Hypoxia augments apnea-induced peripheral vasoconstriction in humans

Area of Science:

• Cardiovascular Physiology
• Autonomic Nervous System Regulation
• Respiratory Physiology

Background:

• Obstructive apnea and voluntary breath-holding transiently elevate muscle sympathetic nerve activity (MSNA) and arterial pressure.
• The precise roles of blood flow and vascular resistance changes in apnea-induced hypertension remain unclear.

Purpose of the Study:

• To investigate the contribution of blood flow and vascular resistance changes to apnea-induced arterial pressure increases.
• To examine the influence of varying oxygen levels (hypoxia and hyperoxia) on these responses.

Main Methods:

• Measurements included heart rate, mean arterial pressure (MAP), peroneal microneurography for MSNA, and Doppler velocimetry for femoral artery blood velocity (V(FA)) in humans.
• Leg blood flow (Q) and vascular resistance (R) were calculated during voluntary end-expiratory apnea under room air, hypoxic, and hyperoxic conditions.
• Apnea-induced changes in MSNA, MAP, Q, and R were analyzed and compared across different inspired oxygen fractions.

Main Results:

• Voluntary apnea elevated MSNA and MAP, with responses being most pronounced during hypoxia and least during hyperoxia.
• Apnea consistently led to decreased leg blood flow (Q) and increased vascular resistance (R).
• The magnitude of Q decrease and R increase during apnea was greatest under hypoxia and smallest under hyperoxia.

Conclusions:

• Voluntary apnea induces vasoconstriction, partly mediated by the sympathetic nervous system.
• The intensity of apnea-induced vasoconstriction is modulated by oxygen levels, suggesting a significant role for arterial chemoreceptor stimulation.
• These findings elucidate the autonomic and vascular mechanisms underlying blood pressure regulation during breath-holding and apnea.