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Chronic stress has been linked to a range of adverse health effects, including muscle wasting or atrophy. Stress-induced muscle wasting is associated with increased susceptibility to injury, decreased strength, and metabolic dysfunction. Studies in mice have shown that chronic stress leads to severe loss of lean body mass, hyperglycemia, and dyslipidemia, with similar results observed in humans. The mechanism underlying this association is not yet fully understood, but it is believed to involve the dysregulation of various hormones and inflammatory pathways, ultimately contributing to a decrease in muscle mass and negative health outcomes.
| Characteristics | Values |
|---|---|
| Inflammatory conditions | IL-6 secretion and action are coupled with increased muscle wasting, often acting in combination with cortisol and other molecules to promote atrophy |
| HPA axis | Hyperactivation associated with hypercortisolemia and subclinical systemic inflammation disrupts the metabolism of muscle mass |
| Myostatin | A member of the transforming growth factor-b family that is associated with protein degradation; its expression increases in response to daily psychological stress |
| Myogenin | A transcription factor that regulates muscle size; its absence results in reduced body and muscle fiber size |
| mTORC1 Signaling | Chronic stress inhibits this signaling pathway, leading to skeletal muscle atrophy |
| Lean body mass | Stress can decrease lean body mass in both humans and rodents, leading to adverse metabolic profiles and increased susceptibility to musculoskeletal injuries |
| Immune system | Chronic stress suppresses the immune system, making individuals more susceptible to illness |
| Insulin resistance | Chronic stress damages cells, making them resistant to insulin, which can lead to increased hunger and an elevated risk of type 2 diabetes |
| Cortisol | High levels of cortisol are associated with prolonged muscle tension, reduced blood flow, and a build-up of lactic acid, resulting in less elastic muscles |
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What You'll Learn
Chronic stress and muscle atrophy in mice
Chronic stress has been shown to cause muscle atrophy in mice. In experiments, male mice were subjected to four weeks of chronic stress, which resulted in decreased body weight, a decrease in the size of the hind limb muscles, and a decrease in U-CRE levels. This indicates that chronic stress induces muscle atrophy.
The study also revealed atrophy of type 2b skeletal muscle fibres in response to chronic stress. Type 2a fibres tended to decrease, but chronic stress had no impact on type 1 muscle fibres. Chronic stress increased the expression of REDD1, FoxO1, FoxO3, KLF15, Atrogin1, and FKBP5, which are all associated with muscle atrophy. In contrast, chronic stress did not affect the expression of myostatin or myogenin.
Another experiment used corticotropin-releasing factor-overexpressing (CRF-OE) mice as a model of chronic stress. These mice exhibited increased plasma corticosterone levels and Cushing's syndrome. The CRF-OE mice had significantly lower skeletal muscle mass, average cross-sectional myofiber area, and total muscle protein content than their wild-type counterparts. The skeletal muscles of CRF-mice also exhibited decreased expression of factors involved in the IGF-1/AKT/mTOR protein synthesis pathway, which is essential for muscle growth and maintenance.
Overall, these studies demonstrate that chronic stress can cause muscle atrophy in mice, likely due to the inhibition of mTORC1 signalling and the increased expression of atrophy-related genes and proteins. The effects of chronic stress on muscle atrophy may also be mediated through MSTN-dependent signalling pathways, as suggested by studies using MSTN null mice.
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Stress-induced decrease in lean body mass
Chronic stress has been linked to a decrease in lean body mass in both humans and rodents. This decrease in lean body mass can have adverse health effects, such as an increased risk of musculoskeletal injury and a higher susceptibility to mechanical strain-induced damage. This is because stressed muscles are smaller and weaker, making them less capable of producing and sustaining the same level of force as an unstressed muscle.
Several studies on mice have shown that chronic stress is associated with skeletal muscle atrophy, or muscle wasting. In one study, mice exposed to chronic stress through methods such as restraints or cage switching exhibited decreased body and muscle mass. Similarly, another study found that chronically stressed mice experienced a significant decrease in the cross-sectional area of type 2b skeletal muscle fibers. These findings suggest that chronic stress can lead to muscle atrophy and a decrease in lean body mass in mice.
The mechanism behind stress-induced decrease in lean body mass involves the disruption of muscle metabolism. During chronic stress, there is an increase in muscle-originating IL-6, a myokine that regulates energy metabolism. IL-6 often acts in combination with cortisol and other molecules to promote atrophy. Additionally, chronic stress can lead to hypercortisolism, which is associated with muscle wasting and insulin resistance. Insulin resistance can further contribute to an adverse metabolic profile, leading to increased energy storage in adipose tissue and a higher risk of obesity.
The impact of chronic stress on lean body mass is not limited to mice. Human studies have shown that 28 days of bed rest, which can be a consequence of chronic stress, can result in a significant loss of lean leg mass. This decrease in lean body mass may contribute to a shift in body composition that promotes obesity and an increased risk of diabetes. Additionally, a reduction in lean muscle mass can decrease the platform for glucose uptake, further contributing to the development of diabetes. Therefore, stress-induced decrease in lean body mass can have significant health implications in humans.
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Stress and muscle-wasting hormones
Stress can have a significant impact on muscle health and body composition. Studies have shown that chronic stress can lead to muscle wasting or atrophy, particularly in skeletal muscle. This is associated with increased levels of muscle-wasting hormones such as cortisol, also known as corticosterone in rodents, and inflammatory molecules such as IL-6.
Cortisol is a steroid hormone that is released in response to stress. While it has anti-inflammatory properties, high levels of cortisol over an extended period can disrupt the natural healing process and lead to "prolonged muscle tension, reduced blood flow, and a build-up of lactic acid". Cortisol is catabolic, meaning it breaks down molecules, and can therefore inhibit protein synthesis, making muscle-building more difficult. This is particularly relevant in skeletal muscle, which is an important endocrine organ that secretes factors with endocrine actions associated with inflammatory processes.
Chronic stress can also cause hypercortisolism, which is associated with muscle wasting. In addition, studies have shown that repeated stress can decrease lean body mass in both humans and rodents, leading to smaller, weaker muscles that are more susceptible to injury. This decrease in lean muscle mass can contribute to a shift in body composition that promotes obesity and increases the risk of diabetes.
The specific molecular mechanisms by which chronic stress leads to muscle wasting are still being investigated. However, it is clear that stress-related inflammation markers and hormones play a significant role in muscle health and can have adverse effects on overall health and disease outcomes.
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Stress-related inflammation and bone health
Chronic psychological stress affects many body systems, including the skeleton. Stress-related inflammation markers have proven to be efficient in predicting changes in bone mineral density, i.e. osteopenia or osteoporosis. Low-grade inflammation and hyperactivation of the sympathetic nervous system during psychological stress are physiological changes detrimental to bone health. Inflammation is one of the important secondary risk factors for osteoporosis, as observed in various inflammatory conditions.
Biological factors in depression, a disease of stress system imbalance, include the inflammatory-mood pathway, hypothalamic-pituitary-adrenal (HPA) axis dysregulation, metabolic dysfunction, and serotonin’s direct and indirect effects on bone cells, causing osteopenia and/or osteoporosis. The pathophysiology lies within the vicious cycle of constant subclinical inflammation, increased pro-inflammatory cytokines, and disruption of bone remodelling balance. Other molecules, such as IGFBP1 and FGF21, are also implicated in bone remodelling.
The level of neuropeptide Y, a neurotransmitter of the sympathetic nervous system, increases during mental stress and is associated with resilience to stress. Overexpression of neuropeptide Y inhibits bone formation and enhances bone loss. The action of neuropeptide Y on bone is mediated by hypothalamic Y1 and osteoblastic Y2 receptors. Neuromedin U is another neuropeptide associated with stress behaviour and stress-related hormones. In preclinical studies, neuromedin U knocked-out mice were found to have increased bone mass due to increased bone formation. These neuropeptides may work together during chronic stress to induce bone loss.
Stress can also lead to unhealthy dietary trends, which will impact bone health. Higher perceived stress is associated with increased consumption of soda, coffee, energy drinks, salty snacks, frozen food, and fast food. Stress-related decreased eating was also observed in subjects. Higher fruit and vegetable intakes have been associated with increased bone mineral density and reduced fracture risk. This association could be mediated by the presence of vitamins and polyphenols in fruits and vegetables, which act as antioxidants and anti-inflammatory agents, promoting osteoblasts' survival and suppressing osteoclast formation.
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Stress and muscle-building/weight loss
Chronic stress has been linked to muscle wasting or atrophy. This is because stress causes hypercortisolism, or high levels of cortisol, which can lead to "prolonged muscle tension, reduced blood flow, and a build-up of lactic acid", making muscles "less elastic". This can also cause insulin resistance, which can lead to an increased risk of type 2 diabetes and obesity. Insulin resistance disrupts the metabolism of muscle mass.
Stress-induced decreases in lean body mass may have adverse outcomes. Firstly, a decrease in lean mass may contribute to an adverse metabolic profile by decreasing substrate oxidation due to a reduction in the amount of metabolically active tissue, which may result in greater energy storage in adipose tissue. Secondly, chronic psychological stress may increase susceptibility to musculoskeletal injury by creating smaller, weaker muscles that are less capable of producing and/or sustaining an equivalent level of force as an unstressed muscle.
In addition, studies have shown that repeated stress or inactivity results in a loss of body weight and muscle mass. Inactivity may be caused by the "insulin resistance" that comes with chronic stress, which can make you feel constantly hungry.
To counteract the negative impact of stress on muscle-building and weight loss, it is recommended to reduce caffeine, alcohol, and sugar consumption. It is also beneficial to practice low-intensity aerobic exercise, such as walking, jogging, swimming, cycling, or yoga. Good nutrition, supplements, and quality rest and sleep will also help to rebalance cortisol levels.
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Frequently asked questions
Yes, chronic stress can cause muscle wasting, also known as atrophy.
Chronic stress can cause muscle wasting through the inhibition of mTORC1 signalling, which is a critical growth-promoting pathway. It can also disrupt the metabolism of muscle mass.
Stress-induced muscle wasting can have several adverse health outcomes, including an increased risk of musculoskeletal injury, obesity, and type 2 diabetes.
The effects of chronic stress on muscle wasting can be mitigated through low-intensity aerobic exercise, good nutrition, supplements, and quality rest and sleep.
