Biomedical subjects

R L Pardy

Publications and source records attributed to R L Pardy.

At least 55 records · Page 3Linked to original sources

PubMed1988

Respiratory muscle training.

The application of skeletal muscle training principles to the respiratory muscles is a relatively new field. Strength and endurance training of the respiratory muscles can be achieved in normal humans and in patients with neuromuscular and chronic obstructive pulmonary diseases. Careful monitoring is required throughout a training program to ensure that the respiratory muscles are, in fact, being trained. This is a promising area, although further research is necessary to determine the indications for respiratory muscle training. Furthermore, it is still necessary to determine the optimal mode of training.

Breathing Exercises↗

PubMed1987

Measurement of inspiratory muscle performance with incremental threshold loading.

We found that breathing strategies affect measurement of sustainable inspiratory pressure (SIP). After allowing time for learning, the maximum sustainable inspiratory pressure (SIPmax) was 46% greater than SIP. We therefore developed a test of ventilatory muscle performance that used progressive 2-minute increments in threshold inspiratory resistance. Subjects started with a low load and continued to breathe until they could no longer inspire. With increasing load there was a fall in minute ventilation and time of inspiration, and an increase in oxygen consumption and PETCO2. Power was greatest when loads were 55 to 75% of maximum static inspiratory pressure (MIP). The inspiratory mouth pressure corresponding to the greatest load achieved (PmPeak) was the same in trained and naive subjects. PmPeak/MIP was reproducible and was not influenced by fixing subjects' breathing frequency. We concluded that tests of ventilatory muscle performance should allow subjects to develop breathing strategies to handle high inspiratory loads. Two-minute incremental loading is a simple assessment of ventilatory muscle performance and the test may have clinical application where reproducibility is necessary.

Adult↗

PubMed1986

Leukocytosis of exercise: role of cardiac output and catecholamines.

The effect of propranolol (5 mg iv) on the leukocytosis of exercise was studied in seven normal young males. Leukocyte counts, plasma norepinephrine (NE), epinephrine (E), and cardiac output were measured at rest and in the steady state of several submaximal work loads when subjects exercised on a cycle ergometer. The results in control experiments were compared with those obtained on a different day with propranolol. Propranolol decreased heart rate at all work loads (P less than 0.001) but had no effect on the increase in cardiac output at increasing work loads. Plasma NE and E levels were similar at rest and in exercise in control and propranolol studies. There was no effect of propranolol on the increase in leukocyte counts with increasing work loads. Although propranolol did not affect the increase in total leukocyte count, the increase in lymphocyte count at higher work loads was less with propranolol. We conclude that the demargination of leukocytes from the pulmonary circulation in exercise is probably a mechanical effect of the increase in cardiac output. However, we have not excluded a contribution from a humoral event that would decrease the adherence of leukocytes to endothelium during exercise. The smaller increase in lymphocytes at higher work loads in the presence of propranolol suggests that catecholamines affect the lymphocyte count over and above their effect on cardiac output.

Adult↗

PubMed1985

Diaphragmatic fatigue in normoxia and hyperoxia.

Diaphragmatic fatigue was induced in six normal young men inspiring against a variable alinear resistance. Breathing pattern was rigidly controlled (tidal volume 0.75 liter, 12 breaths . min-1). Fatigue was defined as an inability to continue to generate a target transdiaphragmatic pressure (Pdi = 0.65 - 0.84 Pdimax). Diaphragmatic electromyogram (EMG, esophageal electrode) and perceived effort (PE, open-ended scale) were recorded. Subjects were tested on an identical resistance inspiring air or 100% O2 in random order on different days. They were unaware of the gas mixture inspired. Mean endurance time (tlim) +/- SE for air was 4.1 +/- 1.4 min and for O2 was 8.6 +/- 2.7 min (P less than 0.005). The increased tlim in O2 was associated with a delay in onset of EMG changes heralding diaphragmatic fatigue and a decrease in PE at any time during the study compared with the level of PE in air. Arterial O2 saturation (ear oximeter) remained at the resting level of 99.0 +/- 0.2% in O2 and decreased from the resting level of 97.2 +/- 0.2% by 2.8 +/- 0.7% (P less than 0.01) in air. The end-tidal CO2 fraction increased to a similar degree in air and O2 studies. We conclude that when breathing pattern, minute ventilation, and Pdi are held constant during inspiratory resistive loading, breathing O2 delays the onset of diaphragm fatigue and decreases PE.

Adult↗

PubMed1985

Effects of separate rib cage and abdominal restriction on exercise performance in normal humans.

We assessed the effects of selective restriction of movements of the rib cage (Res,rc) and abdomen (Res,ab) on ventilatory pattern, transdiaphragmatic pressure (Pdi), and electrical activity of the diaphragm (Edi) in five normal subjects exercising at a constant work rate (80% of maximum power output) on a cycle ergometer till exhaustion. Restriction of movements was achieved by an inelastic corset applied tightly around the rib cage or abdomen. Edi was recorded by an esophageal electrode, rectified, and then integrated, and peak values during inspiration were measured. Each subject exercised at the same work rate on 3 days: with Res,rc, with Res,ab, and without restriction (control). Res,rc but not Res,ab reduced exercise time (tlim). Up to tlim, minute ventilation (VE) was similar in all three conditions. At any level of VE, however, Res,rc decreased tidal volume and inspiratory and expiratory time, whereas Res,ab had no effect on the pattern of breathing. Res,ab was associated with higher inspiratory Pdi swings at any level of VE, whereas peak Edi was similar to control. Inspiratory Pdi swings were the same with Res,rc as control, but the peak Edi for a given Pdi was greater with Res,rc (P less than 0.05). During Res,rc the abdominal pressure swings in expiration were greater than with Res,ab and control. We conclude that Res,rc altered the pattern of breathing in normal subjects in high-intensity exercise, decreased diaphragmatic contractility, increased abdominal muscle recruitment in expiration, and reduced tlim. On the other hand, Res,ab had no effect on breathing pattern or tlim but was associated with increased diaphragmatic contractility.

Abdomen↗

PubMed1985

Inspiratory muscle function with restrictive chest wall loading during exercise in normal humans.

The effects of selective restriction of rib cage (Res,rc) and abdominal wall (Res,ab) movements on endurance of short-term constant-load heavy exercise and on diaphragmatic function during such exercise were examined in five normal young men. An inelastic surgical corset was used to achieve Res,rc and Res,ab. Subjects exercised on a cycle ergometer at 80% of their maximum power output to exhaustion on three occasions: with Res,rc, with Res,ab, and without restriction of chest wall movements (control). Transdiaphragmatic (Pdi), esophageal, and gastric pressures were measured. Electromyogram of the diaphragm was recorded by an esophageal electrode, and the ratio of the power content of a high-frequency to low-frequency band (H/L ratio) was measured. In addition, maximum Pdi (Pdimax) pre- and immediately postexercise was recorded. Res,rc was associated with a shorter endurance time, a progressive decline of the H/L ratio, and a significant reduction of Pdimax postexercise, whereas no such changes were found with Res,ab. We conclude that diaphragmatic function was well defended with abdominal wall loading, whereas limitation of rib cage expansion reduced diaphragmatic endurance during exercise. The diaphragmatic tension-time index (TTdi) in exercise was always less than the critical value of 0.15 found by Bellemare and Grassino (J. Appl. Physiol. 53: 1190-1195, 1982) when subjects inspired against large resistive loads at normal minute ventilations. We suggest that the higher inspiratory flow rate (P less than 0.05) and breathing frequency (P less than 0.05) account for the occurrence of diaphragmatic fatigue in exercise with Res,rc when the TTdi was 0.06 +/- 0.02.

Abdominal Muscles↗

PubMed1985

Mechanical impedance as determinant of inspiratory neural drive during exercise in humans.

Five healthy males exercised progressively with small 2-min increments in work load. We measured inspiratory drive (occlusion pressure, P0.1), pulmonary resistance (RL), dynamic pulmonary compliance (Cdyn), transdiaphragmatic pressure (Pdi), and diaphragmatic electromyogram (EMGdi). Minute ventilation (VE), mean inspiratory flow rate (VT/TI), and P0.1 all increased exponentially with increased work load, but P0.1 increased at a faster rate than did VT/TI or VE. Thus effective impedance (P0.1/VT/TI) rose throughout exercise. The increasing P0.1 was mostly due to augmented Pdi and coincided with increased EMGdi during this initial portion of inspiration. We found no consistent change in RL or Cdyn throughout exercise. With He breathing (80% He-20% O2), RL was reduced at all work loads; P0.1 fell in comparison with air-breathing values and VE, VT, and VT/TI rose in moderate and heavy work; and P0.1/VT/TI was unchanged with increasing exercise loads. Step reductions in gas density at a constant work load of any intensity showed an immediate reduction in the rate of rise of EMGdi and Pdi followed by increased VT/TI, breathing frequency, and hypocapnia. These changes were maintained during prolonged periods of unloading and were immediately reversible on return to air breathing. These data are consistent with the existence of a reflex effect on the magnitude of inspiratory neural drive during exercise that is sensitive to the load presented by the normal mechanical time constant of the respiratory system. This "load" is a significant determinant of the hyperpneic response and thus of the maintenance of normocapnia during exercise.

Abdomen↗

PubMed1985

Ventilatory muscle function during exercise in air and oxygen in patients with chronic air-flow limitation.

Ventilatory muscle function was examined at rest and during exercise on a cycle ergometer in 8 patients with moderate to severe chronic air-flow limitation (FEV1, 32 +/- 4% predicted) in air and in oxygen. The diaphragmatic electromyogram (EMG) was measured using an esophageal electrode. In addition, measurements of esophageal (Pes), gastric (Pga), and transdiaphragmatic (Pdi) pressures and abdominal wall movements were made. Patients exercised to exhaustion at a constant submaximal workload (80% of maximal power output) inspiring air or 40% O2 in random order on separate days. At end-exercise in air, tidal inspiratory Pes swings were 36 +/- 4% of static maximal inspiratory Pes, and inspiratory Pdi swings were 45 +/- 7% of the static maximal Pdi. Arterial oxygen saturation decreased from 91 +/- 2% at rest to 80 +/- 5% at end-exercise in air. During exercise in air, 5 patients demonstrated a persistent and greater than 20% fall in the ratio of high frequency (150 to 350 Hz) to low frequency (20 to 46 Hz) power (H/L) of the diaphragmatic EMG, indicating impending diaphragmatic fatigue, and 2 patients had paradoxical motion of the abdominal wall. Exercise time at the same constant work load increased from 3.0 +/- 0.6 min in air to 6.4 +/- 1.2 min in O2 (p less than 0.005). At the comparable time during exercise in O2 to end-exercise in air, minute ventilation was less by 13% (p less than 0.005), which was entirely attributable to a lower frequency of breathing. Mean inspiratory and expiratory flows and heart rate were all significantly lower.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗

PubMed1984

Ventilatory muscles during exercise in air and oxygen in normal men.

To determine whether normal ventilatory muscles fatigue during short-term high-intensity exercise, we measured diaphragmatic electromyogram (EMG, esophageal electrode), and pleural (Ppl), gastric (Pga), and transdiaphragmatic (Pdi) pressures in seven normal young men. On separate days, the subjects performed exercise to exhaustion at a constant work load (80% maximum power output) inspiring air or 40% O2. Before and after exercise, Pdimax and maximum expiratory pressure at the mouth (PEmax) were measured. At 0.5-2 min postexercise, there was a decrease in Pdimax in both air (P less than 0.02) and O2 studies (P less than 0.05). There was some recovery in Pdimax from 2-5 min postexercise in air (P less than 0.05) and complete recovery 2-5 min postexercise in O2. PEmax did not change postexercise. During exercise in air, the EMG predicted diaphragmatic fatigue in five subjects using a 20% fall of the ratio of high-frequency (150-350 Hz) to low-frequency) (20-46 Hz) power (H/L) as the criterion. Further evidence of diaphragmatic fatigue during exercise in air in two subjects was the decrease in end-inspiratory Pdi toward end exercise. There was an increase in exercise time with O2 (P less than 0.05). The improved performance in O2 was associated with a delay in the fall in H/L and the absence of the decrease in end-inspiratory Pdi in those subjects in whom such changes were observed in air.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1984

Near-maximal voluntary hyperpnea and ventilatory muscle function.

Because of its potential relevance to heavy exercise we studied the ventilatory muscle function of five normal subjects before, during, and after shortterm near-maximal voluntary normocapnic hyperpnea. Measurements of pleural and abdominal pressures and diaphragm electromyogram (EMG) during hyperpnea and of maximum respiratory pressures before and after hyperpnea were made at four levels of ventilation: 76, 79, and 86% maximal voluntary ventilation (MVV) and at MVV. Measurements of pleural and abdominal pressures and diaphragm electromyogram (EMG) during hyperpnea and of maximum respiratory pressures before and after hyperpnea were made. The pressure-stimulation frequency relationship of the diaphragm obtained by unilateral transcutaneous phrenic nerve stimulation was studied in two subjects before and after hyperpnea. Decreases in maximal inspiratory (PImax) and transdiaphragmatic (Pdimax) strength were recorded posthyperpnea at 76 and 79% MVV. Decreases in the pressure-frequency curves of the diaphragm and the ratio of high-to-low frequency power of the diaphragm EMG occurred in association with decreases in Pdimax. Analysis of the pressure-time product (P X dt) for the inspiratory and expiratory muscles individually indicated the increasing contribution of expiratory muscle force to the attainment of higher levels of ventilation. Demonstrable ventilatory muscle fatigue may limit endurance at high levels of ventilation.

Abdomen↗

PubMed1984

Relaxation rate of mouth pressure with sniffs at rest and with inspiratory muscle fatigue.

The relaxation rate of transdiaphragmatic pressure (Pdi) after voluntary contractions of the diaphragm slows with fatigue. We determined a range of values for the relaxation rate of mouth pressure (Pm) after voluntary contractions of the inspiratory muscles in 27 normal men and women at various lung volumes at rest. Values were similar for both sexes. The relaxation rates were similar at functional residual capacity (FRC) and below FRC, but were greater above FRC (p less than 0.05). In addition, we studied the effect of diaphragmatic fatigue induced by inspiratory resistive loading on the relaxation rates of Pdi and Pm with voluntary contractions of the inspiratory muscles in 6 subjects. With fatigue, the relaxation rates of Pdi and Pm both decreased by similar amounts, indicating that a decrease in the relaxation rate of Pm is as useful a predictor of inspiratory muscle fatigue as a decrease in the relaxation rate of Pdi has been shown to be for the diaphragm. The relaxation rate of Pm varies widely in normal subjects at rest, so isolated values do not indicate whether fatigue is present or developing. However, this may be predicted if relaxation rate decreases with serial measurements.

Adult↗

PubMed1984

The ventilatory pump in exercise.

The response of the ventilatory pump during exercise in health and in patients with COPD is reviewed. The authors' hope is that the pump's response to the stress of exercise will be seen to be efficiently matched to the demands placed on it, even though in disease or under some extreme circumstances in normal subjects it may be stretched to (or beyond) its capacity. From a review of the literature, suggestions are made for directions for future research.

Abdominal Muscles↗

PubMed1983

Changes in relaxation rate with diaphragmatic fatigue in humans.

Maximum relaxation rate (MRR) and the time constant of relaxation (tau) of transdiaphragmatic pressure (Pdi) was measured in four male subjects and compared with the high-to-low frequency ratio (H/L) of the diaphragmatic electromyogram (EMG) as a predictor of diaphragmatic fatigue. Pdi and inspiratory time-to-total breath duration ratios (TI/TT) were varied, and TT and tidal volume were held constant; inspiratory resistances were used to increase Pdi. Studies were performed at various tension-time indices (TTdi = Pdi/Pdimax X TI/TT). Base-line MRR/Pdi was 0.0100 +/- 0.0004 (SE) ms-1, and baseline tau was 53.2 +/- 3.2 ms. At TTdi greater than 0.20, MRR and H/L decreased and tau increased, with maximum changes at the highest TTdi. At TTdi less than 0.20, there was no change in H/L, MRR, or tau. The time course of changes in H/L correlated with those of MRR and tau under fatiguing conditions. In this experimental setting, change in relaxation rate was as useful a predictor of diaphragmatic fatigue as fall in H/L of the diaphragmatic EMG.

Adult↗

PubMed1983

Expiratory threshold load under extracorporeal circulation: effects of vagal afferents.

Nine anesthetized dogs breathed against an expiratory threshold load (ETL) applied by switching the expiratory circuit into a column of H2O to a depth of 20-30 cm. Arterial blood gas tensions were maintained in the normal range by placing the dogs under arteriovenous bypass to avoid any uncontrolled chemostimulation. There was an increase in integrated electromyogram activity of the diaphragm with the ETL. This was rarely observed after cold block of the vagus nerves which also reduced the evoked expiratory activity. The ventilatory response to hypercapnia was greatly depressed under loaded breathing whether vagal afferents were intact or blocked by cold. Both inspiratory drive and ventilatory timing were affected, suggesting that the central integration of chemosensitive afferents was altered. Proof of supraspinal projections of proprioceptive inputs from abdominal muscles was provided by the demonstration of changes in ventilatory timing during selective activation of muscle spindles in abdominal muscles by high-frequency mechanical vibration applied to the linea alba. Thus these observations suggest that during ETL breathing, a possible interaction exists between chemoreflex drive and proprioceptive afferents.

Afferent Pathways↗

PubMed1983

Vagal feedback with expiratory threshold load under extracorporeal circulation.

In 11 anesthetized dogs placed under extracorporeal circulation, the vagal feedback was tested by electrical stimulation of the vagus nerves with cold block of their caudal part and by passive lung hyperinflation. The apneic response to such vagal stimulation progressively disappeared during expiratory threshold load breathing but then returned to control values some minutes after the load was removed. This suppression of the inhibitory response to stimulation of the vagus nerves was usually observed when vagal afferents were intact or blocked by cold. However, it was not observed whether no evoked activity continued in expiratory muscles after the cold block, or after suppression of all proprioceptive muscular afferents after transection of the spinal cord at C6 level. These results strongly suggest that enhancement of proprioceptive inputs to the respiratory centers counteracts the vagally mediated inspiratory "off-switch" mechanisms.

Abdominal Muscles↗

PubMed1983

Changes in rate of relaxation of sniffs with diaphragmatic fatigue in humans.

The rate of relaxation of the diaphragm after stimulated (4 subjects) and voluntary (8 subjects) contractions was compared in normal young men. Stimulated contractions were induced by supramaximal unilateral phrenic nerve stimulation and voluntary contractions by short, sharp sniffs of varying tensions against an occluded airway. The rate of relaxation of the diaphragm was calculated from the rate of decline of transdiaphragmatic pressure (Pdi). In both conditions the maximum relaxation rate (MRR) was proportional to the peak transdiaphragmatic pressure (Pdi), whereas the time constant (tau) of the later exponential decline in Pdi was independent of Pdi. The mean +/- SE rate constant of relaxation (MRR/Pdi) was 0.0078 +/- 0.0002 ms-1 and the mean tau was 57 +/- 3.8 ms for stimulated contractions. The rate of relaxation after sniffs was not different, and it was not affected by either the lung volume at which occluded sniffs were performed (in the range of residual volume to functional residual capacity + 1 liter) or by the relative contribution gastric pressure made to Pdi. After diaphragmatic fatigue was induced by inspiring against a high alinear resistance there was a decrease in relaxation rate. In the 1st min postfatigue MRR/Pdi decreased (0.0063 +/- 0.0003 ms-1; P less than 0.005) and tau increased (83 +/- 5 ms; P less than 0.005). Both values returned to prefatigue levels within 5 min of the end of the studies. We conclude that the sniff may prove to be clinically useful in the detection of diaphragmatic fatigue.

Adult↗

PubMed1983

Endurance of hyperventilation in chronic airflow limitation.

The capacity to sustain an increase in ventilation (VE) sufficient to decrease the end-tidal partial pressure of carbon dioxide (PETCO2) by about 10 mm Hg was studied in six hypercapnic patients with moderate to severe chronic airflow limitation (CAL). Patients could continue such an increased VE for a finite time (range 5 to 54 minutes). During hyperventilation (H), ventilation was approximately doubled and represented 77.1 +/- 8.4 (mean +/- SE) percent of maximum voluntary ventilation, mean oxygen consumption (VO2) increased 44 percent (p less than 0.005) and mean inspiratory pleural pressure (Ppl) swings were 43.8 +/- 10.5 percent of maximum Ppl. Four patients achieved reductions of PETCO2 less than 10 mm Hg, and two patients achieved or exceeded the target decrease in PETCO2. The decrease in PaCO2 was correlated with the wasted ventilation ratios (VD/VT) during H, the greatest decrease in PaCO2 being related to the lowest VD/VT (p less than 0.05). Electromyographic (EMG) evidence of inspiratory muscle fatigue developed in four of the six patients during H. Five normal subjects achieved an equal or greater decrease in PETCO2, and none showed EMG evidence of inspiratory muscle fatigue. We conclude that, although impaired gas exchange limits the capacity to voluntarily reduce the PaCO2, the development of respiratory muscle fatigue in some patients with CAL may also contribute by limiting the capacity to sustain the substantial increase in respiratory muscle work done in the attempt.

Adult↗

PubMed1982

Control of breathing in chronic obstructive pulmonary disease. The effect of histamine inhalation.

In 7 normocapnic and 6 hypercapnic patients with chronic obstructive pulmonary disease (COPD), we confirmed the recently reported observation that hypercapnic and/or hypoxemic patients with COPD breathe with a shorter inspiratory time (TI) and a smaller tidal volume (VT) than normocapnic and/or normoxemic patients with COPD. Both hypercapnic and normocapnic groups were exposed to doubling concentrations of aerosolized histamine, and FEV1 was measured 30 and 90 s after each 2-min exposure. A provocative concentration (PC20) of histamine was defined as that which produced a 20% decrease in FEV1. At PC20, minute ventilation and VT decreased in both groups. The decrease in VT was significantly greater in the normocapnic patients. Inspiratory flow (VT/TI) did not change in either group. Although breathing frequency (f) and inspiratory time (TI) did not change in the hypercapnic group, f increased and TI decreased significantly in the normocapnic patients. The same results were obtained when patients were separated into hypoxemic and "normoxemic" groups. At PC20, therefore, the pattern of breathing of the hypercapnic and/or hypoxemic patients showed only small variations, whereas in the normocapnic and/or "normoxemic" patients, the breathing pattern showed greater changes, becoming similar to that of the hypercapnic and/or hypoxemic patients during control breathing. We speculated, therefore, that activation of histamine-sensitive receptors in the airways could be involved in the pathophysiology of the rapid shallow breathing present at rest in hypercapnic and/or hypoxemic patients with COPD.

Aged↗