Has stress been preventing you from reaching your fitness goals? We’ve all heard about how stress plays some big crucial roles in how our bodies respond to our diet and training strategies. But if you’re anything like me, I need the science.

What and HOW exactly does stress impact the body?

We’re all about the evidence and the physiology here at BUILD – because if we can understand WHAT is going on in our bodies as a result of stress (or anything else for that matter), maybe we can find strategies to help our bodies mitigate those negative impacts.

Here’s how stress impacts how your body uses insulin, and therefore how it impacts your metabolism, which prevents you from reaching your fitness goals.

You want your body to use your insulin optimally – that is, to shuttle the sugars (from the carbs you eat) out of your bloodstream and into the cells of your body, namely the muscle cells. It’s here that it can be used for energy production, whether immediately or stored for later use as energy. The alternative to this is that they’re stored as body fat. This is a whole ‘nother process, but the take-away is that we want our bodies to be fat-burning machines, not fat-storing machines. And how well your insulin works in your body – aka how insulin sensitive your cells are – is largely responsible for this.

So… back to stress and your insulin sensitivity.

One of the primary pathways that stress impacts it is the activation of the hypothalamic-pituitary-adrenal (HPA) axis, which leads to increased secretion of stress hormones such as cortisol. Cortisol, in turn, can disrupt normal glucose metabolism and insulin signalling, leading to reduced insulin sensitivity and increased risk of insulin resistance.

The H-P-what??

The hypothalamic-pituitary-adrenal (HPA) axis is a complex neuroendocrine system in the body and it plays a key role in how your body responds to stress. It involves communication between the hypothalamus (a region in the brain), the pituitary gland (a small gland located at the base of the brain), and the adrenal glands (small glands on top of the kidneys).

It all starts with a trigger. When your body senses stress of any kind, whether physical, emotional, real or even perceived, the HPA axis is activated. The hypothalamus then releases a hormone called corticotropin-releasing hormone (CRH), which then signals the pituitary gland to release adrenocorticotropic hormone (ACTH). ACTH then stimulates the adrenal glands to produce and release stress hormones, primarily cortisol.

In the right amounts, at the right times, cortisol is actually a good thing because it initiates a lot of things within the body to give us the energy and focus needed to tackle the threat. It immediately increases blood sugar levels (which gives us the energy for fight or flight), suppresses the immune system (to save energy for the fight or flight), increases heart rate, and regulates inflammation – just to name a few.

But [big but] prolonged or chronic activation of the HPA axis and sustained elevation of cortisol levels has detrimental effects on health, including reduced insulin sensitivity, carb metabolism, and other physiological processes. This can contribute to the development of conditions such as insulin insensitivity and subsequent weight gain, poor energy, and even metabolic and cardiovascular conditions.

Wanna really nerd out on the science?

The function of insulin signalling can be hindered by cortisol as it interferes with the translocation of glucose transporter type 4 (GLUT4) to the cell membrane, disabling glucose uptake into cells. Furthermore, cortisol has the potential to diminish the phosphorylation of insulin receptor substrate 1 (IRS-1), an important protein involved in insulin signaling, resulting in insensitivity towards insulin. Furthermore, muscle protein breakdown can be triggered by cortisol, leading to a rise in the release of amino acids into the bloodstream. These amino acids may then clash with glucose for cellular absorption, leading to a compounded insulin resistance.

Wanna know more about insulin insensitivity? Click here! 

 

References:

Kyrou, I., Tsigos, C., & Mavroghenis, I.K. (2021). Stress, visceral obesity, and metabolic complications: The cortisol-cortisone shuttle hypothesis. Obesity Reviews, 22(1), e13195. doi:10.1111/obr.13195

Black, P.H. (2002). Stress and the inflammatory response: A review of neurogenic inflammation. Brain, Behavior, and Immunity, 16(6), 622-653. doi:10.1016/S0889-1591(02)00021-1

Adam, T.C., & Epel, E.S. (2007). Stress, eating and the reward system. Physiology & Behavior, 91(4), 449-458. doi:10.1016/j.physbeh.2007.04.011

Pervanidou, P., & Chrousos, G.P. (2012). Stress and obesity/metabolic syndrome in childhood and adolescence. International Journal of Pediatric Obesity, 7(Suppl 2), 21-28. doi:10.3109/17477166.2012.700920
Chrousos, G.P. (2000). The role of stress and the hypothalamic-pituitary-adrenal axis in the pathogenesis of the metabolic syndrome: Neuro-endocrine and target tissue-related causes. International Journal of Obesity and Related Metabolic Disorders, 24(Suppl 2), S50-S55. doi:10.1038/sj.ijo.0801392
Reynolds, R.M. (2010). Glucocorticoid excess and the developmental origins of disease: Two decades of testing the hypothesis – 2010 Curt Richter Award Winner. Psychoneuroendocrinology, 35(4), 580-592. doi:10.1016/j.psyneuen.2009.09.012
Stimson, R.H., & Walker, B.R. (2010). Glucocorticoids and 11β-hydroxysteroid dehydrogenase type 1 in obesity and the metabolic syndrome. Minerva Endocrinologica, 35(4), 109-125. PMID: 21085283

 

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