COUPLING OF EXTERNAL TO CELLULAR RESPIRATION

这项研究的重点是外部与细胞的耦合 运动时的呼吸。 进行锻炼的能力取决于 心肺系统的动态反应。 这些支持 肌肉细胞正常利用氧气，消除二氧化碳和 还有酸碱调节。 现在测量技术的最新进展 可以检查肺泡 O2 的动态细节， 运动时的二氧化碳运输。 从概念上讲，气体交换动力学由三个功能组成部分组成 对运动的反应：心动力阶段（第一个 25 秒，第一阶段）， 增加静脉血中 O2 提取量和 CO2 负荷的时期 （15 秒至约 3-4 分钟，第二阶段），以及超过 3-4 分钟的时间 气体交换达到低于乳酸阈值的稳态，但是 继续升至阈值以上（第三阶段）。 本项目将检验三个主要假设：1) 肺泡 O2 运输动力学可用于表征心血管状态 运动期间的功能，2) 繁重工作期间的 O2 消耗有一个 似乎与乳酸代谢机制有关的成分 这会导致运动的 O2 成本增加，3）CO2 输出 动力学可用于测量运动肌肉呼吸商和 代谢（乳酸）酸的碳酸氢盐缓冲速率。 对于第一个假设，我们将研究正常受试者或患有以下疾病的患者 特定的生理缺陷会干扰正常的 外部呼吸与细胞呼吸的耦合。 测试第二个 假设，我们将探索调节 III 期 VO2 的因素 繁重的工作。 检查第三个假设，测量乳酸 HCO3 正常受试者的二氧化碳交换动态将作为基础 二氧化碳排放量（高于和低于）的决定因素的模型分析 乳酸阈值。 这些研究利用了生理学家的技能， 医生、计算机科学家和工程师。 O2 吸收和 CO2 输出随时间的变化 运动是特定心血管和代谢的表现 机制。 因此，反应模式的异常提供了 有关功能障碍部位的重要信息。 了解这些机制可能会为更多的研究提供基础。 运动患者的合理诊断和治疗方法 限制。

This research has as its focus the coupling of external to cellular respiration during exercise. The ability to perform exercise depends on the dynamic responses of the cardiorespiratory system. These support normal oxygen utilization by the muscle cells, elimination of its CO2 and also acid-base regulation. Recent advances in measurement technology now makes it possible to examine the details of the dynamics of alveolar O2 and CO2 transport in response to exercise. Conceptually there are three functional components of gas exchange dynamics in response to exercise: the cardiodynamic phase (first 25 sec, phase I), the period of increasing O2 extraction and CO2 loading into venous blood (15 sec to approx 3-4 min, phase II), and the period beyond 3-4 min where gas exchange achieves a steady-state below the lactate threshold, but continues to rise above the threshold (phase III). Three major hypotheses will be examined in this project: 1) Alveolar O2 transport dynamics can be used to characterize the state of cardiovascular function during exercise, 2) O2 consumption during heavy work has a component which seems to be linked to mechanisms of lactate metabolism and which causes the O2 cost of the exercise to increase, 3) CO2 output kinetics can be used to measure exercising muscle respiratory quotient and the rate of bicarbonate buffering of metabolic (lactic) acid. For the first hypothesis, we will study normal subjects or patients with particular physiological defects which should interfere with the normal coupling of external to cellular respiration. To test the second hypothesis, we will explore factors which modulate the phase III VO2 during heavy work. To examine the third hypothesis, measurement of lactate, HCO3 and CO2 exchange dynamics in normal subjects will be used as the basis of model analysis of the determinants of CO2 output, both above and below the lactate threshold. These studies utilize the skills of physiologists, physicians, computer scientists and engineers. The time-related changes in O2 uptake and CO2 output in response to exercise are manifestations of specific cardiovascular and metabolic mechanisms. Abnormalities of the response patterns therefore provide important information regarding the site(s) of functional impairment. Understanding these mechanisms is likely to provide the basis for a more rational approach to diagnosis and treatment of patients with exercise limitation.