ROLE OF 02 TRANSPORT IN DETERMINING V02 MAX OF MUSCLE

这个项目涉及的一般问题是， 最大摄氧量（V02 max）实际上代表了 工作肌肉中O2可用性的特定限制，或 是否有其他因素介入。 这个问题源于 观察结果显示，全身VO 2 max在 高氧运动和增加红细胞浓度， 减少适度缺氧，而努力显示平行 工作肌最大摄氧量的变化未能显示 期待的回应。 然而，这些测量很难 在完整的运动动物中， 采用隔离循环的原位没有达到最高的VO 2 肌肉可以到达。 这个项目将使用腓肠肌- 麻醉犬和猫的跖肌，循环 在原地隔离。 将使用两种强直收缩模式：1）a 25分钟渐进式格式至VO 2 max，渐进模式 练习，和2）4分钟的重复格式，一个模型的4 分钟最大测试。 每个变量的O2供应到 肌肉、氧张力（PaO 2）、氧含量（CaO 2）和血流量（Q） 将通过1）增加或减少O2在 吸入气体的值高于和低于室内空气（海平面）; 2） 通过使用浓缩红细胞或葡聚糖进行置换来改变红细胞质量 用于血液交换和3）改变流量。 具体目标是：（1） 以确定是否肌肉VO 2 max在进行性 全身高氧和缺氧改变收缩; 2） 以确定重复收缩中的肌肉V02 max是否 全身高氧和缺氧的变化; 3）确定 两种收缩类型中肌肉的V02 max是否 改变由局部高氧和缺氧产生的小气体 交换器在肌肉的动脉供应; 4）看看是否 用其自身静脉血用P02再灌注肌肉 恢复到含氧量正常的水平改变V02; 5）确定是否 具有不同纤维类型组成的猫的肌肉响应 与狗的主要测试肌肉相同;以及6）确定 线粒体细胞色素氧化酶氧饱和度 收缩在高氧和缺氧条件下。 在 除了V02，CO2输出（Vco 2），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 将被衡量。 结果将显示1）是否整个身体 局部高氧和缺氧产生相同的变化， Vo 2 max和是否涉及循环因素; 2）是否 疲劳是较长收缩格式的一个因素; 3）是否 不同纤维类型的肌肉反应相似; 4）是否 代谢物洗脱是一个因素，5）当细胞色素氧化酶 变得明显不饱和。 这最后一点至关重要 确定特定O2存在的测量 限制Vo 2。

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.