As researchers probe the physiology underlying noise’s cardiovascular consequences, they’re zeroing in on a culprit: dramatic changes to the endothelium, the inner lining of arteries and blood vessels. This lining can go from a healthy state to one that’s “activated,” and inflamed, with potentially serious ramifications.
When sound reaches the brain, it activates two important regions: the auditory cortex, which interprets noise, and the amygdala, which manages emotional responses to it. As noise gets louder, and especially during sleep, the amygdala activates a stress response—even if the person isn’t aware of it.
Once initiated, this response releases hormones such as adrenaline and cortisol into the body. Some arteries constrict; others dilate. Blood pressure rises, and sugars and fats flood the bloodstream for quick use by the muscles. The cascading stress response also prompts the creation of harmful molecules that cause oxidative stress and inflammation in the lining of blood vessels. This dysfunctional endothelium meddles with blood flow and affects numerous other processes that, when impaired, contribute to a range of cardiovascular illnesses, including high blood pressure, plaque buildup in arteries, obesity, and diabetes.
Studies on people and mice show that the endothelium doesn’t work as efficiently after just a few days of nighttime airplane-noise exposure, suggesting that loud noise isn’t a concern only for people already at risk for heart and metabolic problems. Healthy adults subjected to recordings of trains during their slumber had impaired blood-vessel function almost immediately, according to a 2019 study published by Münzel and his colleagues in Basic Research in Cardiology.
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