Ventilatory long-term facilitation at rest increases the feedforward contribution to subsequent exercise ventilatory...

Area of Science:

• Respiratory physiology
• Neuroscience
• Exercise physiology

Background:

• The respiratory control system demonstrates neural plasticity, adapting ventilatory control based on prior stimuli.
• Understanding how resting respiratory plasticity influences exercise ventilation is crucial for respiratory control research.

Purpose of the Study:

• To test if ventilatory long-term facilitation (LTF), induced by hypercapnic acute intermittent hypoxia (AIH) at rest, enhances subsequent ventilatory responses during steady-state exercise.
• To investigate the impact of AIH-induced LTF on exercise hyperpnea, system gain, and end-tidal PCO2 regulation.

Main Methods:

• Fourteen healthy adults underwent pulmonary function testing.
• Participants were exposed to either AIH (15, 1-min hypoxic episodes with room air intervals) or a Sham condition.
• Mild hypercapnia was maintained during and after AIH/Sham. Ventilatory responses to steady-state cycle exercise (30, 60, 90 W) were measured post-intervention.

Main Results:

• AIH induced significant ventilatory long-term facilitation (LTF) compared to Sham.
• While minute ventilation during exercise was not significantly different, the ventilatory/CO2 production relationship (system gain) and feedforward exercise gain were significantly increased post-AIH.
• End-tidal PCO2 was regulated lower across all exercise workloads following AIH compared to Sham.

Conclusions:

• Ventilatory plasticity induced at rest via hypercapnic AIH alters subsequent ventilatory responses during mild to moderate steady-state exercise.
• AIH-induced LTF increases the feedforward component of exercise hyperpnea and improves end-tidal PCO2 control during exercise.
• Respiratory motor plasticity at rest can influence physiological responses during other conditions, such as exercise.