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Respiratory Muscle Strength (respiratory + muscle_strength)

Distribution by Scientific Domains
Medical Sciences80%

Selected Abstracts

Inspiratory muscle performance in endurance athletes and sedentary subjects

RESPIROLOGY, Issue 2 2001
Peter R. Eastwood
Objective: The aim of this study was to determine whether whole-body endurance training is associated with increased respiratory muscle strength and endurance. Methodology: Respiratory muscle strength (maximum inspiratory pressure (PImax)) and endurance (progressive threshold loading of the inspiratory muscles) were measured in six marathon runners and six sedentary subjects. Results: PImax was similar between the two groups of subjects but the maximum threshold pressure achieved was greater in marathon runners (90 ± 8 vs 78 ± 10% of PImax, respectively, mean ± SD, P < 0.05). During progressive threshold loading, marathon runners breathed with lower frequency, higher tidal volume, and longer inspiratory and expiratory time. At maximum threshold pressure, marathon runners had lower arterial O2 saturation, but perceived effort (Borg scale) was maximal in both groups. Efficiency of the respiratory muscles was similar in both groups being 2.0 ± 1.7% and 2.3 ± 1.8% for marathon runners and sedentary subjects, respectively. Conclusions: The apparent increase in respiratory muscle endurance of athletes was a consequence of a difference in the breathing pattern adopted during loaded breathing rather than respiratory muscle strength or efficiency. This implies that sensory rather than respiratory muscle conditioning may be an important mechanism by which whole-body endurance is increased. [source]

Respiratory muscle strength and muscle endurance are not affected by acute metabolic acidemia

CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 6 2009
Tessa A. C. Nizet
Summary Respiratory muscle fatigue in asthma and chronic obstructive lung disease (COPD) contributes to respiratory failure with hypercapnia, and subsequent respiratory acidosis. Therapeutic induction of acute metabolic acidosis further increases the respiratory drive and, therefore, may diminish ventilatory failure and hypercapnia. On the other hand, it is known that acute metabolic acidosis can also negatively affect (respiratory) muscle function and, therefore, could lead to a deterioration of respiratory failure. Moreover, we reasoned that the impact of metabolic acidosis on respiratory muscle strength and respiratory muscle endurance could be more pronounced in COPD patients as compared to asthma patients and healthy subjects, due to already impaired respiratory muscle function. In this study, the effect of metabolic acidosis was studied on peripheral muscle strength, peripheral muscle endurance, airway resistance, and on arterial carbon dioxide tension (PaCO2). Acute metabolic acidosis was induced by administration of ammonium chloride (NH4Cl). The effect of metabolic acidosis was studied on inspiratory and expiratory muscle strength and on respiratory muscle endurance. Effects were studied in a randomized, placebo-controlled cross-over design in 15 healthy subjects (4 male; age 33·2 ± 11·5 years; FEV1 108·3 ± 16·2% predicted), 14 asthma patients (5 male; age 48·1 ± 16·1 years; FEV1 101·6 ± 15·3% predicted), and 15 moderate to severe COPD patients (9 male; age 62·8 ± 6·8 years; FEV1 50·0 ± 11·8% predicted). An acute metabolic acidemia of BE ,3·1 mmol.L,1 was induced. Acute metabolic acidemia did not significantly affect strength or endurance of respiratory and peripheral muscles, respectively. In all subjects airway resistance was significantly decreased after induction of metabolic acidemia (mean difference ,0·1 kPa.sec.L,1 [95%-CI: ,0·1 ,,0·02]. In COPD patients PaCO2 was significantly lowered during metabolic acidemia (mean difference ,1·73 mmHg [,3·0 ,,0·08]. In healthy subjects and in asthma patients no such effect was found. Acute metabolic acidemia did not significantly decrease respiratory or peripheral muscle strength, respectively muscle endurance in nomal subjects, asthma, or COPD patients. Metabolic acidemia significantly decreased airway resistance in asthma and COPD patients, as well as in healthy subjects. Moreover, acute metabolic acidemia slightly improved blood gas values in COPD patients. The results suggest that stimulation of ventilation in respiratory failure, by induction of metabolic acidemia will not lead to deterioration of the respiratory failure. [source]

Inspiratory muscle performance in endurance athletes and sedentary subjects

RESPIROLOGY, Issue 2 2001
Peter R. Eastwood
Objective: The aim of this study was to determine whether whole-body endurance training is associated with increased respiratory muscle strength and endurance. Methodology: Respiratory muscle strength (maximum inspiratory pressure (PImax)) and endurance (progressive threshold loading of the inspiratory muscles) were measured in six marathon runners and six sedentary subjects. Results: PImax was similar between the two groups of subjects but the maximum threshold pressure achieved was greater in marathon runners (90 ± 8 vs 78 ± 10% of PImax, respectively, mean ± SD, P < 0.05). During progressive threshold loading, marathon runners breathed with lower frequency, higher tidal volume, and longer inspiratory and expiratory time. At maximum threshold pressure, marathon runners had lower arterial O2 saturation, but perceived effort (Borg scale) was maximal in both groups. Efficiency of the respiratory muscles was similar in both groups being 2.0 ± 1.7% and 2.3 ± 1.8% for marathon runners and sedentary subjects, respectively. Conclusions: The apparent increase in respiratory muscle endurance of athletes was a consequence of a difference in the breathing pattern adopted during loaded breathing rather than respiratory muscle strength or efficiency. This implies that sensory rather than respiratory muscle conditioning may be an important mechanism by which whole-body endurance is increased. [source]

Mechanical ventilatory constraints during incremental cycle exercise in human pregnancy: implications for respiratory sensation

THE JOURNAL OF PHYSIOLOGY, Issue 19 2008
Dennis Jensen
The aim of this study was to identify the physiological mechanisms of exertional respiratory discomfort (breathlessness) in pregnancy by comparing ventilatory (breathing pattern, airway function, operating lung volumes, oesophageal pressure (Poes)-derived indices of respiratory mechanics) and perceptual (breathlessness intensity) responses to incremental cycle exercise in 15 young, healthy women in the third trimester (TM3; between 34 and 38 weeks gestation) and again 4,5 months postpartum (PP). During pregnancy, resting inspiratory capacity (IC) increased (P < 0.01) and end-expiratory lung volume decreased (P < 0.001), with no associated change in total lung capacity (TLC) or static respiratory muscle strength. This permitted greater tidal volume (VT) expansion throughout exercise in TM3, while preserving the relationship between contractile respiratory muscle effort (tidal Poes swing expressed as a percentage of maximum inspiratory pressure (PImax)) and thoracic volume displacement (VT expressed as a percentage of vital capacity) and between breathlessness and ventilation . At the highest equivalent work rate (HEWR = 128 ± 5 W) in TM3 compared with PP: , tidal Poes/PImax and breathlessness intensity ratings increased by 10.2 l min,1 (P < 0.001), 8.8%PImax (P < 0.05) and 0.9 Borg units (P < 0.05), respectively. Pulmonary resistance was not increased at rest or during exercise at the HEWR in TM3, despite marked increases in mean tidal inspiratory and expiratory flow rates, suggesting increased bronchodilatation. Dynamic mechanical constraints on VT expansion (P < 0.05) with associated increased breathlessness intensity ratings (P < 0.05) were observed near peak exercise in TM3 compared with PP. In conclusion: (1) pregnancy-induced increases in exertional breathlessness reflected the normal awareness of increased and contractile respiratory muscle effort; (2) mechanical adaptations of the respiratory system, including recruitment of resting IC and increased bronchodilatation, accommodated the increased VT while preserving effort,displacement and breathlessness, relationships; and (3) dynamic mechanical ventilatory constraints contributed to respiratory discomfort near the limits of tolerance in late gestation. [source]

Respiratory muscle strength and muscle endurance are not affected by acute metabolic acidemia

CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 6 2009
Tessa A. C. Nizet
Summary Respiratory muscle fatigue in asthma and chronic obstructive lung disease (COPD) contributes to respiratory failure with hypercapnia, and subsequent respiratory acidosis. Therapeutic induction of acute metabolic acidosis further increases the respiratory drive and, therefore, may diminish ventilatory failure and hypercapnia. On the other hand, it is known that acute metabolic acidosis can also negatively affect (respiratory) muscle function and, therefore, could lead to a deterioration of respiratory failure. Moreover, we reasoned that the impact of metabolic acidosis on respiratory muscle strength and respiratory muscle endurance could be more pronounced in COPD patients as compared to asthma patients and healthy subjects, due to already impaired respiratory muscle function. In this study, the effect of metabolic acidosis was studied on peripheral muscle strength, peripheral muscle endurance, airway resistance, and on arterial carbon dioxide tension (PaCO2). Acute metabolic acidosis was induced by administration of ammonium chloride (NH4Cl). The effect of metabolic acidosis was studied on inspiratory and expiratory muscle strength and on respiratory muscle endurance. Effects were studied in a randomized, placebo-controlled cross-over design in 15 healthy subjects (4 male; age 33·2 ± 11·5 years; FEV1 108·3 ± 16·2% predicted), 14 asthma patients (5 male; age 48·1 ± 16·1 years; FEV1 101·6 ± 15·3% predicted), and 15 moderate to severe COPD patients (9 male; age 62·8 ± 6·8 years; FEV1 50·0 ± 11·8% predicted). An acute metabolic acidemia of BE ,3·1 mmol.L,1 was induced. Acute metabolic acidemia did not significantly affect strength or endurance of respiratory and peripheral muscles, respectively. In all subjects airway resistance was significantly decreased after induction of metabolic acidemia (mean difference ,0·1 kPa.sec.L,1 [95%-CI: ,0·1 ,,0·02]. In COPD patients PaCO2 was significantly lowered during metabolic acidemia (mean difference ,1·73 mmHg [,3·0 ,,0·08]. In healthy subjects and in asthma patients no such effect was found. Acute metabolic acidemia did not significantly decrease respiratory or peripheral muscle strength, respectively muscle endurance in nomal subjects, asthma, or COPD patients. Metabolic acidemia significantly decreased airway resistance in asthma and COPD patients, as well as in healthy subjects. Moreover, acute metabolic acidemia slightly improved blood gas values in COPD patients. The results suggest that stimulation of ventilation in respiratory failure, by induction of metabolic acidemia will not lead to deterioration of the respiratory failure. [source]