A study in functional coordination of intercostal and abdominal muscles during forced expiration
Project/Area Number |
62570352
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Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
Respiratory organ internal medicine
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Research Institution | Tokai University |
Principal Investigator |
KONDO Tetsuri School of Medicine, Tokai University (Assistant Professor), 医学部, 講師 (90147132)
|
Co-Investigator(Kenkyū-buntansha) |
MIYAIRI Akira School of Medicine, Tokai Univ. (Assistant) (30200116)
YAMABAYASHI Hajime School of Medicine, Tokai Univ. (Professor) (60055697)
OHTA Yasuyo School of Medicine, Tokai Univ. (Professor) (90055939)
|
Project Period (FY) |
1987 – 1988
|
Project Status |
Completed (Fiscal Year 1988)
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Budget Amount *help |
¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1988: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1987: ¥1,300,000 (Direct Cost: ¥1,300,000)
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Keywords | Forced expiration / Expiratory muscle / Control of respiration / Fatigue / 筋電図 / 気道閉塞 / 努力呼気 / 呼吸筋 |
Research Abstract |
Activity of the respiratory muscle during forced expiration was studied with a newly designed EMG amplifier. This amplifier was improved in safety, response frequency, gain, input impedance and noises. The preliminary animal experiments demonstrated that hypercapnia produced recruitment of the large motor units for abdominal motoneurons. The rate coding was a predominant mechanism for phrenic motoneuron pool. In the main experiment, respiratory flow, EMG of intercostal muscle (IC), external oblique (EO) and internal oblique (IO) abdominal muscle were analyzed in 11 healthy volunteers. The pattern of EMG activity during forced expiration could be classified according to the shape, i.e., taper- or hill-shaped. The taper-shaped was found in 7 of 9 subjects for IC, 2 of 6 for EO, and 8 of 11 for IO. Twenty consecutive trials without intermission did not alter the flow-volume curve, activity of respiratory muscle or frequency component (i.e. H/L ratio). When expiratory circuit was obstructed for a short interval during forced expiration, activity of respiratory muscle reduced for a short period. The latencies from the onset of airway obstruction to the reduction in EMG activity were 61.5-100 msec in IC, 61.5-106.5 msec in EO, and 58.0-92.3 msec in IO. These values were not much different in any given subject. During such transient airway obstruction the rise in pleural pressure was slight but mouth pressure was large. Airway anesthesia with xylocaine did not altered the latency. In conclusion, pattern of respiratory muscle activity for forced expiration is predetermined and is specific for each muscles. Repetitive trials to 20 times did not cause respiratory muscle fatigue. Negative feedback from receptors in airway or in respiratory muscle was highly suggested.
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Report
(3 results)
Research Products
(8 results)