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 锻炼的能力取决于 心肺系统的动态反应。 这些支撑 肌肉细胞的正常氧利用率，消除其CO2， 还有酸碱调节。 测量技术的最新进展 使得有可能检查肺泡O2动力学的细节， 二氧化碳运输对运动的响应。 从概念上讲，气体交换动力学有三个功能组成部分 对运动的反应：心脏动力学阶段（前25秒，阶段I）， 增加静脉血O2提取和CO2负荷的时期 (15秒至约3-4分钟，阶段II），以及超过3-4分钟的时间段，其中 气体交换在乳酸阈值以下达到稳定状态，但是 继续高于阈值（第三阶段）。 本研究将探讨三个主要假设：1）肺泡氧 运输动力学可用于表征心血管系统的状态， 2）在繁重的工作中，O2的消耗量 似乎与乳酸代谢机制有关的成分， 这导致运动的O2成本增加，3）CO2输出 动力学可用于测量运动肌肉呼吸商， 代谢（乳酸）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 特殊的生理缺陷会干扰正常的 外部呼吸与细胞呼吸的耦合。 为了测试第二 假设，我们将探讨调节III相VO 2的因素， 繁重的工作。 为了检验第三个假设，测量乳酸，HCO 3 和正常受试者的CO2交换动力学将被用作 模型分析的决定因素的二氧化碳输出，无论是以上和以下的 乳酸阈 这些研究利用生理学家的技能， 医生、计算机科学家和工程师。 O2吸收和CO2输出的时间相关变化 运动是特定的心血管和代谢的表现 机制等 因此，响应模式的摘要提供了 关于功能损害部位的重要信息。 了解这些机制可能会为更深入地研究 运动病人的合理诊治 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.