Biomedical subjects

B J Morgan

Publications and source records attributed to B J Morgan.

At least 19 recordsLinked to original sources

PubMed2001

Fatiguing inspiratory muscle work causes reflex reduction in resting leg blood flow in humans.

1. We recently showed that fatigue of the inspiratory muscles via voluntary efforts caused a time-dependent increase in limb muscle sympathetic nerve activity (MSNA) (St Croix et al. 2000). We now asked whether limb muscle vasoconstriction and reduction in limb blood flow also accompany inspiratory muscle fatigue. 2. In six healthy human subjects at rest, we measured leg blood flow (.Q(L)) in the femoral artery with Doppler ultrasound techniques and calculated limb vascular resistance (LVR) while subjects performed two types of fatiguing inspiratory work to the point of task failure (3-10 min). Subjects inspired primarily with their diaphragm through a resistor, generating (i) 60 % maximal inspiratory mouth pressure (P(M)) and a prolonged duty cycle (T(I)/T(TOT) = 0.7); and (ii) 60 % maximal P(M) and a T(I)/T(TOT) of 0.4. The first type of exercise caused prolonged ischaemia of the diaphragm during each inspiration. The second type fatigued the diaphragm with briefer periods of ischaemia using a shorter duty cycle and a higher frequency of contraction. End-tidal P(CO2) was maintained by increasing the inspired CO(2) fraction (F(I,CO2)) as needed. Both trials caused a 25-40 % reduction in diaphragm force production in response to bilateral phrenic nerve stimulation. 3. .Q(L) and LVR were unchanged during the first minute of the fatigue trials in most subjects; however, .Q(L) subsequently decreased (-30 %) and LVR increased (50-60 %) relative to control in a time-dependent manner. This effect was present by 2 min in all subjects. During recovery, the observed changes dissipated quickly (< 30 s). Mean arterial pressure (MAP; +4-13 mmHg) and heart rate (+16-20 beats min(-1)) increased during fatiguing diaphragm contractions. 4. When central inspiratory motor output was increased for 2 min without diaphragm fatigue by increasing either inspiratory force output (95 % of maximal inspiratory pressure (MIP)) or inspiratory flow rate (5 x eupnoea), .Q(L), MAP and LVR were unchanged; although continuing the high force output trials for 3 min did cause a relatively small but significant increase in LVR and a reduction in .Q(L). 5. When the breathing pattern of the fatiguing trials was mimicked with no added resistance, LVR was reduced and .Q(L) increased significantly; these changes were attributed to the negative feedback effects on MSNA from augmented tidal volume. 6. Voluntary increases in inspiratory effort, in the absence of diaphragm fatigue, had no effect on .Q(L) and LVR, whereas the two types of diaphragm-fatiguing trials elicited decreases in .Q(L) and increases in LVR. We attribute these changes to a metaboreflex originating in the diaphragm. Diaphragm and forearm muscle fatigue showed very similar time-dependent effects on LVR and .Q(L).

Adult↗

PubMed2001

Age, sex, density, winter weather, and population crashes in Soay sheep.

Quantifying the impact of density, extrinsic climatic fluctuations, and demography on population fluctuations is a persistent challenge in ecology. We analyzed the effect of these processes on the irregular pattern of population crashes of Soay sheep on the St. Kilda archipelago, United Kingdom. Because the age and sex structure of the population fluctuates independently of population size, and because animals of different age and sex respond in different ways to density and weather, identical weather conditions can result in different dynamics in populations of equal size. In addition, the strength of density-dependent processes is a function of the distribution of weather events. Incorporating demographic heterogeneities into population models can influence dynamics and their response to climate change.

Aging↗

PubMed2001

Abalone I: analyzing mark-recapture-recovery data incorporating growth and delayed recovery.

Abalone are semimobile marine gastropods that form the basis of Australia's second most valuable fishery. A site off the coast of Port Arthur, Tasmania, was visited on six occasions. On each occasion, any unmarked live abalone found were marked with a unique identification number and were recorded. Any previously marked abalone found had its identification number and whether or not it was still alive recorded. This results in integrated mark-recapture-recovery data, as in Catchpole et al. (1998, Biometrics 54, 33-46). During the study period, abalone grew in size, and we model the survival of individuals as a function of their size, estimated from a fitted growth curve. The shells of dead animals are long lasting, and we extend existing methodology to allow for the possibility that an animal found dead may have been dead but overlooked for several visits.

Animals↗

PubMed2001

On the near-singularity of models for animal recovery data.

Certain probability models sometimes provide poor descriptions when fitted to data by maximum likelihood. We examine one such model for the survival of wild animals, which is fitted to two sets of data. When the model behaves poorly, its expected information matrix, evaluated at the maximum likelihood estimate of parameters, has a 'small' smallest eigenvalue. This is due to the fitted model being similar to a parameter-redundant submodel. In this case, model parameters that are precisely estimated have small coefficients in the eigenvector corresponding to the smallest eigenvalue. Approximate algebraic expressions are provided for the smallest eigenvalue. We discuss the general applicability of these results.

Animals↗

PubMed2001

Exposure to hypoxia produces long-lasting sympathetic activation in humans.

The relative contributions of hypoxia and hypercapnia in causing persistent sympathoexcitation after exposure to the combined stimuli were assessed in nine healthy human subjects during wakefulness. Subjects were exposed to 20 min of isocapnic hypoxia (arterial O(2) saturation, 77-87%) and 20 min of normoxic hypercapnia (end-tidal P(CO)(2), +5.3-8.6 Torr above eupnea) in random order on 2 separate days. The intensities of the chemical stimuli were manipulated in such a way that the two exposures increased sympathetic burst frequency by the same amount (hypoxia: 167 +/- 29% of baseline; hypercapnia: 171 +/- 23% of baseline). Minute ventilation increased to the same extent during the first 5 min of the exposures (hypoxia: +4.4 +/- 1.5 l/min; hypercapnia: +5.8 +/- 1.7 l/min) but declined with continued exposure to hypoxia and increased progressively during exposure to hypercapnia. Sympathetic activity returned to baseline soon after cessation of the hypercapnic stimulus. In contrast, sympathetic activity remained above baseline after withdrawal of the hypoxic stimulus, even though blood gases had normalized and ventilation returned to baseline levels. Consequently, during the recovery period, sympathetic burst frequency was higher in the hypoxia vs. the hypercapnia trial (166 +/- 21 vs. 104 +/- 15% of baseline in the last 5 min of a 20-min recovery period). We conclude that both hypoxia and hypercapnia cause substantial increases in sympathetic outflow to skeletal muscle. Hypercapnia-evoked sympathetic activation is short-lived, whereas hypoxia-induced sympathetic activation outlasts the chemical stimulus.

Adult↗

PubMed2001

Effect of burst-mode transcutaneous electrical nerve stimulation on peripheral vascular resistance.

BACKGROUND AND PURPOSE: Based on changes in skin temperature alone, some authors have proposed that postganglionic sympathetic vasoconstrictor fibers can be stimulated transcutaneously. Our goal was to determine the effects of low-frequency (2 bursts per second), burst-mode transcutaneous electrical nerve stimulation (TENS) on calf vascular resistance, a more direct marker of sympathetic vasoconstrictor outflow than skin temperature, in subjects with no known pathology. SUBJECTS: Fourteen women and 6 men (mean age=31 years, SD=13, range=18-58) participated in this study. METHODS: Calf blood flow, arterial pressure, and skin temperature were measured while TENS was applied over the common peroneal and tibial nerves. RESULTS: Blood flow immediately following stimulation was not affected by TENS applied just under or just above the threshold for muscle contraction. Transcutaneous electrical nerve stimulation applied at 25% above the motor threshold caused a transient increase in calf blood flow. Regardless of stimulation intensity, TENS had no effect on arterial pressure; therefore, calf vascular resistance decreased only during the trial that was 25% above the motor threshold. Regardless of stimulation intensity, TENS failed to alter dorsal or plantar skin temperature. DISCUSSION AND CONCLUSION: These results demonstrate that the effects of TENS on circulation depend on stimulation intensity. When the intensity was sufficient to cause a moderate muscle contraction, a transient, local increase in blood flow occurred. Cooling of the dorsal and plantar skin occurred in both the stimulated and control legs, most likely because skin temperature acclimatized to ambient room temperature, rather than because of any effect of TENS on circulation. The data, therefore, call into question the idea that postganglionic sympathetic efferent fibers are stimulated when TENS is applied at clinically relevant intensities to people without symptoms of cardiovascular or neuromuscular pathology.

Adolescent↗

PubMed2001

Evaluation of an educational intervention for military tobacco users.

This study evaluated the short-term effect of a one-time tobacco hazard education intervention on tobacco use and intention to quit among military tobacco users. Of the 151 Army infantry soldiers who received the intervention, 60 (40%) participated in a 1-month follow-up survey. Respondents' reported pre-intervention tobacco habits included 51% smoking, 22% smokeless tobacco use, and 27% both. A one-group, posttest-only design demonstrated a decline in tobacco use in more than half of tobacco users: 14% quit, and 37% decreased use. However, 46% stayed the same, and 3% increased use. A statistically significant difference in tobacco use existed among the three subgroups of tobacco users (p = 0.004). Smokeless-tobacco-only users were more likely to quit than smoking-only or combined users. Eighty percent had positive thoughts or actions toward quitting tobacco use after the intervention. Results suggest that a one-time tobacco education intervention can positively influence tobacco use in the short term and motivate tobacco users toward quitting.

Chi-Square Distribution↗

PubMed2000

Fatiguing inspiratory muscle work causes reflex sympathetic activation in humans.

We tested the hypothesis that reflexes arising from working respiratory muscle can elicit increases in sympathetic vasoconstrictor outflow to limb skeletal muscle, in seven healthy human subjects at rest. We measured muscle sympathetic nerve activity (MSNA) with intraneural electrodes in the peroneal nerve while the subject inspired (primarily with the diaphragm) against resistance, with mouth pressure (PM) equal to 60 % of maximal, a prolonged duty cycle (TI/TTot) of 0.70, breathing frequency (fb) of 15 breaths min-1 and tidal volume (VT) equivalent to twice eupnoea. This protocol was known to reduce diaphragm blood flow and cause fatigue. MSNA was unchanged during the first 1-2 min but then increased over time, to 77 +/- 51 % (s.d.) greater than control at exhaustion (mean time, 7 +/- 3 min). Mean arterial blood pressure (+12 mmHg) and heart rate (+27 beats min-1) also increased. When the VT, fb and TI/TTot of these trials were mimicked with no added resistance, neither MSNA nor arterial blood pressure increased. MSNA and arterial blood pressure also did not change in response to two types of increased central respiratory motor output that did not produce fatigue: (a) high inspiratory flow rate and fb without added resistance; or (b) high inspiratory effort against resistance with PM of 95 % maximal, TI/TTot of 0.35 and fb of 12 breaths min-1. The heart rate increased by 5-16 beats min-1 during these trials. Thus, in the absence of any effect of increased central respiratory motor output per se on limb MSNA, we attributed the time-dependent increase in MSNA during high resistance, prolonged duty cycle breathing to a reflex arising from a diaphragm that was accumulating metabolic end products in the face of high force output plus compromised blood flow.

Adult↗

PubMed2000

On the Bayesian analysis of ring-recovery data.

Vounatsou and Smith (1995, Biometrics 51, 687-708) describe the modern Bayesian analysis of ring-recovery data. Here we discuss and extend their work. We draw different conclusions from two major data analyses. We emphasize the extreme sensitivity of certain parameter estimates to the choice of prior distribution and conclude that naive use of Bayesian methods in this area can be misleading. Additionally, we explain the discrepancy between the Bayesian and classical analyses when the likelihood surface has a flat ridge. In this case, when there is no unique maximum likelihood estimate, the Bayesian estimators are remarkably precise.

Animals↗

PubMed2000

Neurocirculatory consequences of intermittent asphyxia in humans.

We examined the neurocirculatory and ventilatory responses to intermittent asphyxia (arterial O(2) saturation = 79-85%, end-tidal PCO(2) =3-5 Torr above eupnea) in seven healthy humans during wakefulness. The intermittent asphyxia intervention consisted of 20-s asphyxic exposures alternating with 40-s periods of room-air breathing for a total of 20 min. Minute ventilation increased during the intermittent asphyxia period (14.2 +/- 2.0 l/min in the final 5 min of asphyxia vs. 7.5 +/- 0.4 l/min in baseline) but returned to the baseline level within 2 min after completion of the series of asphyxic exposures. Muscle sympathetic nerve activity increased progressively, reaching 175 +/- 12% of baseline in the final 5 min of the intervention. Unlike ventilation, sympathetic activity remained elevated for at least 20 min after removal of the chemical stimuli (150 +/- 10% of baseline in the last 5 min of the recovery period). Intermittent asphyxia caused a small, but statistically significant, increase in heart rate (64 +/- 4 beats/min in the final 5 min of asphyxia vs. 61 +/- 4 beats/min in baseline); however, this increase was not sustained after the return to room-air breathing. These data demonstrate that relatively short-term exposure to intermittent asphyxia causes sympathetic activation that persists after removal of the chemical stimuli. This carryover effect provides a potential mechanism whereby intermittent asphyxia during sleep could lead to chronic sympathetic activation in patients with sleep apnea syndrome.

Adult↗

PubMed2000

Circulatory responses to voluntary and electrically induced muscle contractions in humans.

BACKGROUND AND PURPOSE: Transcutaneous electrical nerve stimulation (TENS) increases regional blood flow when applied at intensities sufficient to cause skeletal muscle contraction. It is not known whether increases in blood flow elicited by TENS differ from those caused by voluntary muscle contraction. The purpose of this study, therefore, was to compare the hemodynamic effects of these 2 types of muscle contraction. SUBJECTS AND METHODS: Fourteen people with no known pathology, aged 18 to 49 years (mean=28, SD=8), served as subjects. Calf blood flow (venous occlusion plethysmography), heart rate (electrocardiogram), blood pressure (automated sphygmomanometry), and force (footplate transducer) were measured during electrically induced and voluntary contractions. RESULTS: Both modes of exercise caused rapid, but short-lived vasodilation (calf vascular resistance [mean(SEM]: (53%(3% for voluntary contractions versus (57%(4% for electrically induced contractions). The vasodilation caused by electrically induced contractions persisted for at least 15 seconds in the postexercise period, whereas the vasodilation elicited by voluntary contractions had resolved by this time point. CONCLUSION AND DISCUSSION: The hemodynamic changes elicited by voluntary and electrically induced muscle contractions are similar in magnitude but different in duration.

Adult↗

PubMed1999

Role of respiratory motor output in within-breath modulation of muscle sympathetic nerve activity in humans.

We measured muscle sympathetic nerve activity (MSNA, peroneal microneurography) in 5 healthy humans under conditions of matched tidal volume, breathing frequency, and end-tidal CO(2), but varying respiratory motor output as follows: (1) passive positive pressure mechanical ventilation, (2) voluntary hyperventilation, (3) assisted mechanical ventilation that required the subject to generate -2.5 cm H(2)O to trigger each positive pressure breath, and (4) added inspiratory resistance. Spectral analyses showed marked respiratory periodicities in MSNA; however, the amplitude of the peak power was not changed with changing inspiratory effort. Time domain analyses showed that maximum MSNA always occurred at end expiration (25% to 30% of total activity) and minimum activity at end inspiration (2% to 3% of total activity), and the amplitude of the variation was not different among conditions despite marked changes in respiratory motor output. Furthermore, qualitative changes in intrathoracic pressure were without influence on the respiratory modulation of MSNA. In all conditions, within-breath changes in MSNA were inversely related to small changes in diastolic pressure (1 to 3 mm Hg), suggesting that respiratory rhythmicity in MSNA was secondary to loading/unloading of carotid sinus baroreceptors. Furthermore, at any given diastolic pressure, within-breath MSNA varied inversely with lung volume, demonstrating an additional influence of lung inflation feedback on sympathetic discharge. Our data provide evidence against a significant effect of respiratory motor output on the within-breath modulation of MSNA and suggest that feedback from baroreceptors and pulmonary stretch receptors are the dominant determinants of the respiratory modulation of MSNA in the intact human.

Action Potentials↗

PubMed1999

Arousal from sleep shortens sympathetic burst latency in humans.

1. Bursts of sympathetic activity in muscle nerves are phase-locked to the cardiac cycle by the sinoaortic baroreflexes. Acoustic arousal from non-rapid eye movement (NREM) sleep reduces the normally invariant interval between the R-wave of the electrocardiogram (ECG) and the peak of the corresponding sympathetic burst; however, the effects of other forms of sleep disruption (i.e. spontaneous arousals and apnoea-induced arousals) on this temporal relationship are unknown. 2. We simultaneously recorded muscle sympathetic nerve activity in the peroneal nerve (intraneural electrodes) and the ECG (surface electrodes) in seven healthy humans and three patients with sleep apnoea syndrome during NREM sleep. 3. In seven subjects, burst latencies were shortened subsequent to spontaneous K complexes (1.297 +/- 0.024 s, mean +/- s. e.m.) and spontaneous arousals (1.268 +/- 0.044 s) compared with latencies during periods of stable NREM sleep (1.369 +/- 0.023 s). In six subjects who demonstrated spontaneous apnoeas during sleep, apnoea per se did not alter burst latency relative to sleep with stable electroencephalogram (EEG) and breathing (1.313 +/- 0.038 vs. 1.342 +/- 0.026 s); however, following apnoea-induced EEG perturbations, burst latencies were reduced (1.214 +/- 0.034 s). 4. Arousal-induced reduction in sympathetic burst latency may reflect a temporary diminution of baroreflex buffering of sympathetic outflow. If so, the magnitude of arterial pressure perturbations during sleep (e.g. those caused by sleep disordered breathing and periodic leg movements) may be augmented by arousal.

Adult↗

PubMed1999

Daytime blood pressure elevation after nocturnal hypoxia.

The purpose of this study was to investigate whether nocturnal hypoxia causes daytime blood pressure (BP) elevation. We hypothesized that overnight exposure to hypoxia leads the next morning to elevation in BP that outlasts the hypoxia stimulus. We studied the effect on BP of two consecutive night exposures to hypobaric hypoxia in 10 healthy normotensive subjects. During the hypoxia nights, subjects slept for 8 h in a hypobaric chamber at a simulated altitude of 4,000 m (barometric pressure = 462 mmHg). Arterial O(2) saturation and electrocardiogram were monitored throughout the night. For 30 min before the nocturnal simulated ascent and for 4 h after return to baseline altitude the next morning, BP was measured every 5 min while the subject was awake. The same measurements were made before and after 2 normoxic nights of sleep in the hypobaric chamber at ambient barometric pressure (745 mmHg). Principal components analysis was applied to evaluate patterns of BP response after the second night of hypoxia and normoxia. A distinct pattern of diastolic BP (DBP) elevation was observed after the hypoxia night in 9 of the 10 subjects but in none after the normoxia night. This pattern showed a mean increase of 4 mmHg in DBP compared with the presleep-awake baseline in the first 60 min and a return to baseline by 90 min. We conclude that nocturnal hypoxia leads to a carryover elevation of daytime DBP.

Adolescent↗

PubMed1998

Blood pressure perturbations caused by subclinical sleep-disordered breathing.

We studied the acute effects of apneas and hypopneas on blood pressure in a nonclinic population of middle-aged adults. Arterial pressure was measured noninvasively (photoelectric plethysmography) during an overnight, in-laboratory polysomnographic study in 72 men and 23 women enrolled in the Wisconsin Sleep Cohort Study, a population-based study of sleep-disordered breathing. Sleep-disordered breathing events (272 apneas and 1469 hypopneas) were observed in 92% of subjects. The across-subject mean decreases in arterial O2 saturation were 9+/-8% (SD) for apneas (17+/-8 seconds duration) and 4+/-3% for hypopneas (21+/-6 seconds duration; 41+/-17% of baseline ventilation). In both apneas and hypopneas, even those with only 1% to 3% O2 desaturations, blood pressure decreased during the event, followed by an abrupt increase in the postevent recovery period. Mean values for peak changes in blood pressure (difference between the maximum during the recovery period and the minimum during the event) were 23+/-10 mm Hg for systolic and 13+/-6 mm Hg for diastolic pressure. The strongest predictors of the pressor responses to apneas and hypopneas were (in order of importance): magnitude of the ventilatory overshoot, length of the event, magnitude of changes in heart rate and arterial O2 saturation, and presence or absence of electroencephalographic arousal. We speculate that these fluctuations may play a role in the pathogenesis of hypertension in individuals with subclinical sleep-disordered breathing.

Cohort Studies↗

PubMed1997

Effect of transcutaneous electrical nerve stimulation on the pressor response to static handgrip exercise.

BACKGROUND AND PURPOSE: A proposed mechanism for the pain-relieving properties of transcutaneous electrical nerve stimulation (TENS) is gating of impulses carried by group III and IV afferent nerve fibers. The purpose of this study was to determine the effects of TENS on the pressor response to static exercise, a response mediated by group III and IV muscle afferents. SUBJECTS: Sixteen subjects (9 men, 7 women) with no known history of cardiovascular, neurologic, or musculoskeletal disease participated. METHODS: We measured arterial pressure, heart rate, and sympathetic activity during sustained, 25% maximal handgrip exercise. Each subject performed the handgrip exercise with and without conventional TENS applied to the ipsilateral forearm and, in a separate trial, to the contralateral leg. RESULTS: The sympathetically mediated pressor response to handgrip exercise was blunted when TENS was applied to the ipsilateral forearm, but not when TENS was applied to the contralateral leg. CONCLUSION AND DISCUSSION: These data support the concept that central transmission of neural impulses traveling in group III and IV fibers can be modulated by other afferent inputs converging on the same spinal level.

Adult↗

PubMed1997

Ventilatory response to induced auditory arousals during NREM sleep.

Sleep state instability is a potential mechanism of central apnea/hypopnea during non-rapid eye movement (NREM) sleep. To investigate this postulate, we induced brief arousals by delivering transient (0.5 second) auditory stimuli during stable NREM sleep in eight normal subjects. Arousal was determined according to American Sleep Disorders Association (ASDA) criteria. A total of 96 trials were conducted; 59 resulted in cortical arousal and 37 did not result in arousal. In trials associated with arousal, minute ventilation (VE) increased from 5.1 +/- 1.24 minutes to 7.5 +/- 2.24 minutes on the first posttone breath (p = 0.001). However, no subsequent hypopnea or apnea occurred as VE decreased gradually to 4.8 +/- 1.5 l/minute (p > 0.05) on the fifth posttone breath. Trials without arousal did not result in hyperpnea on the first breath nor subsequent hypopnea. We conclude that 1) auditory stimulation resulted in transient hyperpnea only if associated with cortical arousal; 2) hypopnea or apnea did not occur following arousal-induced hyperpnea in normal subjects; 3) interaction with fluctuating chemical stimuli or upper airway resistance may be required for arousals to cause sleep-disordered breathing.

Acoustic Stimulation↗

PubMed1997

Neural mechanism of the pressor response to obstructive and nonobstructive apnea.

Obstructive and nonobstructive apneas elicit substantial increases in muscle sympathetic nerve activity and arterial pressure. The time course of change in these variables suggests a causal relationship; however, mechanical influences, such as release of negative intrathoracic pressure and reinflation of the lungs, are potential contributors to the arterial pressure rise. To test the hypothesis that apnea-induced pressor responses are neurally mediated, we measured arterial pressure (photoelectric plethysmography), muscle sympathetic nerve activity (peroneal microneurography), arterial O2 saturation (pulse oximeter), and end-tidal CO2 tension (gas analyzer) during sustained Mueller maneuvers, intermittent Mueller maneuvers, and simple breath holds in six healthy humans before, during, and after ganglionic blockade with trimethaphan (3-4 mg/min, titrated to produce complete disappearance of sympathetic bursts from the neurogram). Ganglionic blockade abolished the pressor responses to sustained and intermittent Mueller maneuvers (-4 +/- 1 vs. +15 +/- 3 and 0 +/- 2 vs. +15 +/- 5 mmHg) and breath holds (0 +/- 3 vs. +11 +/- 3, all P < 0.05). We conclude that the acute pressor response to obstructive and nonobstructive voluntary apnea is sympathetically mediated.

Adult↗