摘要:

It is commonly held that the structural capacity of the nonnal lung is “overbuilt” and exceeds the demand for pulmonary O2and CO2transport in the healthy, exercising human. On the other hand, the adaptability of pulmonary system structures to habitual physical training is substantially less than are other links in the O2transport system. Accordingly, in some highly fit, and even in some not sofit habitually active individuals, the lung's diffusion suiface, airways, and/or chest-wall musculature are underbuilt relative to the demand for maximal O2transport. Two specific pulmonary limitations to exercise performance are proposed: (1) exercise-induced arterial hypoxemia secondary to excessive widening of the alveolar to arterial O2difference, inadequate hyperventilation, and metabolic acidosis; and (2) highly fatiguing levels of respiratory muscle work which effectively steals blood flow from locomotor muscles via sympathetically mediated reflexes and heightens the perception of limb discomfort and dyspnea. In this brief review, we describe the characteristics and causes of each of these proposed pulmonary limitations and their consequences to maximal O2uptake and exercise performa

ISSN:1066-7814    

DOI:h2003-066

出版商:NRC Research Press    

年代:2003

数据来源: NRC

ISSN:1066-7814    

DOI:h2003-067

出版商:NRC Research Press    

年代:2003

数据来源: NRC