Respiration during exercise in conscious laryngectomized humans

1989 ◽  
Vol 66 (5) ◽  
pp. 2071-2078 ◽  
Author(s):  
W. N. Gardner ◽  
M. S. Meah

We compared respiratory patterning at rest and during steady cycle exercise at work rates of 30, 60, and 90 W in 7 male chronically laryngectomized subjects and 13 normal controls. Breathing was measured with a pneumotachograph and end-tidal PCO2 by mass spectrometer. Inspired air was humidified and enriched to 35% O2. Peak flow, volume, and times for the inspiratory and expiratory half cycles, time for expiratory flow, minute ventilation, and mean inspiratory flow were computer averaged over at least 40 breaths at rest and during the last 2 min of 5-min periods at each work rate. During the transition from rest to exercise and with increasing work rate in both groups, there was an increase in respiratory rate and depth with selective and progressive shortening of expiratory time; these responses were not significantly different between the two groups, but there was a suggestion that respiratory “drive” as quantitated by mean inspiratory flow may limit in the laryngectomized subjects at high work rates. Time for expiratory flow increased on transition from rest to exercise and then decreased in both groups as the work rate increased; it was shorter in the laryngectomy than control group at all levels. In the laryngectomized subjects there was significantly more breath-by-breath scatter in some variables at rest, but there was no difference during exercise. It is concluded that chronic removal of the larynx and upper airways in mildly hyperoxic conscious humans has only subtle and, therefore, functionally insignificant effects on breathing during moderate exercise. Evidence is provided that the upper airways can modulate expiratory flow but not expiratory time during exercise.

1999 ◽  
Vol 98 (1) ◽  
pp. 91-101
Author(s):  
Takahiro URUMA ◽  
Hiroshi KIMURA ◽  
Akira KOJIMA ◽  
Kiyoshi HASAKO ◽  
Shigeru MASUYAMA ◽  
...  

In order to evaluate the applicability of volume acceleration (AI) at the onset of inspiration as an index of neuromuscular output, CO2 rebreathing in six healthy subjects and incremental-load exercise in eight healthy subjects was performed while measuring AI and mouth occlusion pressure (P0.1). During CO2 rebreathing, AI increased linearly with end-tidal CO2 partial pressure and P0.1. During incremental-load exercise, P0.1 and AI increased exponentially with minute ventilation and mean inspiratory flow, and AI increased linearly with P0.1. Dyspnoea sensation at rest and exercise with or without the circuit system in eight healthy subjects was examined. Dyspnoea sensation increased markedly with the circuit system in some subjects. Incremental-load exercise was carried out by 13 healthy subjects and 21 patients with chronic obstructive pulmonary disease (COPD) to evaluate the difference in AI as respiratory drive between the two groups in the absence of a respiratory circuit. In patients with COPD, AI responses to minute ventilation, mean inspiratory flow and carbon dioxide output (co2) were greater than those in healthy subjects. In patients with COPD, the AI response to co2 was greater in those with a lower FEV1.0 (forced expiratory volume in 1.0 s), but the ventilatory response to co2 was lower in those with a lower FEV1.0. These data suggest that AI reflects neuromuscular output during CO2 rebreathing and incremental-load exercise under conditions where mechanical properties of the respiratory system are expected to be involved. During exercise, flow increased markedly, and the influence of the resistance of the respiratory circuit also increased. Therefore the use of AI has the advantage of less resistance (no respiratory circuit) and less additional respiratory effort, in comparison with the use of P0.1, especially in patients with COPD.


1984 ◽  
Vol 56 (6) ◽  
pp. 1627-1632 ◽  
Author(s):  
H. Kimura ◽  
F. Hayashi ◽  
A. Yoshida ◽  
S. Watanabe ◽  
I. Hashizume ◽  
...  

We studied 10 male subjects who were administered chlormadinone acetate (CMA), a potent synthetic progesterone, to clarify the physiological basis of its respiratory effects. Arterial blood gas tension, resting ventilation, and respiratory drive assessed by ventilatory and occlusion pressure response to CO2 with and without inspiratory flow-resistive loading were measured before and 4 wk after CMA administration. In all subjects, arterial PCO2 decreased significantly by 5.7 +/- 0.6 (SE) Torr with an increase in minute ventilation by 1.8 +/- 0.6 l X min-1, whereas no significant changes were seen in O2 uptake. During unloaded conditions, both slopes of occlusion pressure and ventilatory response to CO2 increased, being statistically significant in the former but showing nonsignificant trends in the latter. Furthermore, inspiratory flow-resistive loading (16 cmH2O X l(-1) X s) increased both slopes more markedly after CMA. The magnitudes of load compensation, assessed by the ratio of loaded to unloaded slope of the occlusion pressure response curve, were increased significantly. We concluded CMA is a potent respiratory stimulant that increases the CO2 chemosensitivity and neuromechanical drives in the load-compensation mechanism.


1981 ◽  
Vol 50 (3) ◽  
pp. 552-560 ◽  
Author(s):  
J. A. Hirsch ◽  
B. Bishop

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.


1998 ◽  
Vol 84 (1) ◽  
pp. 3-12 ◽  
Author(s):  
S. Meza ◽  
E. Giannouli ◽  
M. Younes

Meza, S., E. Giannouli, and M. Younes. Control of breathing during sleep assessed by proportional assist ventilation. J. Appl. Physiol. 84(1): 3–12, 1998.—We used proportional assist ventilation (PAV) to evaluate the sources of respiratory drive during sleep. PAV increases the slope of the relation between tidal volume (Vt) and respiratory muscle pressure output (Pmus). We reasoned that if respiratory drive is dominated by chemical factors, progressive increase of PAV gain should result in only a small increase in Vt because Pmus would be downregulated substantially as a result of small decreases in[Formula: see text]. In the presence of substantial nonchemical sources of drive [believed to be the case in rapid-eye-movement (REM) sleep] PAV should result in a substantial increase in minute ventilation and reduction in [Formula: see text] as the output related to the chemically insensitive drive source is amplified severalfold. Twelve normal subjects underwent polysomnography while connected to a PAV ventilator. Continuous positive air pressure (5.2 ± 2.0 cmH2O) was administered to stabilize the upper airway. PAV was increased in 2-min steps from 0 to 20, 40, 60, 80, and 90% of the subject’s elastance and resistance. Vt, respiratory rate, minute ventilation, and end-tidal CO2pressure were measured at the different levels, and Pmus was calculated. Observations were obtained in stage 2 sleep ( n = 12), slow-wave sleep ( n = 11), and REM sleep ( n = 7). In all cases, Pmus was substantially downregulated with increase in assist so that the increase in Vt, although significant ( P < 0.05), was small (0.08 liter at the highest assist). There was no difference in response between REM and non-REM sleep. We conclude that respiratory drive during sleep is dominated by chemical control and that there is no fundamental difference between REM and non-REM sleep in this regard. REM sleep appears to simply add bidirectional noise to what is basically a chemically controlled respiratory output.


2016 ◽  
Vol 2 (4) ◽  
pp. 00062-2016 ◽  
Author(s):  
Mariann H.L. Bentsen ◽  
Morten Eriksen ◽  
Merete S. Olsen ◽  
Trond Markestad ◽  
Thomas Halvorsen

Reliable, accurate and noninvasive methods for measuring lung function in infants are desirable. Electromagnetic inductance plethysmography has been used to perform infant spirometry and VoluSense Pediatrics (VSP) (VoluSense, Bergen, Norway) represents an updated version of this technique. We aimed to examine its accuracy compared to a validated system measuring airflow via a facemask using an ultrasonic flowmeter.We tested 30 infants with postmenstrual ages between 36 to 43 weeks and weights from 2.3 to 4.8 kg, applying both methods simultaneously and applying VSP alone. Agreement between the methods was calculated using Bland–Altman analyses and we also estimated the effect of applying the mask.Mean differences for all breathing parameters were within ±5.5% and limits of agreement between the two methods were acceptable, except perhaps for peak tidal expiratory flow (PTEF). Application of the facemask significantly increased tidal volume, minute ventilation, PTEF, the ratio of inspiratory to expiratory time and the ratio of expiratory flow at 50% of expired volume to PTEF.VSP accurately measured tidal breathing parameters and seems well suited for tidal breathing measurements in infants under treatment with equipment that precludes the use of a facemask.


1998 ◽  
Vol 85 (6) ◽  
pp. 2213-2219 ◽  
Author(s):  
Thorsten Schäfer ◽  
Marianne E. Schläfke

Rapid eye movements during rapid-eye-movement (REM) sleep are associated with rapid, shallow breathing. We wanted to know whether this effect persisted during increased respiratory drive by CO2. In eight healthy subjects, we recorded electroencephalographic, electrooculographic, and electromyographic signals, ventilation, and end-tidal[Formula: see text] during the night. Inspiratory[Formula: see text] was changed to increase end-tidal [Formula: see text] by 3 and 6 Torr. During normocapnia, rapid eye movements were associated with a decrease in total breath time by −0.71 ± 0.19 (SE) s ( P < 0.05) because of shortened expiratory time (−0.52 ± 0.08 s, P < 0.001) and with a reduced tidal volume (−89 ± 27 ml, P < 0.05) because of decreased rib cage contribution (−75 ± 18 ml, P < 0.05). Abdominal (−11 ± 16 ml, P = 0.52) and minute ventilation (−0.09 ± 0.21 ml/min, P = 0.66) did not change. In hypercapnia, however, rapid eye movements were associated with a further shortening of total breath time. Abdominal breathing was also inhibited (−79 ± 23 ml, P< 0.05), leading to a stronger inhibition of tidal volume and minute ventilation (−1.84 ± 0.54 l/min, P < 0.05). We conclude that REM-associated respiratory changes are even more pronounced during hypercapnia because of additional inhibition of abdominal breathing. This may contribute to the reduction of the hypercapnic ventilatory response during REM sleep.


1997 ◽  
Vol 83 (1) ◽  
pp. 82-88 ◽  
Author(s):  
Bharath S. Krishnan ◽  
Ron E. Clemens ◽  
Trevor A. Zintel ◽  
Martin J. Stockwell ◽  
Charles G. Gallagher

Krishnan, Bharath S., Ron E. Clemens, Trevor A. Zintel, Martin J. Stockwell, and Charles G. Gallagher. Ventilatory response to helium-oxygen breathing during exercise: effect of airway anesthesia. J. Appl. Physiol. 83(1): 82–88, 1997.—The substitution of a normoxic helium mixture (HeO2) for room air (Air) during exercise results in a sustained hyperventilation, which is present even in the first breath. We hypothesized that this response is dependent on intact airway afferents; if so, airway anesthesia (Anesthesia) should affect this response. Anesthesia was administered to the upper airways by topical application and to lower central airways by aerosol inhalation and was confirmed to be effective for over 15 min. Subjects performed constant work-rate exercise (CWE) at 69 ± 2 (SE) % maximal work rate on a cycle ergometer on three separate days: twice after saline inhalation ( days 1 and 3) and once after Anesthesia ( day 2). CWE commenced after a brief warm-up, with subjects breathing Air for the first 5 min (Air-1), HeO2 for the next 3 min, and Air again until the end of CWE (Air-2). The resistance of the breathing circuit was matched for Air and HeO2. Breathing HeO2 resulted in a small but significant increase in minute ventilation (V˙i) and decrease in alveolar [Formula: see text] in both the Saline (average of 2 saline tests; not significant) and Anesthesia tests. Although Anesthesia had no effect on the sustained hyperventilatory response to HeO2breathing, theV˙i transients within the first six breaths of HeO2 were significantly attenuated with Anesthesia. We conclude that theV˙i response to HeO2 is not simply due to a reduction in external tubing resistance and that, in humans, airway afferents mediate the transient but not the sustained hyperventilatory response to HeO2 breathing during exercise.


1995 ◽  
Vol 78 (2) ◽  
pp. 449-457 ◽  
Author(s):  
G. A. Fontana ◽  
T. Pantaleo ◽  
F. Bongianni ◽  
F. Cresci ◽  
F. Lavorini ◽  
...  

We investigated the effects of prostaglandin synthesis blockade on the changes in breathing pattern, mean blood pressure (MBP), and heart rate (HR) elicited by 3 min of static handgrip at 30% of the maximum voluntary contraction in 12 healthy volunteers. Before each handgrip trial, subjects were treated with intravenous administration of either saline placebo (control) or 1 mg/kg of ketoprofen. Muscle tension and integrated electromyographic activity of exercising muscles remained fairly constant during each trial. In agreement with our earlier findings, during control handgrip minute ventilation progressively increased (P < 0.01) due to a rise in tidal volume and, to a lesser extent, in respiratory frequency. Mean inspiratory flow, MBP, and HR also increased (P < 0.01). End-tidal PCO2 decreased (P < 0.05) during the late phases of control handgrip bouts. Ketoprofen administration reduced serum thromboxane B2 levels (from 57.5 +/- 7.0 to 1.6 +/- 0.4 pg/ml; P < 0.01) and significantly attenuated mean increases in minute ventilation (40.25 +/- 0.60%), tidal volume (37.78 +/- 7.48%), respiratory frequency (55.94 +/- 17.92%), inspiratory flow (42.66 +/- 5.11%), MBP (22.33 +/- 6.82%), and HR (11.04 +/- 2.75%) during the 3rd min of handgrip. End-tidal PCO2 remained close to normocapnic levels. In agreement with previous animal investigations, the present results show that arachidonic acid metabolites are involved in the regulation of the cardiovascular responses to static efforts in humans, possibly through a stimulatory action on muscle receptors. Furthermore, they provide the first experimental evidence that products of the cyclooxygenase metabolic pathway play a role in the mediation of the respiratory adjustments elicited by this form of exercise.


1978 ◽  
Vol 45 (4) ◽  
pp. 495-501 ◽  
Author(s):  
B. Bishop ◽  
J. Hirsch ◽  
M. Thursby

This study is a breath-by-breath analysis of the effects of 5, 10, and 15 cmH2O positive-pressure breathing (PPB) on man's steady-state breathing pattern. Inspiratory (TI), expiratory (TE), and cycle (TT) durations, tidal volumes (VT), minute ventilation (VE), mean inspiratory flow rate (VT/TI), and mean expiratory flow rate (VT/TE) were determined from pneumotachograph and Wedge spirometer recordings before and during steady states on PPB. End-tidal CO2 was continuously recorded. Seventeen adults, seated in a full body-box, breathed quietly for 8 min through a mouthpiece on a bag-in-box. Pressure in the body-box was lowered to the desired level prior to 4 min of stress. On all pressure levels, end-expiratory volume, VT, VE, VT/TI, and VT/TE increased; end-tidal CO2, TE, and TT decreased with no consistent change in TI. Calculated alveolar ventilations indicated that the increases in VE were true hyperventilations. Each individual increased VE by using a unique combination of VT, TI, and TE. End-expiratory volume increased less and expiratory flow increased more than would occur passively. Hence, it is concluded that active reflexes account for the resistance of the systems to the passive distention, the facilitation of expiratory flow, and the shortening of TE.


2000 ◽  
Vol 10 (3) ◽  
pp. 201-207 ◽  
Author(s):  
Gernot Buheitel ◽  
Michael Hofbeck ◽  
Stephan Gerling ◽  
Andreas Koch ◽  
Helmut Singer

AbstractObjectiveTo investigate cardiopulmonary performance in patients after a Fontan procedure, comparing it to patients following a Senning operation.MethodsWe studied 21 children, with a mean age of 11.1 years, after a total cavopulmonary anastomosis, comparing them to 13 with complete transposition after a Senning procedure, having a mean age of 11.8 years, and 21 control subjects with a mean age of 11.2 years. All were tested on a bicycle ergospirometer.ResultsPeak consumption of oxygen, maximal work rate, peak oxygen pulse and endexpiratory pressure of carbon dioxide at a work rate of 1.5 Watt/kg were lowest in patients with a modified Fontan procedure, and highest in the control group (p≤ 0.0278). Production of carbon dioxide, and minute ventilation at a work rate of 1.5 Watt/kg, was highest in the patients after Fontan procedure, and lowest in the healthy subjects (p≤ 0.0163). Production of carbon dioxide per single breath was lower in those having a Fontan procedure (28.9 ml) than in the two other groups (35.1 ml; p = 0.0243). The tidal volume showed no significant differences between the three groups.ConclusionsThe reaction to exercise was identical qualitatively in both groups of patients, and comparable to the behaviour of patients with chronic heart failure. Quantitatively, the results of the patients following a Senning procedure lay between those of control subjects and those who had undergone a Fontan operation. The only exception was dead space ventilation, where the patients after a Fontan procedure differed from the two other groups because of their increased ventilation-perfusion mismatch.


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