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Biomedical subjects

J A Dempsey

Publications and source records attributed to J A Dempsey.

At least 55 records · Page 3Linked to original sources
PubMed1997

Pulmonary-locomotory interactions in exercising dogs and horses.

In exercising quadrupeds, limb movement is often coupled with breathing frequency. This finding has lead some investigators to conclude that locomotory forces, associated with foot plant, abdominal visceral displacements or lumbo-sacral flexion, are the primary determinants of airflow generation. Analysis of respiratory muscle electrical activation (EMG) and contraction profiles in chronically instrumented dogs and horses, along with measurements of esophageal pressure (Pes) changes and limb movements, provide evidence that each breath during the exercise hyperpnea is determined by respiratory neuromuscular events. Specifically: (1) Phasic diaphragmatic EMG and tidal shortening are always synchronous with decreases in Pes; (2) decrements in Pes are always associated with inspiratory flow generation; and (3) strict phase coupling between breathing and stride frequency is not obligatory. Thus, although locomotory-associated forces may minimally assist with flow generation, they are not the primary determinants of breathing during exercise.

Animals↗
PubMed1997

Automated detection and classification of sleep-disordered breathing from conventional polysomnography data.

Efficient automated detection of sleep-disordered breathing (SDB) from routine polysomnography (PSG) data is made difficult by the availability of only indirect measurements of breathing. The approach we used to overcome this limitation was to incorporate pulse oximetry into the definitions of apnea and hypopnea. In our algorithm, 1) we begin with the detection of desaturation as a fall in oxyhemoglobin saturation level of 2% or greater once a rate of descent greater than 0.1% per second (but less than 4% per second) has been achieved and then ask if an apnea or hypopnea was responsible; 2) an apnea is detected if there is a period of no breathing, as indicated by sum respiratory inductive plethysmography (RIP), lasting at least 10 seconds and coincident with the desaturation event; and 3) if there is breathing, a hypopnea is defined as a minimum of three breaths showing at least 20% reduction in sum RIP magnitude from the immediately preceding breath followed by a return to at least 90% of that "baseline" breath. Our evaluation of this algorithm using 10 PSG records containing 1,938 SDB events showed strong event-by-event agreement with manual scoring by an experienced polysomnographer. On the basis of manually verified computer desaturations, detection sensitivity and specificity percentages were, respectively, 73.6 and 90.8% for apneas and 84.1 and 86.1% for hypopneas. Overall, 93.1% of the manually detected events were detected by the algorithm. We have designed an efficient algorithm for detecting and classifying SDB events that emulates manual scoring with high accuracy.

Adult↗
PubMed1997

Ventilatory effects of specific carotid body hypocapnia and hypoxia in awake dogs.

Specific carotid body (CB) hypocapnia in the-10-Torr (less than eupneic) range reduced ventilation in the awake and sleeping dog to the same degree as did CB hyperoxia [CB PO2 (PCBO2); > 500 Torr; C.A. Smith, K.W. Saupe, K. S. Henderson, and J. A. Dempsey. J. Appl. Physiol. 79:689-699, 1995], suggesting a powerful inhibitory effect of hypocapnia at the carotid chemosensor over a range of PCO2 encountered commonly in physiological hyperpneas. The primary purpose of this study was to assess the ventilatory effect of CB hypocapnia on the ventilatory response to concomitant CB hypoxia. The secondary purpose was to assess the relative gains of the CB and central chemoreceptors to hypocapnia. In eight awake female dogs the vascularly isolated CB was perfused with hypoxic blood (mild, PCBO2 approximately equal to 50 Torr or severe, PCBO2 approximately equal to 36 Torr) in a background of normocapnia or hypocapnia (10 Torr less than eupneic arterial PCO2) in the perfusate. The systemic (and brain) circulation was normoxic throughout, and arterial PCO2 was not controlled (poikilocapnia). With CB hypocapnia, the peak ventilation (range 19-27 s) in response to hypoxic CB perfusion increased 48% (mild) and 77% (severe) due to increased tidal volume. When CB hypocapnia was present, these increases in ventilation were reduced to 21 and 27%, respectively. With systemic hypocapnia, with the isolated CB maintained normocapnic and hypoxic for > 70 s, the steady-state poikilocapnic ventilatory response (i.e., to systemic hypocapnia alone) decreased 15% (mild CB hypoxia) and 27% (severe CB hypoxia) from the peak response, respectively. We conclude that carotid body hypocapnia can be a major source of inhibitory feedback to respiratory motor output during the hyperventilatory response to hypoxic carotid body stimulation.

Animals↗
PubMed1997

Respiratory muscle work compromises leg blood flow during maximal exercise.

We hypothesized that during exercise at maximal O2 consumption (VO2max), high demand for respiratory muscle blood flow (Q) would elicit locomotor muscle vasoconstriction and compromise limb Q. Seven male cyclists (VO2max 64 +/- 6 ml.kg-1.min-1) each completed 14 exercise bouts of 2.5-min duration at VO2max on a cycle ergometer during two testing sessions. Inspiratory muscle work was either 1) reduced via a proportional-assist ventilator, 2) increased via graded resistive loads, or 3) was not manipulated (control). Arterial (brachial) and venous (femoral) blood samples, arterial blood pressure, leg Q (Qlegs; thermodilution), esophageal pressure, and O2 consumption (VO2) were measured. Within each subject and across all subjects, at constant maximal work rate, significant correlations existed (r = 0.74-0.90; P < 0.05) between work of breathing (Wb) and Qlegs (inverse), leg vascular resistance (LVR), and leg VO2 (VO2legs; inverse), and between LVR and norepinephrine spillover. Mean arterial pressure did not change with changes in Wb nor did tidal volume or minute ventilation. For a +/-50% change from control in Wb, Qlegs changed 2 l/min or 11% of control, LVR changed 13% of control, and O2 extraction did not change; thus VO2legs changed 0.4 l/min or 10% of control. Total VO2max was unchanged with loading but fell 9.3% with unloading; thus VO2legs as a percentage of total VO2max was 81% in control, increased to 89% with respiratory muscle unloading, and decreased to 71% with respiratory muscle loading. We conclude that Wb normally incurred during maximal exercise causes vasoconstriction in locomotor muscles and compromises locomotor muscle perfusion and VO2.

Adult↗
PubMed1997

Superior laryngeal nerve section alters responses to upper airway distortion in sleeping dogs.

We investigated the effect of superior laryngeal nerve (SLN) section on expiratory time (TE) and genioglossus electromyogram (EMGgg) responses to upper airway (UA) negative pressure (UANP) in sleeping dogs. The same dogs used in a similar intact study (C. A. Harms, C. A., Y.-J. Zeng, C. A. Smith, E. H. Vidruk, and J. A. Dempsey. J. Appl. Physiol. 80: 1528-1539, 1996) were bilaterally SLN sectioned. After recovery, the UA was isolated while the animal breathed through a tracheostomy. Square waves of negative pressure were applied to the UA from below the larynx or from the mask (nares) at end expiration and held until the next inspiratory effort. Section of the SLN increased eupneic respiratory frequency and minute ventilation. Relative to the same dogs before SLN section, sublaryngeal UANP caused less TE prolongation while activation of the genioglossus required less negative pressures. Mask UANP had no effect on TE or EMGgg activity. We conclude that the SLN 1) is not obligatory for the reflex prolongation of TE and activation of EMGgg activity produced by UANP and 2) plays an important role in the maintenance of UA stability and the pattern of breathing in sleeping dogs.

Animals↗
PubMed1997

Neural-mechanical coupling of breathing in REM sleep.

During rapid-eye-movement (REM) sleep the ventilatory response to airway occlusion is reduced. Possible mechanisms are reduced chemosensitivity, mechanical impairment of the chest wall secondary to the atonia of REM sleep, or phasic REM events that interrupt or fractionate ongoing diaphragm electromyogram (EMG) activity. To differentiate between these possibilities, we studied three chronically instrumented dogs before, during, and after 15-20 s of airway occlusion during non-REM (NREM) and phasic REM sleep. We found that 1) for a given inspiratory time the integrated diaphragm EMG (Di) was similar or reduced in REM sleep relative to NREM sleep; 2) for a given Di in response to airway occlusion and the hyperpnea following occlusion, the mechanical output (flow or pressure) was similar or reduced during REM sleep relative to NREM sleep; 3) for comparable durations of airway occlusion the Di and integrated inspiratory tracheal pressure tended to be smaller and more variable in REM than in NREM sleep, and 4) significant fractionations (caused visible changes in tracheal pressure) of the diaphragm EMG during airway occlusion in REM sleep occurred in approximately 40% of breathing efforts. Thus reduced and/or erratic mechanical output during and after airway occlusion in REM sleep in terms of flow rate, tidal volume, and/or pressure generation is attributable largely to reduced neural activity of the diaphragm, which in turn is likely attributable to REM effects, causing reduced chemosensitivity at the level of the peripheral chemoreceptors or, more likely, at the central integrator. Chest wall distortion secondary to the atonia of REM sleep may contribute to the reduced mechanical output following airway occlusion when ventilatory drive is highest.

Air Pressure↗
PubMed1996

Frequency and volume thresholds for inhibition of inspiratory motor output during mechanical ventilation.

We quantified volume and frequency thresholds necessary for the inhibition of respiratory motor output during prolonged normocapnic mechanical ventilation in healthy subjects during wakefulness (n = 7) and NREM sleep (n = 5). Subjects were ventilated at eupneic frequency (fR) with 3 min step-wise increases in tidal volume (VT), or at eupneic VT with step-wise increases in fR, or by combinations of these two parameters. Inhibition of respiratory motor output was determined using mask pressure and, when available, esophageal pressure and diaphragmatic EMG. During wakefulness, the volume threshold (at eupneic fR) averaged 969 +/- 94 ml or 1.3-1.4 times the average eupneic tidal volume; the frequency threshold (at eupneic VT was 14.1 +/- 0.7 min-1 or 1.2 times the average eupneic frequency. The volume threshold was reduced when MV was provided at an fR above the eupneic value, and the frequency threshold was decreased when MV was provided at a VT above the eupneic level. During NREM sleep (n = 5) the volume threshold for inhibition was 835 +/- 108 ml or 1.4-1.5 times eupneic VT. The inhibitory thresholds for VT and fR were reproducible upon repeat trials within subjects. We conclude that inhibition of respiratory motor output during prolonged normocapnic mechanical ventilation in wakefulness or NREM sleep is highly sensitive to changes in ventilator VT, fR and their combination.

Adult↗
PubMed1996

Apnea prolongation via short-term inhibition.

Central apneas during sleep are frequently of longer duration than predicted and persist despite high levels of chemical stimuli. We provide evidence that suggests that this apnea prolongation represents a central inertia in the control system mediated by reciprocal inhibition of inspiration.

Animals↗
PubMed1996

Respiratory muscle perfusion and energetics during exercise.

The oxygen cost of breathing and blood flow requirements of the respiratory muscles during exercise are discussed along with the implications for limitation of locomotor muscle and exercise performance. Findings show that the oxygen cost of the hyperpnea achieved during very heavy exercise may approach 15% or more of VO2max under conditions that require extraordinary levels of ventilatory work. These conditions include those in the highly trained endurance athlete (at VE > 150 l.min-1), the older athlete at VE of 110-120 l.min-1), and athletic cursorial mammals at VO2max--all of whom experience significant expiratory flow limitation and sometimes even complete ventilatory limitation during heavy or maximum exercise. Rates of blood flow to the respiratory muscles under these peak exercise conditions may equal or exceed those to the limb locomotor muscles. The hypothesis is advanced that excessive requirements of ventilatory work (and therefore VO2 and blood flow) during heavy exercise may cause reflex vasoconstriction of locomotor muscles resulting in curtailment of endurance exercise performance.

Animals↗
PubMed1996

Respiratory muscle fatigue during exercise: implications for performance.

Heavy whole-body exercise, requiring a 10- to 15-fold increase in minute ventilation, encroaches on the capacities of the respiratory muscle system to respond. Recently, using the technique of bilateral phrenic nerve stimulation, it has been shown that heavy endurance exercise (> 85% of VO2max) lasting > 8-10 min causes diaphragmatic fatigue (15-30% reduction in transdiaphragmatic pressures when electrically stimulated at low frequencies [1-20 Hz] supramaximally). The fatigue appears to be due to an interaction of diaphragmatic work (i.e., pressure production) combined with effects related to exercise intensity (i.e., increased blood flow competition with the locomotor muscles and increased production of metabolic by-products) and requires > 60 min for recovery. Fitness (i.e., as implied from VO2max) appears to allow greater diaphragmatic work for a similar degree of fatigue. Unloading the respiratory muscles (with helium/oxygen gas or using a pressure-assist device) during heavy exercise < 90-95% of VO2max does not appear to alter exercise time, VO2max, or minute ventilation, implying that respiratory muscle fatigue plays little role in altering human performance at these work intensities. However, unloading the respiratory system with helium at work intensities > 90-95% of VO2max has been shown to improve exercise time. This would imply that respiratory muscle fatigue may play a role in limiting human performance at the extremes of human performance or that other factors related to the respiratory system (i.e., alterations in the sensation of dyspnea or mechanical load) may play an important role.

Diaphragm↗
PubMed1996

Negative pressure-induced deformation of the upper airway causes central apnea in awake and sleeping dogs.

We investigated the effects of negative pressure (NP) in the isolated upper airway (UA) in three unanesthetized dogs. The UA was isolated, and the dogs breathed through an endotracheal tube while wearing a fitted fiberglass snout mask. NP (-2 to -32 cmH2O) was applied in a square wave below the larynx or at the snout at end expiration and was held until inspiratory effort during wakefulness, non-rapid-eye-movement (NREM) sleep, and rapid-eye-movement (REM) sleep. During all states of consciousness, NP applied to the UA prolonged expiratory time (TE) 1) below a threshold of -8 to -10 cmH2O, which coincided with closure of the oro- and/or velopharynx; and 2) in a progressive fashion at more negative pressures than threshold, up to a mean apneic length of 324% of the control value (or 13.9 s) at -30 cmH2O. TE prolongation was less during REM sleep at a given NP (P < 0.05). Augmented tonic genioglossal electromyographic activity also occurred with the applied NP during wakefulness and NREM sleep but not with REM sleep. NP (-20 to -32 cmH2O) applied as a brief pulse (300-500 ms) during NREM sleep caused transient airway occlusion, terminated the breath during inspiration, and prolonged TE when applied at end expiration. Central apneas always persisted beyond the termination of the UA closure. TE prolongation in response to NP persisted in the presence of a topical anesthetic nebulized through the UA sufficient to abolish the laryngeal gag reflexes. We conclude that UA closure and deformation will cause significant TE prolongation during all states of consciousness and activation of the genioglossus muscle during wakefulness and NREM sleep but not during REM sleep.

Animals↗
PubMed1996

Breathing during exercise in dogs--passive or active?

The activation patterns of the costal and crural diaphragm and transversus abdominis muscle and their relationship to esophageal pressure (Pes) changes and footplant were examined in five chronically instrumented dogs which breathed at high frequencies at rest and during exercise. In two tracheostomized dogs, measurements were made of diaphragmatic length via sonomicrometry and of airflow and were related to diaphragmatic electrical activity and Pes. Dogs exhibited either a high-frequency breathing pattern, characterized by Pes changes occurring at 2-6 Hz, or a mixed-frequency breathing pattern, characterized by low-amplitude Pes oscillations (4-6 Hz) superimposed on a slower breathing rate of 0.5-1 Hz. Regardless of the type of breathing pattern elected or of the various breathing-to-stride frequency ratios observed during exercise, decreases in Pes were always associated with phasic electromyographic activity of the costal and crural diaphragm and with phasic diaphragmatic muscle shortening. The transversus abdominis electromyographic activity coincided with an increasing Pes from peak negative values in resting dogs and exhibited both an expiratory and a locomotory modulation during exercise. Although footplant may have contributed to some airflow generation when dogs utilized the mixed-frequency pattern, these data demonstrate that the movement of air into and out of the lungs in stationary or exercising dogs requires phasic neural activation of the diaphragm and other respiratory muscles.

Animals↗
PubMed1996

Aerobic fitness effects on exercise-induced low-frequency diaphragm fatigue.

We used bilateral phrenic nerve stimulation (BPNS; at 1, 10, and 20 Hz at functional residual capacity) to compare the amount of exercise-induced diaphragm fatigue between two groups of healthy subjects, a high-fit group [maximal O2 consumption (VO2max) = 69.0 +/- 1.8 ml.kg-1.min-1, n = 11] and a fit group (VO2max = 50.4 +/- 1.7 ml.kg-1.min-1, n = 13). Both groups exercised at 88-92% VO2max for about the same duration (15.2 +/- 1.7 and 17.9 +/- 2.6 min for high-fit and fit subjects, respectively, P > 0.05). The supramaximal BPNS test showed a significant reduction (P < 0.01) in the BPNS transdiaphragmatic pressure (Pdi) immediately after exercise of -23.1 +/- 3.1% for the high-fit group and -23.1 +/- 3.8% (P > 0.05) for the fit group. Recovery of the BPNS Pdi took 60 min in both groups. The high-fit group exercised at a higher absolute workload, which resulted in a higher CO2 production (+26%), a greater ventilatory demand (+16%) throughout the exercise, and an increased diaphragm force output (+28%) over the initial 60% of the exercise period. Thereafter, diaphragm force output declined, despite a rising minute ventilation, and it was not different between most of the high-fit and fit subjects. In summary, the high-fit subjects showed diaphragm fatigue as a result of heavy endurance exercise but were also partially protected from excessive fatigue, despite high ventilatory requirements, because their hyperventilatory response to endurance exercise was reduced, their diaphragm was utilized less in providing the total ventilatory response, and possibly their diaphragm aerobic capacity was greater.

Adult↗
PubMed1996

Sleep-induced breathing instability. University of Wisconsin-Madison Sleep and respiration Research Group.

We present a view of the neuromechanical regulation of breathing and causes of breathing instability during sleep. First, we would expect transient increases in upper airway resistance to be a major cause of transient hypopnea. This occurs in sleep because a hypotonic upper airway is more susceptible to narrowing and because the immediate excitatory increase in respiratory motor output in response to increased loads is absent in non-REM sleep. Secondly, sleep predisposes to an increased occurrence of ventilatory "overshoots", in part because abruptly changing sleep states cause transient changes in upper airway resistance and in the gain of the respiratory controller. Following these ventilatory overshoots, breathing stability will be maintained if excitatory short-term potentiation is the prevailing influence. On the other hand, apnea and hypopnea will occur if inhibitory mechanisms dominate following the ventilatory overshoot. These inhibitory mechanisms include: a) hypocapnia-if transient, will inhibit carotid chemoreceptors and cause hypopnea, but if prolonged will inhibit medullary chemoreceptors and cause apnea; b) a persistent inhibitory effect from lung stretch; c) baroreceptor stimulation, from a transient rise in systemic blood pressure immediately following termination of apnea or hypopnea may partially suppress the accompanying hyperpnea; d) depression of central respiratory motor output via prolonged brain hypoxia. Once apneas are initiated, reinitiation of inspiration is delayed even though excitatory stimuli have risen well above their apneic thresholds, and these prolonged apneas are commonly accompanied by tonic EMG activation of expiratory muscles of the chest wall and upper airway.

Adult↗
PubMed1995

An integrative view of limitations to muscular performance.

First we describe the changing site of limitation to maximal O2 transport with increasing fitness in mammals. The capacity for diffusion and airway/parenchymal flow rate and volume are markedly overbuilt in the sedentary subject's lung, but undergo little change with increased training/fitness; accordingly, as demand for O2 transport increases in the highly fit, the limits for maximal diffusion and ventilation are surpassed or met at maximal exercise. Secondly, low-frequency diaphragmatic fatigue occurred with by heavy endurance exercise. This fatigue resulted from increased diaphragmatic work together with the major contribution from the secondary effects of increased locomotor muscle activity; namely, metabolic acidosis and increased requirement for blood flow.

Exercise↗
PubMed1995

The assessment of upper airway patency during apnea using cardiogenic oscillations in the airflow signal.

We investigated the relationship between airway patency and the occurrence of cardiogenic related oscillations in the airflow signal during 67 apneas occurring in non-rapid eye movement sleep in eight subjects. Spontaneously occurring apneas and apneas induced by mechanical ventilation were analyzed. Airway occlusion was determined by direct observation of the pharyngeal lumen using fiberoptic endoscopy. The presence or absence of cardiogenic oscillations was determined from an expanded airflow signal by an investigator blinded to the airway patency. Of the total 67 apneas, complete airway occlusion occurred during 51, and the airway remained patent throughout in 16. Cardiogenic oscillations were seen throughout 39 of the 51 occluded apneas and throughout 9 of the 16 apneas with the airway patent. There was no relationship between the occurrence of cardiogenic oscillations and airway patency. In addition, in a canine model where the upper airway was anatomically isolated, cardiogenic oscillations were evident during apneas in pressure signals recorded from the isolated upper airway and in airflow signals at the tracheal stoma. We conclude that cardiogenic oscillations cannot be used to predict airway patency during apnea.

Adult↗
PubMed1995

The physical map of the chromosome of a serogroup A strain of Neisseria meningitidis shows complex rearrangements relative to the chromosomes of the two mapped strains of the closely related species N. gonorrhoeae.

A physical map of the chromosome of N. meningitidis Z2491 (serogroup A, subgroup IV-1) has been constructed. Z2491 DNA was digested with NheI, SpeI, SgfI, PacI, BglII, or PmeI, resulting in a limited number of fragments that were resolved by contour-clamped homogeneous electric field (CHEF) electrophoresis. The estimated genome size for this strain was 2,226 kb. To construct the map, probes corresponding to single-copy genes or sequences were used on Southern blots of chromosomal DNA digested with the different mapping enzymes and subjected to CHEF electrophoresis. By determining which fragments from different digests hybridized to each specific probe, it was possible to walk back and forth between digests to form a circular macrorestriction map. The intervals between mapped restriction sites range from 10 to 143 kb in size. A total of 117 markers have been placed on the map; 75 represent identified genes, with the remaining markers defined by anonymous cloned fragments of neisserial DNA. Comparison of the arrangement of genetic loci in Z2491 with that in gonococcal strain FA1090, for which a physical map was previously constructed, revealed complex genomic rearrangements between the two strains. Although gene order is generally conserved over much of the chromosome, a region of approximately 500 kb shows translocation and/or inversion of multiple blocks of markers between the two strains. Even within the relatively conserved portions of the maps, several genetic markers are in different positions in Z2491 and FA1090.

Base Sequence↗