RESUMEN
The effects on exercise performance of physiotherapy (PT) (8 patients) were compared with those of inspiratory muscle training (IMT) (9 patients) in severe chronic airflow limitation. Exercise performance was measured by 3 tests: the distance walked in 12 min, peak oxygen uptake on a progressive multistage exercise test, and endurance time at two thirds of maximal power output. Measurements were repeated after a 1-month control period during which no change was observed apart from an increase in the distance walked in 12 min in the PT group. The PT patients then performed graded exercise in a physiotherapy program 3 times weekly, whereas the IMT patients trained for 30 min daily, inspiring against a resistance. Measurements were repeated after 1 and 2 months of training. Physiotherapy was associated with insignificant increases in exercise performance, whereas IMT produced both an increase in endurance time and in the distance walked in 12 min. We concluded that a simple at-home training program of inspiratory muscles was more effective than this particular physiotherapy program in improving exercise performance of some patients with severe chronic airflow limitation.
Asunto(s)
Terapia por Ejercicio/métodos , Enfermedades Pulmonares Obstructivas/terapia , Músculos , Aptitud Física , Respiración , Terapia Respiratoria/métodos , Anciano , Humanos , Enfermedades Pulmonares Obstructivas/diagnóstico , Persona de Mediana Edad , Esfuerzo FísicoRESUMEN
Using a simple, inexpensive, at-home program, 12 patients with moderate-to-severe chronic air flow limitation trained their inspiratory muscles. All showed increased inspiratory muscle endurance with no change in inspiratory muscle strength. Seven of the twelve patients increased their endurance time for submaximal exercise beyond the 90% confidence limits determined by 2 pretraining tests (i.e., a more than 40% increase in endurance time). The same group of 7 patients increased the maximal power output (p less than 0.005) and peak oxygen uptake (p less than 0.05) on a progressive exercise test after 2 months of training and increased the distance walked in 12 min after both 1 (p less than 0.005) and 2 (p less than 0.005) months of training. In 6 of the 7 patients in this group, the pretraining submaximal exercise tests were accompanied by electromyographic changes heralding inspiratory muscle fatigue. Their increased endurance time post-training was associated with a delay or absence of these changes. In the other group of 5 patients, who showed no change in exercise performance with training, electromyographic changes heralding inspiratory muscle fatigue were never observed in submaximal exercise tests. We concluded that although the endurance of the inspiratory muscles of patients with chronic airflow limitation is increased, specific training of the inspiratory muscles is usually associated with improved exercise performance only in those who demonstrate electromyographic changes heralding inspiratory muscle fatigue during exercise.
Asunto(s)
Terapia por Ejercicio/métodos , Enfermedades Pulmonares Obstructivas/terapia , Músculos , Respiración , Terapia Respiratoria/métodos , Anciano , Electromiografía , Femenino , Volumen Espiratorio Forzado , Capacidad Residual Funcional , Humanos , Enfermedades Pulmonares Obstructivas/diagnóstico , Masculino , Persona de Mediana Edad , Esfuerzo Físico , Capacidad VitalRESUMEN
During CO2 rebreathing we measured ventilation and the pressure generated during the first 0.1 sec of inspiratory effort against a closed airway (P 0.1) in 12 asthmatics during acute exacerbation, 10 normal subjects, and 10 patients with chronic obstructive pulmonary disease. In normal subjects, the ventilatory responst to CO2 correlated with the P 0.1 response measured as delta In P 0.1. Patients with chronic obstructive pulmonary disease showed depressed responses to CO2 in terms of both ventilation and deltaIn P0.1. However, P 0.1 values in the patients with chronic obstructive pulmonary disease were greater than those of the normal subjects when they were compared at an alveolar PCO2 of 60 mm Hg. Asthmatics' responses to CO2 were similar to those of patients with chronic obstructive pulmonary disease. When measured at an alveolar PCO2 of 60 mm Hg, asthmatics' P 0.1 values were greater than those of both normal subjects and patients with chronic obstructive pulmonary disease. As the asthmatics' airway obstruction decreased so did their P 0.1. The asthmatics, and to a lesser extent the patients with chronic obstructive pulmonary disease, demonstrated increased inspiratory muscle activity that could not be explained on the basis of chemical drive or alterations in functional residual capacity. In the case of the asthmatics it was possible that the increased inspiratory muscle activity was a response to airway obstruction.
Asunto(s)
Obstrucción de las Vías Aéreas/fisiopatología , Asma/fisiopatología , Enfermedades Pulmonares Obstructivas/fisiopatología , Presión , Adulto , Anciano , Análisis de los Gases de la Sangre , Dióxido de Carbono/administración & dosificación , Enfermedad Crónica , Femenino , Volumen Espiratorio Forzado , Humanos , Capacidad Inspiratoria , Pulmón/fisiopatología , Masculino , Persona de Mediana Edad , Músculos/fisiopatología , Relación Ventilacion-PerfusiónAsunto(s)
Pulmón/fisiopatología , Diálisis Renal , Uremia/fisiopatología , Adulto , Resistencia de las Vías Respiratorias , Peso Corporal , Dióxido de Carbono/sangre , Enfermedad Crónica , Humanos , Fallo Renal Crónico/fisiopatología , Oxígeno/sangre , Perfusión , Capacidad de Difusión Pulmonar , Ventilación Pulmonar , Radioisótopos , Fumar , Espirometría , Factores de Tiempo , Capacidad Vital , Agua , XenónRESUMEN
Because maximum expiratory flow-volume rates in normal subjects are dependent on gas density, the resistance between alveoli and the point at which dynamic compression begins (R(us)) is mostly due to convective acceleration and turbulence. We measured maximum expiratory flow-volume (MEFV) curves in asthmatics and chronic bronchitics breathing air and He-O(2). In the latter and in some asthmatics, MEFV curves did not change, indicating that R(us) is mostly due to laminar flow. Therefore, the point at which dynamic compression begins must be further upstream than in normal subjects and the site of obstruction must be in small airways. In other asthmatics, flow increased normally indicating obstruction in larger airways. The response to He-O(2) did not correlate with initial values of pulmonary resistance, the initial MEFV curves or the response to bronchodilators. We conclude that the site of airway obstruction varies among asthmatics and that the site of obstruction is not detectable by measurement of the usual parameters of lung mechanics.