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 心脏呼吸系统的动态反应。这些支持 肌肉细胞的正常氧气利用，其二氧化碳的排出和 还有酸碱调节。当前测量技术的最新进展 使得研究肺泡氧气动力学的细节成为可能 运动对二氧化碳运输的响应。 从概念上讲，气体交换动力学有三个功能组件 对运动的反应：心脏动力学阶段(前25秒，阶段I)， 静脉血氧摄取和二氧化碳负荷增加的时期 (15秒到大约3-4分钟，第二阶段)，以及超过3-4分钟的时间，其中 气体交换在乳酸阈值以下达到稳定状态，但 继续上升到门槛以上(第三阶段)。 本项目将检验三个主要假说：1)肺泡氧气 转运动力学可以用来表征心血管状态 在运动中的功能，2)在繁重的工作中消耗氧气 似乎与乳酸代谢机制有关的成分和 这会导致运动的氧气成本增加，3)二氧化碳排放 运动学可以用来测量运动肌肉的呼吸商和 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 特殊的生理缺陷，应该干扰正常的 外部呼吸与细胞呼吸的耦合。测试第二个 假设，我们将探索调节第三相VO2的因素 繁重的工作。为了检验第三个假设，乳酸盐的测量，HCO3 并将正常受试者的二氧化碳交换动力学作为研究的基础 二氧化碳排放量决定因素的模型分析，无论是在 乳酸盐阈值。这些研究利用了生理学家的技术， 医生、计算机科学家和工程师。 氧摄取和二氧化碳输出随时间的变化 运动是特定的心血管和代谢的表现 机械装置。因此，反应模式的异常提供了 有关功能受损部位(S)的重要信息。 了解这些机制可能会为更多的 合理对待运动患者的诊断和治疗 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.