Stress can be deadly!

Stress is a general term meaning homeostatic disorder, i.e. an environmental disorder that is optimal for the body. Stress now has a bad reputation, but is part of the natural adaptive mechanisms and physiological response such as fight or flight. For the immediate response, type II fibers are prepared with large energy resources that can be quickly consumed (eg, phosphocreatine, glycogen – stored glucose).

While chronic stress is harmful to health, short-term allows to cope with the challenges. In addition, it was discovered that short-term, low stress promotes protection against pathogens, strengthens the immune system. While the situation is highly unfavorable, when high concentrations of cortisol are still present, short-term, even a few dozen-fold increase in the concentration of “stress hormone” (eg within tens of minutes after intervals) does not have a negative effect on the system. Similarly, short-term cooling or exposure to high temperature, although they exert different hormonal responses (effects on free and total testosterone, ACTH, cortisol, prolactin, thyroid T4, T3, TSH, hematology profile, hemoglobin, hematocrit) 3,4 are not associated with diseases . The situation is completely different,when exposure to cold water or heat is prolonged. Both of these variants in extreme circumstances are associated with increased mortality (eg hypothermia and related phenomena or cardiovascular complications and dehydration occurring at high temperature). The body’s powerful cooling down can kill even within minutes. Similarly, it should not be considered in the binary system (i.e. either something is “only positive” or “only negative”) the impact of training on health.

How short-term and how chronic stress affect obesity?

It has been shown that short-term stress induces the first and secondarily immunological response. “Strengthening” refers to changes in dendritic cells, activation and effects on the maturation of neutrophils, macrophages and lymphocytes, as well as local and systemic production of cytokines. In turn, chronic stress interferes with the proportions of type 1 and 2 cytokines, induces chronic inflammatory lesions of low intensity and affects immunosuppression (inhibits the quantity, migration, activity and immunoprotective functions of specialized cells). 1 Chronic stress increases the susceptibility to certain types of cancer by affecting type I cytokines, T-lymphocytes and suppression of T-cell function.

“Cytokines … affect the growth and survival of cancer cells, regulate tumor infiltration by leukocytes, stimulate the formation of new blood vessels (angiogenesis), participate in the formation of extracellular matrix and in the multistage process of distant metastasis formation and regulate the immune response” 5

For example, TGF-α, TGFβ, IL-4, IL-10 and VEGF have immunosuppressive effects. 5

Long-lasting stress promotes obesity as it affects

leptin concentration (this means a disturbance in the feeling of satiety, in normal conditions high leptin concentration limits the supply of food),

the concentration of ghrelin (=> “wolf hunger”),

concentration of TNF-alpha, IL-1, IL-8 and inhibition of TGF-beta production (in normal conditions, cortisol suppresses the production of pro-inflammatory factors such as TNF-α, IL-12 and interferon gamma, and promotes the production of anti-inflammatory IL-4, IL-10 and transforming growth factor beta. However, in a situation of chronic stress, these phenomena are disturbed!), 18

resistin concentration,

TNF-alpha concentration (effect on insulin resistance), 19

amount of neuropeptide Y (NPY); the neuropeptide Y is a leptin antagonist – it increases appetite), 19

cortisol concentration (indirectly affects the accumulation of, for example, visceral fat, it has an effect on stimulating the appetite, the so-called stress eating),

leptin concentration (this means a disturbance in the feeling of satiety, in normal conditions high leptin concentration limits the supply of food),

the concentration of ghrelin (=> “wolf hunger”),

concentration of TNF-alpha, IL-1, IL-8 and inhibition of TGF-beta production (in normal conditions, cortisol suppresses the production of pro-inflammatory factors such as TNF-α, IL-12 and interferon gamma, and promotes the production of anti-inflammatory IL-4, IL-10 and transforming growth factor beta. However, in a situation of chronic stress, these phenomena are disturbed!), 18

resistin concentration,

TNF-alpha concentration (effect on insulin resistance), 19

amount of neuropeptide Y (NPY); the neuropeptide Y is a leptin antagonist – it increases appetite), 19

cortisol concentration (indirectly affects the accumulation of, for example, visceral fat, it has an effect on stimulating the appetite, the so-called stress eating),

In contrast, short-term stress stimulates the adrenal medulla (=> adrenaline) and the release of noradrenaline into the synaptic cleft, which promotes appetite suppression. 19, 20

Inflammation and cancer

Many cytokines, pro-inflammatory factors, affect cancer. The same compounds are formed during intense physical exercise or under chronic stress (eg IL-6, IL-8). 21.22 In the studies of Nieman DC et al. From 2013, 8 athletes practiced three days in a row with an intensity of 70% VO2max (for 2.5 hours per day). They examined how training affects creatine kinase, inflammatory factors (CRP, IL-6, IL-8, IL-10, MCP) and immunity. It was found that runners had much greater muscle damage from cyclists. Also, inflammatory factors were at a much higher level in runners than in cyclists (CRP higher by 87%, IL-6 by 256%, IL 8 by 61%, IL-10 by 32%, MCP by 29%).

The acute phase protein – CRP, C-reactive protein (C-reactive protein) is produced by the liver. Elevated levels of c-reactive protein indicate increased inflammation, viral and bacterial infection, high concentrations are associated with, for example, burns.

IL-6 – a highly pro-inflammatory cytokine administered as having anti-inflammatory activity 10 “Studies conducted in mice with experimentally induced infections, allergic inflammation or arthritis show a more complex picture, because depending on the model, IL-6 promotes cell formation Th1 or Th2 and differently affect the inflammatory response … The pro-inflammatory or anti-inflammatory properties of IL-6 depend on the specificity of tissue and inflammation-inducing factors that create a microenvironment that produces, among others, a set of cytokines that co-determine the direction of T lymphocyte differentiation “9; Currently, it is known that its main role is to participate in the immune response and inflammatory response and in the formation of blood,

IL-8 – proinflammatory cytokine,

IL-10 – anti-inflammatory cytokine.

MCP- has been shown to be involved in the pathogenesis of psoriatic diseases, rheumatoid arthritis and atherosclerosis. 11

And now the most interesting is the relationship between cytokines and tumors. How is this possible? Cancerous tissues are unable to function without a constant blood supply. Although tumors are resistant to hypoxia and have been shown to obtain energy through anaerobic (most likely they need lactate), they must have access to the bloodstream (if only to source nutrients and remove unnecessary metabolites). 17 This process of creating new vessels is called angiogenesis. Cancer cells themselves produce a variety of factors, because the neovascularization of tumor or angiogenesis (the formation of new blood vessels) is stimulated eg by IL-6, VEGF (vascular endothelial growth factor), TGF (alpha and beta growth factor forming), or IL-6 , IL-8.

And now the most interesting

The formation of new blood vessels can be induced by

vascular endothelial growth factor – VEGF (vascular endothelial growth factor),

essential fibroblast growth factor (bFGF, basic fibroblast growth factor); sometimes erroneously called basic (error in translation), 17

TNF-α (tumor necrosis factor) – corresponds to, e.g. for tumor neovascularization or angiogenesis. Paradoxically, it can be highly harmful to the heart inducing apoptosis, contrary to its name – it affects, among others, on the increase in TNF-a mortality, it is involved in the production of other pro-inflammatory cytokines, such as IL-6, IL-1, which exacerbate the myocardial metabolic disturbances caused by TNF-α, 16

IL-6 (pro-inflammatory cytokine, according to some data also with a small anti-inflammatory effect). Neoplasms secrete large amounts of IL-6, which are fundamental for the growth of pathologically changed tissues and metastasis (including angiogenesis, proliferation, attachment and invasion). In in vitro studies with norepinephrine, increased synthesis and release of IL-6 in human ovarian tumor cells has been observed (eg (eg, SKOV3ip1, Hey-A8 and EG),

essential fibroblast growth factor (bFGF, basic fibroblast growth factor); sometimes erroneously called basic (error in translation), 17

IL-8 – proinflammatory cytokine,

PDGF – endothelial cell growth factor derived from platelets,

TGF-α and β (Transforming growth factor alpha and beta); “In many papers, the important role played by TGF-beta in various diseases, i.e. osteoporosis, Alzheimer’s disease, breast cancer, diabetic retinopathy, myocardial infarction, or autoimmune diseases, has been confirmed, 14

TNF-α (tumor necrosis factor) – corresponds to, e.g. for tumor neovascularization or angiogenesis. Paradoxically, it can be highly harmful to the heart inducing apoptosis, contrary to its name – it affects, among others, on the increase in TNF-a mortality, it is involved in the production of other pro-inflammatory cytokines, such as IL-6, IL-1, which exacerbate the myocardial metabolic disturbances caused by TNF-α, 16

G-CSF.

Both aerobic and strength training have an impact on the formation of new blood vessels (but this does not mean anything bad under normal conditions). Aerobic training activated the genes responsible for the growth of new blood vessels and increased efficiency. Strength exercises caused the growth of new blood vessels, but also influenced the gene responsible for the increase in the volume of muscle tissue 12-13. It was also found that VEGF-A (growth factor of new blood vessels) increased three times after aerobic training and twice after strength training.

Inflammation and sudden deaths of athletes

A chronic inflammation with sudden cardiac death (SCD) 6 was also associated, and what is most interesting, the most deaths due to SCD are noted in endurance disciplines and team sports.

In 820 cases of sudden cardiac death:

98 (11.94%) of other disciplines.

251 (30.57%) concerned cycling,

175 (21.32%) concerned running,

107 (13.03%) related to playing football,

41 (4.99%) concerned marching in the field, hiking,

31 (3.78%) related to swimming,

29 (3.53%) related to retina,

18 (2.19%) related to rugby,

15 (1.83%) related to tennis,

11 (1.34%) related to diving,

11 (1.34%) concerned judo,

10 (1.22%) concerned handball,

8 (0.97%) concerned alpine skiing,

6 (0.73%) related to table tennis,

5 (0.61%) related to bodybuilding,

5 (0.61%) related to retina,

98 (11.94%) of other disciplines.

Chronic stress and muscle building

At the end, chronic stress, of course, is not conducive to the building of muscle mass, but rather to the body’s fatness. This affects the deterioration of the silhouette composition in the perspective of months (years). Chronic inflammation interferes with training, easier overtraining, fatigue and worsening of strength results. Stress also affects sleep disorders, which limits the increase in strength and weight. What to do? You have to approach the situation you deal with every day differently. Do not treat everything in terms of success or failure and there is nothing intermediate! Chronic stress has been linked to cancer, depression and cardiovascular diseases. For sure, the less you get stressed, the longer you will live.

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