What is sleep apnea?

Sleep apnea is a sleep disorder characterized by pauses in breathing or shallow breaths during sleep. These pauses can last from a few seconds to minutes and may occur multiple times throughout the night. Sleep apnea can disrupt normal sleep patterns and lead to symptoms such as daytime fatigue, excessive daytime sleepiness, and irritability.


There are two main types of sleep apnea:


  • Obstructive Sleep Apnea (OSA): This is the most common form of sleep apnea and occurs when the muscles in the throat relax excessively during sleep, causing the airway to collapse or become blocked. As a result, airflow is restricted or completely blocked, leading to pauses in breathing (apneas) or shallow breathing (hypopneas). OSA is often associated with snoring, choking, or gasping sounds during sleep.


  • Central Sleep Apnea (CSA): In central sleep apnea, the brain fails to send proper signals to the muscles that control breathing during sleep. This results in a lack of effort to breathe, leading to pauses in breathing. CSA is less common than OSA and is often associated with medical conditions such as heart failure, stroke, or neurological disorders.


Risk factors for sleep apnea include obesity, male gender, older age, family history of sleep apnea, smoking, and nasal congestion. Untreated sleep apnea can have serious consequences, including increased risk of cardiovascular disease, hypertension, stroke, diabetes, and accidents due to daytime sleepiness.


What is the relationship between sleep apnea and oxidative stress?

The relationship between sleep apnea and oxidative stress is multifaceted and involves complex interactions between intermittent hypoxia, inflammation, and oxidative damage. Here’s how sleep apnea contributes to oxidative stress:


  • Intermittent Hypoxia: In obstructive sleep apnea (OSA), repeated episodes of partial or complete obstruction of the upper airway lead to intermittent hypoxia (decreased oxygen levels) during sleep. These cycles of hypoxia followed by reoxygenation result in oxidative stress. When oxygen levels drop, cells undergo a state of ischemia-reperfusion, where tissues are deprived of oxygen followed by a sudden influx of oxygen upon resumption of airflow. This process leads to the generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS), which contribute to oxidative damage to cellular structures.


  • Inflammation: Sleep apnea is associated with chronic low-grade inflammation, characterized by elevated levels of inflammatory markers such as C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha). Inflammatory pathways activated by sleep apnea further promote oxidative stress by stimulating the production of ROS and RNS within cells.


  • Endothelial Dysfunction: Sleep apnea can impair endothelial function, leading to endothelial dysfunction. The endothelium, which lines blood vessels, plays a crucial role in regulating vascular tone, inflammation, and oxidative stress. Dysfunction of the endothelium results in increased production of ROS and decreased bioavailability of nitric oxide (NO), a vasodilator that helps maintain blood vessel health.


  • Oxidative Damage: Prolonged exposure to oxidative stress in individuals with sleep apnea can lead to oxidative damage to lipids, proteins, and DNA. Lipid peroxidation, protein oxidation, and DNA damage contribute to cellular dysfunction and tissue injury, particularly in organs vulnerable to oxidative stress such as the heart, brain, and blood vessels.


  • Systemic Effects: Oxidative stress associated with sleep apnea has systemic effects beyond the respiratory system. It can contribute to the development and progression of cardiovascular disease, metabolic disorders, neurocognitive impairment, and other comorbidities associated with sleep apnea.


Overall, sleep apnea-induced oxidative stress plays a significant role in the pathophysiology of sleep apnea-related complications and contributes to the overall burden of disease in affected individuals.