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Biomedical subjects

C G Gallagher

Publications and source records attributed to C G Gallagher.

At least 37 records · Page 2Linked to original sources
PubMed1995

Superior laryngeal nerve blockade and inspiratory resistive load detection in normal subjects.

The site for detection of added inspiratory resistive loads is unknown, but recent evidence suggests that the airways may play an important role. The aim of this study was to discern whether the larynx has an important independent role in conscious detection of added inspiratory resistive loads. A randomized double-blind placebo-controlled study of the effect of superior laryngeal nerve blockade on inspiratory resistive load-detection threshold was carried out in 12 normal subjects (7 women; mean age 27.5 yr; range 18-45 yr). Baseline (preinjection) detection thresholds were similar on the lidocaine [0.58 +/- 0.16 (SE) cmH2O.l-1.s] and saline (0.53 +/- 0.12 cmH2O.l-1.s; P = 0.28) days. There was no significant difference in load-detection thresholds after injection between lidocaine (0.60 +/- 0.15 cmH2O.l-1.s) and saline (0.55 +/- 0.10 cmH2O.l-1.s; P = 0.68). Thus, the larynx does not appear to be an important independent airway site for conscious inspiratory resistive load detection.

Adolescent↗
PubMed1995

Low-dose nebulized morphine does not improve exercise in interstitial lung disease.

Recent reports have suggested that low-dose nebulized morphine may improve exercise tolerance in patients with interstitial lung disease (ILD) by acting on peripheral opioid-sensitive pulmonary receptors. We therefore examined whether the administration of low-dose nebulized morphine would influence dyspnea or the breathing pattern during exercise of subjects with ILD and improve their exercise performance. Each of six subjects with ILD underwent three maximal incremental cycle ergometer tests, each test separated from the last by at least 3 d. Each exercise test was similar except that 30 min before exercise, the subjects received nebulized saline (control), morphine 2.5 mg, or morphine 5.0 mg, respectively, in double-blinded fashion. No significant differences were noted in exercise duration, maximal workload, or sense of dyspnea at the end of exercise in the control test and the tests with either morphine 2.5 mg or morphine 5.0 mg. Nor were significant differences noted in resting, submaximal, or end-exercise measurements of oxygen uptake (VO2), carbon dioxide output (VCO2), end-tidal CO2 (PETCO2), oxygen saturation (SaO2), minute ventilation (VI), respiratory frequency (f), tidal volume (VT), or heart rate (HR) in the three tests. Low-dose nebulized morphine did not alter the subjects' breathing pattern or affect the relationship between dyspnea and ventilation during exercise. No significant side effects were noted. The administration of low-dose nebulized morphine to subjects with ILD neither relieves their dyspnea during exercise nor improves their maximal exercise performance.

Double-Blind Method↗
PubMed1995

Inspiratory muscle weakness in chronic heart failure: role of nutrition and electrolyte status and systemic myopathy.

Inspiratory muscle weakness has been demonstrated in ambulatory, stable chronic heart failure (CHF) and may contribute to dyspnea during daily living. However, the mechanisms underlying this weakness are unknown. Malnutrition and electrolyte depletion are recognized complications of CHF that may impair skeletal muscle function, and limb muscle weakness and myopathic changes have also been demonstrated in CHF. We examined whether nutrition and electrolyte status contribute to the reduced skeletal muscle strength and whether inspiratory muscle weakness in CHF is part of general skeletal muscle weakness. We measured maximum inspiratory and expiratory mouth pressures as indices of respiratory muscle strength, maximum hand-grip strength as an index of limb muscle strength, anthropometric indices, serum albumin, and total lymphocyte count as indices of nutritional status, and serum electrolytes in 15 stable patients with chronic cardiac pump failure who had no evidence of primary lung disease, and in 15 age-and-sex-matched healthy controls. As compared with the matched controls, the CHF patients had reduced inspiratory muscle strength (p < 0.0025), but their expiratory and limb muscle strength were not significantly reduced. CHF patients were not malnourished; they were heavier than matched controls because of increased body fat (p < 0.05). Serum sodium was significantly lower in the CHF patients than in the controls (p < 0.01), but was within the normal range in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1994

Differential ventilatory control during constant work rate and incremental exercise.

The purpose of this study was to determine whether the tachypneic breathing pattern of constant work rate, heavy exercise (CWE) is unique to CWE or whether it represents the usual pattern of the respiratory control system at high levels of ventilation (VI). We compared breathing pattern in ten healthy subjects (age 20-29 years) during CWE and maximal incremental exercise (MIE) on a bicycle ergometer. Work rate was constant at 76% of maximum work rate in CWE and progressively increased by 25 watts/minute until exhaustion during MIE. Breathing pattern was examined at matched levels of VI equivalent to 80% and about 100% of maximum VI during CWE (97.1 and 121.4 L.min-1, respectively). Exercise duration (mean+standard deviation) was 13 +/- 6 and 12 +/- 1 min during CWE and MIE, respectively (P = NS). Tidal volume (VT) fell by an average of 0.20 L towards the end of CWE, but was maintained relatively high and constant towards the end of MIE. At high, but not lower, matched levels of VI breathing pattern during CWE was significantly more rapid and shallow than that during MIE. The tachypnoea of CWE did not correlate with the progressive rise in VI, oxygen uptake or cardiac frequency during CWE. We conclude that (1) CWE is associated with a tachypneic influence that is absent or less during incremental exercise; this tachypnea is most marked at the end of CWE. (2) The tachypnoea of CWE is not part of a generalized rate accelerating process during CWE. The mechanism(s) underlying the tachypnoea are unclear but it may be related to inspiratory muscle fatigue, pulmonary oedema, and/or altered respiratory mechanics.

Adult↗
PubMed1994

Lung volumes and expiratory flow limitation during exercise in interstitial lung disease.

Lung volumes were measured at rest and during exercise by an open-circuit N2-washout technique in patients with interstitial lung disease (ILD). Exercise tidal flow-volume (F-V) curves were also compared with maximal F-V curves to investigate whether these patients demonstrated flow limitation. Seven patients underwent 4 min of constant work rate bicycle ergometer exercise at 40, 70, and 90% of their previously determined maximal work rates. End-expiratory lung volume and total lung capacity were measured at rest and near the end of each period of exercise. There was no significant change in end-expiratory lung volume or total lung capacity when resting measurements were compared with measurements at 40, 70, and 90% work rates. During exercise, expiratory flow limitation was evident in four patients who reported stopping exercise because of dyspnea. In the remaining patients who discontinued exercise because of leg fatigue, no flow limitation was evident. In all patients, the mean ratio of maximal minute ventilation to maximal ventilatory capacity (calculated from maximal F-V curves) was 67%. We conclude that lung volumes during exercise do not significantly differ from those at rest in this population and that patients with ILD may demonstrate expiratory flow limitation during exercise. Furthermore, because most patients with ILD are not breathing near their maximal ventilatory capacity at the end of exercise, we suggest that respiratory mechanics are not the primary cause of their exercise limitation.

Airway Obstruction↗
PubMed1994

Oxygen improves maximal exercise performance in interstitial lung disease.

We examined whether arterial hypoxemia impairs incremental exercise performance in subjects with interstitial lung disease (ILD). Seven subjects underwent two incremental exercise tests on a bicycle ergometer in random order; one while breathing room air (RA), and the other while breathing 60% O2. Maximal exercise performance was impaired in all subjects: maximal oxygen uptake (peak VO2) was 56 +/- 4% predicted (+/- SEM); and all subjects demonstrated significant arterial oxygen desaturation during exercise breathing RA (mean 11 +/- 1%). Breathing 60% O2 during exercise resulted in a significant increase in peak VO2 (RA: 1.32 +/- 0.05 L/min; O2: 1.58 +/- 0.08 L/min; p < 0.05), exercise duration (RA: 390 +/- 21 s; O2: 458 +/- 24 s; p < 0.01) and maximal work load (RA: 112 +/- 6 watts; O2: 129 +/- 6 watts; p < 0.005). There was no significant difference in maximal minute ventilation (VI) achieved at the end of both tests. At matched ventilation (90% peak VI from the RA test), respiratory frequency (f) was significantly higher (RA: 33 +/- 2 breaths/min; O2: 35 +/- 2 breaths/min; p < 0.05), and tidal volume (VT) significantly lower (RA: 1.72 +/- 0.15 L; O2: 1.64 +/- 0.12; p < 0.05) when subjects exercised breathing oxygen. We conclude that arterial hypoxemia significantly impairs incremental exercise performance in subjects with ILD, but that mechanisms other than arterial oxygen desaturation are responsible for the rapid, shallow breathing pattern these subjects adopt during exercise.

Adult↗
PubMed1994

Dead space loading and exercise limitation in patients with interstitial lung disease.

STUDY DESIGN: We tested the hypothesis that maximal exercise performance in subjects with interstitial lung disease (ILD) is limited by respiratory factors. Assuming this is so, ventilatory stimulation by added dead space (VD) should impair exercise capacity. METHODS: Six subjects with ILD each underwent three maximal incremental exercise studies on a bicycle ergometer; control 1, added VD, and control 2. During the VD study, external VD (500 ml) was added to the circuit, and results obtained were compared with the mean results from the control studies. RESULTS: Exercise duration (TLIM) was significantly less in the VD study when compared to the control study (369 +/- 50 vs 439 +/- 55, p < 0.05), as was work rate (102 +/- 13 vs 125 +/- 14 W, p < 0.05) and peak oxygen uptake per minute (VO2) (1.08 +/- 0.09 vs 1.43 +/- 0.14 L/min, p < 0.05). At end-exercise, the Borg scale was higher in the VD study when compared to the control study (6 +/- 1 vs 5 +/- 1, p < 0.05), while no significant difference in minute ventilation (VI) or oxygen desaturation was noted. When compared to the control study at matched times during exercise, the addition of VD resulted in a significant increase in VI while no significant change was noted in VO2, carbon dioxide output (VcO2), or heart rate (HR). CONCLUSION: The decrease observed in TLIM, work rate, and peak VO2 with added VD, associated with a lack of change in VI or oxygen desaturation at end-exercise, suggests that exercise limitation in ILD is primarily due to respiratory factors.

Adult↗
PubMed1994

Clinical exercise testing in interstitial lung disease.

Clinical exercise testing has become an essential tool used in the early diagnosis, in the monitoring of treatment effectiveness, and in the assessment of impairment owing to ILD. Despite the assorted causes, the responses to exercise demonstrated by these diseases are generally similar. Although much has been learned about how these diverse diseases functionally impair the exercise capacity of the patient, further study is required if we are to understand fully the various physiologic abnormalities manifested by patients with ILD during exercise.

Biomechanical Phenomena↗
PubMed1994

Exercise limitation and clinical exercise testing in chronic obstructive pulmonary disease.

Clinical exercise testing is an important tool in assessment of exercise limitation in COPD patients, in assessment of physiologic and psychological factors that contribute to exercise limitation, and in the differential diagnosis of cardiorespiratory disease. Further studies that examine the clinical utility of exercise testing are needed because there are currently insufficient data regarding the utility of many exercise variables.

Acidosis, Respiratory↗
PubMed1993

Reproducibility of incremental maximal cycle ergometer testing in patients with restrictive lung disease.

BACKGROUND: Exercise testing has become an important tool in the diagnosis and treatment of restrictive lung disease. The reproducibility of variables measured during exercise testing was examined in subjects with stable restrictive lung disease. METHODS: Six subjects, who had never previously undergone exercise testing, each underwent three maximal incremental exercise studies on a bicycle ergometer conducted during a 28 day period. RESULTS: Data collected at rest, before exercise, were not significantly different during the three study days. Comparison of results at the end of the exercise tests from the three studies also revealed no evidence of a significant learning effect. Reproducibility of exercise performance by subjects was assessed by the coefficient of variation. The mean within subject coefficient of variation at the end of the exercise tests was 5.6% for work rate, 7.9% for exercise duration, and 9.5% for dyspnoea. The mean within subject coefficient of variation obtained at the end of the exercise tests was 5.3% for oxygen uptake (VO2), 2.5% for oxygen saturation (SaO2), 4.0% for heart rate (HR), 5.5% for minute ventilation (VE), 5.8% for respiratory frequency (f), and 4.6% for tidal volume (VT). The mean within subject coefficient of variation at 40% and 70% of maximal work rates for VO2 was 5.7% and 5.6% respectively, for SaO2 1.3% and 1.5%, for HR 4.8% and 4.0%, for VE 6.3% and 6.6%, for f 10.1% and 7.8%, and for VT 6.0% and 4.5%. CONCLUSIONS: Variables measured during clinical exercise testing in subjects with restrictive lung disease are highly reproducible. No significant learning effect was found on repeated testing in subjects who had never previously undergone exercise testing.

Adult↗
PubMed1993

Lack of importance of the superior laryngeal nerves in citric acid cough in humans.

The relative importance of laryngeal afferents in the cough reflex in humans is unknown. This study was designed to investigate the importance of superior laryngeal nerve afferents in the cough reflex induced by inhaled nebulized citric acid in awake humans. Nine healthy volunteers had their cough thresholds to inhaled nebulized citric acid measured after superior laryngeal nerve conduction blockade and after a sham nerve block. Of the nine subjects, four showed no change in cough threshold after superior laryngeal nerve anesthesia, three showed increased cough threshold after nerve block compared with no block, and two showed decreased cough threshold after nerve block. The geometric means of the cough thresholds for the nerve block vs. sham block tests were 16 +/- 13 (SD) and 15 +/- 8% citric acid, respectively. There was no statistically significant difference (Wilcoxon signed-rank test) between the cough thresholds with and without superior laryngeal nerve block (P > 0.05). We conclude that, in the awake human, superior laryngeal nerve afferents do not play a necessary role in initiation of citric acid-induced cough.

Administration, Inhalation↗
PubMed1993

Carotid chemoreceptors and respiratory adaptations to dead space loading during incremental exercise.

Dead space (VD) loading has been shown to cause an increase in tidal volume and a decrease in respiratory frequency at moderate to high levels of ventilation (VI) during exercise (J. Appl. Physiol. 70: 55-62, 1991). This study examined the role of carotid chemoreceptors (CC) in the breathing pattern response to added VD during maximal incremental exercise; we used hyperoxia to silence the CC. Nine healthy subjects exercised on a bicycle ergometer on 4 different days while inspiring air with VD (AVD) and without VD [air control (AC)] and while inspiring 100% O2 with VD (O2VD) and without VD (O2C). Equipment resistance for VD and control studies was identical, and the exercise tests were done in a randomized order. At a matched level of VI equivalent to 75% VI at the end of the AC experiments (102 l/min), the breathing pattern in the AVD and O2VD tests was significantly deeper and slower (P < 0.05) than that in the AC and O2C tests. The difference in tidal volume between AVD and AC tests (delta = 0.26 +/- 0.16 liter) was not significantly different from that between O2VD and O2C tests (delta = 0.23 +/- 0.23 liter). The breathing pattern was the same in the AC and O2C tests. It is concluded that the altered breathing pattern with VD loading is not mediated by the CC.

Adaptation, Physiological↗
PubMed1992

Effect of physical training on breathing pattern during progressive exercise.

It has been suggested that physical training causes a slower, deeper breathing pattern at a given level of ventilation, but there is no convincing evidence to support this. We examined breathing pattern during maximal incremental exercise on a cycle ergometer in 7 males before and after 3-4 weeks of cycle endurance training (TRAINING), and in 6 males before and after a similar period of unaltered physical activity (CONTROL); all subjects were healthy and previously sedentary. After physical training there was a significant increase in peak oxygen uptake, and significant reductions in carbon dioxide output, heart rate (fHR) and minute ventilation (VI) at submaximal workloads; peak VI was significantly increased whereas peak fHR was unchanged. At matched VI levels (moderate, moderately-high, high) the TRAINING subjects' breathing pattern was not significantly altered; there was a power of at least 80% to detect a significant (> 0.30 L) increase in tidal volume (P < 0.05) at moderately high and high ventilation levels. There was no change in the CONTROL subjects' maximal exercise performance, or breathing pattern at matched VI levels, over the same period. Short-term, activity-specific physical training does not significantly affect the breathing pattern adopted by normal humans during progressive exercise.

Adult↗
PubMed1992

Inspiratory muscle weakness and dyspnea in chronic heart failure.

Dyspnea is a common, disabling symptom in chronic heart failure, yet the underlying mechanisms remain unknown. The respiratory muscle pump is composed of skeletal muscles whose strength directly influences the pump's performance. Respiratory muscle weakness is important in the dyspnea experienced by some patients with pulmonary disease; however, the role of the respiratory muscle pump in the dyspnea of chronic heart failure has not previously been examined. To assess respiratory muscle strength and its relation to dyspnea during daily activity, we measured maximum inspiratory and expiratory mouth pressures as indices of respiratory muscle strength and the baseline dyspnea index in nine stable, chronic cardiac pump failure patients who had no evidence of primary lung disease, and in nine age- and sex-matched healthy control subjects. The chronic heart failure patients, when compared with their matched control subjects, had reduced inspiratory and expiratory muscle strength, and both inspiratory and expiratory muscle strength were significantly correlated with dyspnea during daily activity (r2 = 0.80, p = 0.001 and r2 = 0.45, p = 0.05, respectively). Inspiratory muscle strength accounted for all of the variance in dyspnea that was correlated with respiratory muscle strength when the relative contributions of inspiratory and expiratory muscle strength were examined. There was no correlation between lung volumes or spirometry and dyspnea in the heart failure patients. These findings indicate that patients with stable chronic heart failure have inspiratory and expiratory muscle weakness and further suggest that the respiratory muscle pump significantly contributes to the dyspnea during the activities of daily living.

Activities of Daily Living↗
PubMed1991

Respiratory adaptations to dead space loading during maximal incremental exercise.

We examined the effects of dead space (VD) loading on breathing pattern during maximal incremental exercise in eight normal subjects. Addition of external VD was associated with a significant increase in tidal volume (VT) and decrease in respiratory frequency (f) at moderate and high levels of ventilation (VI); at a VI of 120 l/min, VT and f with added VD were 3.31 +/- 0.33 liters and 36.7 +/- 6.7 breaths/min, respectively, compared with 2.90 +/- 0.29 liters and 41.8 +/- 7.3 breaths/min without added VD. Because breathing pattern does not change with CO2 inhalation during heavy exercise (Gallagher et al. J. Appl. Physiol. 63: 238-244, 1987), the breathing pattern response to added VD is probably a consequence of alteration in the PCO2 time profile, possibly sensed by the carotid body and/or airway-pulmonary chemoreceptors. The increase in VT during heavy exercise with VD loading indicates that the tachypneic breathing pattern of heavy exercise is not due to mechanical limitation of maximum ventilatory capacity at high levels of VT.

Adaptation, Physiological↗
PubMed1991

Corticosteroid therapy and respiratory muscle function in humans.

We examined the effects of prednisone administration on respiratory muscle function in humans using a double-blind study with a placebo control group. A total of 16 normal subjects were randomized to receive 20 mg prednisone daily (n = 8) or placebo daily (n = 8) for 2 wk. Inspiratory muscle strength (Pimax), expiratory muscle strength (PEmax), diaphragmatic strength (Pdimax), and inspiratory muscle endurance were measured at the beginning and end of the study. There was no significant change with treatment for Pimax (-145 +/- 7 to -138 +/- 6 cm H2O), PEmax (171 +/- 17 to 169 +/- 14 cm H2O), Pdimax (194 +/- 11 to 196 +/- 12 cm H2O), or endurance (76 +/- 3 to 77 +/- 4%) for the prednisone group and no significant difference between the two groups. We conclude that prednisone in moderate dosage has no significant effect on respiratory muscle function in humans, at least in the short term.

Adult↗
PubMed1990

Exercise and chronic obstructive pulmonary disease.

Patients with chronic obstructive pulmonary disease have abnormal respiratory mechanics, respiratory muscle function, gas exchange, and cardiovascular function during exercise. Their impaired exercise tolerance is at least partly due to altered respiratory mechanics, but factors that increase ventilation during exercise indirectly contribute to exercise limitation. Clinical exercise testing is a very important tool in the assessment of exercise capacity, assessment of factors that contribute to exercise limitation, and differential diagnosis of cardiopulmonary disease.

Exercise↗