Augmented Ventilatory Response Research Articles

Augmented ventilatory response to sustained normocapnic hypoxia following 100% O2 breathing in humans.

The presence of hyperoxic hyperventilation seems to have been well confirmed in humans by Becker et al (1995) when the PETco2 is maintained at a normocapnic level. They also observed that augmented ventilation at higher than the control level still continued even 15 min after termination of hyperoxia, suggesting that a humoral agent might be involved to stimulate ventilation.KeywordsCarotid BodyMetabotropic Glutamate ReceptorVentilatory ResponseSustained HypoxiaPlasma Glutamine ConcentrationThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Effects of pregnancy and chronic exercise on respiratory responses to graded exercise

Effects of cycle ergometer conditioning (heart rate 143 +/- 2 beats/min, 25 min/session, 3 sessions/wk) during the second and third trimesters of pregnancy were studied in 18 healthy previously sedentary women. A nonexercising control group (n = 9) was also studied. Graded exercise tests were conducted for both groups at approximately 17, 27, and 37 wk of gestation and at 20 wk postpartum. Both groups exhibited augmented ventilatory responses to exercise throughout pregnancy. Significant aerobic conditioning effects observed in the exercised group between entry and third trimester of pregnancy testing included a 17% increase in oxygen pulse at peak exercise, reduction in the respiratory exchange ratio during standard submaximal exercise, and an increase in work rate at the onset of blood lactate accumulation. Onset of blood lactate accumulation did not change significantly in the control group. Respiratory exchange ratio at peak exercise was higher in postpartum tests compared with those conducted in late gestation in both groups. Peak postexercise lactate levels were also significantly lower in second and third trimesters of pregnancy testing compared with postpartum in the control group. This effect appeared to be prevented by physical conditioning in the exercised group. The study results support the hypothesis that moderate aerobic conditioning increases maximal aerobic power and the capacity for sustained submaximal exercise. Chronic exercise also appeared to help to preserve anaerobic working capacity in late gestation.

Comparison of ventilatory response between dead space and CO2 breathing in humans.

Ventilatory response during external dead space (tube) breathing and CO2 inhalation for given increase in PETCO2 were compared at different levels of PETO2 (hyperoxia, normoxia, and hypoxia) in human subjects. At all the PETO2 levels studied, magnitude of increment in minute ventilation (VE) and tidal volume were larger in the dead space breathing than in the CO2 inhalation. The slope of CO2-ventilation response line was significantly steeper in the dead space breathing only in the hypoxic condition. There was no significant difference in frequency response to CO2 between the two methods. These results suggested that augmented ventilatory response to CO2 in the dead space breathing occurs in the condition of peripheral chemoreceptor activation.

Augmented Ventilatory Response to Exercise in Pulmonary Hypertension

The ventilatory response to submaximal exercise, defined as the slope of minute ventilation over carbon dioxide production (VE/VCO2), was determined in 12 normal subjects, ten patients with pulmonary hypertension before and after heart-lung transplantation, and eight patients following heart transplantation. Patients with pulmonary hypertension show an augmented ventilatory response compared to normal subjects (pulmonary hypertension [mean, 57.7 +/- 6.8 (SE) ml/ml VCO2; normal subjects, 22.3 +/- 1.4 ml/ml VCO2; p less than 0.001]). Following heart-lung transplantation, VE/VCO2 slope fell to 24.7 +/- 1.6 ml/ml VCO2, a value which is not significantly different than the value in normal subjects. Patients after heart transplantation show a mean slope value of 25.3 +/- 1.3 ml/ml VCO2, which is not significantly different than the normal value or the value found after heart-lung transplantation. The augmented ventilatory response to exercise did not correlate with the usual chemical modulators of ventilation (arterial pH, arterial carbon dioxide tension, or arterial oxygen tension). These results suggest the following: the existence of a neural system in patients with pulmonary hypertension which results in an augmentation of ventilatory drive in response to exercise; the augmented ventilatory response reflects excessive neural activity of pulmonary afferents during exercise; narrow regulation of the ventilatory response to exercise in normal subjects which is preserved in the denervated lung, indicating that pulmonary afferents are not critical to ventilatory control during exercise in the normal subject; and the possible use of measurements of the ventilatory response to exercise as a noninvasive screening test for pulmonary hypertension.