Written by Kranti Kaur

At some point in our lives, everyone has experienced the gut-wrenching symptoms that anxiety brings along: an elevated heart rate, sweaty palms, and perspiration before a big presentation or when faced with adversity. It is established that an elevated heart rate is a symptom of anxiety, but could the relationship work backwards? Just as anxiety leads to increased heart rate, could having an increased heart rate induce feelings of anxiety as well?

A study published in the Journal of Neuroscience attempted to answer this question by elevating heart rates in twins using isoproterenol– a drug routinely used to treat heart failure by cautiously increasing heart rate. After having ingested the drug, participants were asked whether they felt panicky or anxious. However, the results of this study did not result in a definitive answer to the research question, considering that isoproterenol causes changes across the entire body, not just the heart. Therefore, another study was needed that focused solely on the heart to truly help answer this question.         

A recent study by Karl Deisseroth, a neuroscientist at Stanford University, showed that artificially elevating heart rate in mice causes an increase in anxiety levels. This study used optogenetics, a method of controlling and monitoring biological functions of different parts of an organism such as cells or organs with the use of genetic engineering and optical systems. This allowed for researchers to isolate heart rate as the independent variable, which was better than using a drug that can cause changes in other parts of the body as well.

Using optogenetics, Deisseroth and his colleagues made the mice’s hearts light sensitive. They put a vest on the mice that emitted red light which passed through the body of the mouse until it reached the heart and caused the heart muscle cells to fire, causing the heart to beat. With the use of the vest, researchers were able to control the heart rate of the mice. When they pressed a lever, mice were taught to expect a shock that led to a water reward. The results of the study found that when the mice had elevated heart rates, they were not as willing to explore open areas or press the lever as they normally would, which suggested a level of anxiety. However, in different contexts, the artificially elevated heart rate had no effect on mouse anxiety. Deisseroth’s findings suggest that the heart rate alone does not determine anxious symptoms: rather, there is an interaction between the heart and the brain that results in anxiety.

Recent studies, along with the findings from the previous mice study, suggest links between cardiac processes, anxiety, and alterations in the insular cortex of the brain. To confirm this, and to identify other neurons with increased activation as a result of increased heart rate, Deisseroth and his colleagues used a pacemaker to measure and reveal neural activity. Findings revealed that the expression in many cerebral regions was positively correlated with heart rate. These regions include the insular cortex, as previously suggested, along with the prefrontal cortex, brainstem, nucleus tractus solitarius (NTS), and the neurons in the locus coeruleus (LC). The insular cortex has a critical role in both regulating emotions and interpreting physiological symptoms, demonstrating the importance this region has in anxiety and anxiety-like symptoms. Additionally, the NTS and LC are critical for mechanisms related to stress, which is commonly associated with anxiety. These correlations demonstrate the importance of neural mechanisms in anxiety symptoms along with cardiac pacing.

While both heart rate levels and neural mechanisms are correlated with anxiety-like behavior, they rely on each other to have a significant impact. This was concluded in 2021 when Deisseroth and his colleagues at Stanford tested whether hindering function in the insular cortex of the brain led to less drastic effects in anxiety symptoms when elevating heart rate. The inhibition of the insular region was achieved by targeting the medial prefrontal cortex (mPFC) and the posterior insular cortex (pIC) of mice using the inhibitory protein channelrhodopsin. The medial prefrontal cortex has been associated with cardiovascular arousal, which is related to the increased heart rate that occurs when an individual experiences anxiety. Moreover, the posterior insular cortex is involved in interpreting sensory signals from the heart and regulating anxiety-linked behaviors. When mice had these brain regions inhibited and their heart rate increased, results showed that mice demonstrated less anxiety symptoms when compared with mice with increased heart rate and full neurological function in the insular region. These mice were more willing to explore and more likely engage in risky scenarios. With the interconnectivity with these cerebrum regions and cardiac functions, it is no surprise that both need to be effectively activated to induce the anxiety behaviors.

The results of this study suggest that increasing heart rate can lead to anxious symptoms with the interaction of the heart and brain. This conclusion could also suggest that anxious symptoms may be controlled and lessened by decreasing heart rate. In other words, decreasing heart rate can be a possible treatment for disorders like anxiety and even depression. However, more research would have to be conducted to demonstrate this trend empirically. Even though there is not much research that can demonstrate this, it is common practice to take deep breaths to decrease anxiousness which definitely helps some, if not most, people. It is definitely possible for this research to open a new form of treatment that is significantly less expensive than current treatments. This is especially important because disorders such as anxiety and depression tend to have a long course and can be highly expensive to treat.