ROLE OF 02 TRANSPORT IN DETERMINING V02 MAX OF MUSCLE

这个项目解决了这样一个普遍的问题，即 身体运动，最大摄氧量(V02max)确实代表着 工作肌肉中氧气利用率的特定限制或 是否有其他因素介入。这个问题产生于 观察显示，整个身体的最大摄氧量在 高氧运动和红细胞浓度升高以及 由于轻度缺氧而减少，同时努力表现出平行的 工作肌肉最大摄氧量的变化未能显示出 预期的反应。然而，这些测量很难 制作完整的运动动物，并利用肌肉进行研究 隔离循环的原位没有达到最高的VO2 肌肉可以伸展到。这个项目将使用腓肠肌- 麻醉犬和猫的足底肌伴循环 就地隔离。将使用两种强直性收缩模式：1)a 25分钟进步式VO2max，进步式的典范 练习，以及2)4分钟的重复形式，一个4分钟的模型 分钟最大试验。氧气的每个变量提供给 肌肉、O2张力(PaO2)、O2含量(CaO2)和血流量(Q) 将通过1)增加或减少O2的分数来改变 吸入气体高于和低于室内空气的数值(在海平面上)；2) 输注包装红细胞或葡聚糖改变红细胞质量 用于血液交换和3)改变血流。具体目标是1) 以确定进展期肌肉的最大摄氧量 全身高氧和低氧改变收缩；2) 以确定重复收缩中的肌肉V02max是否 由全身高氧和缺氧引起的变化；3)确定 两种收缩类型的肌肉的V02max是否为 由少量气体引起的局部高氧和低氧改变 肌肉动脉供血中的交换器；4)观察 P02静脉血对肌肉的再灌流作用 恢复到常氧水平改变V02；5)以确定 猫的肌肉中含有不同类型的纤维成分 与狗的主要测试肌肉相同；6)确定 线粒体细胞色素氧化酶氧饱和度的变化 高氧和低氧条件下的收缩。在……里面 除VO2外，还包括二氧化碳输出(VCO2)、乳酸输出(L)、肌肉 (乳酸)/(丙酮酸)和血浆肾上腺素和去甲肾上腺素 将会被测量。结果将显示1)全身是否 局部高氧和低氧会产生相同的变化 VO2max和是否涉及循环因素；2)是否 疲劳是较长收缩形式的一个因素；3)是否 不同纤维类型的肌肉反应相似；4)是否 代谢产物洗脱是一个因素，当细胞色素氧化酶 会显著降低饱和度。这最后一个是至关重要的 测定比氧存在时的测量 VO2的局限性。

This project addresses the general question of whether, in whole body exercise, maximal O2 uptake (V02max) really represents a specific limitation of O2 availability in the working muscle or whether some other factor intervenes. This question arises from observations that show whole body VO2max is elevated during exercise by hyperoxia and increased red cell concentration and decreased by modest hypoxia, while efforts to show parallel changes in working muscle VO2max have failed to show the expected response. However, these measurements are difficult to make in intact exercising animals, and studies using muscles in situ with isolated circulation have not achieved the highest VO2 the muscles can reach. This project will use the gastrocnemius- plantaris muscles of anesthetized dogs and cats with circulations isolated in situ. Two tetanic contraction modes will be used: 1) a 25 minute progessive format to VO2max, a model of progressive exercise, and 2) a 4 minute repetitive format, a model of a 4 minute maximal test. Each of the variables of O2 supply to the muscles, O2 tension (PaO2), O2 content (CaO2) and blood flow (Q) will be varied by 1) increasing or deceasing the fractions of O2 in inspired gas to values above and below room air (at sea level); 2) changing red cell mass by transfusing packed red cells or dextran for blood exchange and 3) changing flow. The specific aims are 1) to ascertain whether muscle VO2max in the progressive contractions is changed by whole body hyperoxia and hypoxia; 2) to determine if muscle V02max in the repetitive contractions is changed by whole body hyperoxia adn hypoxia; 3) to ascertain whether V02max of the muscles in both contraction types is changed by local hyperoxia and hypoxia produced by a small gas exchanger in the arterial supply of the muscles; 4) to see whether reperfusion of the muscle with its own venous blood with P02 restored to normoxic levels changes V02; 5) to establish whether muscles of the cat with a different fiber type composition respond the same as the main test muscle of the dog; and 6) to determine the O2 saturation of mitochondial cytochrome oxidase during contractions under the hyperoxic and hypoxic conditions. In addition to V02, CO2 output (Vco2), lactate output (L), muscle (lactate)/(pyruvate) and plasma epinephrine and norepinephrine will be measured. The results will show 1) whether whole body and local hyperoxia and hypoxia produce the same changes in Vo2max and whether a circulating factor is involved; 2) whether fatigue is a factor in the longer contraction format; 3) whether muscles of differing fiber types respond similarily; 4) whether metabolite washout is a factor and 5) when cytochrome oxidase becomes significantly desaturated. This last is the crucial measurement in determining the presence of specific O2 limitation of Vo2.