LACTATE AND GLUCOSE EXCHANGE ACROSS THE FOREARM, LEGS, AND SPLANCHNIC BED DURING AND AFTER PROLONGED LEG EXERCISE
LACTATE AND GLUCOSE EXCHANGE ACROSS THE FOREARM, LEGS, AND SPLANCHNIC BED DURING AND AFTER PROLONGED LEG EXERCISE
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DOI：
10.1172/jci110440
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发表时间：
1982-01-01
影响因子：
15.9
通讯作者：
FELIG, P
中科院分区：
文献类型：
--
作者：
AHLBORG, G;FELIG, P
对健康受试者在腿部运动(自行车测功机)3-3.5h、最大摄氧量58%和运动后40min恢复期内，测定腿部和内脏床上葡萄糖和乳酸的净交换以及前臂这些底物的动脉-深静脉(A-DV)差。腿部葡萄糖摄取量在运动期间增加了16倍，在整个运动期间超过了内脏葡萄糖输出。后者在90min达到峰值(3.5倍基础值)，3h下降60%。结果，血糖下降40%，3.5h时50%的受试者达到明显的低血糖(血糖45 mg/dl)。内脏乳酸摄取量在运动中逐渐增加，3h时达到基础值的4倍，同时动脉血乳酸升高至1.5 mM。超过90分钟的运动后，腿部的乳酸没有显著的净产出。在整个运动过程中，前臂的A-DV乳酸差值逐渐变得更负，在3.5h时达到基础水平的3倍。运动过程中动脉乳酸的增加与血浆肾上腺素的增加成正比，肾上腺素的增加是基础水平的9倍。在恢复期间，内脏乳酸摄取量进一步上升到基础速率的6倍，而腿部的乳酸产量并不比基础状态下大。前臂A-DV乳酸差值甚至比运动时更负，达到基础值的4倍。在运动和恢复过程中，前臂对血糖的摄取占前臂乳酸释放的比例不超过25%-67%。恢复期间的腿部葡萄糖摄取量比基础状态高3-5倍，因为血浆胰岛素浓度比基础状态低60%，并与0.7的呼吸交换比率相关。在最大摄氧量为58%的长时间腿部运动中，内脏葡萄糖产生和腿部葡萄糖利用之间的失衡导致血糖下降，可能会达到健康受试者的低血糖水平。内脏床对乳酸的摄取显著增加，这不能归因于运动腿乳酸产量的增加。乳酸是由前臂肌肉释放的，与其他相对不活跃的肌肉一起，可能是长时间腿部运动期间和之后乳酸周转增加的重要来源。前臂的A-DV乳酸差值越来越负，不能用血糖的摄取来解释，这表明在腿部运动过程中和之后，前臂肌肉中的糖原分解。在恢复期间，腿部葡萄糖摄取量的增加与低胰岛素血症有关，这表明胰岛素敏感性的增加，使得以前锻炼肌肉时在没有食物摄入的情况下糖原得以补充。恢复期间前臂乳酸产量增加和腿部葡萄糖摄取增加的证据增加了这样一种可能性，即腿部运动后，相对不活跃的肌肉(例如前臂的肌肉)中的糖原储存减少，而先前锻炼的腿部肌肉中的糖原储存增加。
The net exchange of glucose and lactate across the leg and the splanchnic bed and the arterial-deep venous (A-DV) differences for these substrates in the forearm were determined in healthy [human] subjects during 3-3.5 h of leg exercise (bicycle ergometer) at 58% maximum O2 uptake and during a 40-min postexercise recovery period. Leg glucose uptake rose 16-fold during exercise and throughout the exercise period exceeded splanchnic glucose output. The latter reached a peak increment (3.5 times basal) at 90 min and fell by 60% during the 3rd h. As a result, blood glucose declined 40%, reaching frank hypoglycemia (blood glucose, < 45 mg/dl) in 50% of subjects at 3.5 h. Splanchnic lactate uptake rose progressively during exercise to values 4 times the basal rate at 3 h in association with a rise in arterial lactate to 1.5 mM. There was no significant net output of lactate from the legs beyond 90 min of exercise. The A-DV lactate difference in the forearm became progressively more negative throughout exercise, reaching values 3 times the basal level at 3.5 h. The rise in arterial lactate during exercise was proportional to the elevation in plasma epinephrine, which rose 9-fold. During recovery, splanchnic lactate uptake rose further to values 6 times the basal rate, whereas lactate output by the legs was no greater than in the basal state. The A-DV lactate difference in the forearm became even more negative than during exercise, reaching values 4 times basal. During exercise as well as recovery, forearm uptake of blood glucose could account for no more than 25-67% of forearm lactate release. Leg glucose uptake during recovery ws 3- to 5-fold higher than in the basal state in the face of plasma insulin concentrations that were 60% below basal and in association with a respiratory exchange ratio of 0.7. During prolonged leg exercise at 58% maximum O2 uptake an imbalance between splanchnic glucose production and leg glucose utilization results in a fall in blood glucose that may reach hypoglycemic levels in healthy subjects. There is a marked increase in the uptake of lactate by the splanchnic bed that cannot be attributed to increased output of lactate from the exercising legs. Lactate is released by forearm muscle and, together with other relatively inactive muscle, may be an important source of the increased lactate turnover during and after prolonged leg exercise. The increasingly negative A-DV lactate difference in the forearm cannot be accounted for by uptake of blood glucose, suggesting the breakdown of glycogen in forearm muscle during and after leg exercise. Increased glucose uptake by the legs in association with hypoinsulinemia during recovery suggests an increase in insulin sensitivity that permits glycogen repletion in previously exercising muscle in the absence of food ingestion. The evidence for increased lactate output in the forearm and augmented glucose uptake in the legs during recovery raises the possibility that after leg exercise glycogen stores decrease in muscle that was relatively inactive (e.g., that of the forearm) while they increase in the previously exercising leg muscles.