The limitation of exercise ventilation during speech

1981 ◽  
Vol 46 (2) ◽  
pp. 137-147 ◽  
Author(s):  
J.H. Doust ◽  
J.M. Patrick
Keyword(s):  
1987 ◽  
Vol 73 (s17) ◽  
pp. 3P-3P ◽  
Author(s):  
G E Packe ◽  
W Freeman ◽  
R M Cayton
Keyword(s):  

1985 ◽  
Vol 58 (6) ◽  
pp. 1783-1787 ◽  
Author(s):  
L. J. Folinsbee ◽  
J. F. Bedi ◽  
S. M. Horvath

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.


2020 ◽  
Vol 107 (3) ◽  
pp. 431-443
Author(s):  
J.A. Loeppky ◽  
R.M. Salgado ◽  
A.C. Sheard ◽  
D.O. Kuethe ◽  
C.M. Mermier

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.


1989 ◽  
Vol 67 (3) ◽  
pp. 1119-1124 ◽  
Author(s):  
S. R. Hopkins ◽  
D. C. McKenzie

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.


1963 ◽  
Vol 18 (1) ◽  
pp. 19-24 ◽  
Author(s):  
J. Howland Auchincloss ◽  
John Sipple ◽  
Robert Gilbert

The ventilatory response to treadmill exercise was studied in normal and obese subjects, with an analysis of both the steady and unsteady states of exercise. Ventilation, oxygen consumption, carbon dioxide production, respiratory quotient, and alveolar and mixed expired gas concentrations were measured directly or computed. During the steady state of exercise obese subjects increased their ventilation sufficiently to maintain normal alveolar carbon dioxide tensions. During the first 2 min of exercise hypoventilation was more pronounced in obese subjects and in certain individuals resulted in mild reductions in alveolar oxygen tensions. Obese individuals exercised less efficiently than nonobese as manifested by excessive energy expenditure in relation to weight. Steady-state exercise PaCoCo2 values were higher in those subjects previously shown to be relatively insensitive to inhalation of 5% CO2 but failed to correlate with the speed of ventilatory responsiveness.


1999 ◽  
Vol 86 (2) ◽  
pp. 611-616 ◽  
Author(s):  
Susana Mota ◽  
Pere Casan ◽  
Franchek Drobnic ◽  
Jordi Giner ◽  
Olga Ruiz ◽  
...  

In some trained athletes, maximal exercise ventilation is believed to be constrained by expiratory flow limitation (FL). Using the negative expiratory pressure method, we assessed whether FL was reached during a progressive maximal exercise test in 10 male competition cyclists. The cyclists reached an average maximal O2 consumption of 72 ml ⋅ kg−1 ⋅ min−1(range: 67–82 ml ⋅ kg−1 ⋅ min−1) and ventilation of 147 l/min (range: 122–180 l/min) (88% of preexercise maximal voluntary ventilation in 15 s). In nine subjects, FL was absent at all levels of exercise (i.e., expiratory flow increased with negative expiratory pressure over the entire tidal volume range). One subject, the oldest in the group, exhibited FL during peak exercise. The group end-expiratory lung volume (EELV) decreased during light-to-moderate exercise by 13% (range: 5–33%) of forced vital capacity but increased as maximal exercise was approached. EELV at peak exercise and at rest were not significantly different. The end-inspiratory lung volume increased progressively throughout the exercise test. The conclusions reached are as follows: 1) most well-trained young cyclists do not reach FL even during maximal exercise, and, hence, mechanical ventilatory constraint does not limit their aerobic exercise capacity, and 2) in absence of FL, EELV decreases initially but increases during heavy exercise.


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

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