Recruitment and rate-coding strategies of the human genioglossus muscle.
Single motor unit (SMU) analysis provides a means to examine the motor control of a muscle. SMUs in the genioglossus show considerable complexity, with several different firing patterns. Two of the primary stimuli that contribute to genioglossal activation are carbon dioxide (CO(2)) and negative pressure, which act through chemoreceptor and mechanoreceptor activation, respectively. We sought to determine how these stimuli affect the behavior of genioglossus SMUs. We quantified genioglossus SMU discharge activity during periods of quiet breathing, elevated CO(2) (facilitation), and continuous positive airway pressure (CPAP) administration (inhibition). CPAP was applied in 2-cmH(2)O increments until 10 cmH(2)O during hypercapnia. Five hundred ninety-one periods (each ∼ 3 breaths) of genioglossus SMU data were recorded using wire electrodes(n = 96 units) from 15 awake, supine subjects. Overall hypercapnic stimulation increased the discharge rate of genioglossus units (20.9 ± 1.0 vs. 22.7 ± 0.9 Hz). Inspiratory units were activated ∼ 13% earlier in the inspiratory cycle, and the units fired for a longer duration (80.6 ± 5.1 vs. 105.3 ± 4.2% inspiratory time; P < 0.05). Compared with baseline, an additional 32% of distinguishable SMUs within the selective electrode recording area were recruited with hypercapnia. CPAP led to progressive SMU inhibition; at ∼ 6 cmH(2)O, there were similar numbers of SMUs active compared with baseline, with peak frequencies of inspiratory units close to baseline, despite elevated CO(2) levels. At 10 cmH(2)O, the number of units was 36% less than baseline. Genioglossus inspiratory phasic SMUs respond to hypercapnic stimulation with changes in recruitment and rate coding. The SMUs respond to CPAP with derecruitment as a homogeneous population, and inspiratory phasic units show slower discharge rates. Understanding upper airway muscle recruitment/derecruitment may yield therapeutic targets for maintenance of pharyngeal patency.
Division of Sleep Medicine, Sleep Disorders Program, Brigham and Women's Hospital, 221 Longwood Ave., Boston, MA 02115, USA. JSABOISKY@partners.org
Julian P
JP
Saboisky
Amy S
AS
Jordan
Danny J
DJ
Eckert
David P
DP
White
John A
JA
Trinder
Christian L
CL
Nicholas
Shiva
S
Gautam
Atul
A
Malhotra
D000200:Action Potentials; D000328:Adult; D002245:Carbon Dioxide / Q000378:metabolism; D002628:Chemoreceptor Cells / Q000378:metabolism; D045422:Continuous Positive Airway Pressure; D004576:Electromyography; D005260:Female; D006801:Humans; D006935:Hypercapnia / Q000378:metabolism / Q000503:physiopathology*; D001239:Inhalation; D008297:Male; D008465:Mechanoreceptors / Q000378:metabolism; D009046:Motor Neurons / Q000378:metabolism; D009434:Neural Pathways / Q000378:metabolism / Q000503:physiopathology; D011312:Pressure; D012891:Sleep Apnea Syndromes / Q000503:physiopathology; D013997:Time Factors; D014059:Tongue / Q000294:innervation*
D002245:Carbon Dioxide