
Myokines are cytokines or small proteins produced and released by skeletal muscle cells in response to muscular contractions. They are involved in exercise-associated metabolic changes, tissue regeneration and repair, as well as the maintenance of healthy bodily functions. Myokines have been shown to have beneficial effects on neurodegenerative diseases and muscle wasting conditions. However, there is limited research on the impact of myokines on muscle degeneration, and further studies are needed to fully understand their role.
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What You'll Learn
- Myokines are synthesised and released by skeletal muscle cells in response to physical exercise
- Myokines can have both beneficial and detrimental effects on cardiac structure and function in heart failure
- Myokines can be used to treat neurodegenerative diseases, such as Alzheimer's and Parkinson's
- Myokines are involved in the control of muscle size and may alleviate muscle wasting
- Myokines can influence the function and survival of pancreatic β-cells

Myokines are synthesised and released by skeletal muscle cells in response to physical exercise
Myokines are muscle-derived factors that are synthesised and released by skeletal muscle cells in response to physical exercise. They are defined as peptides or proteins secreted by skeletal muscle cells. Myokines exert autocrine, paracrine, and endocrine functions, influencing the muscle itself and distant organs.
The secretion of myokines is triggered by physical exercise, with aerobic exercise in humans leading to significant structural alterations in the brain. Exercise-induced myokines have been shown to have therapeutic potential in treating muscle wasting and neurodegenerative diseases. For example, apelin, a myokine induced by exercise, is involved in neutralising age-associated muscle wasting. Additionally, myokines such as BDNF and neurotrophic factor-4 promote the survival and function of motoneurons, making them important for the adaptation of skeletal muscle to increased physical workload.
The major physiological function of myokines is to protect and enhance the functionality and exercise capacity of skeletal muscle. They control adaptive processes in skeletal muscle by regulating fuel oxidation, hypertrophy, angiogenesis, inflammatory processes, and the extracellular matrix. Myokines also play a role in immunomodulation, cell signalling, expression, and differentiation. Furthermore, they are involved in metabolic changes associated with exercise and training adaptation.
Myokines are essential components of whole-body homeostasis and may be associated with physical frailty through sarcopenia and sedentary behaviour. They can influence the function and survival of pancreatic β-cells and play a role in bone mineralization, cell-matrix interactions, and collagen binding. Additionally, myokines have been shown to inhibit cancer cell proliferation and suppress tumour growth. Overall, myokines are important mediators of physical fitness and the beneficial effects of exercise on the body.
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Myokines can have both beneficial and detrimental effects on cardiac structure and function in heart failure
Myokines are cytokines or small proteins produced and released by skeletal muscle cells in response to muscular contractions. They have been shown to have both beneficial and detrimental effects on cardiac structure and function in heart failure.
On the one hand, myokines have been linked to improved cardiac function and structure. For example, physical exercise triggers the secretion of myokines, which have been associated with a reduction in age-related oxidative damage, chronic inflammation, and improved mitochondrial function. These effects can positively impact the cardiovascular system, potentially reducing the risk of heart failure. Additionally, myokines such as decorin play a role in muscle growth and can offset muscle wasting by inducing mitochondriogenesis and fostering muscle regeneration. This can help maintain cardiac muscle health and function.
On the other hand, myokines have also been associated with detrimental effects in the context of heart failure. Certain myokines, such as LIF, have been implicated in cancer-associated muscle wasting, which can include cardiac muscle degeneration. Furthermore, conditions such as untreated diabetes, chronic obstructive pulmonary disease, and aging can lead to dysregulated secretion of myokines, contributing to cardiac muscle dysfunction and potentially increasing the risk of heart failure.
The complex interplay of myokines and their effects on cardiac structure and function in heart failure is an active area of research. While some myokines may have detrimental effects, others could be leveraged as therapeutic agents to improve cardiac health and slow the progression of heart failure. Further studies are needed to fully understand the role of myokines in heart failure and to develop myokine-based treatments.
In conclusion, myokines can indeed have both beneficial and detrimental effects on cardiac structure and function in heart failure. While some myokines promote cardiac health and function, others may contribute to cardiac muscle degeneration and dysfunction. A better understanding of myokines and their regulation has the potential to inform the development of personalized physical training and myokine-based interventions for individuals with heart failure.
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Myokines can be used to treat neurodegenerative diseases, such as Alzheimer's and Parkinson's
Myokines are molecules synthesized and secreted by skeletal muscle in response to physical exercise. They are essential components of whole-body homeostasis and can influence the function and survival of other organs in the body.
Neurodegenerative diseases (NDs) are disorders characterized by the progressive degeneration of the nervous system. Examples include Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. Currently, there are no disease-modifying treatments for most NDs. However, studies have shown that exercise has beneficial effects on NDs, and this is believed to be due to the release of myokines during physical activity.
Myokines can influence NDs through various regulatory mechanisms, including cell survival, neurogenesis, neuroinflammation, proteostasis, oxidative stress, and protein modification. For example, Cathepsin B (CTSB), a myokine increased by aerobic exercise, has been found to have neuroprotective effects. Additionally, BDNF and CX3CL1 overexpression induced neurogenesis in Alzheimer's disease model mice and enhanced the therapeutic effects of engrafted stem cells. Apelin, another exercise-induced myokine, is involved in neutralizing age-associated muscle wasting, which is often seen in NDs.
In summary, myokines have the potential to be used as a therapeutic treatment for neurodegenerative diseases, such as Alzheimer's and Parkinson's. Further studies are needed to fully understand the role of each myokine and their interactions, but the current research highlights the importance of the muscle-brain axis and the beneficial effects of exercise-induced myokines on NDs.
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Myokines are involved in the control of muscle size and may alleviate muscle wasting
Myokines are cytokines or small proteins produced and released by skeletal muscle cells in response to muscular contractions. They are involved in the control of muscle size and may alleviate muscle wasting.
Myokines are essential components of whole-body homeostasis. They have autocrine, paracrine, and/or endocrine effects, influencing the function and survival of other organs in the body. For example, myokines can influence the function and survival of pancreatic β-cells, protecting them from the harmful effects of pro-inflammatory cytokines. Myokines are also involved in the regulation of metabolism, angiogenesis, and inflammation.
The secretion of myokines is triggered by physical exercise, which can induce structural alterations in the brain and improve synaptic transmission in the hippocampus. Exercise-induced myokines have been shown to have therapeutic potential for muscle wasting. For instance, decorin, a myokine released during muscular contraction, plays a role in muscle growth by directly binding to and inhibiting myostatin, a known negative regulator of muscle mass. Similarly, interleukin-15 (IL-15), which accumulates in the muscles as a result of regular exercise training, has been found to promote myoblast differentiation and increase muscle mass. In addition, apelin, an exercise-induced myokine, is involved in neutralizing age-associated muscle wasting.
The benefits of exercise in alleviating muscle wasting are also associated with the release of muscle-derived myokines, which create a healthy anti-inflammatory environment and reduce age-related loss of muscle mass and function. Furthermore, exercise-induced myokines have been found to have beneficial effects on neurodegenerative diseases (NDs) by exerting regulatory effects on cell survival, neurogenesis, neuroinflammation, proteostasis, oxidative stress, and protein modification.
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Myokines can influence the function and survival of pancreatic β-cells
Myokines are cytokines or small proteins produced and released by skeletal muscle cells in response to muscular contractions or exercise. They have autocrine, paracrine, and endocrine effects, influencing various organs and biological functions, including the pancreas.
The pancreas, particularly the pancreatic β-cells, is of interest due to its role in insulin production and glucose homeostasis. Myokines have been shown to influence the function and survival of these pancreatic β-cells, which are often targeted for destruction in type 1 diabetes (T1D). Type 2 diabetes (T2D), on the other hand, is associated with impaired metabolism and deficient glucose disposal, and myokines play a role in reducing the risk of insulin resistance in this context.
Several studies have reported the protective effects of specific myokines on pancreatic β-cells. Angiogenin and osteoprotegerin, for example, are type II muscle-specific myokines that safeguard β-cells from the harmful effects of pro-inflammatory cytokines. This protection is particularly relevant in the context of diabetes, where these cytokines can induce β-cell dysfunction and contribute to the disease's progression. Additionally, the myokine follistatin, when administered chronically, has been shown to prevent apoptosis and promote the proliferation of rat β-cells.
The interplay between myokines and pancreatic β-cells is complex and influenced by factors such as muscle type and metabolic status. For instance, the impact of myokines on β-cells differs between Type I and Type II primary myotubes, with distinct mRNA and myokine signatures influencing their sensitivity to TNF-alpha-induced insulin resistance. Furthermore, physical activity and exercise influence myokine production and secretion, with some myokines, like IL-6, exhibiting increased levels proportional to the length of exercise and the amount of muscle mass engaged. This suggests that exercise-induced myokines may play a therapeutic role in mitigating β-cell dysfunction and improving glucose homeostasis.
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Frequently asked questions
Myokines are cytokines or small proteins produced and released by skeletal muscle cells in response to muscular contractions or physical exercise.
No, myokines do not promote muscle degeneration. On the contrary, they help reduce age-related loss of muscle mass and function. Myokines are involved in the control of muscle size and may be important to be restored to normal levels to alleviate muscle wasting in various conditions.
Examples of myokines include decorin, myostatin, irisin, interleukin-15 (IL-15), and apelin.
Myokines have multiple benefits, including regulating metabolism, angiogenesis, and inflammation. They are also involved in tissue regeneration, repair, and immunomodulation. Additionally, myokines have been shown to have positive effects on neurodegenerative diseases and neuronal health.
Physical exercise triggers the secretion of myokines by muscle cells. Different types of exercises, such as aerobic training and strength training, can lead to the release of different clusters of myokines, providing varying benefits.












