Elevated exercise ventilation in mild COPD is not linked to enhanced central chemosensitivity

2021 ◽  
Vol 284 ◽  
pp. 103571
Author(s):  
Devin B Phillips ◽  
Nicolle J Domnik ◽  
Amany F Elbehairy ◽  
Megan E Preston ◽  
Kathryn M Milne ◽  
...  
Keyword(s):  
Central Chemosensitivity ◽  
Exercise Ventilation

Changes in Resting Airflow and Exercise Ventilation in Asthma

1987 ◽  
Vol 73 (s17) ◽  
pp. 3P-3P ◽  
Author(s):  
G E Packe ◽  
W Freeman ◽  
R M Cayton
Keyword(s):  
Exercise Ventilation

The limitation of exercise ventilation during speech

1981 ◽  
Vol 46 (2) ◽  
pp. 137-147 ◽  
Author(s):  
J.H. Doust ◽  
J.M. Patrick
Keyword(s):  
Exercise Ventilation

Pulmonary response to threshold levels of sulfur dioxide (1.0 ppm) and ozone (0.3 ppm)

1985 ◽  
Vol 58 (6) ◽  
pp. 1783-1787 ◽  
Author(s):  
L. J. Folinsbee ◽  
J. F. Bedi ◽  
S. M. Horvath
Keyword(s):  
Sulfur Dioxide ◽  
Pulmonary Response ◽  
Rest Periods ◽  
Pollutant Concentrations ◽  
Thoracic Gas Volume ◽  
Exercise Ventilation ◽  
Before And After ◽  
Residual Capacity ◽  
Gas Volume ◽  
Male Subjects

We exposed 22 healthy adult nonsmoking male subjects for 2 h to filtered air, 1.0 ppm sulfur dioxide (SO2), 0.3 ppm ozone (O3), or the combination of 1.0 ppm SO2 + 0.3 ppm O3. We hypothesized that exposure to near-threshold concentrations of these pollutants would allow us to observe any interaction between the two pollutants that might have been masked by the more obvious response to the higher concentrations of O3 used in previous studies. Each subject alternated 30-min treadmill exercise with 10-min rest periods for the 2 h. The average exercise ventilation measured during the last 5 min of exercise was 38 1/min (BTPS). Forced expiratory maneuvers were performed before exposure and 5 min after each of the three exercise periods. Maximum voluntary ventilation, He dilution functional residual capacity, thoracic gas volume, and airway resistance were measured before and after the exposure. After O3 exposure alone, forced expiratory measurements (FVC, FEV1.0, and FEF25–75%) were significantly decreased. The combined exposure to SO2 + O3 produced similar but smaller decreases in these measures. There were small but significant differences between the O3 and the O3 + SO2 exposure for FVC, FEV1.0, FEV2.0, FEV3.0, and FEF25–75% at the end of the 2-h exposure. We conclude that, with these pollutant concentrations, there is no additive or synergistic effect of the two pollutants on pulmonary function.

scholarly journals Variations in exercise ventilation in hypoxia will affect oxygen uptake

2020 ◽  
Vol 107 (3) ◽  
pp. 431-443
Author(s):  
J.A. Loeppky ◽  
R.M. Salgado ◽  
A.C. Sheard ◽  
D.O. Kuethe ◽  
C.M. Mermier
Keyword(s):  
Individual Variation ◽  
Ambient Pressure ◽  
Work Of Breathing ◽  
Linear Equations ◽  
Mechanical Efficiency ◽  
Individual Response ◽  
Hypoxic Ventilatory Response ◽  
Gross Efficiency ◽  
Exercise Ventilation ◽  
Progressive Exercise

AbstractReports of VO2 response differences between normoxia and hypoxia during incremental exercise do not agree. In this study VO2 and VE were obtained from 15-s averages at identical work rates during continuous incremental cycle exercise in 8 subjects under ambient pressure (633 mmHg ≈1,600 m) and during duplicate tests in acute hypobaric hypoxia (455 mmHg ≈4,350 m), ranging from 49 to 100% of VO2 peak in hypoxia and 42–87% of VO2 peak in normoxia. The average VO2 was 96 mL/min (619 mL) lower at 455 mmHg (n.s. P = 0.15) during ramp exercises. Individual response points were better described by polynomial than linear equations (mL/min/W). The VE was greater in hypoxia, with marked individual variation in the differences which correlated significantly and directly with the VO2 difference between 455 mmHg and 633 mmHg (P = 0.002), likely related to work of breathing (Wb). The greater VE at 455 mmHg resulted from a greater breathing frequency. When a subject's hypoxic ventilatory response is high, the extra work of breathing reduces mechanical efficiency (E). Mean ∆E calculated from individual linear slopes was 27.7 and 30.3% at 633 and 455 mmHg, respectively (n.s.). Gross efficiency (GE) calculated from mean VO2 and work rate and correcting for Wb from a VE–VO2 relationship reported previously, gave corresponding values of 20.6 and 21.8 (P = 0.05). Individual variation in VE among individuals overshadows average trends, as also apparent from other reports comparing hypoxia and normoxia during progressive exercise and must be considered in such studies.

Role of peripheral chemoreceptors and central chemosensitivity in the regulation of respiration and circulation.

1982 ◽  
Vol 100 (1) ◽  
pp. 23-40 ◽  
Author(s):  
R G O'Regan ◽  
S Majcherczyk
Keyword(s):  
The Body ◽  
Ion Concentration ◽  
Regulation Of Respiration ◽  
Acid Base Balance ◽  
Acid Base ◽  
Vascular Effects ◽  
Peripheral Chemoreceptor ◽  
Hydrogen Ion Concentration ◽  
Central Chemosensitivity ◽  
Base Balance

Adjustments of respiration and circulation in response to alterations in the levels of oxygen, carbon dioxide and hydrogen ions in the body fluids are mediated by two distinct chemoreceptive elements, situated peripherally and centrally. The peripheral arterial chemoreceptors, located in the carotid and aortic bodies, are supplied with sensory fibres coursing in the sinus and aortic nerves, and also receive sympathetic and parasympathetic motor innervations. The carotid receptors, and some aortic receptors, are essential for the immediate ventilatory and arterial pressure increases during acute hypoxic hypoxaemia, and also make an important contribution to respiratory compensation for acute disturbances of acid-base balance. The vascular effects of peripheral chemoreceptor stimulation include coronary vasodilation and vasoconstriction in skeletal muscle and the splanchnic area. The bradycardia and peripheral vasoconstriction during carotid chemoreceptor stimulation can be lessened or reversed by effects arising from a concurrent hyperpnoea. Central chemoreceptive elements respond to changes in the hydrogen ion concentration in the interstitial fluid in the brain, and are chiefly responsible for ventilatory and circulatory adjustments during hypercapnia and chronic disturbances of acid-base balance. The proposal that the neurones responsible for central chemoreception are located superficially in the ventrolateral portion of the medulla oblongata is not universally accepted, mainly because of a lack of convincing morphological and electrophysiological evidence. Central chemosensitive structures can modify peripheral chemoreceptor responses by altering discharges in parasympathetic and sympathetic nerves supplying these receptors, and such modifications could be a factor contributing to ventilatory unresponsiveness in mild hypoxia. Conversely, peripheral chemoreceptor drive can modulate central chemosensitivity during hypercapnia.

Hypoxic ventilatory response and arterial desaturation during heavy work

1989 ◽  
Vol 67 (3) ◽  
pp. 1119-1124 ◽  
Author(s):  
S. R. Hopkins ◽  
D. C. McKenzie
Keyword(s):  
Maximal Exercise ◽  
Ventilatory Response ◽  
Pulmonary Ventilation ◽  
Ideal Gas ◽  
Respiratory Drive ◽  
O2 Uptake ◽  
Arterial Blood ◽  
Arterial Desaturation ◽  
Exercise Ventilation ◽  
Arterial O2 Saturation

Arterial desaturation in athletes during intense exercise has been reported by several authors, yet the etiology of this phenomenon remains obscure. Inadequate pulmonary ventilation, due to a blunted respiratory drive, has been implicated as a factor. To investigate the relationship between the ventilatory response to hypoxia, exercise ventilation, and arterial desaturation, 12 healthy male subjects [age, 23.8 +/- 3.6 yr; height, 181.6 +/- 5.6 cm; weight, 73.7 +/- 6.2 kg; and maximal O2 uptake (VO2max), 63.0 +/- 2.2 ml.kg-1 min-1] performed a 5-min treadmill test at 100% of VO2max, during which arterial blood samples and ventilatory data were collected every 15 s. Alveolar PO2 (PAO2) was determined using the ideal gas equation. On a separate occasion the ventilatory response to isocapnic hypoxia was measured. Arterial PO2 decreased by an average of 29 Torr during the test, associated with arterial desaturation [arterial O2 saturation (SaO2) 92.0%]. PAO2 was maintained; however, alveolar-arterial gas pressure difference increased progressively to greater than 40 Torr. Minimal hypocapnia was observed, despite marked metabolic acidosis. There was no significant correlation observed between hypoxic drives and ventilation-to-O2 uptake ratio or SaO2 (r = 0.1 and 0.06, respectively, P = NS). These data support the conclusions that hypoxic drives are not related to maximal exercise ventilation or to the development of arterial desaturation during maximal exercise.

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