Inspiratory muscle training in chronic airflow limitation: Effect on exercise performance
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Date
1997
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Abstract
The effect of inspiratory muscle training (IMT) on exercise capacity in patients with chronic airflow limitation (CAL) has been debated. The present study was planned to further investigate the effects of IMT on exercise performance.
Twenty patients (aged 62+/-1 yrs; forced expiratory volume in one second/forced vital capacity (FEV1/FVC) 36+/-2%) were trained 30 min daily for 6 days a week during 10 weeks, with either 30% (Group 1) or 10% (Group 2) of peak maximal inspiratory pressure (PI,max) as a training load. Exercise performance was evaluated by the distance walked in 6 min (6MWD) and by changes in oxygen consumption (V'O-2 and minute ventilation (V'E) during a progressive exercise test. Changes in PI,max and dyspnoea were also measured.
Results showed a significant increment in peak PI,max in both groups, whereas dyspnoea and 6MWD improved only in Group 1 (p<0.05 and p<0.01, respectively). No increment in maximal workload or in peak V'O-2 was observed in either group. Patients in Group 1, however, showed a reduction in V'E and V'O-2, for the same exercise. A correlation between changes in V'E and V'O-2 during a workload of 75 kpm . min(-1) was observed in Group 1 (r=0.92; p<0.001).
We conclude that inspiratory muscle training using a load of 30% peak maximal inspiratory pressure, improves dyspnoea, increases walking capacity and reduces the metabolic cost of exercise.
Twenty patients (aged 62+/-1 yrs; forced expiratory volume in one second/forced vital capacity (FEV1/FVC) 36+/-2%) were trained 30 min daily for 6 days a week during 10 weeks, with either 30% (Group 1) or 10% (Group 2) of peak maximal inspiratory pressure (PI,max) as a training load. Exercise performance was evaluated by the distance walked in 6 min (6MWD) and by changes in oxygen consumption (V'O-2 and minute ventilation (V'E) during a progressive exercise test. Changes in PI,max and dyspnoea were also measured.
Results showed a significant increment in peak PI,max in both groups, whereas dyspnoea and 6MWD improved only in Group 1 (p<0.05 and p<0.01, respectively). No increment in maximal workload or in peak V'O-2 was observed in either group. Patients in Group 1, however, showed a reduction in V'E and V'O-2, for the same exercise. A correlation between changes in V'E and V'O-2 during a workload of 75 kpm . min(-1) was observed in Group 1 (r=0.92; p<0.001).
We conclude that inspiratory muscle training using a load of 30% peak maximal inspiratory pressure, improves dyspnoea, increases walking capacity and reduces the metabolic cost of exercise.
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Keywords
chronic airflow limitation, chronic obstructive pulmonary disease, dyspnoea, exercise capacity, muscle training