min of exercise at 101 +/- 3 W, which elicited 51.1 +/- 1% of the sea level peak O2 uptake (65 +/- 2% of both acute altitude and acclimatization peak O2 uptake). Glucose and lactate arteriovenous differences across the legs and arms and leg blood flow were measured. Leg G increased during exercise compared with rest, at altitude compared with sea level, and after acclimatization. Leg G accounted for 27-36% of Rd at rest and essentially all glucose Rd during exercise. A shunting of the blood glucose flux to active muscle during exercise at altitude is indicated. With acute altitude exposure, at 5 min of exercise L was elevated compared with sea level or after acclimatization, but from 15 to 45 min of exercise the pattern and magnitude of L from the legs varied and followed neither the pattern nor the magnitude of responses in arterial lactate concentration or Ra. Leg L accounted for 6-65% of lactate Ra at rest and 17-63% during exercise, but the percent Ra from L was not affected by altitude. Tracer-measured lactate extraction by legs accounted for 10-25% of lactate Rd at rest and 31-83% during exercise. Arms released lactate under all conditions except during exercise with acute exposure to high altitude, when the arms consumed lactate. Both active and inactive muscle beds demonstrated simultaneous lactate extraction and release. We conclude that active skeletal muscle is the predominant site of glucose disposal during exercise and at high altitude but not the sole source of blood lactate during exercise at sea level or high altitude.
我们假设，运动期间以及适应高海拔（4300米）后观察到的血糖消失率（Rd）增加可能归因于腿部的葡萄糖净摄取量（G），并且到达高原时动脉乳酸浓度和乳酸生成率（Ra）增加以及随后适应过程中的降低是由肌肉乳酸净释放量（L）的变化引起的。为了评估这些假设，对7名健康男性[23±2（标准误）岁，72.2±1.6千克]进行了研究，他们采用控制饮食，在空腹状态下于海平面、急性暴露于4300米高度以及适应4300米高度3周后进行了测试。受试者接受了[6,6-D2]葡萄糖（布鲁克斯等人，《应用生理学杂志》70: 919 - 927, 1991）和[3-13C]乳酸（布鲁克斯等人，《应用生理学杂志》71: 333 - 341, 1991）的一次性连续输注，并至少休息90分钟，随后立即进行45分钟功率为101±3瓦的运动，该运动引发的摄氧量为海平面峰值摄氧量的51.1±1%（急性高原和适应高原后的峰值摄氧量均为65±2%）。测量了腿部和手臂的葡萄糖和乳酸动静脉差值以及腿部血流量。与休息时相比，运动期间、高原时与海平面相比以及适应后腿部的G均增加。腿部的G在休息时占Rd的27 - 36%，在运动期间基本上占所有葡萄糖Rd。这表明在高原运动期间血糖通量向活跃肌肉发生了分流。急性暴露于高原时，运动5分钟时腿部的L与海平面或适应后相比升高，但在运动15至45分钟期间，腿部L的模式和幅度有所变化，既不跟随动脉乳酸浓度或Ra的模式，也不跟随其幅度。腿部的L在休息时占乳酸Ra的6 - 65%，在运动期间占17 - 63%，但来自L的Ra百分比不受海拔影响。示踪剂测量的腿部乳酸摄取量在休息时占乳酸Rd的10 - 25%，在运动期间占31 - 83%。除急性暴露于高原运动期间手臂消耗乳酸外，在所有其他条件下手臂均释放乳酸。活跃和不活跃的肌肉床均表现出同时摄取和释放乳酸。我们得出结论：活跃的骨骼肌是运动期间和高原时葡萄糖处置的主要部位，但不是海平面或高原运动期间血液乳酸的唯一来源。
