Poortmans J R, Vanderstraeten J
Institut Supérieur d'Education Physique et de Kinésithérapie, Université Libre de Bruxelles, Belgium.
Sports Med. 1994 Dec;18(6):419-37. doi: 10.2165/00007256-199418060-00006.
Exercise induces profound changes in renal haemodynamics and protein excretion. The rate of ultrafiltration across the glomerular capillary is determined by the imbalance between the transcapillary hydraulic and colloid osmotic pressure gradients. Despite a major reduction in the renal plasma flow, the filtration fraction can double with maximal exercise, preserving the transfer of metabolites or substances through the glomerulus. Tubular processes and excretion rates are modified by exercise. Despite large increases in plasma lactate during strenuous exercise, renal excretion plays a limited role in lactate metabolism. Apparently, the mechanism of transcellular transport of lactate is saturated during severe exercise. Urea reabsorption is enhanced during prolonged exercise, and this process may act to limit the dehydration of an individual. As uric acid transport is also carrier-mediated, it appears that there is no saturation of the carrier system during prolonged exercise. Postexercise proteinuria is directly related to the intensity of exercise rather than to its duration. This excretion of excess proteins is a transient state with a half-time decay of about 1 hour. The increased clearance of plasma proteins suggests an increased glomerular permeability and a partial inhibition of tubular reabsorption. Studies suggest that exercise decreases the glomerular electrostatic barrier and facilitates transfer of macromolecules. Postexercise proteinuria appears to be age-dependent. Nephropathy is a common observation in the diabetic patient. In young and adult diabetic patients, exhaustive physical exercise does not provoke an enhanced dysfunction of the kidney to what is already found in healthy individuals. Heart and kidney transplant patients have a lesser postexercise proteinuria as compared with healthy individuals.
运动可引起肾脏血流动力学和蛋白质排泄的深刻变化。肾小球毛细血管超滤过率取决于跨毛细血管的液压和胶体渗透压梯度之间的失衡。尽管肾血浆流量大幅减少，但在最大运动量时滤过分数可增加一倍，从而保持代谢产物或物质通过肾小球的转运。运动可改变肾小管功能和排泄率。尽管剧烈运动时血浆乳酸大幅增加，但肾脏排泄在乳酸代谢中作用有限。显然，在剧烈运动期间，乳酸的跨细胞转运机制会饱和。长时间运动期间尿素重吸收增强，这一过程可能有助于限制个体脱水。由于尿酸转运也是载体介导的，因此在长时间运动期间载体系统似乎不会饱和。运动后蛋白尿与运动强度直接相关，而非与运动持续时间相关。这种过量蛋白质的排泄是一种短暂状态，半衰期约为1小时。血浆蛋白清除率增加表明肾小球通透性增加和肾小管重吸收部分受抑制。研究表明，运动可降低肾小球静电屏障并促进大分子转运。运动后蛋白尿似乎与年龄有关。糖尿病患者中肾病很常见。在年轻和成年糖尿病患者中，力竭性体育锻炼不会使肾脏功能障碍比健康个体中已有的情况更严重。与健康个体相比，心脏和肾脏移植患者运动后蛋白尿较少。
