Breathing In Man Research Articles

Association of Alcohol Consumption and Sleep Disordered Breathing In Men And Women

Experimental evidence indicates that alcohol use near bedtime may exacerbate sleep disordered breathing (SDB). However, scarce research has examined the relation between moderate habitual alcohol use and objectively assessed SDB, and it is unclear whether patients with SDB, or those at risk for SDB, should be counseled to avoid alcohol regardless of proximity to bedtime. In this population-based epidemiology study, our objective is to measure the association of SDB with usual alcohol consumption habits. Men (N = 775) and women (N = 645)--initially randomly selected from a working population--participating in the Wisconsin Sleep Cohort Study were evaluated for alcohol consumption and SDB. The apnea-hypopnea index (AHI, events/hour) was determined by in-laboratory polysomnography. AHI > 5 defined "mild or worse" SDB and AHI > 15 defined "moderate or worse" SDB. Alcohol consumption (drinks/day) was assessed by questionnaire. Potential confounding or interacting variables such as smoking, body mass index, and medication use, were measured by clinical assessment and questionnaire. Relative to men who consumed less alcohol, for each increment of one drink per day, men who consumed more alcohol had 25% greater odds of mild or worse SDB (OR = 1.25, 95% CI = 1.07-1.46, p = 0.006). Among women, minimal to moderate alcohol consumption was not significantly associated with increased risk of SDB. In men, increased usual alcohol consumption was associated with increased risk of mild or worse SDB. Persons with SDB might benefit from generally reduced alcohol consumption and not just avoidance near bedtime.

A high prevalence of sleep disordered breathing in men with mild symptomatic chronic heart failure due to left ventricular systolic dysfunction

Sleep disordered breathing (SDB) is common in severe chronic heart failure (CHF) and is associated with increased morbidity and mortality. The prevalence of SDB in mild symptomatic CHF is unknown. The aim of this study was to determine the prevalence and characteristics of SDB in male patients with NYHA class II symptoms of CHF. 55 male patients with mild symptomatic CHF underwent assessment of quality of life, echocardiography, cardiopulmonary exercise, chemoreflex testing and polysomnography. 53% of the patients had SDB. 38% had central sleep apnoea (CSA) and 15% had obstructive sleep apnoea. SDB patients had steeper VE/VCO(2) slope [median (inter-quartile range) 31.1 (28-37) vs. 28.1 (27-30) respectively; p=0.04], enhanced chemoreflexes to carbon dioxide during wakefulness [mean+/-sd: 2.4+/-1.6 vs. 1.5+/-0.7 %VE Max/mmHg CO(2) respectively; p=0.03], and significantly higher levels of brain natriuretic peptide and endothelin-1 compared to patients without SDB. No differences in left ventricular ejection fraction, percent predicted peak oxygen uptake, or symptoms of SDB were observed. A high prevalence of SDB was found in men with mild symptomatic CHF. Patients with SDB could not be differentiated by symptoms or by routine cardiac assessment making clinical diagnosis of SDB in CHF difficult.

P0077 Experimental sleep fragmentation induces disordered breathing in men but not women

P0077 Experimental sleep fragmentation induces disordered breathing in men but not women

Transtornos respiratórios do sono e fibromialgia

Fibromyalgia is a chronic, painful condition that is diagnosed by identifying chronic, diffuse muscular-skeletal pain upon compression of at least eighteen determined anatomical points. Although not constituting diagnostic criteria, sleep fragmentation events, such as brief awakenings (arousals), increased oscillations in the cyclic alternating pattern of sleep, and alpha-wave intrusion into non-rapid eye movement sleep, are common in individuals with sleep disorders. Among the various manifestations of fibromyalgia, nonrestorative sleep is an important aspect that necessitates the investigation of primary sleep disorders in the evaluation of affected patients. The association between fibromyalgia and sleep disordered breathing was first described in 1986 in a report stating that three out of eleven patients with sleep apnea met the criteria for fibromyalgia. In seven of those patients, polysomnography revealed a pattern of fragmented sleep similar to the alpha-delta pattern. (1) Subsequent studies can be divided into those that evaluated sleep disordered breathing in patients with fibromyalgia and those that evaluated the manifestations of fibromyalgia in patients with sleep apnea. Sleep disordered breathing in patients with fibromyalgia has been more widely studied. Among the various articles, one significant 1993 study was conducted with twenty fibromyalgia patient and ten healthy volunteers. The authors found no difference between the two groups in terms of the frequency of apnea-hypopnea indices higher than five events per hour of sleep (20% of the cases in each group). However, they also found that the patients with sleep apnea presented greater sleep fragmentation. (2) According to the results of another 1993 study, fibromyalgia symptoms suggest sleep disordered breathing in men but not in women. The authors used polysomnography to evaluate thirteen men and

Relationships of craniofacial morphology and body mass index with sleep-disordered breathing in Japanese men.

Obesity is an established risk factor for sleep-disordered breathing, but the impact of craniofacial morphology is uncertain. The aim of this study was to assess the impact of craniofacial morphology and body weight on sleep-disordered breathing in Japanese men. A cross-sectional study. We measured body mass index, seven cephalometric variables, and 3% oxygen desaturation index recorded by a pulse oximeter in 313 Japanese men aged 20 to 65 years who attended a sleep clinic. We defined craniofacial score as the sums of quartile points (0-3) for distance from sella to nasion and that from hyoid bone to mandibular plane. The mean value of 3% oxygen desaturation index and odds ratios of 3% oxygen desaturation index 15 or greater progressively increased with craniofacial score as well as body mass index. Multivariate odds ratios associated with craniofacial score were higher in men with body mass index 25.0 kg/m or greater (odds ratio = 4.2, 95% confidence interval [CI] = 2.1-8.6) than in men with lower body mass index (odds ratio = 1.6, 95% CI = 0.7-3.6). Our results imply the importance of cephalometric assessment in overweight patients.

Modeling the bifurcating flow in an asymmetric human lung airway

In a former paper, the inspiratory flow characteristics in a three-generation symmetric bifurcation airway have been numerically investigated using a control volume method to solve the fully three-dimensional laminar Navier-Stokes equations. The present paper extends the work to deal with asymmetric airway extracted from the 5th–11th branches of the model of Weibel (Morphometry of the Human Lung. New York Academic Press, Verlag, 1963) in order to more appropriately model human air passage. Computations are carried out in the Reynolds number range 200–1600, corresponding to mouth-air breathing rates ranging from 0.27 to 2.16 l/s, representative for an averaged height man breathing from quiet to vigorous state. Particular attentions are paid to establishing relations between the Reynolds number and the overall flow characteristics, including flow patterns and pressure drop. The study shows that the ratios of airflow rate through the medial branches to that of their mother branches are the same, and this is also true for the ratios of airflow rate through the lateral branches. This partially explains why regular human breathing is not affected by airways of different sizes.

Chest wall kinematics during chemically stimulated breathing in healthy man.

Chest wall compartment kinematics and respiratory muscle coordinate activity, during either hypercapnia or hypoxia, have not been comparatively assessed in healthy humans. We assessed the displacement volume of the chest wall (Vcw) in 5 normal subjects during hypoxic-normocapnic and hypercapnic-hyperoxic rebreathing by using linearized magnetometers. Vcw was divided into displacement volumes of the rib cage (Vrc) and the abdomen (Vab). Esophageal (Pes) and gastric (Pga) pressures were simultaneously recorded and transdiaphragmatic pressure (Pdi) was calculated by subtracting Pes from Pga. Pressure swings (sw) from end expiration (EE) to end inspiration (EI) were also calculated. During both hypoxia and hypercapnia, from quiet breathing to 40 L/min VE, Vrc,EI increased consistently but Vrc,EE, and Vab,EI did not. Moreover, Vab,EE decreased significantly during hypercapnia and remained unchanged during hypoxia. PesEI decreased (more negative values) and PesEE increased (less negative values) during either stimulus, while PgaEE increased with hypercapnia. Pdisw, calculated as the difference between PdiEE and PdiEI, increased significantly with both hypercapnia and hypoxia ( p = 0.002 for both). On the plot of Pes vs Pga, the slope of a line from end expiratory to end inspiratory lung volume between 20 and 40 L/min VE progressively increased during hypercapnia indicating increasing rib cage muscle (RCM) contribution to inspiratory pressure swings relative to the diaphragm. From these results we conclude that in healthy man: (i) with both chemical stimuli RCM contribution accounts for increase in Vrc displacement; (ii) with hypercapnia, the decrease in Vab,EE displacement indicates abdominal muscle (ABM) contribution to tidal volume; (iii) RCM and ABM assist the diaphragmatic function during hypercapnic stimulation.

Modeling the bifurcating flow in a human lung airway

The inspiratory flow characteristics in a three-generation lung airway have been numerically investigated using a control volume method to solve the fully three-dimensional laminar Navier–Stokes equations. The three-generation airway is extracted from the fifth to seventh branches of the model of Weibel (Morphometry of the Human Lung, Academic Press, New York, Springer, Berlin, 1963) with in-plane and 90° off-plane configurations. Computations are carried out in the Reynolds number range of 200–1600, corresponding to mouth-air breathing rates ranging from 0.27 to 2.16 l/s, or an averaged height of a man breathing from quiet to vigorous state. Particular attention is paid to establishing relations between the Reynolds number and the overall flow characteristics, including flow patterns and pressure drop. The ratio of airflow rate through the medial branch to that of the lateral branch for an in-plane airway increases as Re 0.227. However, the total pressure drop coefficient varies as Re −0.497 for an in-plane airway and as Re −0.464 for an off-plane airway. These pressure drop results are in good agreement with the experimentally measured behavior of Re −0.5 and are more accurate than the numerically determined behavior of Re −0.61 assuming the airways to be approximated by two-dimensional channels.

Iliac Arteriovenous Fistula With Renal Insufficiency, Ascites, Hepatomegaly, and Abnormal Liver Test Results

Iliac Arteriovenous Fistula With Renal Insufficiency, Ascites, Hepatomegaly, and Abnormal Liver Test Results

Sleep-disordered breathing and glucose metabolism in hypertensive men: a population-based study.

Diabetes mellitus and obstructive sleep apnoea (OSA) are two prevalent medical problems. Both are strongly associated with obesity and hypertension. The aim of this study was to investigate whether the association between OSA and diabetes is entirely dependent on obesity in hypertensive men. A population-based study. The municipality of Uppsala, Sweden. Subjects and methods. In 1994, 2668 men aged 40-79 years answered a questionnaire regarding snoring, sleep disturbances and somatic diseases. An age-stratified sample of 116 hypertensive men was selected for a whole-night sleep study. Twenty-five of them had diabetes, defined as reporting regular medical controls for diabetes or having a fasting blood glucose > or =6.1 mmol L(-1). The prevalence of severe OSA, defined as apnoea-hypopnoea index (AHI) > or =20 h(-1) was significantly higher in diabetic patients than in normoglycaemic subjects (36 vs. 14.5%, P < 0.05). The sample was divided into four groups based on the presence or absence of severe OSA and the presence or absence of central obesity, defined as waist-to-hip ratio (WHR) > or =1.0. In a logistic regression model with the non-OSA, WHR <1.0 as the reference group, the adjusted odds ratio (95% confidence interval) for diabetes was 11.8 (2.0-69.8) in the OSA, WHR > or =1.0 group, whilst it was 3.6 (0.9-14.8) in the non-OSA, WHR > or =1.0 group and 5.7 (0.3-112) in the OSA, WHR <1.0 group. In a linear regression model, after adjustment for WHR, there was a significant relationship between variables of sleep-disordered breathing and fasting insulin, glucose and haemoglobin A1c. We conclude that, in hypertensive men, although obesity is the main risk factor for diabetes, coexistent severe OSA may add to this risk. Sleep breathing disorders, independent of central obesity, may influence plasma insulin and glycaemia.

The contribution of chemoreflex drives to resting breathing in man.

The contribution of automatic drives to breathing at rest, relative to behavioural drives such as "wakefulness", has been a subject of debate. We measured the combined central and peripheral chemoreflex contribution to resting ventilation using a modified rebreathing method that included a prior hyperventilation and addition of oxygen to maintain isoxia at a P(ET,O2) (end-tidal partial pressure of oxygen) of 100 mmHg. During rebreathing, ventilation was unrelated to P(ET,CO2) (end-tidal partial pressure of carbon dioxide) in the hypocapnic range, but after a threshold P(ET,CO2) was exceeded, ventilation increased linearly with P(ET,CO2). We considered the sub-threshold ventilation to be an estimate of the behavioural drives to breathe (mean +/- S.E.M. = 3.1 +/- 0.5 l min(-1)), and compared it to ventilation at rest (mean +/- S.E.M. = 9.1 +/- 0.7 l min(-1)). The difference was significant (Student's paired t test, P < 0.001). We also considered the threshold P(CO2) observed during rebreathing to be an estimate of the chemoreflex threshold at rest (mean +/- S.E.M. = 42.0 +/- 0.5 mmHg). However, P(ET,CO2) during rebreathing estimates mixed venous or tissue P(CO2), whereas the resting P(ET,CO2) during resting breathing estimates P(a,CO2) (arterial partial pressure of carbon dioxide). The chemoreflex threshold measured during rebreathing was therefore reduced by the difference in P(ET,CO2) at rest and at the start of rebreathing (the plateau estimates the mixed venous P(CO2) at rest) in order to make comparisons. The corrected chemoreflex thresholds (mean +/- S.E.M. = 26.0 +/- 0.9 mmHg) were significantly less (paired Student's t test, P < 0.001) than the resting P(ET,CO2) values (mean +/- S.E.M. = 34.3 +/- 0.5 mmHg). We conclude that both the behavioural and chemoreflex drives contribute to resting ventilation. Experimental Physiology (2001) 86.1, 109-116.

Obstructive sleep apnea syndrome: Anesthetic implications in the cardiac surgical patient

PATIENTS with obstructive sleep apnea syndrome (OSAS) are characterized by excessive daytime sleepiness, snoring, and fragmentation of nighttime sleep. They are usually obese and have upper airway edema. The prevalence of sleep apnea syndrome among the general population is 1% to 4%, 1 Young T Palta M Dempsey J et al. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med. 1993; 328: 1230-1235 Crossref PubMed Scopus (8385) Google Scholar but in patients with ischemic heart disease (IHD), it has been reported in 30%. 2 Mooe T Rabben T Wiklund U et al. Sleep-disordered breathing in men with coronary artery disease. Chest. 1996; 109: 659-663 Crossref PubMed Scopus (310) Google Scholar A study by Maekawa et al 3 Maekawa M Shiomi T Usui K et al. Prevalence of ischaemic heart disease among patients with sleep apnea syndrome. Psychiatry Clin Neurosci. 1998; 52: 219-220 Crossref PubMed Scopus (20) Google Scholar found that IHD was seen as a complication in about one quarter of sleep apnea syndrome patients. Sleep apnea syndrome aggravates coronary risk factors promoting IHD 3 Maekawa M Shiomi T Usui K et al. Prevalence of ischaemic heart disease among patients with sleep apnea syndrome. Psychiatry Clin Neurosci. 1998; 52: 219-220 Crossref PubMed Scopus (20) Google Scholar and causes coronary spasm. 4 Akasaka K Akiba Y Ishii Y et al. Association between sleep apnea syndrome and coronary artery disease. Nippon Kyobu Shikkan Gakkai Zasshi. 1997; 35: 16-21 PubMed Google Scholar Abnormal breathing patterns during sleep have been reported to trigger cardiac arrhythmias. 5 Dark D Pingleton S Kerby G et al. Breathing pattern abnormalities and arterial oxygen desaturation during sleep in the congestive heart failure syndrome. Chest. 1987; 91: 833-836 Crossref PubMed Scopus (108) Google Scholar

Carbon Dioxide Tracing for Face Mask Disconnects

To the Editor: The use of strapped on masks in the operating room has grown in recent years as more surgery is performed under regional or local anesthesia. We report a helpful signal on the carbon dioxide tracing that can alert the anesthesiologist that the tubing from the oxygen mask has come detached from the oxygen source. Immediately after the disconnection occurs, the end-tidal carbon dioxide tracing becomes noticeably larger (Figure 1a). Undoubtedly, the additional rebreathing of carbon dioxide that occurs explains the greater magnitude of the curve. The tracing returns to its normal size once the oxygen is reconnected.Figure 1: End-tidal carbon dioxide tracings for a man breathing oxygen from a nonrebreathing mask (a) with a 10-L oxygen flow or from a nasal cannula (b) with a 2-L oxygen flow and gas sampled from a 14-gauge IV catheter thrust into the nasal cannula.A similar but more subtle change is seen if a disconnection occurs while the end-tidal carbon dioxide tracing is obtained from an IV catheter thrust into a nasal cannula (Figure 1b). The large quantity of room air that is entrained obscures the effect of the extra carbon dioxide that is not washed away by the oxygen. Evan Goodman, MD Pat A. Johnson, CRNA Department of Anesthesiology; Case Western Reserve University and University Hospitals of Cleveland; Cleveland Heights, OH 44118

Effects of mechanical unloading/loading on respiratory loop gain and periodic breathing in man

We investigated the effect of mechanical unloading and loading on Cheyne–Stokes respiration (CSR) in seven intubated patients with preexisting CSR. For mechanical loading patients had to breathe against the resistance of the endotracheal tube. For mechanical unloading patients were supported with a volume-proportional pressure support in the proportional assist ventilation (PAV) mode whilst the flow-dependent (nonlinear) endotracheal tube resistance was continuously compensated for by means of the automatic tube compensation (ATC) mode. Mechanical unloading aggravated CSR as revealed by a prolongation of apnea time and by an increase in the so-called strength index whereas mechanical loading shortened apnea time and decreased strength index. To test whether the observed changes are caused by the effect of mechanical unloading/loading on respiratory loop gain (relationship between minute ventilation and arterial CO 2 tension), the response of respiratory loop gain on mechanical unloading/loading was determined in five healthy subjects (without CSR). In each subject, mechanical unloading increased respiratory loop gain whereas mechanical loading decreased it.

Control of breathing in man; insights from the ‘locked-in’ syndrome

Control of breathing was studied in a patient with a lesion in the ventral pons; no volitional behaviour, including voluntary breathing acts, was possible (locked-in syndrome, LIS). Spontaneous breathing via a tracheostomy maintained a normal P et CO 2 of 39–40 mmHg. Variability of ventilatory parameters awake was similar to that seen in five tracheostomized control subjects during stage IV sleep but much smaller than during resting wakefulness. Emotion associated with laughter caused disturbances of breathing. The ventilatory response to CO 2 was normal and was associated with ‘hunger for air’ when the P et CO 2 was 49–50 mmHg. Mechanical ventilation to reduce P et CO 2 by as little as 1 mmHg resulted in apnoea when the ventilator was disconnected; breathing resumed when P et CO 2 crossed the threshold of 39–40 mmHg. These results demonstrate the functional dependence of the human medullary respiratory oscillator on a threshold level of P co 2 in the absence of cortico-bulbar input, even during wakefulness. The absence of such input may explain the regularity of breathing.

Sleep-Disordered Breathing in Men With Coronary Artery Disease

To examine the occurrence of sleep apnea and nocturnal hypoxemia in men with symptomatic coronary artery disease (CAD) and to evaluate the relationship between disordered breathing and coronary artery disease. Case-control study. Cases were randomly selected from men undergoing coronary angiography because of angina pectoris. Controls were age matched and selected from the population registry. Pulse oximetry, oronasal thermistors, body position indicator, and recording of body and respiratory movements were used to quantify desaturations and apneas. Norrland University Hospital, a referral center for northern Sweden. One hundred forty-two men with angina pectoris and angiographically verified CAD and 50 controls without known heart disease. The number of arterial oxygen desaturations of 4% or more per hour of sleep, oxygen desaturation index (ODI), and the number of apneas or hypopneas per hour of sleep, apnea-hypopnea index (AHI). Men with CAD had a high occurrence of sleep-disordered breathing measured as ODI of 5 or more, 39% (n=55), or AHI of 10 or more, 37% (n=50), while, the same proportions in controls were 22% (n=11, p<0.05) and 20% (n=10, p<0.05). Mean values of ODI in cases and controls were 6.4 and 2.7, respectively (p<0.001). Multiple logistic regression analysis identified ODI, AHI, body mass index, and hypertension as significant predictors of CAD (p<0.05). Sleep- disordered breathing is common in men with CAD. A significant association between sleep apnea with nocturnal hypoxemia and CAD remains after adjustment for age, hypertension, body mass index, diabetes, and smoking.

Coordination Between Breathing and Finger Tracking in Man.

Arm and leg movements are known to produce temporal pattern changes of breathing. This can be interpreted as coordination, as defined by von Holst (1939). The aim of the present study was to find whether breathing exerts an influence in a reverse direction on a nonrespiratory movement as well. A pursuit tracking test was used, and test individuals (N = 19) were instructed to track a visually presented step function by flexion or extension of their right index finger. Velocity and precision of the step responses proved to be dependent on their relation to the breathing time course; the differences between inspiratory and expiratory responses were smaller than those within each half-cycle. The movements were performed more rapidly and more precisely in about the middle of each half-cycle than immediately after the respiratory phase transition or during the second half of each inspiration or expiration. Discontinuous short-lasting motor actions exerted a coordinative influence on respiration comparablewith that of periodical events: Breaths coinciding with step responses were shortened, preferably when the preset step was given early in the inspiration. It was hypothesized that the reciprocal effect between both motor actions changes periodically. In the first part of each respiratory half-cycle, the respiratory rhythm exerts only a weak influence on additional movements, but it can be altered easily by simultaneous motor processes. Toward the respiratory phase-switching, the respiratory rhythm behaves more stably against coordinative influences and becomes capable of impairing an additional movement.

Evidence for limbic system activation during CO2-stimulated breathing in man.

1. The role of supra-brainstem structures in the ventilatory response to inhaled CO2 is unknown. The present study uses positron emission tomography (PET), with infusion of H2(15)O, to measure changes in relative regional cerebral blood flow (rCBF) in order to identify sites of increased neuronal activation during CO2-stimulated breathing (CO2-SB) in awake man. 2. Five male volunteers were scanned during CO2-SB (mean +/- S.E.M.; end-tidal PCO2, 50.3 +/- 1.7 mmHg; respiratory frequency, 16.4 +/- 2.7 min-1; tidal volume, 1.8 +/- 0.2 l). As control, scans were performed during 'passive' isocapnic (elevated fraction of inspired CO2) positive pressure ventilation (end-tidal PCO2, 38.4 +/- 1.0 mmHg; respiratory frequency, 15.5 +/- 2.2 min-1; tidal volume, 1.6 +/- 0.2 l). With CO2-SB, all subjects reported dyspnoea. 3. The anatomical locations of the increases in relative rCBF (CO2-SB versus control) were obtained using magnetic resonance imaging. 4. Group analysis identified neuronal activation within the upper brainstem, midbrain and hypothalamus, thalamus, hippocampus and parahippocampus, fusiform gyrus, cingulate area, insula, frontal cortex, temporo-occipital cortex and parietal cortex. No neuronal activation was seen within the primary motor cortex (at sites previously shown to be associated with volitional breathing). 5. These results suggest neuronal activation within the limbic system; this activation may be important in the sensory and/or motor respiratory responses to hypercapnia in awake man.

Control of the respiratory cycle in conscious humans.

There is no simple model for control of breathing in man. There are a number of degrees of freedom in the respiratory cycle. In inspiration, these include tidal volume (VTI), inspiratory time (TI) and mean inspiratory flow (MIF or VTI/TI), and in expiration, expiratory time (TE). We have developed a new technique to clamp and vary these variables individually or in combination to determine the strength of the mechanisms limiting change of each variable, and the hierarchy of control between variables. Subjects breathed into and from an open circuit via a mouthpiece and pneumotachograph and variables were measured breath-by-breath on-line by computer. Subjects coincided two bleeps of different pitches activated by the computer, one triggered at a fixed VTI and one at a fixed time after the start of inspiration (i.e. TI, expiration being initiated at this point. The threshold for each bleep could be varied from the keyboard without the subjects’ knowledge and were slowly applied to reduce subject awareness of the induced change. End-tidal PCO2 (PET,CO2) was held constant by manipulation of the inspired gas. We performed 4 sets of experiments in various combinations of 17 normal subjects in mild hyperoxia at a constant PET,CO2 slightly above resting. Each lasted 3/4–1 hour. The first experiment examined the range over which VTI and MIF could be increased and decreased by changing the threshold for the VTI bleep in 50–100 ml steps every 3 minutes at constant TE Subjects tracked the bleeps without difficulty as VTI increased by 500 ml but were not able to reduce VTI by more than 20 ml below the resting value, associated with a reduction in MIF of 12%. In a second series of experiments, TI was changed by ñ 800 msec at constant VTI using a similar technique; no difficulty was experienced in either direction, TI changing from, on average, 1.48 to 2.91 sec. In a third series of experiments, VT, and TI were reduced together from starting values at inspired PCO2 of 1, 3 and 5% to keep MIF constant while reducing VTI. At each level of chemical drive, VTI overshot the bleeps and could not be reduced below the free breathing resting value. These experiments show that timing can be changed over a wide range, that VTI and MIF can increase without difficulty, but that it is impossible to reduce VTI by more than a small amount below the resting values as dictated by the chemical drive. In a fourth series of experiments, we studied rapid shallow breathing without feedback control at constant PET,CO2 in 4 subjects. VTI fell without difficulty for prolonged periods to about 1/2 resting but end-expiratory volume as measured by a respiratory inductive plethysmograph increased to keep peak absolute tidal volume constant. In summary, these results suggest that in conscious humans, the major role of the control mechanism is to prevent a fall of tidal volume below that dictated by the chemical drive, presumably to ensure the maintenance of metabolic requirements. Mechanisms controlling timing are of lesser importance, consistent with the needs for non-metabolic functions of breathing such as speech. When VTI is forced to decrease by a programmed manoeuvre such as panting, end-expiratory volume increases to keep absolute volume constant.

Middle cerebral artery blood flow velocity studied during quiet breathing, reflex hypercapnic breathing and volitionally copied eucapnic breathing in man. Voluntary control of breathing.

The cerebrovascular circulation can be assessed non-invasively in man using transcranial doppler (TCD) velocimetry (1). The change in flow velocity pulse wave is proportional to the change in blood flow in that vessel, assuming cross sectional area of the artery studied to be constant. Such changes have been shown to correlate well with changes in cerebral perfusion in response to hypercapnia (3). TCD estimates of cerebral blood flow is increased when subjects performed both physical and cognitive activities (6) or when they were presented with visual stimuli (2). This suggests that TCD is capable of detecting changes in cerebral blood flow which accompany cerebral activity. In this study we have tested the hypothesis that volitionally controlled breathing is accompanied by an increase in middle cerebral artery (MCA) blood flow velocity (bfv) independent of changes in PCO2.