To determine the role of postinspiratory inspiratory activity of the diaphragm in the biphasic ventilatory response to hypoxia in unanesthetized rats, we examined diaphragmatic activity at its peak (DI), at the end of expiration (DE), and ventilation in adult unanesthetized rats during poikilocapnic hypoxia (10 % O2) sustained for 20 min. Hypoxia induced an initial increase in ventilation followed by a consistent decline. Tidal volume (VT), frequency of breathing (fR), DI and DE at first increased, then VT and DE decreased, while fR and DI remained enhanced. Phasic activation of the diaphragm (DI - DE) increased significantly at 10, 15 and 20 min of hypoxia. These results indicate that 1) the ventilatory response of unanesthetized rats to sustained hypoxia has a typical biphasic character and 2) the increased end-expiratory activity of the diaphragm limits its phasic inspiratory activation, but this increase cannot explain the secondary decline in tidal volume and ventilation., H. Maxová, M. Vízek., and Obsahuje bibliografii
Time delay in the mediation of ventilation (VE) by arterial CO2 pressure (PaCO2) was studied during recovery from short impulse-like exercises with different work loads of recovery. Subjects performed two tests including 10-s impulse like exercise with work load of 200 watts and 15-min recovery with 25 watts in test one and 50 watts in test two. V . E, end tidal CO2 pressure (PETCO2) and heart rate (HR) were measured continuously during rest, warming up, exercise and recovery. PaCO2 was estimated from PETCO2 and tidal volume (VT). Results showed that predicted arterial CO2 pressure (PaCO2 pre) increased during recovery in both tests. In both tests, VE increased and peaked at the end of exercise. VE decreased in the first few seconds of recovery but started to increase again. The highest correlation coefficient between PaCO2 pre and V . E was obtained in the time delay of 7 s (r=0.854) in test one and in time delays of 6 s (r=0.451) and 31 s (r=0.567) in test two. HR was significantly higher in test two than in test one. These results indicate that PaCO2 pre drives VE with a time delay and that higher work intensity induces a shorter time delay., R. Afroundeh, T. Arimitsu, R. Yamanaka, C. S. Lian, K. Shirakawa, T. Yunoki, T. Yano., and Obsahuje bibliografii
The article reports on a newly realized experimental ground heat exchanger (GHE) which has been built up as an accessory of an experimental low-energy dwelling of Faculty of Mechanical Engineering, Brno University of Technology (FME BUT)., and analyzes some aspects of its project, especially the choice of proper tubing. Based on a simplified computational model, the impact of four most employed tubing types on a performance and an effectivness of the GHE has been judged and benefits of particular tubing types were compared with their investment costs. Finally, using of KG-Systém (PVC)® SN4 was evaluated as the best variant. and Obsahuje seznam literatury a názvosloví
The purpose of the present study was to examine whether excessive CO2 output (V.co2excess) is dominantly attributable to hyperventilation during the period of recovery from repeated cycling sprints. A series of four 10-sec cycling sprints with 30-sec passive recovery periods was performed two times. The first series and second series of cycle sprints (SCS) were followed by 360-sec passive recovery periods (first recovery and second recovery). Increases in blood lactate (ΔLa) were 11.17±2.57 mM from rest to 5.5 min during first recovery and 2.07±1.23 mM from the start of the second SCS to 5.5 min during second recovery. CO2 output (V.co2) was significantly higher than O2 uptake (V.o2) during both recovery periods. This difference was defined as V.co2excess. V.co2excess was significantly higher during first recovery than during second recovery. V.co2excess was added from rest to the end of first recovery and from the start of the second SCS to the end of second recovery (CO2excess). ΔLa was significantly related to CO2excess (r=0.845). However, ventilation during first recovery was the same as that during second recovery. End-tidal CO2 pressure (PETco2) significantly decreased from the resting level during the recovery periods, indicating hyperventilation. PETco2 during first recovery was significantly higher than that during second recovery. It is concluded that V.co2excess is not simply determined by ventilation during recovery from repeated cycle sprints., T. Yano ... [et al.]., and Obsahuje seznam literatury
We investigated ventilation (V . E) control factors during recovery from light impulse-like exercise (100 watts) with a duration of 20 s. Blood ions and gases were measured at rest and during recovery. V . E, end tidal CO2 pressure (PETCO2) and respiratory exchange ratio (RER) were measured continuously during rest, exercise and recovery periods. Arterial CO2 pressure (PaCO2 pre) was estimated from PETCO2 and tidal volume (VT). RER at 20 s of exercise and until 50 s during recovery was significantly lower than RER at rest. Despite no change in arterialized blood pH level, PaCO2 pre was significantly higher in the last 10 s of exercise and until 70 s during recovery than the resting value. V . E increased during exercise and then decreased during recovery; however, it was elevated and was significantly higher than the resting value until 155 s (p<0.05). There was a significant relationship between V . E and PaCO2 pre during the first 70 s of recovery in each subject. The results suggest that PaCO2 drives V . E during the first 70 s of recovery after light impulse-like exercise. Elevated V . E in the interval from 70 s until 155 s during recovery might be due to neural factors., R. Afroundeh, ... [et al.]., and Obsahuje seznam literatury