Ventilatory Response to CO 2 During Work at Normal and at Low Oxygen Tensions

and values for both were reduced with the acid-base disturbances seen in the first 10 days after birth. Evidence was given which suggested that the response of the new-born lamb to inhaled C02 was similar to that of man acclimatized to a P-02 of 70-75 mm Hg.5. In the lightly anaesthetized lamb, bilateral section of the sinus nerves caused a small reduction in the sensitivity to inhaled 5 % C02 in air, an increase in the respiratory lag and a reduction in the rate at which v increased.6. It was concluded that, in the new-born lamb, the carotid chemo-* Supported in part by USPHS grant HE 06285.

Section: Discussionmentioning

confidence: 99%

The respiratory response of the new‐born lamb to inhaled CO₂ with and without accompanying hypoxia*

Purves¹

1966

“…The relations between expiratory ventilation (PE) and the end-tidal partial pressure of CO2 (PETC2 ), which are the C02 response lines, have been determined during exercise at various steady oxygen tensions by several groups (Asmussen & Nielsen, 1957; Bhattacharyya, Cunningham, Goode, Howson & Lloyd, 1970;Masson & Lahiri, 1974). During exercise, the mean slope of the CO2 response line in euoxia and hyperoxia is about the same as during rest.…”

Section: Introductionmentioning

confidence: 99%

Dynamics of the ventilatory response in man to step changes of end‐tidal carbon dioxide and of hypoxia during exercise.

Macfarlane¹,

Cunningham²

1992

SUMMARY1. Four human subjects exercised in hypoxia (end-tidal partial pressure Of 02 (PET, 02) ca 55 Torr; heart rate ca 100-130 beats min-), and the contribution to the respiratory drive of the peripheral and central chemoreflex pathways have been separated on the basis of the latencies and the time courses of the responses to sudden changes of stimulus.2. The subjects were exposed to repeated end-tidal step changes in PCO2 of ca 3-3 5 Torr (at nearly constant PET, 02 ) and P02 (between ca 55 and 230 Torr) at three regions along the expiratory ventilation VE-PET°2 response line (hypocapnia, eucapnia, hypercapnia). The dynamics of the ventilatory responses were calculated using a two-compartment non-linear least-squares optimization method.3. The component of the response attributable to the peripheral chemoreflex loop may in some subjects contribute up to 75% of the ventilatory drive during mild hypocapnic hypoxic exercise and ca 72 % of the total gain following steps Of PET, CO, during hypoxic exercise. These data support the notion that the effectiveness of the peripheral chemoreceptor pathway is enhanced in moderate exercise.4. During hypoxic exercise, the time delays and time constants attributed to the peripheral chemoreflex pathways (ca 3-5 and 9 s respectively) and to the central chemoreflex pathways (ca 9-5 and 47 s respectively) are some of the shortest reported.5. The dynamics of the peripheral and central chemoreflex pathways appeared to be largely independent of each other.6. There was a notable absence of systematic change of inspiratory and expiratory durations during the step-induced transients.

“…In contrast to the earlier work which has largely been done during air breathing, in our experiments exercise was studied on a background of either hypoxia or hyperoxia. Exercise is known markedly to amplify the hypoxia-induced peripheral chemoreflex (Asmussen & Nielsen, 1957;Cunningham et al 1968;Masson & Lahiri, 1974). Our study consequently permits a comparison of the effects of propranolol on the dynamic response of ventilation to step changes from rest to work in a condition with enhanced chemoreceptor activity and in a condition in which chemoreceptor activity is attenuated or absent.…”

Section: Introductionmentioning

confidence: 98%

Effects of beta‐adrenergic blockade on the ventilatory responses to hypoxic and hyperoxic exercise in man.

Conway¹,

Petersen²

1987

SUMMARY1. The ventilatory responses to step changes from rest to 100 W cycling exercise were studied in five healthy human subjects. Exercise was performed in hypoxia (end-tidal 02 pressure, PET,02' 50-55 mmHg), a condition characterized by a marked enhancement of arterial chemoreceptor activity, and in hyperoxia (PETo°2 > 250 mmHg), a condition in which arterial chemoreceptor activity is largely suppressed. The subjects were studied at each 02 level after placebo and after an oral dose of 120 mg propranolol.2. The magnitude of phase 1, the immediate, rapid ventilatory response at the onset of work, was unaffected by hypoxia and at both oxygen levels it was also unaffected by propranolol.3. Phase 2, analysed from 20 to 120 s after the onset of exercise, was significantly affected by both 02 level and fl-blockade. The kinetics of the ventilatory changes in this phase were well described in all four conditions by a simple exponential function. The overall mean time constants after placebo were shorter in hypoxia (31-0 s) than in hyperoxia (40-2 s), and at each 02 level longer after propranolol, in hypoxia 61-3 s and in hyperoxia 106-0 s 4. Continuous analysis of gas sampled at the mouth with a mass spectrometer showed constancy of end-tidal Pco2 throughout the step change in hypoxia both with and without f-blockade. In contrast, in both hyperoxic conditions PETCo2 rose, mainly in phase 2, to a value 5-6 mmHg higher than the starting value. 5. The steady-state ventilation was higher in hypoxia than in hyperoxia, and endtidal CO2 pressure, PETC02, correspondingly lower. Neither ventilation nor Pco2were, however, affected by propranolol in either condition. 6. It is concluded that the arterial chemoreceptors are important for both the rate of adaptation of ventilation to a new rate of metabolism during a step change of work rate, and for the matching of ventilation to C02 flow which normally ensures isocapnia. The further slowing of the dynamics of the ventilatory response in hyperoxia as well as the preserved isocapnia in hypoxia after fl-blockade argue against any major role of f8-adrenergic mechanisms for these functions of the arterial chemoreceptors. The observed effects are considered to be secondary to the reduced cardiac output and an increased CO2 storage initially during exercise following fiadrenergic blockade.