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James Duffin

Publications and source records attributed to James Duffin.

At least 19 recordsLinked to original sources
PubMed2006

Long-term facilitation of breathing is absent after episodes of hypercapnic hypoxia in awake humans.

Despite the failure by many previous investigators to demonstrate a long-term facilitation of breathing following episodes of hypoxia in awake humans, we attempted to produce it using a pattern of hypercapnic hypoxic episodes similar to that experienced by obstructive sleep apnoea patients, reasoning that if long-term facilitation was relevant to these patients then it is appropriate to test the effectiveness of such episodes. Ten subjects drawn from the University student population were instrumented to measure ventilation, heart rate and end-tidal PCO2 and PO2 breath-by-breath while seated in a comfortable reclining chair. After an initial resting period breathing room air they experienced fifteen, 30-s episodes breathing 6% O2 and 5% CO2 separated by 90 s of breathing air. We examined the measured variables for an hour after the episodes but found no trends toward an increase in ventilation or decrease in end-tidal PCO2 that would indicate the presence of a long-term facilitation. We therefore concluded that long-term facilitation of ventilation was not demonstrated in awake humans using this pattern of stimuli.

Adaptation, Physiological↗
PubMed2005

Transmission of respiratory rhythm: midline-crossing connections at the level of the phrenic motor nucleus?

We used three methods to test for the existence of transmission of respiratory rhythm across the midline at the level of the phrenic motor nucleus in rats using the in situ preparation over a range of ages from neonatal to juvenile. Stimulus-triggered averages of phrenic activity for stimuli applied to one side of the spinal cord at C2 and C3 produced large peaks in the ipsilateral averages but no discernible peaks in the contralateral averages, unless the stimulating microelectrode was placed close to the midline in the ventral funiculus. Following mid-sagittal section of the medulla, respiratory rhythm was maintained for all ages, with bursts occurring on one phrenic nerve that were absent on the other. Cross-correlations of left and right phrenic discharges displayed peaks indicative of short time-scale synchronisation before the medullary transections but not afterwards. We therefore could not find evidence for transmission of respiratory rhythm across the midline at the phrenic motoneurone level; we did find evidence that that transmission via ipsilaterally descending axons of medullary phrenic pre-motor neurones is present at all ages.

Age Factors↗
PubMed2005

Rapid increases in ventilation accompany the transition from passive to active movement.

We used a novel movement transition technique to look for evidence of a rapid onset drive to breathe related to the active component of exercise in humans. Ten volunteers performed the following transitions in a specially designed tandem exercise chair apparatus: rest to passive movement, passive to active movement, and rest to active movement. The transition from rest to active exercise was accompanied by an immediate increase in ventilation, as was the transition from rest to passive leg movement (Delta = 6.06 +/- 1.09 l min(-1), p < 0.001 and Delta = 3.30 +/- 0.57 l min(-1), p = 0.002, respectively). When subjects actively assumed the leg movements, ventilation again increased immediately and significantly (Delta = 2.55 +/- 0.52 l min(-1), p = 0.032). Ventilation at the first point of active exercise was the same when started either from rest or from a background of passive leg movement (p = 1.00). We conclude that the use of a transition from passive to active leg movements in humans recruits a ventilatory drive related to the active component of exercise, and this can be discerned as a rapid increase in breathing.

Adult↗
PubMed2005

Role of acid-base balance in the chemoreflex control of breathing.

This paper uses a steady-state modeling approach to describe the effects of changes in acid-base balance on the chemoreflex control of breathing. First, a mathematical model is presented, which describes the control of breathing by the respiratory chemoreflexes; equations express the dependence of pulmonary ventilation on Pco(2) and Po(2) at the central and peripheral chemoreceptors. These equations, with Pco(2) values as inputs to the chemoreceptors, are transformed to equations with hydrogen ion concentrations [H(+)] in brain interstitial fluid and arterial blood as inputs, using the Stewart approach to acid-base balance. Examples illustrate the use of the model to explain the regulation of breathing during acid-base disturbances. They include diet-induced changes in sodium and chloride, altitude acclimatization, and respiratory disturbances of acid-base balance due to chronic hyperventilation and carbon dioxide retention. The examples demonstrate that the relationship between Pco(2) and [H(+)] should not be neglected when modeling the chemoreflex control of breathing. Because pulmonary ventilation controls Pco(2) rather than the actual stimulus to the chemoreceptors, [H(+)], changes in their relationship will alter the ventilatory recruitment threshold Pco(2), and thereby the steady-state resting ventilation and Pco(2).

Acid-Base Equilibrium↗
PubMed2005

Effects of concurrent inspiratory and expiratory muscle training on respiratory and exercise performance in competitive swimmers.

The efficiency of the respiratory system presents significant limitations on the body's ability to perform exercise due to the effects of the increased work of breathing, respiratory muscle fatigue, and dyspnoea. Respiratory muscle training is an intervention that may be able to address these limitations, but the impact of respiratory muscle training on exercise performance remains controversial. Therefore, in this study we evaluated the effects of a 12-week (10 sessions week(-1)) concurrent inspiratory and expiratory muscle training (CRMT) program in 34 adolescent competitive swimmers. The CRMT program consisted of 6 weeks during which the experimental group (E, n = 17) performed CRMT and the sham group (S, n = 17) performed sham CRMT, followed by 6 weeks when the E and S groups performed CRMT of differing intensities. CRMT training resulted in a significant improvement in forced inspiratory volume in 1 s (FIV1.0) (P = 0.050) and forced expiratory volume in 1 s (FEV1.0) (P = 0.045) in the E group, which exceeded the S group's results. Significant improvements in pulmonary function, breathing power, and chemoreflex ventilation threshold were observed in both groups, and there was a trend toward an improvement in swimming critical speed after 12 weeks of training (P = 0.08). We concluded that although swim training results in attenuation of the ventilatory response to hypercapnia and in improvements in pulmonary function and sustainable breathing power, supplemental respiratory muscle training has no additional effect except on dynamic pulmonary function variables.

Adolescent↗
PubMed2005

Overnight changes of chemoreflex control in obstructive sleep apnoea patients.

We hypothesized that the numerous episodes of hypoxia, hypercapnia and arousal experienced by obstructive sleep apnoea (OSA) patients induce overnight changes in respiratory chemoreflexes. A modification of the Read rebreathing technique assessed chemoreflex characteristics in the evening and the morning of patients undergoing diagnostic assessment for OSA in a clinical sleep laboratory. Two groups were studied: those with apnoea-hypopnoea indices (AHI) greater than 30 composed the OSA group (n = 12), and those with AHI indices less than 10 composed the non-OSA group (n = 12). There was a significant (approximately 30%) overnight increase in chemoreflex sensitivities, without changes in thresholds, in the OSA group. In the non-OSA group there was a significant overnight reduction in chemoreflex thresholds (approximately 5%), without changes in sensitivities. We suggest that these changes affect the stability of the chemoreflex control system in opposite ways as the night proceeds: destabilizing breathing for patients in the OSA group, and stabilising breathing for patients in the non-OSA group.

Adult↗
PubMed2005

The initial phase of exercise hyperpnoea in humans is depressed during a cognitive task.

Increased wakefulness is known to suppress the initial ventilatory response to passive movement and the steady-state ventilatory response to exercise. However, the effect of increased wakefulness upon the integrated ventilatory response at the onset of exercise is not known. We hypothesized that increasing wakefulness via a cognitive task would attenuate the initial ventilatory response to exercise, and so we examined the response to active leg extensions under two conditions: with and without concurrently solving a puzzle. At rest before exercise, subjects demonstrated greater minute ventilation while solving a puzzle (mean +/- S.E.M., 12.38 +/- 0.55 versus 10.12 +/- 0.51 l min(-1), P < 0.001), due to a higher mean breathing frequency (mean +/- S.E.M., 17.1 +/- 0.93 versus 13.6 +/- 0.59 breaths min(-1), P < 0.001). At the start of exercise, subjects did not increase their ventilation significantly while solving the puzzle (P = 0.170), but did by a mean +/-s.e.m. of 6.16 +/- 1.12 l min(-1) (P < 0.001) when not puzzle solving. The ventilation achieved at the start of exercise in absolute terms was also lower while solving the puzzle (14.6 +/- 1.1 versus 16.3 +/- 1.3 l min(-1), P = 0.047). Despite differences in the rapid ventilatory response to exercise between conditions, the steady-state responses were not different. We conclude that the performance of a cognitive task decreases the initial phase of exercise hyperpnoea, and suggest that this might occur because of either a competitive interaction between drives to breathe or a behavioural distraction from the 'task' of exercise.

Adaptation, Physiological↗
PubMed2005

Changes in respiratory control after 5 days at altitude.

These experiments examined changes in the chemoreflex control of breathing and acid-base balance after 5 days at altitude (3480 m) in six healthy males. The partial pressures of carbon dioxide (P(CO2)) at which ventilation increased during isoxic hypoxic and hyperoxic modified rebreathing tests at sea level fell significantly at altitude by mean+/-S.E.M. of 12.8+/-2.51 mmHg and 9.5+/-1.77 mmHg, respectively, but response slopes above threshold were unchanged. Altitude exposure produced a respiratory alkalosis evidenced by a decrease in mean resting end-tidal P(CO2) from 41+/-0.84 mmHg at sea level to 32+/-2.04 mmHg at altitude, but pH did not increase significantly from its sea level value. Blood samples were analyzed to discover acid-base changes, using a modification of the equations for acid-base balance proposed by [Stewart, P.A., 1983. Modern quantitative acid-base chemistry. Can. J. Physiol. Pharmacol. 61, 1444-1461]. While strong ion difference at altitude was not significantly different from its sea level value, albumin concentration was increased significantly from 38.6+/-0.30 g L(-1) to 49.8+/-0.76 g L(-1). We suggest that the respiratory alkalosis was produced by a fall in the chemoreflex threshold and pH was corrected by an elevation in the concentration of weakly dissociated protein anions.

Acclimatization↗
PubMed2004

Anxiety sensitivity as a predictor of panic attacks.

Anxiety sensitivity (AS) is the fear of physical symptoms of anxiety and related sensations believed to have harmful consequences. AS may play a central role in the nature and etiology of panic disorder (PD) and the genesis of panic attacks. We collected Anxiety Sensitivity Index (ASI) scores from PD patients and controls to determine if AS accurately predicts panic. ASIs were completed prior to panic induction using the modified Read rebreathing test in both hypoxic and hyperoxic conditions. Total scores first-order factors, and individual item ASI scores were correlated with panic presence (Spearman correlation) for each of the hypoxic and hyperoxic rebreathing tests for both study populations. Control subjects' data correlated significantly for items 4, 8, and 11 of the ASI for the hyperoxic (n=9; r(S)=0.63, 0.70, and 0.63, respectively) and items 4 and 8 for the hypoxic rebreathing tests (n = 9; r(S) = 0.63 and 0.70, respectively). Panic patients' data correlated significantly for item 1 of the ASI for hyperoxic tests (n=8; r(S)=0.76) and item 5 for the hypoxic tests (n = 8; r(S) = 0.95). Total ASI scores or first-order factors (physical, social concerns, and mental incapacitation) scores of either study group did not correlate significantly with panic presence. AS may not be a reliable predictor of panicogenic responses to CO2-induced panic in either PD or normal control populations. AS may not be an ultimate causal element in eliciting panic attacks.

Adult↗
PubMed2004

Developmental changes in transmission of respiratory rhythm in the rat.

We used cross-correlation to examine the short time-scale synchronisation of left and right phrenic nerve discharges in in-situ preparations of rats over a range of ages, to investigate the development of respiratory rhythm transmission to phrenic motoneurones. We found central peaks in the cross-correlograms, indicative of short time-scale synchronisation, at all ages (2-41 days), whose half-amplitude widths varied inversely with age (40-1.8 ms). In 10 preparations < or =5-days-old the central peaks were unaffected by a mid-sagittal section from C3 to C6. Carbenoxalone (CBX), a gap junction blocker, and its inactive analogue glycyrrhzic acid (GZA), eliminated central peaks in preparations younger than 12 days but not in older preparations. We concluded that in rats older than approximately 12 days short time-scale synchronisation is produced by bilaterally-projecting axons of medullary pre-motor neurones, whereas in younger rats it is due to pre-synaptic synchronisation of left and right medullary pre-motor neurones. While the latter mechanism may be gap junction connections, these experiments cannot unequivocally demonstrate it.

Action Potentials↗
PubMed2004

Cardio-respiratory measures following isocapnic voluntary hyperventilation.

In some individuals, breathing is greater than at rest following voluntary hyperventilation. Most previous investigations have employed short hyperventilation periods; here we examine the time course of cardio-respiratory measures before, during, and after a 5-min voluntary hyperventilation, maintaining isocapnia throughout. We examined the possible co-involvement of the cardiovascular system; hypothesising that post-hyperventilation hyperpnoea results from an increase in autonomic arousal. In four subjects (two males, two females) of 18 (nine males, nine females) we observed a post-hyperventilation hyperpnoea, characterised by a slow decline of ventilation toward resting levels with a time constant of 109.0 +/- 16.1s. By contrast, heart rate, and systolic and diastolic blood pressure were unchanged from rest during and after voluntary hyperventilation for all subjects. We concluded that males and females were equally likely to exhibit post-hyperventilation hyperpnoea, and suggest that they may be characterised by an increased resting heart rate and the choice of breathing frequency to increase ventilation during the voluntary hyperventilation. We further concluded that post-hyperventilation hyperpnoea is rare, but when present is a strong and lasting phenomenon, and that it is not the result of an increased autonomic arousal.

Adult↗
PubMed2004

Respiratory response to passive limb movement is suppressed by a cognitive task.

Feedback from muscles stimulates ventilation at the onset of passive movement. We hypothesized that central neural activity via a cognitive task source would interact with afferent feedback, and we tested this hypothesis by examining the fast changes in ventilation at the transition from rest to passive leg movement, under two conditions: 1) no task and 2) solving a computer-based puzzle. Resting breathing was greater in condition 2 than in condition 1, evidenced by an increase in mean +/- SE breathing frequency (18.2 +/- 1.1 vs. 15.0 +/- 1.2 breaths/min, P = 0.004) and ventilation (10.93 +/- 1.16 vs. 9.11 +/- 1.17 l/min, P < 0.001). In condition 1, the onset of passive movement produced a fast increase in mean +/- SE breathing frequency (change of 2.9 +/- 0.4 breaths/min, P < 0.001), tidal volume (change of 233 +/- 95 ml, P < 0.001), and ventilation (change of 6.00 +/- 1.76 l/min, P < 0.001). However, in condition 2, the onset of passive movement only produced a fast increase in mean +/- SE breathing frequency (change of 1.3 +/- 0.4 breaths/min, P = 0.045), significantly smaller than in condition 1 (P = 0.007). These findings provide evidence for an interaction between central neural cognitive activity and the afferent feedback mechanism, and we conclude that the performance of a cognitive task suppresses the respiratory response to passive movement.

Adult↗
PubMed2004

Functional organization of respiratory neurones: a brief review of current questions and speculations.

This article presents a short overview of current knowledge about the medullary respiratory neurones and the generation of breathing rhythm. The background respiratory neurophysiology of the medulla and pons is briefly reviewed, with some current ideas about the organization of the pontine-medullary respiratory control system and its development. Questions and speculations about the organization and generation of respiratory rhythm are included, with a view to stimulating experiments to provide answers.

Animals↗
PubMed2004

The effects of carbon monoxide on respiratory chemoreflexes in humans.

As protection against low-oxygen and high-carbon-dioxide environments, the respiratory chemoreceptors reflexly increase breathing. Since CO is also frequently present in such environments, it is important to know whether CO affects the respiratory chemoreflexes responsiveness. Although the peripheral chemoreceptors fail to detect hypoxia produced by CO poisoning, whether CO affects the respiratory chemoreflex responsiveness to carbon dioxide is unknown. The responsiveness of 10 healthy male volunteers were assessed before and after inhalation of approximately 1200 ppm CO in air using two iso-oxic rebreathing tests; hypoxic, to emphasize the peripheral chemoreflex, and hyperoxic, to emphasize the central chemoreflex. Although mean (SEM) COHb values of 10.2 (0.2)% were achieved, no statistically significant effects of CO were observed. The average differences between pre- and post-CO values for ventilation response threshold and sensitivity were -0.5 (0.9) mmHg and 0.8 (0.3) L/min/mmHg, respectively, for hyperoxia, and 0.7 (1.1) mmHg and 1.2 (0.8) L/min/mmHg, respectively, for hypoxia. The 95% confidence intervals for the effect of CO were small. We conclude that environments with low levels of CO do not have a clinically significant effect acutely on either the central or the peripheral chemoreflex responsiveness to carbon dioxide.

Adult↗
PubMed2004

Epidural catheter penetration of human dural tissue: in vitro investigation.

BACKGROUND: Factors contributing to subarachnoid catheter passage after epidural placement are not well understood. This study explored mechanisms that might explain its occurrence. METHODS: Human cadaveric dura was mounted on a model and pressurized to physiologic levels. In a standardized fashion, a 20-gauge Portex three-port, closed end (nonflexible) tip catheter was passed through an epidural needle mounted on a micromanipulator at a 90 degree angle, attempting to penetrate dura with the catheter. Attempts then followed with a 19-gauge Arrow Flex Tip Plus single-port catheter. Subarachnoid catheter passage was compared in (1) intact dura, (2) clinically occult versus obvious epidural needle punctures, and (3) single 25-gauge Whitacre spinal needle punctures after combined spinal-epidural placement. RESULTS: Neither catheter penetrated intact dura: Portex, 0 of 300 attempts (0.0000; 95% confidence interval [CI]: 0.0000, 0.0158); Arrow, 0 of 300 attempts (0.0000; 95% CI: 0.0000, 0.0158). In clinically occult epidural needle punctures, the 20-gauge Portex catheter penetrated 1 of 3 specimens in 1 of 14 attempts (0.0714; 95% CI: 0.0021, 0.3583). The 19-gauge Arrow did not pass (0 of 15 attempts, 0.0000; 95% CI: 0.0000, 0.2535). In clinically obvious epidural needle punctures, the Portex passed in 6 of 33 attempts (0.1818; 95% CI: 0.0760, 0.3608) and the Arrow passed in 1 of 35 attempts (0.0286; 95% CI: 0.0012, 0.1662). Neither catheter passed through a single 25-gauge spinal needle puncture after an uncomplicated combined spinal-epidural: Portex, 0 of 90 attempts (0.0000; 95% CI: 0.0000, 0.0510); Arrow, 0 of 90 attempts (0.0000; 95% CI: 0.0000, 0.0510). CONCLUSIONS: Catheter passage is unlikely in the presence of intact dura or after an uncomplicated combined spinal-epidural. Unintentional subarachnoid passage suggests dural damage with the epidural needle.

Adult↗
PubMed2003

A commentary on eupnoea and gasping.

This commentary discusses the differences between patterns of bursting activity recorded from the phrenic nerves of different species, in several experimental preparations and under differing conditions. The spectrum of bursting activity patterns varies from that termed eupnoic to that termed gasping. Taking the pattern of activity recorded in the least reduced preparation as a standard for normality, i.e. eupnoea, consideration is given to the possible factors affecting the pattern of bursting activity in progressively reduced preparations. An examination of the conditions of these preparations leads to the conclusion that tissue gas exchange is a major determinant of bursting pattern, and consideration is given to the possible differences in respiratory rhythm generation that can be inferred from these different patterns.

Aging↗
PubMed2003

Connections between respiratory neurones in the neonatal rat transverse medullary slice studied with cross-correlation.

In the transverse medullary slice prepared from neonatal rats the hypoglossal nerve rootlets exhibit a bursting 'respiratory' rhythm as do neurones in the pre-Bötzinger complex (PBC). We used cross-correlation analysis of the rhythmic multiunit discharges recorded from hypoglossal nerve rootlets, hypoglossal nucleus neurones and PBC neurones to investigate the connections between these groups. All cross-correlograms computed between left and right hypoglossal nerves, and between hypoglossal neurones and contralateral hypoglossal nerves, displayed central peaks with broad half-amplitude widths (mean +/- S.D. of 29.6 +/- 10.4 and 37.3 +/- 6.0 ms, respectively), which we interpreted as evidence for activation from a common source. Five of the 18 cross-correlograms computed between left and right PBC neurones displayed peaks either side of time zero with narrower half-amplitude widths (mean +/- S.D. of 9.3 +/- 1.9 ms) superimposed on broader central peaks, which we interpreted as evidence for mutual excitation and common activation, respectively. Cross-correlograms computed between PBC neurones and contralateral hypoglossal neurones or nerves did not display consistent features, but some of those computed between PBC and ipsilateral hypoglossal neurones (two of eight) or nerves (two of five) displayed peaks with broad half-amplitude widths (mean +/- S.D. of 36.8 +/- 6.9 ms), offset from time zero by 6 ms (except for one at 18 ms), which we interpreted as evidence for excitation of hypoglossal neurones and motoneurones by PBC neurones. We concluded that rhythm is synchronised between left and right sides by mutual excitatory connections between left and right PBC neurones. The rhythm is transmitted to ipsilateral hypoglossal neurones by a paucisynaptic pathway. Both hypoglossal neurones and PBC neurones receive a common activation from as yet unidentified sources.

Animals↗