New research reveals that activity among neurons that keeps heart rate low is reduced among the people with sleep apnea.
The study titled “Chronic intermittent hypoxia‐hypercapnia blunts heart rate responses and alters neurotransmission to cardiac vagal neurons” was published in the Journal of Physiology
A summary reported that researchers at the George Washington University state that in sleep apnea, neurons in the brainstem that controls heart rate experience a reduced activity. This diminished neuronal activity then activates increased heart rate, blood pressure and also the risk of adverse cardiovascular events in OSA patients.
Lack of oxygen during these incidents puts the sufferers in lighter state of sleep or brief wakefulness for restoration of normal breathing. Cycles of interrupted breathing and arousal from sleep can occur as frequently as once per minute.
“Lack of sleep leaves the mind and body tired, leading to poor mental and physical performance, and if untreated OSA increases a person’s risk of developing hypertension and irregular heartbeats,” said lead study author Dr David Mendelowitz. “Therefore it is very important that we have discovered some of the underlying mechanisms that could injure the heart and other cardiovascular tissues.”
The team explored these mechanisms in rats, by mimicking OSA for four weeks and studying the changes in blood pressure, heart rate, and synaptic activity in parasympathetic neurons that control heart rate.
Future work will need to build from this foundation and focus on finding targets to restore the usual cardio-protective function of these neurons to help reduce the risk of arrhythmias, elevated heart rate, and blood pressure that occur with this disease.
