Rate of Acclimatization to Chronic Hypercapnia in Man

Clark, JM; Sinclair, Ruth; Welch, B. E.

doi:10.1016/b978-0-12-434750-2.50052-6

Cited by 16 publications

(20 citation statements)

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“…The findings are in accord with those reported by Chapin et al (1955), who found increased values for Pa,co, after breath-holding in two subjects exposed to 3% CO, for 2 h. In their studies the breath-holding Pa,co, reached a maximum value in 8-13 h. More recently studies of ventilation and acid-base data in prolonged experimental hypercapnia have been reported in normal man (Clark et al, 1971). On exposure to CO, the subjects of Clark et al (1971) showed a rapid increase in both ventilation and Pa,co,, the latter reaching a maximum at 20 h after exposure.…”

Section: Discussionsupporting

confidence: 91%

“…Although it has been suggested that the respiratory rate of work might be a better indicator of the respiratory response to CO, than ventilation (Eldridge & Davies, 1959;Brodowsky, MacDonell & Cherniak, 1960), few studies of work measurements have been reported (Kellog, Pace, Archibald & Waughan, 1957;Flenley & Millar, 1967, 1968Martin, Perrault, Morinet, Puchelle & Sadoul, 1969). These studies suggest that the respiratory response to CO, reaches a plateau after 10 min, the so-called 'steady-state' response, and this is supported by the observation of Brackett, Cohen & Schwartz (1965), who found that a steady state of acid-base equilibrium was achieved after 10 min in normal men exposed to 7% inspired Studies of response to CO, after longer periods of exposure have suggested that some adaptation of ventilation occurs in the first 24 h (Chapin, Otis & Rahn, 1955;Falchuk, Lamb & Tenney, 1966;Clark, Sinclair & Welch, 1971), but the changes reported after longer periods have been variable (Schaeffer, 1963;Clark et al, 1971).…”

Section: Introductionmentioning

confidence: 83%

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The Respiratory Response to Inhaled Carbon Dioxide in Man after 3 Hours Exposure to 3% Carbon Dioxide

et al. 1978

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1. The respiratory response to inhaled 3% and 6% CO2 was measured in 10 normal subjects after a 3 h acclimatization period to 3% CO2 in an environmental chamber. Control studies were carried out after a 3 h period of breathing air in the chamber. 2. At the end of the acclimatization period studies were carried out during 20 min periods breathing 3% CO2, 6% CO2 and air. 3. At 2-min intervals during the studies measurements were made of tidal volume (Vt), breathing frequency (fR), minute ventilation (Ve), viscous pulmonary rate of work (Wp) and total viscous rate of work across the lungs and apparatus (Wt). Blood gas tensions were measured at the end of this period. 4. After acclimatization to 3% CO2 there was a significant shift in the response curves Ve/Pa,CO2 and Wt/Pa,CO2 such that subjects showed higher Pa,CO2 values for given values of Ve or Wt. There was no significant change in the slope of the response curves. 5. No correlation was found between the slope of the response curve after the control period breathing air and the degree of shift of the response curve. 6. There was no difference in respiratory pattern or in pulmonary resistance. 7. Similar results were found in two subjects studied after 24 h acclimatization to 3% CO2 but one subject also showed a significant change in the slope of the Ve/Pa,CO2 curve.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 83%

The Respiratory Response to Inhaled Carbon Dioxide in Man after 3 Hours Exposure to 3% Carbon Dioxide

et al. 1978

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“…over the long term (Schaefer, 1963;Schaefer et al, 1963;Clark et al, 1971;Guillerm and Radziszewski, 1979;Jennings and Davidson, 1984;Burgraff et al, 2018Burgraff et al, , 2019. This time-dependent physiologic change suggests an adaptation or acclimatization to long-term hypercapnia.…”

Section: Neuroplasticity Underlying Adaptation To Long-term Hypercapniamentioning

confidence: 99%

“…Acute hypercapnia causes an increase in ventilatory drive by peripherally and centrally mediated chemoreflex mechanisms Smith et al, 2010). Long-term hypercapnia shows a biphasic ventilatory response in humans, dogs, goats and rodents, consisting of an initial increase in ventilatory drive in the first 8 h (rodents), 24 h (goats and dogs), 5 days (human) followed by a sustained decrease in this response (21-44 days) (Schaefer, 1963;Schaefer et al, 1963;Clark et al, 1971;Pingree, 1977;Lai et al, 1981;Jennings and Davidson, 1984;Burgraff et al, 2018;Burgraff et al, 2019). The mechanism underlying physiological adaptation to long-term hypercapnia is not clearly understood.…”

Section: Introductionmentioning

confidence: 99%

Adaptation of Respiratory-Related Brain Regions to Long-Term Hypercapnia: Focus on Neuropeptides in the RTN

et al. 2019

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Long-term hypercapnia is associated with respiratory conditions including obstructive sleep apnea, chronic obstructive pulmonary disease and obesity hypoventilation syndrome. Animal studies have demonstrated an initial (within hours) increase in ventilatory drive followed by a decrease in this response over the long-term (daysweeks) in response hypercapnia. Little is known about whether changes in the central respiratory chemoreflex are involved. Here we investigated whether central respiratory chemoreceptor neurons of the retrotrapezoid nucleus (RTN), which project to the respiratory pattern generator within the ventral respiratory column (VRC) have a role in the mechanism of neuroplasticity associated with long-term hypercapnia. Adult male C57BL/6 mice (n = 5/group) were used. Our aims were (1) to determine if galanin, neuromedin B and gastrin-releasing peptide gene expression is altered in the RTN after long-term hypercapnia. This was achieved using qPCR to measure mRNA expression changes of neuropeptides in the RTN after short-term hypercapnia (6 or 8 h, 5 or 8% CO 2 ) or long-term hypercapnia exposure (10 day, 5 or 8% CO 2 ), (2) in the mouse brainstem, to determine the distribution of preprogalanin in chemoreceptors, and the cooccurrence of the galanin receptor 1 (GalR1:Gi-coupled receptor) with inhibitory GlyT2 ventral respiratory column neurons using in situ hybridization (ISH) to better characterize galaninergic RTN-VRC circuitry, (3) to investigate whether long-term hypercapnia causes changes to recruitment (detected by cFos immunohistochemistry) of respiratory related neural populations including the RTN neurons and their galaninergic subset, in vivo. Collectively, we found that hypercapnia decreases neuropeptide expression in the RTN in the short-term and has the opposite effect over the long-term. Following long term hypercapnia, the number of RTN galanin neurons remains unchanged, and their responsiveness to acute chemoreflex is sustained; in contrast, we identified multiple respiratory related sites that exhibit blunted chemoreflex activation. GalR1 was distributed in 11% of preBötC and 30% of BötC glycinergic neurons. Our working hypothesis is that during long-term hypercapnia, galanin co-release from RTN neurons may counterbalance glutamatergic inputs to respiratory centers to downscale energetically wasteful hyperventilation, thereby having a role in neuroplasticity by contributing to a decrease in ventilation, through the inhibitory effects of galanin.

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“…I n a review Dempsey & Forster (1982) summarized studies on ventilation during extended exposures to increased inspired CO, in this way: 'The hyperpnea during chronic exposure equals or exceeds the hyperpnea during acute CO, exposure. O n the other hand, Clark et al (1971) found Pzc0, to be only 0.7 kPa above control G. . T h e studies of Pace, are also conflicting.…”

mentioning

confidence: 81%

Arterial PCO₂ and pH in man during 3 days' exposure to 2.8 kPa CO₂ in the inspired gas

Nicolaysen

Ellingsen

Owe³

et al. 1989

Acta Physiologica Scandinavica

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It has not been firmly established how respiration adapts to long-term CO2 exposure in man. We have therefore exposed five healthy human subjects to 2.8 kPa CO2 in the inspired gas for about 70 h in a chamber with controlled atmospheric conditions at ambient pressure PCO2 and pH were determined in arterial or arterialized venous blood drawn before, during and after the exposure. One subject was studied twice. We found that PaCO2 increased acutely and then increased further within the 5- to 24-h period of exposure to 2.8 kPa CO2. No consistent change was observed during the following 2 days. At the end of exposure the PaCO2 was 0.5 kPa above the pre-exposure level. When the breathing gas was switched back to room air, PaCO2 promptly returned to pre-exposure values. The secondary rise in PaCO2 within the first day would correspond to a decrease in alveolar ventilation of about 10% assuming constant production and elimination of CO2. Arterial pH remained slightly below the pre-exposure level during the entire exposure period. A slight renal compensation resulting in an increase in base excess of about 1 mmol l-1 may have occurred in the middle part of the exposure period. We conclude that a significant, but moderate, respiratory adaptation takes place during the first day of exposure to an increased inspired load of CO2.

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Rate of Acclimatization to Chronic Hypercapnia in Man

Cited by 16 publications

References 20 publications

The Respiratory Response to Inhaled Carbon Dioxide in Man after 3 Hours Exposure to 3% Carbon Dioxide

The Respiratory Response to Inhaled Carbon Dioxide in Man after 3 Hours Exposure to 3% Carbon Dioxide

Adaptation of Respiratory-Related Brain Regions to Long-Term Hypercapnia: Focus on Neuropeptides in the RTN

Arterial PCO₂ and pH in man during 3 days' exposure to 2.8 kPa CO₂ in the inspired gas

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Rate of Acclimatization to Chronic Hypercapnia in Man

Cited by 16 publications

References 20 publications

The Respiratory Response to Inhaled Carbon Dioxide in Man after 3 Hours Exposure to 3% Carbon Dioxide

The Respiratory Response to Inhaled Carbon Dioxide in Man after 3 Hours Exposure to 3% Carbon Dioxide

Adaptation of Respiratory-Related Brain Regions to Long-Term Hypercapnia: Focus on Neuropeptides in the RTN

Arterial PCO2 and pH in man during 3 days' exposure to 2.8 kPa CO2 in the inspired gas

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Arterial PCO₂ and pH in man during 3 days' exposure to 2.8 kPa CO₂ in the inspired gas