Effects of chronic electrical stimulation on paralyzed expiratory muscles

Abstract

Following spinal cord injury, the expiratory muscles develop significant disuse atrophy characterized by reductions in their weight, fiber cross-sectional area, and force-generating capacity. We determined the extent to which these physiological alterations can be prevented with electrical stimulation. Because a critical function of the expiratory muscles is cough generation, an important goal was the maintenance of maximal force production. In a cat model of spinal cord injury, short periods of high-frequency lower thoracic electrical spinal cord stimulation (SCS) at the T(10) level (50 Hz, 15 min, twice/day, 5 days/wk) were initiated 2 wk following spinalization and continued for a 6-mo period. Airway pressure (P)-generating capacity was determined by SCS. Five acute, spinalized animals served as controls. Compared with controls, initial P fell from 43.9 +/- 1.0 to 41.8 +/- 0.7 cmH(2)O (not significant) in the chronic animals. There were small reductions in the weight of the external oblique, internal oblique, transverses abdominis, internal intercostal, and rectus abdominis muscles (not significant for each). There were no significant changes in the population of fast muscle fibers. Because prior studies (Kowalski KE, Romaniuk JR, DiMarco AF. J Appl Physiol 102: 1422-1428, 2007) have demonstrated significant atrophy following spinalization in this model, these results indicate that expiratory muscle atrophy can be prevented by the application of short periods of daily high-frequency stimulation. Because the frequency of stimulation is similar to the expected pattern of clinical use for cough generation, the daily application of electrical stimulation could potentially serve the dual purpose of maintenance of expiratory muscle function and airway clearance.

Fig. 1

Effects of lower thoracic spinal cord stimulation on airway pressure generation over a wide range of lung volumes (expressed as precontractile airway pressures) in the acute animals (control group; ●) and in the chronically stimulated group (×). A: results from a single animal. B: group mean results ± SE. FRC, functional residual capacity. At all lung volumes, the magnitude of airway pressure generation was not significantly different between groups.

Fig. 2

Effects of lower thoracic spinal cord stimulation on airway pressure generation over a wide range of stimulus amplitudes in the acute animals (control group; ●) and in the chronically stimulated group (×). Values are group means ± SE. In both groups, there were progressive increases in airway pressure generation with increasing stimulus amplitude until a plateau was reached at ~15 mA, following which there were no further increases in pressure development. The magnitude of airway pressure generation was somewhat smaller in the chronically stimulated group compared with control animals, but these differences were significant only at stimulus amplitudes of 2and6mA(*P < 0.05 for each).

Fig. 3

Relationship between stimulus frequency (20–100 Hz) and airway pressure generation in the acute animals (control group; ●) and in the chronically stimulated group (×). Values are group means ± SE. In the chronically stimulated group, the magnitude of airway pressure generation during spinal cord stimulation was similar to the control group at all stimulus frequencies.