Moinard J, Yquel R, Manier G
Centre de Pneumologie et Polyclinique Bordeaux-Nord Aquitaine, 17 rue de Rivière, 33000 Bordeaux, France.
Rev Mal Respir. 2004 Nov;21(5 Pt 1):950-60. doi: 10.1016/s0761-8425(04)71477-1.
The modifications of gas exchange on exercise reflect the consequences of the control and limits of adaptation of the respiratory apparatus to the mechanical loads imposed on the muscles and the oxygen requirements of the organism. In the majority of cases, even if the thoraco-pulmonary apparatus is perfectly adapted to the increase in these requirements, the balance between the metabolic demands of the tissues and the pulmonary supply appears difficult to satisfy beyond certain limits without hypoxaemia, particularly in those subjects with a low ventilatory response to exercise. Based on the populations reported in the literature the functional limits of the control of the thoraco-pulmonary system and the possible modifications of the structures of the lung are discussed for each of these mechanisms.
At certain levels of duration and intensity of exercise there is an increase in the alveolar-arterial oxygen gradient [P(A-a)O2] associated inconsistently with a fall in PaO2. It is mainly the use of inert gas techniques that has established over many years the respective roles of the different possible patho-physiological mechanisms: shunt, unequal distribution of VA/Q ratios, limitation of alveolar-capillary diffusion and its components. The inequalities of VA/Q increase at low levels of exercise but beyond certain levels of VO2 limitation of oxygen diffusion may develop. In effect, particularly in subjects capable of high levels of exercise, the interaction between diminished transit time of the red cells in the pulmonary capillaries and possible delay in equilibration of partial pressures between the blood and gas phases may create a limitation of diffusion. This added to the inequalities of distribution of VA/Q and reduction in PVO2 leads, in certain subjects, to a transitory exercise induced hypoxaemia.
New techniques of investigation seem to be necessary to clarify the sources of the observed changes and the development of modifications of pulmonary structure that establish the functional limits of the lungs on exercise. It remains to demonstrate the true impact of these anomalies on the limitation of human performance.
运动时气体交换的改变反映了呼吸器官对肌肉所承受机械负荷及机体氧需求的控制和适应限度的后果。在大多数情况下,即使胸肺器官能很好地适应这些需求的增加,但在某些限度之上,若不出现低氧血症,组织的代谢需求与肺供应之间的平衡似乎难以满足,尤其是在那些运动时通气反应较低的受试者中。基于文献报道的人群,针对每种机制讨论了胸肺系统控制的功能限度以及肺结构可能的改变。
在运动的特定持续时间和强度水平下,肺泡 - 动脉血氧梯度[P(A - a)O2]会增加,且与动脉血氧分压(PaO2)下降的关系并不一致。多年来主要是通过惰性气体技术确定了不同可能病理生理机制的各自作用:分流、通气/血流比值(VA/Q)分布不均、肺泡 - 毛细血管扩散及其组成部分的限制。在低运动水平时VA/Q的不均等增加,但超过一定VO2水平时可能会出现氧扩散受限。实际上,特别是在能够进行高强度运动的受试者中,红细胞在肺毛细血管中通过时间的减少与血气相之间分压平衡可能的延迟之间的相互作用可能会造成扩散限制。这加上VA/Q分布不均和混合静脉血氧分压(PVO2)降低,在某些受试者中会导致短暂的运动性低氧血症。
似乎需要新的研究技术来阐明观察到的变化的来源以及肺结构改变的发展情况,这些改变确立了运动时肺的功能限度。仍有待证明这些异常对人类运动能力限制的真正影响。