Am. J. Respir. Crit. Care Med., Vol 154, No. 1, Jul 1996, 63-67.
Diaphragmatic fatigue following voluntary hyperpnea
JM Mador, A Rodis and J Diaz
Division of Pulmonary and Critical Care Medicine, State University of New York at Buffalo, USA.
The purpose of this study was to determine whether diaphragmatic fatigue
occurs after voluntary hyperpnea to task failure. Ten male subjects were
asked to breathe at minute ventilation (V1) equal or slightly greater than
60% of their 12-s maximum voluntary ventilation (MVV) until task failure.
Transdiaphragmatic pressure (Pdi) was measured during bilateral
supramaximal stimulation of the phrenic nerves before and 10, 30, 60, and
120 min after hyperpnea. For the group, V1 averaged 107.1 +/- 7.1 L/min
(SE) (range, 71-154 L/min), which represented 60 +/- 2% of the MVV. After
voluntary hyperpnea, seven of the 10 subjects displayed at least a 10%
reduction in twitch Pdi during transcutaneous stimulation, while all 10
subjects had a greater than 10% reduction in twitch Pdi during cervical
magnetic stimulation. For the group, transcutaneous twitch Pdi was
significantly decreased from 27.0 +/- 1.9 at baseline to 21.4 +/- 1.7 cm
H2O (p < 0.0001) at 10 min posthyperpnea. Magnetic twitch Pdi was also
significantly decreased from 36.0 +/- 2.1 at baseline to 28.7 +/- 1.9 cm
H2O (p < 0.0001) at 10 min posthyperpnea. Twitch Pdi remained
significantly decreased from baseline for at least 1 h after hyperpnea.
After hyperpnea, the mean percentage decrease from baseline in twitch Pdi
was virtually identical with the two stimulation techniques. The percentage
fall in twitch Pdi after hyperpnea with the two techniques was not
significantly correlated (r = 0.4). In conclusion, long-lasting contractile
fatigue of the diaphragm reliably occurs after voluntary hyperpnea at
levels sufficient to induce task failure. Cervical magnetic stimulation can
detect diaphragmatic fatigue after a fatiguing task, but the results
obtained with this technique may differ from those obtained with
transcutaneous stimulation in individual subjects.
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Copyright © 1996 American Thoracic Society
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