Respiratory abdominal muscle recruitment and chest wall motion in myotonic muscular dystrophy
1 Department of Physical Medicine and Rehabilitation, 2 Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, and 3 Center for Nursing Research, University of California Davis Medical Center, Sacramento, California 95817 Abdominal muscles are selectively active in nor...
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Veröffentlicht in: | Journal of applied physiology (1985) 2001-07, Vol.91 (1), p.395-407 |
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Sprache: | eng |
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Zusammenfassung: | 1 Department of Physical Medicine and Rehabilitation,
2 Division of Pulmonary and Critical Care Medicine,
Department of Internal Medicine, and 3 Center for Nursing
Research, University of California Davis Medical Center, Sacramento,
California 95817
Abdominal muscles are selectively
active in normal subjects during stress and may increase the potential
energy for inspiration by reducing the end-expiratory lung volume
(EELV). We hypothesized that a similar process would occur in
subjects with myotonic muscular dystrophy (MMD), but would be less
effective, because of to their weakness and altered chest wall
mechanics. Fine-wire electromyography (EMG) of the transversus
abdominis (TA), internal oblique (IO), external oblique, and rectus
abdominis was recorded in 10 MMD and 10 control subjects. EMG activity,
respiratory inductive plethysmography, and gastric pressure were
recorded during static pressure measurement and at increasing levels of
inspiratory resistance breathing. EELV was reduced and chest wall
motion was synchronous only in controls. Although the TA and IO were
selectively recruited in both groups, EMG activity of the MMD group was
twice that of controls at the same inspiratory pressure. In MMD
subjects with mildly reduced forced vital capacity, significant
differences can be seen in abdominal muscle recruitment, wall motion,
work of breathing, and ventilatory parameters.
dynamic electromyogram; transversus abdominis; inspiratory
resistance breathing; end-expiratory lung volume |
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ISSN: | 8750-7587 1522-1601 |
DOI: | 10.1152/jappl.2001.91.1.395 |