scholarly journals The physiological mechanism behind the talk test

Kinesiology ◽  
2017 ◽  
Vol 49 (1) ◽  
pp. 3-8 ◽  
Author(s):  
Noortje Creemers ◽  
Jos J. de Koning
Keyword(s):  
Minute Ventilation ◽  
Physiological Mechanism ◽  
Cycle Ergometer ◽  
Potential Mechanism ◽  
Breathing Frequency ◽  
Co2 Output ◽  
Ventilatory Drive ◽  
Aged Subjects ◽  
End Tidal ◽  
End Tidal Co2

The Talk Test (TT) is a very simple marker of exercise intensity, which has been shown to be a useful surrogate of the ventilatory (VT) and respiratory compensation (RCT) thresholds. The purpose of this study was to evaluate a potential mechanism behind the TT. Healthy, college-aged subjects (n=20) performed a maximal and two sub-maximal cycle ergometer tests. The two submaximal tests were performed: with the Talk Test (EXP) and without speaking (the control trial – CON). Oxygen uptake (VO2), CO2 output (VCO2), minute ventilation (VE), breathing frequency (BF), end-tidal CO2 pressure (PETCO2) and TT times were recorded. VO2, VCO2 and VE were reduced during the TT and increased immediately after it. BF was reduced during the TT. PETCO2 values (a surrogate of PaCO2) were highest during the TT and lowest before the TT. The time to complete the TT increased across progressive stages. This study supports the hypothesis that talking causes CO2 retention, which may cause ventilatory drive to increase. Since the ventilatory drive is already high above the VT, the apparent CO2 retention associated with speech may cause talking to become uncomfortable

Effect of inspiratory resistive loading on control of ventilation during progressive exercise

1987 ◽  
Vol 62 (1) ◽  
pp. 134-140 ◽  
Author(s):  
A. D. D'Urzo ◽  
K. R. Chapman ◽  
A. S. Rebuck
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Work Load ◽  
Cycle Ergometer ◽  
Resistive Load ◽  
Co2 Output ◽  
Exercise Ventilation ◽  
Resistive Loading ◽  
End Tidal ◽  
Arterial O2 Saturation

Eight healthy volunteers performed gradational tests to exhaustion on a mechanically braked cycle ergometer, with and without the addition of an inspiratory resistive load. Mean slopes for linear ventilatory responses during loaded and unloaded exercise [change in minute ventilation per change in CO2 output (delta VE/delta VCO2)] measured below the anaerobic threshold were 24.1 +/- 1.3 (SE) = l/l of CO2 and 26.2 +/- 1.0 l/l of CO2, respectively (P greater than 0.10). During loaded exercise, decrements in VE, tidal volume, respiratory frequency, arterial O2 saturation, and increases in end-tidal CO2 tension were observed only when work loads exceeded 65% of the unloaded maximum. There was a significant correlation between the resting ventilatory response to hypercapnia delta VE/delta PCO2 and the ventilatory response to VCO2 during exercise (delta VE/delta VCO2; r = 0.88; P less than 0.05). The maximal inspiratory pressure generated during loading correlated with CO2 sensitivity at rest (r = 0.91; P less than 0.05) and with exercise ventilation (delta VE/delta VCO2; r = 0.83; P less than 0.05). Although resistive loading did not alter O2 uptake (VO2) or heart rate (HR) as a function of work load, maximal VO2, HR, and exercise tolerance were decreased to 90% of control values. We conclude that a modest inspiratory resistive load reduces maximum exercise capacity and that CO2 responsiveness may play a role in the control of breathing during exercise when airway resistance is artificially increased.

Increased normoxic ventilation induced by repetitive hypoxia in conscious dogs

1992 ◽  
Vol 73 (5) ◽  
pp. 2083-2088 ◽  
Author(s):  
K. Y. Cao ◽  
C. W. Zwillich ◽  
M. Berthon-Jones ◽  
C. E. Sullivan
Keyword(s):  
Minute Ventilation ◽  
Recovery Period ◽  
Short Exposure ◽  
Experimental Protocol ◽  
Ventilatory Drive ◽  
The Mean ◽  
End Tidal ◽  
Arterial O2 Saturation ◽  
Conscious Animals ◽  
End Tidal Co2

To determine if a long-lasting increase in normoxic ventilatory drive is induced in conscious animals by repetitive hypoxia, we examined the normoxic [arterial O2 saturation (SaO2) > 93%] ventilatory response following successive episodes of 2-min eucapnic hypoxic challenges (SaO2 = 80%) in awake tracheotomized dogs. End-tidal CO2 was maintained at the resting level during and after repetitive hypoxia. The experimental protocol was performed twice in each of five dogs on separate days. To determine if changes in normoxic ventilation occurred between episodes of repetitive hypoxia, data were compared from six periods (epochs) for all experiments. The mean minute ventilation (VI) during three normoxic periods between episodes of intermittent hypoxia was 135, 154, and 169% of control (P < 0.05). VI during a 30-min recovery period was still higher at 183 and 172% of control (P < 0.05). Normoxic VI between hypoxic and recovery periods was significantly higher than the corresponding values in sham experiments. Our results indicate that a long-lasting increase in normoxic ventilation can be evoked in an awake unanesthetized dog by a short exposure to repetitive hypoxia.

Alteration by hyperoxia of ventilatory dynamics during sinusoidal work

1980 ◽  
Vol 48 (6) ◽  
pp. 1083-1091 ◽  
Author(s):  
R. Casaburi ◽  
R. W. Stremel ◽  
B. J. Whipp ◽  
W. L. Beaver ◽  
K. Wasserman
Keyword(s):  
Gas Exchange ◽  
Work Load ◽  
Cycle Ergometer ◽  
Work Rate ◽  
Phase Lag ◽  
Ventilatory Responses ◽  
Load Tests ◽  
The Mean ◽  
End Tidal ◽  
End Tidal Co2

The effects of hyperoxia on ventilatory and gas exchange dynamics were studied utilizing sinusoidal work rate forcings. Five subjects exercised on 14 occasions on a cycle ergometer for 30 min with a sinusoidally varying work load. Tests were performed at seven frequencies of work load during air or 100% O2 inspiration. From the breath-by-breath responses to these tests, dynamic characteristics were analyzed by extracting the mean level, amplitude of oscillation, and phase lag for each six variables with digital computer techniques. Calculation of the time constant (tau) of the ventilatory responses demonstrated that ventilatory kinetics were slower during hyperoxia than during normoxia (P less than 0.025; avg 1.56 and 1.13 min, respectively). Further, for identical work rate fluctuations, end-tidal CO2 tension fluctuations were increased by hyperpoxia. Ventilation during hyperoxia is slower to respond to variations in the level of metabolically produced CO2, presumably because hyperoxia attenuates carotid body output; the arterial CO2 tension is consequently less tightly regulated.

Effects of elevated oxygen and carbon dioxide partial pressures on respiratory function and cognitive performance

2014 ◽  
Vol 117 (4) ◽  
pp. 406-412 ◽  
Author(s):  
Matthew Gill ◽  
Michael J. Natoli ◽  
Charles Vacchiano ◽  
David B. MacLeod ◽  
Keita Ikeda ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Respiratory Function ◽  
Vision Loss ◽  
Minute Ventilation ◽  
Cycle Ergometer ◽  
Hyperbaric Chamber ◽  
Tunnel Vision ◽  
Partial Pressures ◽  
Ergometer Exercise ◽  
End Tidal

Hyperoxia during diving has been suggested to exacerbate hypercapnic narcosis and promote unconsciousness. We tested this hypothesis in male volunteers (12 at rest, 10 at 75 W cycle ergometer exercise) breathing each of four gases in a hyperbaric chamber. Inspired Po2 (PiO2) was 0.21 and 1.3 atmospheres (atm) without or with an individual subject's maximum tolerable inspired CO2 (PiO2 = 0.055–0.085 atm). Measurements included end-tidal CO2 partial pressure (PetCO2), rating of perceived discomfort (RPD), expired minute ventilation (V̇e), and cognitive function assessed by auditory n-back test. The most prominent finding was, irrespective of PetCO2, that minute ventilation was 8–9 l/min greater for rest or exercise with a PiO2 of 1.3 atm compared with 0.21 atm ( P < 0.0001). For hyperoxic gases, PetCO2 was consistently less than for normoxic gases ( P < 0.01). For hyperoxic hypercapnic gases, n-back scores were higher than for normoxic gases ( P < 0.01), and RPD was lower for exercise but not rest ( P < 0.02). Subjects completed 66 hyperoxic hypercapnic trials without incident, but five stopped prematurely because of serious symptoms (tunnel vision, vision loss, dizziness, panic, exhaustion, or near syncope) during 69 normoxic hypercapnic trials ( P = 0.0582). Serious symptoms during hypercapnic trials occurred only during normoxia. We conclude serious symptoms with hyperoxic hypercapnia were absent because of decreased PetCO2 consequent to increased ventilation.

Anaerobic threshold alterations caused by endurance training in middle-aged men

1979 ◽  
Vol 46 (6) ◽  
pp. 1039-1046 ◽  
Author(s):  
J. A. Davis ◽  
M. H. Frank ◽  
B. J. Whipp ◽  
K. Wasserman
Keyword(s):  
Endurance Training ◽  
Anaerobic Threshold ◽  
Minute Ventilation ◽  
Correlation Coefficients ◽  
Cycle Ergometer ◽  
Work Rate ◽  
Middle Aged ◽  
Co2 Output ◽  
Before And After ◽  
Cycle Endurance

Nine previously sedentary middle-aged males underwent cycle endurance training 45 min/day for 9 wk with an average attendance of 4.1 days/wk. Seven males served as controls. Before and after the training period, the subjects performed three cycle ergometer tests. Work rate was incremented by 15 W/min, to the limit of the subjects' tolerance, in the first two tests; the third test consisted of contant-load cycling at an O2 uptake (VO2) just below the pretraining anaerobic threshold (AT). After training, the AT increased significantly by 44%, expressed as absolute VO2, and by 15%, expressed relative to VO2 max. Significant increases were also noted in VO2max (25%), maximal minute ventilation (19%), and maximal work rate (28%). The test-retest correlation coefficients for the AT (%VO2max) were 0.91, pre- and posttraining. Training did not alter steady-state VO2 during the submaximal exercise test whereas significant decreases occurred in CO2 output, VE, respiratory quotient, and VE/VO2. No changes occurred in the control subjects during this period. These results demonstrate that the AT is profoundly influenced by endurance training in previously sedentary middle-aged males.

scholarly journals Anesthesia and Increased Hypercarbic Drive Impair the Coordination between Breathing and Swallowing

2014 ◽  
Vol 121 (6) ◽  
pp. 1175-1183 ◽  
Author(s):  
Olivia M. D’Angelo ◽  
Daniel Diaz-Gil ◽  
Danuza Nunn ◽  
Jeroen C. P. Simons ◽  
Chloe Gianatasio ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Electrical Stimulation ◽  
Respiratory Tract ◽  
Motor Response ◽  
Minute Ventilation ◽  
Foreign Material ◽  
Randomized Controlled ◽  
Ventilatory Drive ◽  
End Tidal ◽  
Stimulation Of

Abstract Background: Coordination between breathing and swallowing helps prevent aspiration of foreign material into the respiratory tract. The authors examined the effects of anesthesia and hypercapnia on swallowing–breathing coordination. Methods: In a randomized controlled crossover study, general anesthesia with propofol or sevoflurane was titrated using an up-down method to identify the threshold for suppression of the motor response to electrical stimulation of the forearm. Additional measurements included bispectral index, genioglossus electromyogram, ventilation (pneumotachometer), and hypopharyngeal pressure. During wakefulness and at each level of anesthesia, carbon dioxide was added to increase the end-tidal pressure by 4 and 8 mmHg. A swallow was defined as increased genioglossus activity with deglutition apnea and an increase in hypopharyngeal pressure. Spontaneous swallows were categorized as physiological (during expiration or followed by expiration) or pathological (during inspiration or followed by an inspiration). Results: A total of 224 swallows were analyzed. Anesthesia increased the proportion of pathological swallows (25.9% vs. 4.9%) and decreased the number of swallows per hour (1.7 ± 3.3 vs. 28.0 ± 22.3) compared to wakefulness. During anesthesia, hypercapnia decreased hypopharyngeal pressure during inspiration (−14.1 ± 3.7 vs. −8.7 ± 2 mmHg) and increased minute ventilation, the proportion of pathological swallows (19.1% vs. 12.3%), and the number of swallows per hour (5.5 ± 17.0. vs. 1.3 ± 5.5). Conclusions: Anesthesia impaired the coordination between swallowing and respiration. Mild hypercapnia increased the frequency of swallowing during anesthesia and the likelihood of pathological swallowing. During anesthesia, the risk for aspiration may be further increased when ventilatory drive is stimulated.

Sonomicrometric regional diaphragmatic shortening in awake sheep after thoracic surgery

1989 ◽  
Vol 67 (6) ◽  
pp. 2357-2368 ◽  
Author(s):  
A. Torres ◽  
W. R. Kimball ◽  
J. Qvist ◽  
K. Stanek ◽  
R. M. Kacmarek ◽  
...  
Keyword(s):  
Thoracic Surgery ◽  
Tidal Volume ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Quiet Breathing ◽  
Transdiaphragmatic Pressure ◽  
Right Thoracotomy ◽  
Before And After ◽  
End Tidal ◽  
End Tidal Co2

Through a right thoracotomy in seven sheep we chronically implanted sonomicrometry crystals and electromyographic electrodes in the costal and crural diaphragmatic regions. Awake sheep were studied during recovery for 4-6 wk, both during quiet breathing (QB) and during CO2 rebreathing. Tidal volume, respiratory frequency, and esophageal and gastric pressures were studied before and after surgery. Normalized resting length (LFRC) was significantly decreased for the costal segment on postoperative day 1 compared with postoperative day 28. Fractional costal shortening both during QB and at 10% end-tidal CO2 (ETCO2) increased significantly from postoperative days 1 to 28, whereas crural shortening did not change during QB but progressively increased at 10% ETCO2. Maximal costal shortening during electrophrenic stimulation was constant at 40% LFRC during recovery, although maximal crural shortening increased from 23 to 32% LFRC. Minute ventilation, tidal volume, and transdiaphragmatic pressure at 10% ETCO2 increased progressively after thoracotomy until postoperative day 28. Our results suggest there is profound diaphragmatic inhibition after thoracotomy and crystal implantation in sheep that requires at least 3-4 wk for stable recovery.

Breath-by-breath respiratory timing and volume control during periodic breathing

1989 ◽  
Vol 257 (3) ◽  
pp. R653-R660
Author(s):  
D. W. Carley ◽  
C. Maayan ◽  
J. Grimes ◽  
D. C. Shannon
Keyword(s):  
Cross Correlation ◽  
Minute Ventilation ◽  
Periodic Breathing ◽  
Respiratory Pattern ◽  
Volume Control ◽  
Cycle Duration ◽  
Rapid Eye Movement Sleep ◽  
The Mean ◽  
End Tidal ◽  
End Tidal Co2

We examined the control of respiratory pattern during non-rapid-eye-movement sleep-related periodic breathing (PB) in adults, with and without hypoxia. We analyzed 186 cycles of PB from 18 epochs occurring in eight subjects; the mean (+/- SD) cycle duration was 30.8 +/- 8.4 s. Significant oscillations occurred in inspired tidal volume (VT), inspiratory duration (TI), mean inspired flow, inspired minute ventilation, and expiratory duration (TE) (P less than 0.005). For each epoch of PB, moving cross-correlation (MCC) functions were employed to describe the time-dependent intervariable relationships between 1) TI vs. TE, 2) VT vs. TE, and 3) VT vs. breath duration (TT) as synchronization, a strong and consistent intervariable correlation; relative coordination (RC), a weaker interaction characterized by an unstable MCC function oscillating at a subharmonic of the PB frequency; or as independence, with no statistical evidence of interaction. Fourteen epochs showed RC between TI and TE, 11 and 12 of which also showed RC between VT and TE, and VT and TT, respectively. In 4 epochs negative synchronization was exhibited by all three variable pairs. In no case were the oscillations between any pair of variables independent. The modes of coupling between variables were not correlated to O2 saturation, end-tidal CO2 levels, or inspired O2 level. We conclude that during sleep-related PB a nonrandom but weak coupling usually exists between TI and TE, VT and TE, and VT and TT.(ABSTRACT TRUNCATED AT 250 WORDS)

Volume, flow, and timing of each breath during negative airway pressure in humans

1981 ◽  
Vol 50 (3) ◽  
pp. 552-560 ◽  
Author(s):  
J. A. Hirsch ◽  
B. Bishop
Keyword(s):  
Airway Pressure ◽  
Minute Ventilation ◽  
The Body ◽  
Multiple Components ◽  
Respiratory Events ◽  
Inspiratory Activity ◽  
Expiratory Flow ◽  
End Tidal ◽  
Negative Airway Pressure ◽  
End Tidal Co2

We have analyzed the effects of 4-6 min of 5, 10 and 15 cmH2O continuous negative airway pressure breathing (NPB) on steady-state end-expiratory lung volume (delta VR) and breathing pattern. Fourteen healthy adults, seated in a full body box, breathed via a mouthpiece on a bag-in-box. Pressure in the body box was elevated to the desired pressure level. Inspiratory (TI) and expiratory (TE) durations, tidal volume (VT), minute ventilation (VI), mean inspiratory flow (VT/TI), and mean expiratory flow (VT/TE) were calculated from pneumotachometer recordings. The effects of NPB are decreases in delta VR, VT, and VT/TI and increases in VT/TE. The responses to NPB are an increase in breathing frequency, due to a shortened TE, and an increase in inspiratory activity. The decrease in delta VR and the increase in VT/TE are limited by an active retardation of expiratory flow. End-tidal CO2 and VI were not altered significantly during NPB, suggesting no alveolar hyperventilation. Thus multiple components of the human response to NPB are not all engaged at the same levels of NPB. The changes in the timing of respiratory events occur at -5 cmH2O, whereas VT compensation is not seen until -15 cmH2O.

Effect of CO2 on the ventilatory sensitivity to rising body temperature during exercise

2011 ◽  
Vol 110 (5) ◽  
pp. 1334-1341 ◽  
Author(s):  
Keiji Hayashi ◽  
Yasushi Honda ◽  
Natsuki Miyakawa ◽  
Naoto Fujii ◽  
Masashi Ichinose ◽  
...  
Keyword(s):  
Body Temperature ◽  
Prolonged Exercise ◽  
Minute Ventilation ◽  
Regression Line ◽  
Cycle Ergometer ◽  
Blood Velocity ◽  
Esophageal Temperature ◽  
Arterial Blood ◽  
End Tidal ◽  
Respiratory Gases

We examined the degree to which ventilatory sensitivity to rising body temperature (the slope of the regression line relating ventilation and body temperature) is altered by restoration of arterial Pco2 to the eucapnic level during prolonged exercise in the heat. Thirteen subjects exercised for ∼60 min on a cycle ergometer at 50% of peak O2 uptake with and without inhalation of CO2-enriched air. Subjects began breathing CO2-enriched air at the point that end-tidal Pco2 started to decline. Esophageal temperature (Tes), minute ventilation (V̇e), tidal volume (VT), respiratory frequency ( fR), respiratory gases, middle cerebral artery blood velocity, and arterial blood pressure were recorded continuously. When V̇e, VT, fR, and ventilatory equivalents for O2 uptake (V̇e/V̇o2) and CO2 output (V̇e/V̇co2) were plotted against changes in Tes from the start of the CO2-enriched air inhalation (ΔTes), the slopes of the regression lines relating V̇e, VT, V̇e/V̇o2, and V̇e/V̇co2 to ΔTes (ventilatory sensitivity to rising body temperature) were significantly greater when subjects breathed CO2-enriched air than when they breathed room air (V̇e: 19.8 ± 10.3 vs. 8.9 ± 6.7 l·min−1·°C−1, VT: 18 ± 120 vs. −81 ± 92 ml/°C; V̇e/V̇o2: 7.4 ± 5.5 vs. 2.6 ± 2.3 units/°C, and V̇e/V̇co2: 7.6 ± 6.6 vs. 3.4 ± 2.8 units/°C). The increase in V̇e was accompanied by increases in VT and fR. These results suggest that restoration of arterial Pco2 to nearly eucapnic levels increases ventilatory sensitivity to rising body temperature by around threefold.

Sign in / Sign up

Export Citation Format

Share Document