Rubini A, Parmagnani A, Paoli A
University of Padova Department of Biomedical Sciences Via Marzolo 3 35100 Padova Italy.
Acta Physiol Hung. 2014 Jun;101(2):197-204. doi: 10.1556/APhysiol.101.2014.2.8.
We measured respiratory ratio (RR), pulmonary ventilation (VE) and end-tidal carbon dioxide partial pressure (ETPCO2) at rest and during cycling aerobic workloads (20%, 40%, 60% of estimated maximal oxygen uptake). Measurements were taken after overnight fasting and after an oral glucose load. RR, VE and ETPCO2 increased with workload. Glucose load caused RR and VE increments at rest (0.75 ± 0.01 vs. 0.86 ± 0.02, p < 0.01, and 10.8 ± 0.43 vs. 12.1 ± 0.49 l/min, p < 0.01, respectively) and for each workload (20% estimated maximal oxygen uptake: 0.77 ± 0.01 vs. 0.855 ± 0.02, p < 0.01, and 16.2 ± 0.73 vs. 17.7 ± 0.8 l/min, p < 0.01; 40% estimated maximal oxygen uptake: 0.76 ± 0.02 vs. 0.82 ± 0.01, p < 0.01, and 25.9 ± 1.1 vs. 28.3 ± 1.3 l/min, p < 0.05; 60% estimated maximal oxygen uptake: 0.85 ± 0.02 vs. 0.91 ± 0.02, p < 0.01, and 37.4 ± 1.7 vs. 40.9 ± 1.9 l/min, p < 0.05) but ETPCO2 did not change. The differences in RR before and after glucose load became smaller as the workload increased. Linear regression analysis of VE and carbon dioxide output yielded virtually identical results for both fasting and glucose load conditions. We have concluded that: a) for the metabolic carbon dioxide load increment due to glucose-induced RR increment, the physiological response is an increase of VE at all workloads. This response modulates constant ETPCO2 values; b) on workload increment, skeletal muscle increasingly utilises more and more glycogen stores, regardless of the blood glucose availability. This reduces the usefulness of dietary manipulations decreasing carbon dioxide metabolic load during muscular work in respiratory failure; c) the absolute value of metabolic carbon dioxide load exerts a role in ventilation regulation at rest and during aerobic exercise.
我们测量了静息状态以及在有氧骑行负荷（估计最大摄氧量的20%、40%、60%）期间的呼吸商（RR）、肺通气量（VE）和呼气末二氧化碳分压（ETPCO2）。测量在过夜禁食后以及口服葡萄糖负荷后进行。RR、VE和ETPCO2随负荷增加而升高。葡萄糖负荷导致静息状态下RR和VE增加（分别为0.75±0.01对0.86±0.02，p<0.01，以及10.8±0.43对12.1±0.49升/分钟，p<0.01），并且在每个负荷水平下也增加（估计最大摄氧量的20%：0.77±0.01对0.855±0.02，p<0.01，以及16.2±0.73对17.7±0.8升/分钟，p<0.01；估计最大摄氧量的40%：0.76±0.02对0.82±0.01，p<0.01，以及25.9±1.1对28.3±1.3升/分钟，p<0.05；估计最大摄氧量的60%：0.85±0.02对0.91±0.02，p<0.01，以及37.4±1.7对40.9±1.9升/分钟，p<0.05），但ETPCO2没有变化。随着负荷增加，葡萄糖负荷前后RR的差异变小。对VE和二氧化碳排出量进行线性回归分析，在禁食和葡萄糖负荷条件下得出几乎相同的结果。我们得出结论：a）对于葡萄糖诱导的RR增加所导致的代谢性二氧化碳负荷增加，生理反应是在所有负荷水平下VE增加。这种反应调节ETPCO2值保持恒定；b）随着负荷增加，骨骼肌越来越多地利用糖原储备，而不考虑血糖可用性。这降低了在呼吸衰竭时肌肉工作期间通过饮食控制降低二氧化碳代谢负荷的作用；c）代谢性二氧化碳负荷的绝对值在静息和有氧运动期间的通气调节中起作用。
