PubMed Health⌕ Search

Biomedical subjects

E Summers

Publications and source records attributed to E Summers.

At least 19 recordsLinked to original sources

MAP kinase and cAMP filamentation signaling pathways converge on the unusually large promoter of the yeast FLO11 gene.

In Saccharomyces cerevisiae, two major signal transduction pathways, the Kss1 MAPK pathway and the cAMP-regulated pathway, are critical for the differentiation of round yeast form cells to multicellular, invasive pseudohyphae. Here we report that these parallel pathways converge on the promoter of a gene, FLO11, which encodes a cell surface protein required for pseudohyphal formation. The FLO11 promoter is unusually large, containing at least four upstream activation sequences (UASs) and nine repression elements which together span at least 2.8 kb. Several lines of evidence indicate that the MAPK and cAMP signals are received by distinct transcription factors and promoter elements. First, regulation via the MAPK pathway requires the transcription factors Ste12p/Tec1p, whereas cAMP-mediated activation requires a distinct factor, Flo8p. Secondly, mutations in either pathway block FLO11 transcription. Overexpression of STE12 can suppress the loss of FLO8, and overexpression of FLO8 can suppress the loss of STE12. Finally, multiple distinct promoter regions of the FLO11 promoter are required for its activation by either Flo8p or Ste12p/ Tec1p. Thus, like the promoters of the key developmental genes, HO and IME1, the FLO11 promoter is large and complex, endowing it with the ability to integrate multiple inputs.

Calcium-Calmodulin-Dependent Protein Kinases↗

Ras signaling is required for serum-induced hyphal differentiation in Candida albicans.

Serum induces Candida albicans to make a rapid morphological change from the yeast cell form to hyphae. Contrary to the previous reports, we found that serum albumin does not play a critical role in this morphological change. Instead, a filtrate (molecular mass, <1 kDa) devoid of serum albumin induces hyphae. To study genes controlling this response, we have isolated the RAS1 gene from C. albicans by complementation. The Candida Ras1 protein, like Ras1 and Ras2 of Saccharomyces cerevisiae, has a long C-terminal extension. Although RAS1 appears to be the only RAS gene present in the C. albicans genome, strains homozygous for a deletion of RAS1 (ras1-2/ras1-3) are viable. The Candida ras1-2/ras1-3 mutant fails to form germ tubes and hyphae in response to serum or to a serum filtrate but does form pseudohyphae. Moreover, strains expressing the dominant active RAS1(V13) allele manifest enhanced hyphal growth, whereas those expressing a dominant negative RAS1(A16) allele show reduced hyphal growth. These data show that low-molecular-weight molecules in serum induce hyphal differentiation in C. albicans through a Ras-mediated signal transduction pathway.

Amino Acid Sequence↗

Protection against methacholine bronchoconstriction to assess relative potency of inhaled beta2-agonist.

The purposes of this study were to estimate the relative dose potency (RP) of two formulations of salbutamol pressurized metered-dose inhalers (Proventil-HFA and Ventolin-CFC MDIs) to protect against methacholine bronchoconstriction, to validate this method and provide recommendations. The protective effects of 100-, 200-, and 400-micrograms doses of Proventil-HFA were compared with the same doses of Ventolin-CFC in 18 adult asthmatics (mean FEV1, 92% predicted; mean baseline PC20 methacholine, 1.8 mg/ml), in a dose-level blind, balanced, eight-period, crossover, placebo-controlled study. The log-transformed PC20 values after each dose of the drugs were compared by repeated-measures analysis of variance (ANOVA). A significant dose-effect was present (p < 0.0001). Using the Finney assay, the RP of Proventil-HFA compared with Ventolin-CFC was 1.08 (90% CI, 0.81-1.46) (80% power). This was also estimated using a nonlinear Emax model to validate the Finney method. The most precise estimate of RP was obtained with the comparison between 100- and 200-micrograms doses (RP, 1.00; 90% CI, 0.77-1.31). There were no adverse events resulting from the drugs or methacholine. We conclude that Proventil-HFA salbutamol is bioequivalent to Ventolin-CFC salbutamol. Bronchoprotection to methacholine is a valid method of demonstrating bioequivalence. By this method, 100- and 200-micrograms doses of salbutamol inhalations from an MDI will suffice.

Administration, Inhalation↗

Prolonged protection against exercise-induced bronchoconstriction by the leukotriene D4-receptor antagonist cinalukast.

OBJECTIVES: The degree and duration of protection against exercise-induced bronchoconstriction afforded by three doses of a specific leukotriene D4 receptor antagonist, cinalukast, were assessed after an initial dosing and after 1 week of therapy. METHODS: A placebo-controlled crossover study was performed in eight male patients who had mild, stable asthma and exercise-induced bronchoconstriction. Treatment consisted of four 7-day periods of placebo and three dose levels of the drug (10, 50, and 200 mg administered orally). Exercise challenge was performed at 2 hours and 8 hours after treatment on the first and seventh treatment days. The response was measured as the area under the FEV1-time effect curve (AUEC). RESULTS: On the first day of treatment, the mean (+/- SEM) AUEC at 2 hours was 24.2 +/- 3.3 L.min after placebo and was 5.5 +/- 2.2 L.min, 6.3 +/- 2.7 L.min, 3.3 +/- 3.8 L.min after 10 mg, 50 mg, and 200 mg, respectively (p < 0.05 for all values compared with placebo). The AUEC at 8 hours on the first day was 25.1 +/- 4.4 L.min after placebo and was 6.8 +/- 4.1 L.min, 11.2 +/- 2.5 L.min, and 5.0 +/- 2.8 L.min after 10 mg, 50 mg, and 200 mg, respectively (p < 0.05 for all values compared with placebo). The protection afforded by 10 mg of cinaluicast was lost after 7 days of treatment but persisted with 50 mg and 200 mg doses. CONCLUSION: Orally administered cinalukast provides at least 8 hours of protection against exercise-induced bronchoconstriction. This protection is lost with regular treatment for 1 week for the lowest dose studied.

Administration, Oral↗

Quantification of intensity of sensations during muscular work by normal subjects.

Eleven subjects performed a series of 30-s work bouts on a cycle ergometer at power outputs ranging from 20-120% of the work capacity (Wcap) achieved during an incremental cycle to exhaustion and estimated the intensity of several sensations (leg effort, muscle tension, muscle discomfort, muscle pain, and breathing discomfort) by using Borg's category-ratio scale (range 0-10 units). Leg effort was perceived as "just noticeable" at 31 +/- 15% Wcap, muscle tension was just noticeable at 31 +/- 16% Wcap, muscle discomfort was just noticeable at 47 +/- 21% Wcap, breathing discomfort was just noticeable at 52 +/- 19% Wcap, and muscle pain was just noticeable at 58 +/- 33% Wcap. The intensity of all sensations increased in a positively accelerating manner with increases in power output (P < 0.001). Above 60% Wcap, the intensity of leg effort and muscle tension exceeded the intensity of muscle pain (P < 0.01), and above 100% Wcap the intensity of muscle discomfort also exceeded the intensity of muscle pain (P < 0.01). At 120% Wcap, leg effort, muscle tension, and muscle discomfort were rated between "severe" and "very severe" (6.1 +/- 2.2, 6.4 +/- 2.0, and 5.6 +/- 2.1 Borg units, respectively), whereas muscle pain and breathing discomfort were rated between "moderate" and "somewhat severe" (3.6 +/- 2.1 and 3.3 +/- 1.9 Borg units, respectively). These results suggest that subjects have a perception of muscle pain during muscular work that is distinct from perceptions of leg effort, muscle tension, and muscle discomfort.

Adult↗

Symptom intensity and subjective limitation to exercise in patients with cardiorespiratory disorders.

The aim of the study was to compare (1) the intensity of leg effort and dyspnea during exercise and (2) subjective limitations to performance in normal subjects, patients receiving medication for cardiac disorders, patients with pulmonary impairment, patients with pulmonary impairment who were also receiving cardiac medications, patients experiencing chest pain during exercise, and patients who had a reduced exercise capacity but did not have pulmonary impairment and were not receiving cardiac medication. Five hundred seventy-eight subjects rated the intensity of leg effort, discomfort with breathing (dyspnea), and chest pain every minute (Borg scale) during an incremental exercise task (100 kpm/min each minute) to maximum work capacity on a cycle ergometer and following exercise indicated their subjective limitation by completing a simple questionnaire. Leg effort and dyspnea increased systematically with power output in a positively accelerating manner in all groups; both symptoms were significantly more intense in the impaired groups compared with the normal group at submaximal power outputs. In all groups, there was a significant relationship between symptom intensity at submaximal power outputs and the maximal power output achieved. Leg discomfort in combination with breathing discomfort was the predominant subjective limitation in all groups; chest pain in combination with leg and breathing discomfort was the major subjective limitation in individuals with angina. Activation of the sensory systems during exercise is accompanied by a perception of discomfort associated with the peripheral exercising muscles and discomfort with breathing; both discomfort associated with the exercising muscles and discomfort associated with breathing contribute to exercise limitation to a large degree in normal subjects and patients with cardiorespiratory diseases.

Angina Pectoris↗

Muscle strength, symptom intensity, and exercise capacity in patients with cardiorespiratory disorders.

The contribution of muscle strength to symptom intensity and work capacity was examined in normal individuals and patients with cardiorespiratory disorders. Respiratory muscle strengths (maximal inspiratory and expiratory pressures) and peripheral muscle strengths (leg extension, leg flexion, seated bench press, and seated row) were measured in 4,617 subjects referred for clinical exercise testing. Subjects then rated the intensity of leg effort, discomfort with breathing (dyspnea), and chest pain (Borg scale) during an incremental exercise task (100 kpm/min each minute) to capacity on a cycle ergometer. Subjects were classified into groups on the basis of pulmonary function, drug therapy for cardiac disorders, and the presence of chest pain during exercise with electrocardiographic changes indicative of myocardial ischemia. Respiratory and peripheral muscle strengths, normalized for differences in age, sex, and height, were significantly reduced in patients with cardiorespiratory disorders compared with normal individuals. Muscle strength was a significant contributor to symptom intensity and work capacity in both health and disease; a two-fold increase in muscle strength was associated with a 25 to 30% decrease in the intensity of both leg effort and dyspnea and a 1.4- to 1.6-fold increase in work capacity. These results emphasize the need for an integrative approach in the assessment and therapeutic management of exercise intolerance, which considers the contribution of muscle weakness to excessive symptoms and reduced work capacity, in addition to the contribution of ventilatory, gas exchange, and circulatory impairments.

Angina Pectoris↗

Molecular cloning of the yeast OPI3 gene as a high copy number suppressor of the cho2 mutation.

By functional complementation of the auxotrophic requirements for choline of a cdg1, cho2 double-mutant, by transformation with a genomic DNA library in a high copy number plasmid, two different types of complementing DNA inserts were identified. One type of insert was earlier shown to represent the CHO2 structural gene. In this report we describe the molecular and biochemical chemical characterization of the second type of complementing activity. The transcript encoded by the cloned gene was about 1000-nt in length and was regulated in response to the soluble phospholipid precursors, inositol and choline. A gene disruption resulted in no obvious growth phenotype at 23 degrees C or 30 degrees C, but in a lack of growth at 37 degrees C in the presence of monomethylethanolamine. Null-mutants exhibited an inositol-secretion phenotype, indicative of mutations in the lipid biosynthetic pathway. Complementation analysis, biochemical analysis of the phospholipid methylation pathway in vivo, and comparison of the restriction pattern of the cloned gene to published sequences, unequivocally identified the cloned gene as the OPI3 gene, encoding phospholipid-N-methyltransferase in yeast. When present in multiple copies the OPI3 gene efficiently suppresses the phospholipid methylation defect of a cho2 mutation. As a result of impaired synthesis of phosphatidylcholine, the INO1-deregulation phenotype is abolished in cho2 mutants transformed with the OPI3 gene on a high copy number plasmid.(ABSTRACT TRUNCATED AT 250 WORDS)

Cloning, Molecular↗

Factors contributing to dyspnoea during bronchoconstriction and exercise in asthmatic subjects.

The purpose of the present study was to identify: 1) whether dyspnoea during bronchoconstriction and exercise is related, in asthmatic subjects; and 2) to what extent baseline pulmonary function and respiratory muscle strength contribute to dyspnoea under both conditions. One hundred and seventy five consecutive subjects, referred with suspected asthma, rated the intensity of dyspnoea (Borg scale 0-10): 1) during the administration of doubling concentrations of methacholine to 32 mg.ml-1 methacholine, or until the baseline forced expiratory volume in one second (FEV1) was reduced by 20%; and 2) during incremental cycle ergometry (100 kpm.min-1 each minute) to maximal capacity. 138/175 subjects achieved a 20% reduction in their baseline FEV1; 18 of the 138 were excluded, 2 children and 16 with complicating pulmonary disorders (diffusing capacity of the lung for carbon monoxide (DLCO) and/or total lung capacity (TLC) < 70% predicted). The remaining 120 out of 175 constituted the study population. Dyspnoea following a 20% reduction in the baseline FEV1 (Dys20%) was linearly interpolated, using the rating of dyspnoea and the FEV1 at the two final concentrations of methacholine. In the 120 asthmatic subjects, the mean intensity of dyspnoea was "moderate" (2.9, SD 1.91; Borg 0-10) and the intensity across subjects was not significantly related to baseline FEV1, vital capacity (VC), FEV1/VC, DLCO, TLC and maximal static inspiratory pressure (MIP), alone or in combination.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Dyspnea and leg effort during incremental cycle ergometry.

The aim of this study was to establish the perceived magnitude of dyspnea (discomfort associated with breathing) and leg effort experienced by normal subjects during a standardized incremental exercise test to maximal capacity; 460 normal subjects (297 male and 163 female 20 to 70 yr of age) were studied. The perceptual magnitude of both symptoms was rated using simple descriptive phrases (slight, moderate, maximal) tagged to numbers from zero to 10 on the Borg scale, which is an interval scale with ratio properties. Leg effort and dyspnea increased with power output, were higher in women than in men (p less than 0.0001), increased with advancing age (p less than 0.0001), and declined as height increased (p less than 0.0001). Leg effort = 4.82 + 0.007 kpm/min + 1.05 sex + 0.04 age - 0.055 Ht (r = 0.78; SD, 1.80). Dyspnea = 4.96 + 0.006 kpm/min + 0.96 sex + 0.04 age - 0.05 Ht (r = 0.74; SD, 1.80) (m = 1; f = 2). With power output expressed as a percentage of maximal power output (%MPO) both symptoms increased in an alinear manner. Effort = 0.0014 * %MPO1.86 (r = 0.86; SD, 1.50). Dyspnea = 0.0016 * %MPO1.79 (r = 0.81; SD, 1.57). Sex, age, or stature did not contribute to the rating of effort or dyspnea when power output was normalized in this way.

Adult↗

Exercise capacity and ventilatory, circulatory, and symptom limitation in patients with chronic airflow limitation.

Dyspnea, leg effort (Borg 0 to 10 scale), ventilation, and heart rate (VEmax/VEcap; HRmax/HRcap expressed as a percentage of capacity) were measured at maximal exercise (cycle ergometer) in 97 patients with chronic airflow limitation (CAL) (FEV, 46.6 +/- 14.23% of predicted) and compared with 320 matched control subjects. Patients with CAL achieved a maximum power output of 86 +/- 39.5 W (60 +/- 23.2% of predicted) compared with 140 +/- 37.5 W (98 +/- 14.5% of predicted) in controls (p less than 0.0001), VEmax/VEcap was 72 +/- 19.3% compared with 53 +/- 18.6% (p less than 0.0001), and HRmax/HRcap was 76 +/- 13.5% compared with 82 +/- 13% (p less than 0.001). These findings were expected. The median intensity of dyspnea was 6 (severe to very severe) and leg effort was 7 (very severe) in both groups, and these findings were unexpected. The patients with CAL were handicapped by an increase in both dyspnea and peripheral muscular effort relative to the actual power output. The rating of dyspnea exceeded leg effort in 25 (26%) of CAL versus 69 (22%) control subjects: the rating of leg effort exceeded dyspnea in 42 (43%) CAL and 117 (36%) control subjects; both were rated equally in 30 (31%) CAL and 134 (42%) control subjects, respectively (NS). VEmax/VEcap and HRmax/HRcap were not significantly different in those limited by dyspnea, leg fatigue, or a combination of both. All values are expressed +/- SD.

Cardiac Output↗

A method for culturing rat oviduct gamma-aminobutyric acid cells.

A technique for the culture of rat oviduct gamma-aminobutyric acid (GABA) cells is described. The technique involves first explaining the fimbria and preampulla, which are the oviduct divisions with the highest density of GABA cells. The explanted tissue is cultured in a serum-free medium, to propagate the outgrowing cells. Under the experimental conditions we describe, the majority of the cells maintain GABA expression, as determined by immunostaining with a GABA antiserum.

Animals↗

Breathing during prolonged exercise in humans.

1. Six normal subjects cycled to endurance or for 60 min at four work rates (WR 1-4): mean of 34% working capacity (93 watts for 60 min); 43% (120 watts for 56 min); 63% (177 watts for 37 min); and 84% (233 watts for 12 min), to determine how breathing pattern and dyspnoea change during prolonged activity. Four to six minutes were allowed to establish steady state and subsequent changes were considered to be endurance related. 2. Dyspnoea (Borg scale, 0-10) increased with the duration of activity at all work rates. 3. Ventilation (VE) did not change at WR1; increased from 44 to 47 l min-1 at WR2; from 60 to 88 l min-1 at WR3; and from 111 to 132 l min-1 at WR4. Dyspnoea was significantly and independently related to ventilation and duration of activity: dyspnoea = 0.004 VE1.36 time 0.25 (r = 0.81; partial F 202 and 26 respectively). 4. Inspiratory resistance did not increase at any work rate. Dynamic elastance remained constant during WR1, WR2 and WR3 but increased from 7.4 to 9.1 cmH2O l-1 during WR4. 5. Peak inspiratory pressure did not increase, and the increase in VE was accomplished by an increased breathing frequency without change in duty cycle. 6. Duration of activity is an important contributor to dyspnoea independent of changes in respiratory muscle contractile activity.

Adult↗

Effort and dyspnoea during work of varying intensity and duration.

This study quantified the separate contributions of the intensity of exercise and its duration to muscular effort and dyspnoea during cycle ergometry. Six normal subjects estimated the perceived intensity (Borg scale 0-10) of peripheral muscular effort and dyspnoea during incremental exercise to their maximum work capacity (Wcap). On separate days, the same subjects exercised to endurance or 60 min at work rates rated for leg effort on the initial incremental test as: 2 ("slight", 33.1 +/- 1.45% Wcap) (mean +/- SE); 3 ("moderate", omission 83.6 +/- 3.87% Wcap). Perceived leg effort increased by a factor of 4.4 (2(2.13)) with a doubling of work rate and by 1.3 (2(0.39)) with a doubling of duration, as expressed by: Leg effort = k x %Wcap2.13 x Time0.39 (r2 = 0.87) Perceived dysponea increased 5.3-fold with a doubling of work rate and by 1.4-fold with a doubling of duration: Dysponea = k x %Wcap2.41 x Time0.47 (r2 = 0.75) Changes in work intensity, rather than duration, dominated symptom magnitudes such that in the performance of a given task, halving the intensity and doubling the duration of activity reduces the maximal intensity of muscular effort and dyspnoea to less than a third.

Adult↗

Influence of age and stature on exercise capacity during incremental cycle ergometry in men and women.

The present study re-evaluated the accuracy of standards for maximal exercise capacity (Wcap) recently reported from our laboratory by examining the interaction between height and age on Wcap achieved and predicted in 1,071 subjects (732 males and 339 females). They underwent an incremental exercise test on a cycle ergometer using the same incremental protocol and exercise mode as the previous study, and were retrospectively judged to be normal. Although Wcap predicted was either not significantly different (males) or underestimated Wcap by less than 5% (females, p less than 0.05), significant differences were found in subjects at the extremes of the population ranges for height and age. The influences of age 9yr) and height (m) were found to be nonlinear and interactive, as described by the equations: Males: Wcap = 1506*Ht2.70*Age-0.46(r = 0.78) (lower limit 81% pred) Females: Wcap = 969*Ht2.80*Age-0.43(r = 0.77) (lower limit 79% pred) Wcap (kpm/min) predicted by these equations was compared to Wcap achieved by the 100 subjects who took part in the original study; no significant differences were found (paired t test, p less than 0.05). The interactive influences of age and height expressed by the equations are more plausible from a biological point of view than the linear, additive relationships previously described. The equations should be more reliable than previous equations for patients referred for exercise testing.

Aging↗

Inspiratory muscles during exercise: a problem of supply and demand.

The capacity of inspiratory muscles to generate esophageal pressure at several lung volumes from functional residual capacity (FRC) to total lung capacity (TLC) and several flow rates from zero to maximal flow was measured in five normal subjects. Static capacity was 126 +/- 14.6 cmH2O at FRC, remained unchanged between 30 and 55% TLC, and decreased to 40 +/- 6.8 cmH2O at TLC. Dynamic capacity declined by a further 5.0 +/- 0.35% from the static pressure at any given lung volume for every liter per second increase in inspiratory flow. The subjects underwent progressive incremental exercise to maximum power and achieved 1,800 +/- 45 kpm/min and maximum O2 uptake of 3,518 +/- 222 ml/min. During exercise peak esophageal pressure increased from 9.4 +/- 1.81 to 38.2 +/- 5.70 cmH2O and end-inspiratory esophageal pressure increased from 7.8 +/- 0.52 to 22.5 +/- 2.03 cmH2O from rest to maximum exercise. Because the estimated capacity available to meet these demands is critically dependent on end-inspiratory lung volume, the changes in lung volume during exercise were measured in three of the subjects using He dilution. End-expiratory volume was 52.3 +/- 2.42% TLC at rest and 38.5 +/- 0.79% TLC at maximum exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Breathlessness during exercise with and without resistive loading.

The purpose of this study was to quantify the intensity of breathlessness associated with exercise and respiratory resistive loading, with the specific purpose of isolating the quantitative contributions of inspiratory pressure, length, velocity, and frequency of inspiratory muscle shortening and duty cycle to breathlessness. The intensity of inspiratory pressure was quantified by measurement of estimated esophageal pressure (Pes = pressure at the mouth plus lung pressure), the extent of shortening by tidal volume (VT), and the velocity of shortening by inspiratory flow rate (VI). Six normal subjects underwent five incremental (100 kpm X min-1 X min-1) exercise tests on a cycle ergometer to maximum capacity. The first and last test were unloaded and the intervening tests were performed with external added resistances of 33, 57, and 73 cm H2O X l-1 X s in random order. The resistances were selected to provide a range of pressures, tidal volumes, flow rates, and patterns of breathing. At rest and at the end of each minute during exercise the subjects estimated the intensity of breathlessness (psi) by selecting a number ranging from 0 to 10 (Borg rating scale, 0 indicating no appreciable breathlessness and 10 the maximum tolerable sensation). Breathlessness was significantly and independently related to Pes (P less than 0.0001), VI (P less than 0.0001), frequency of breathing (fb) (P less than 0.01), and duty cycle [ratio of inspiratory duration to total breath duration (TI/TT)] (P less than 0.01): psi = 0.11 Pes + 0.61 VI + 1.99 TI/TT + 0.04 fb - 2.60 (r = 0.83). The results suggest that peak pressure (tension), VI (velocity of inspiratory muscle shortening), TI/TT, and fb contribute independently and collectively to breathlessness. The perception of respiratory muscle effort is ideally suited to subserve this sensation. The neurophysiological mechanism purported is a conscious awareness of the intensity of the outgoing motor command by means of corollary discharge within the central nervous system.

Adult↗

Breathlessness and exercise in patients with cardiorespiratory disease.

Previous studies have led to the revival of the hypothesis that breathlessness is the perception of respiratory muscle effort and is present when the tension developed by muscles increases, when the muscles are weak, or when both conditions are present simultaneously. Using a category scale, the intensity of breathlessness was measured in 20 subjects (2 normal subjects and 18 patients) undergoing an incremental exercise test (50 to 100 kpm/min) to maximal capacity. The patients were selected to provide a heterogeneous group of pulmonary diseases, obesity, muscular weakness, and cardiac disease, with a wide variability in exercise capacity (250 to 1,900 kpm/min) and severity of dyspnea. Maximal inspiratory pressure (MIP), pleural pressure (Ppl), the extent of shortening of the inspiratory muscles as indicated by the tidal volume expressed as a percent of vital capacity (VT/VC), the rate of shortening as indicated by flow rate, the frequency of contraction as indicated by breathing frequency (fb), and the duty cycle (TI/Ttot) were measured throughout exercise to assess their relative contribution to the intensity of breathlessness. Using multifactorial analysis, the perception of breathlessness was significantly (p less than 0.01) related to the Ppl, inspiratory flow rate (VI), VT/VC, TI/Ttot, and fb. A multiple linear regression equation that included all these variables explained 69% of the variance, with no single factor being identified as uniquely predominant: Breathlessness = 3.0 (Ppl/MIP) + 1.2 (VI) + 4.5 (VT/VC) + 0.13 (fb) + 5.6 TI/Ttot) - 6.2 (R = 0.83). The intensity of effort required to produce a given pressure increases when the muscle is weak, when the velocity of contraction increases, or when the muscle shortens.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗