Key result
Small voluntary increases in ventilation and low inspiratory threshold loads resulted in a 40% and 25% incidence of premotor potentials, respectively, which was not significantly different from the 0% incidence during resting breathing (p>0.05).
Why the study?
Do small voluntary increases in ventilation or low inspiratory threshold loads elicit respiratory premotor potentials in healthy participants?
Observational (n=15)
No
Do small voluntary increases in ventilation or low inspiratory threshold loads elicit respiratory premotor potentials in healthy participants?
Absolute Event Rate: 40% vs 0%
p-value: p=>0.05
In healthy participants, small voluntary increases in tidal volume or low inspiratory threshold loads do not elicit significant cortical contributions (premotor potentials) compared to resting breathing.
Small ventilatory increases do not significantly elicit premotor potentials; leaves open cortical thresholds in respiratory control.
Respiratory-related premotor potentials from averaged electroencephalography (EEG) over the motor areas indicate cortical activation in healthy participants to maintain ventilation in the face of moderate inspiratory or expiratory loads. These experimental conditions are associated with respiratory discomfort, i.e. dyspnea. Premotor potentials are also observed in resting breathing in patients with reduced automatic respiratory drive or respiratory muscle strength due to respiratory or neurological disease, presumably in an attempt to maintain ventilation. The aim of this study was to determine if small voluntary increases in ventilation or smaller load-capacity imbalances, that generate an awareness of breathing but aren’t necessarily dyspneic, give rise to respiratory premotor potentials in healthy participants. In 15 healthy subjects, EEG was recorded during voluntary large breaths (~3x tidal volume, that were interspersed with smaller non-voluntary breaths in the same trial; in 10 subjects) and breathing with a ‘low’ inspiratory threshold load (~7 cmH20; in 8 subjects). Averaged EEG signals at Cz and FCz were assessed for premotor potentials prior to inspiration. Premotor potential incidence in large breaths was 40%, similar to that in the smaller non-voluntary breaths in the same trial (20%; p > 0.05) and to that in a separate trial of resting breathing (0%; p > 0.05). The incidence of premotor potentials was 25% in the low load condition, similar to that in resting breathing (0%; p > 0.05). In contrast, voluntary sniffs were always associated with a higher incidence of premotor potentials (100%; p < 0.05). We have demonstrated that in contrast to respiratory and neurological disease, there is no significant cortical contribution to increase tidal volume or to maintain the load-capacity balance with a small inspiratory threshold load in healthy participants as detected using event-related potential methodology. A lack of cortical contribution during loading was associated with low ratings of respiratory discomfort and minimal changes in ventilation. These findings advance our understanding of the neural control of breathing in health and disease and how respiratory-related EEG may be used for medical technologies such as brain-computer interfaces.
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Hudson et al. (2018) conducted an observational in Healthy (n=15). Small voluntary increases in ventilation (large breaths) and low inspiratory threshold load vs. Resting breathing was evaluated on Incidence of inspiratory premotor potentials (p=>0.05). Small voluntary increases in ventilation and low inspiratory threshold loads resulted in a 40% and 25% incidence of premotor potentials, respectively, which was not significantly different from the 0% incidence during resting breathing (p>0.05).
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