April 1, 2019, by hjohnson

How exercise can help overcome stress

Written by Lucy Tyler

 

According to mental health charity Mind, it is estimated that there will be approximately 2 million more adults experiencing poor mental health by 2030, compared to 2013 in the UK1. According to the Mental Health Foundation, around 45% of adults in the UK report having poor mental health and medication is the most used treatment. There is mixed opinion on how effective antidepressants are for improving mental health. Studies have shown that antidepressants can improve symptoms in 20% of people and that long-term use of antidepressants can prevent a relapse in around 27% of people. However, they can cause side-effects such as headaches, insomnia, nausea and dizziness, which can discourage people from continuing treatment2. As an alternative to antidepressant medication Maria Toledo-Rodriguez and a team based at the University of Nottingham have investigated a link between exercise and resilience to stressful circumstances and preventing anxiety. Their results suggest that exercise is a viable non-pharmacological method of improving mental health.

Both stress and exercise activate the HPA (hypothalamic-pituitary-adrenal) axis, a pathway that controls the release of stress hormones, corticoids. The HPA axis operates by a negative feedback system, where the final product of a cascade inhibits the production of the first product in the cascade and subsequently prevents further action of the pathway.  In this case, release of corticoids stops the pathway and prevents excessive release of corticoids. If a stress response is prolonged, the release of corticoids is maintained and the feedback becomes dysfunctional, causing the high corticoid levels that characterise disorders such as anxiety or depression.

Several metabolic processes, such as exercise, naturally cause activation of this pathway. However, the timing and strength of HPA activation differs between stress and exercise. Exercise causes a short-term increase in HPA activity, which is beneficial, whereas stress causes a long-term increase in activity and stress hormone production, that is not. Long-term high levels of corticoids can increase risk of diabetes, for example. The type of corticoid released also has an impact on the response. This research specifically investigated glucocorticoid, which is a type of corticoid. A strong association has been found between the number of glucocorticoid receptors expressed in the brain, and the resilience of an individual to stressful stimuli.

The amount of receptor expression changes by a mechanism known as epigenetics. Epigenetics is the concept that DNA can be altered during the lifetime of an individual such that the gene expressed does not change but how much it is expressed does change. The group from the University of Nottingham measured the expression of the glucocorticoid receptor gene in experimental models from stressful and non-stressful conditions, from either active or sedentary lifestyles. Exercising subjects displayed less anxious behaviour in stressful situations and greater expression of glucocorticoid receptors in the hippocampus, a part of the brain that is associated with emotional processing. The group found that exercise causes modifications to DNA that encodes glucocorticoid receptors. This modification is thought to occur by silencing an inhibitory mechanism that prevents DNA expression, known as microRNAs. Exercise silenced the microRNAs and prevented their inhibitory actions on DNA expression. Whether the relationship between exercise alone directly changes the activity of microRNAs and not via other factors remains to be investigated.

These findings indicate a strong link between exercise and resilience to stress and anxiety. The mechanism by which this is thought to occur highlights the importance of thinking about long-term health. It has also been established by research conducted at the University of Nottingham that exercise improves memory later in life3.  What you do now will impact health and wellbeing in later life or in circumstances in the foreseeable future, and leading an active lifestyle will have wider positive impact than just decreasing your risk of cardiovascular disease.

 

References and further reading

To read the original article: Pan-Vazquez, A., Rye, N., Ameri, M., McSparron, B., Smallwood, G., Bickerdyke, J., Rathbone, A., Dajas-Bailador, F. and Toledo-Rodriguez, M., 2015. Impact of voluntary exercise and housing conditions on hippocampal glucocorticoid receptor, miR-124 and anxiety. Molecular brain8(1), p.40.

  1. Sudo, N., Chida, Y., Aiba, Y., Sonoda, J., Oyama, N., Yu, X.N., Kubo, C. and Koga, Y., (2004). Postnatal microbial colonization programs the hypothalamic–pituitary–adrenal system for stress response in mice. The Journal of physiology558(1), pp.263-275.
  2. Foster, J.A. and Neufeld, K.A.M., (2013). Gut–brain axis: how the microbiome influences anxiety and depression. Trends in neurosciences36(5), pp.305-312.
  3. Jessop P and Toledo-Rodriguez M (2018) Hippocampal TET1 and TET2 Expression and DNA Hydroxymethylation Are Affected by Physical Exercise in Aged Mice. Front. Cell Dev. Biol. 6:45. doi: 10.3389/fcell.2018.00045

Picture: Creative Commons License. Source: Pexels.

Posted in EpigeneticsExerciseStress