Differential Activation of Inspiratory Muscles Acting on The Upper Rib Cage in Humans

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Differential activation of the respiratory muscles is probably essential for precise and fine coordination of the respiratory muscle activity during ventilation. Indeed, the abdominal muscles, which squeeze the abdominal component to generate expiratory airflow, have been reported to show differential activation. In contrast, inspiratory muscles acting on the upper rib cage have not been reported to show differential activation. We hypothesized that the scalene (SCLN) muscles and parasternal intercostal (PARA) muscles, which are the most important inspiratory muscles acting on the rib cage, may be activated differentially during inspiration. We conducted an electromyographic (EMG) investigation of the SCLN and PARA muscles, to determine the timing and magnitude of their activation during resting breathing and CO_2 rebreathing in the supine posture in seven awake subjects. The EMGs were recorded using fine wire electrodes having a diameter of 80 μm, fashioned from polyurethane-coated fine platinum wire. The electrodes were inserted into the right SCLN and PARA muscles under high-resolution ultrasound guidance. The raw and moving averaged EMG of the SCLN and PARA muscles, the respiratory airflow and the end-tidal CO_2 (ETCO_2) were recorded. The raw EMG was used to define the onset and end of muscle activity on a breath-by-breath basis. The respiratory air flow signal was used to determine the timing of respiration, and was digitally integrated to obtain minute ventilation. The maximum EMG (EMG_<max>) was obtained for each muscle during a sustained total lung capacity (TLC) maneuver. ETCO_2 increased from a mean of 44.6 (SD 2.3) to a mean of 57.0 (1.6) mmHg during CO_2 rebreathing. Phasic inspiratory EMG activity and post-inspiratory inspiratory activity (PIIA) were observed in the SCLN and PARA muscles of all subjects during resting breathing. The SCLN EMG amplitude increased significantly from 2.6 (2.0) to 7.1 (3.4) % EMGmax (p<0.005), and the PARA EMG amplitude also increased significantly from 10.8 (6.1) to 23.2 (6.9) % EMG_<max> (p<0.001) during CO_2 rebreathing. SCLN EMG activity appeared 0.25 (0.52) and 0.24 (0.35) s after the onset of inspiratory flow, and PARA EMG activity appeared 0.25 (0.17) and 0.26 (0.1 6) s before the onset of inspiratory flow, during resting and CO_2-stimulated breathing, respectively. The timing of onset of EMG activity did not change with increasing ventilation for either the SCLN or the PARA muscles. The magnitude of SCLN PIIA increased significantly from 2.2 (1.8) to 6.1 (3.2) % EMG_<max> (p<0.01), and that of PARA PIIA also increased significantly from 8.2 (5.4) to 16.4 (6.6) % EMG_<max> (p<0.001) during CO_2-stimulated breathing. The ratio of the magnitude of the PIIA to the tidal EMG (PIIA/ EMG_<tic.ai>) for the SCLN muscles was significantly higher than that for the PARA muscles during both resting and CO_2-stimulated breathing (p<0.05). The PIIA/ EMGtidal ratio did not change with increasing ventilation for either the SCLN or the PARA muscles. There was no significant difference in the duration of the PIIA between the SCLN and PARA muscles. These results show that: 1) the parasternal intercostal muscles, but not the scalene muscles, contribute to the initiation of inspiration, 2) the scalene muscles are more active per unit tidal EMG activity than the parasternal intercostal muscles during the post-inspiratory phase, 3) the pattern of activity of neither the scalene nor the parasternal intercostal muscles is influenced by the increase of ventilation induced by CO_2 rebreathing. We conclude that the scalene and parasternal intercostal muscles contribute differentially to ventilatory movements during resting and CO_2-stimulated breathing in humans.
2002-08-31

Differential Activation of Inspiratory Muscles Acting on The Upper Rib Cage in Humans

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