Logan Steele
Muscle atrophy is the wasting or loss of muscle tissue and strength. It can be caused by a variety of factors, including immobility, aging, malnutrition, medications, injuries, or diseases that impact the musculoskeletal or nervous system. Physiologic atrophy, the most common type, is caused by a lack of physical activity, which leads to the body breaking down muscle tissue. Pathologic atrophy is associated with aging, malnutrition, and diseases such as Cushing's disease. Neurogenic atrophy is caused by nerve damage that prevents muscles from contracting. Treatment for muscle atrophy includes physical therapy, functional electrical stimulation, and in some cases, surgery.
| Characteristics | Values |
|---|---|
| Definition | Wasting (thinning) or loss of muscle tissue |
| Loss of muscle mass | 20 to 40 percent |
| Types | Physiologic, pathologic, neurogenic |
| Physiologic atrophy causes | Sedentary lifestyle, malnourishment, inadequate exercise, desk jobs, immobility, old age, etc. |
| Pathologic atrophy causes | Aging, starvation, diseases (Cushing's disease, etc.) |
| Neurogenic atrophy causes | Nerve problems, nerve diseases, spinal cord injury, stroke, etc. |
| Symptoms | Reduced muscle mass, muscle weakness, trouble balancing, difficulty swallowing or speaking, etc. |
| Treatments | Physical therapy, functional electrical stimulation, surgery, targeted mitochondrial therapy, etc. |
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What You'll Learn
Physiologic atrophy is caused by not using muscles enough
Muscle atrophy is the wasting or loss of muscle tissue and can be caused by immobility, aging, malnutrition, medications, or a wide range of injuries or diseases that impact the musculoskeletal or nervous system. It can severely limit a person's mobility, which could lead to muscle disuse and atrophy. Physiologic atrophy, or disuse atrophy, is caused by not using the muscles enough. This type of atrophy can often be reversed with exercise and better nutrition.
Disuse atrophy may affect you if you lead a sedentary lifestyle, are malnourished, don't get enough exercise, have a desk job, are on bed rest, or have a genetic disorder such as muscular dystrophy or Charcot-Marie-Tooth disease. When your muscles don't contract, your body starts breaking them down, causing them to decrease in size and strength. The process of physiologic atrophy can start within two to three weeks of not using your muscles.
The consequences of muscle atrophy can include overall weakness, poor balance, and even frailty. Treatment for muscle atrophy depends on the type and underlying cause but often includes exercise and adequate nutrition. Physical therapy, functional electrical stimulation, and surgery are also treatment options.
To prevent and treat physiologic atrophy, it is important to engage in physical activity, which provides a significant anabolic muscle stimulus. Resistance exercise has been shown to be beneficial in reducing muscle atrophy in older adults. Adequate calories, protein, and nutritional supplements are also crucial to preventing muscle atrophy.
While muscle loss is a natural part of aging, it can occur faster after an injury, illness, or any prolonged period of inactivity, leading to muscle atrophy. It is possible to rebuild lost muscle through a comprehensive program that includes physical therapy, strength training, cardio, flexibility exercises, and a nutrition plan that includes more protein and calories.
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Pathologic atrophy is seen with ageing, starvation, and diseases
Muscle atrophy is the wasting or loss of muscle tissue. People may lose 20 to 40 percent of their muscle and their strength as they age. Pathologic atrophy is caused by ageing, starvation, and disease.
Ageing leads to a loss of lean muscle mass, or atrophy. This is known as sarcopenia. Sarcopenia is likely caused by multiple interacting factors, including changes in hormones, immobility, age-related muscle changes, nutrition, and neurodegenerative changes. The hallmark sign of sarcopenia is the loss of lean muscle mass, but it may be difficult to detect due to obesity, changes in fat mass, or edema. Sarcopenia may also have no symptoms until it is severe. In the elderly, immobility or bed rest can lead to decreased biological reserve and increased vulnerability to stressors, known as the "frailty syndrome". The weakness that accompanies muscle atrophy also leads to a higher risk of falls, fractures, and physical disability.
Starvation and malnutrition can also cause muscle atrophy. Studies have shown that starvation leads to a loss of muscle mass, changes in muscle contractility, and atrophy of muscle fibres. In one study, men undergoing a semi-starvation diet lost on average 16 kg within six months, with muscle mass loss estimated at 41% of the control value. Similarly, anorexic patients also experience muscle atrophy, with work capacity declining by about 50% in females and 70% in males.
Diseases that affect the nerves that connect to muscles can also cause muscle atrophy, known as neurogenic atrophy. Examples of such diseases include Amyotrophic lateral sclerosis (ALS), Guillain-Barre syndrome, carpal tunnel syndrome, spinal cord injury, and multiple sclerosis. In neurogenic atrophy, the nerves are damaged and cannot trigger the muscle contractions needed to stimulate muscle activity.
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Neurogenic atrophy occurs due to nerve problems or diseases
Muscle atrophy is the wasting or thinning of muscle mass. It can be caused by muscle disuse, age, nutrition issues, and genetics. The most obvious sign of muscle atrophy is reduced muscle mass. Other signs and symptoms of muscle atrophy may include:
- One arm or one leg is smaller than the other.
- Weakness in one arm or one leg.
- Numbness or tingling in the arms and legs.
- Trouble walking or balancing.
- Difficulty swallowing or speaking.
- Facial weakness.
- Gradual memory loss.
Neurogenic atrophy is a type of muscle atrophy that occurs due to nerve problems or diseases. It is caused by an injury or disease affecting nerves that connect to the muscles. When these nerves are damaged, they cannot trigger the muscle contractions needed to stimulate muscle activity. As a result, the muscles stop contracting, and the body starts breaking them down, leading to a decrease in muscle size and strength. Neurogenic atrophy is considered the most severe type of muscle atrophy and tends to occur more suddenly than other types.
Diseases and conditions that can affect these nerves and lead to neurogenic atrophy include:
- Amyotrophic lateral sclerosis (ALS)
- Guillain-Barre syndrome
- Carpal tunnel syndrome
- Spinal cord injury
- Multiple sclerosis
- Mitochondrial dysfunction
- Spinal muscular atrophy
- Primary lateral sclerosis
Treatment for neurogenic atrophy aims to address the underlying nerve problems and prevent further muscle loss. A special type of physical therapy called electrical stimulation or functional electrical stimulation (FES) is often used. This involves placing electrodes on the skin over the affected muscles to send electrical impulses that stimulate muscle contractions. Ultrasound therapy and, in some cases, surgery to correct contractures may also be recommended.
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Sarcopenia is age-related muscle atrophy
Sarcopenia, a muscle-wasting syndrome, is characterised by a degenerative loss of skeletal muscle mass, quality, and strength during the ageing process. It is a natural part of getting older, but muscle loss can be accelerated by injury, illness, or a prolonged period of inactivity. The hallmark sign of sarcopenia is the loss of lean muscle mass, which may be difficult to detect due to obesity, changes in fat mass, or oedema. The weakness that accompanies muscle atrophy can lead to a higher risk of falls, fractures, physical disability, and a need for institutional care.
The major cause of sarcopenia is ageing, but other factors such as inactivity, a poor diet, and chronic disease can contribute to the development of the condition. Studies suggest that staying active as you age can significantly reduce the risk of sarcopenia. Spending a lot of time inactive may contribute to muscle loss even if you exercise during other parts of the day. A poor-quality diet also appears to be a contributing factor, with low protein intake suspected to be a cause. As people age, the body has increasing difficulty turning protein into energy, and older adults may require higher amounts of protein to prevent muscle atrophy.
The risk of sarcopenia increases with age, with loss of muscle mass and strength typically occurring from the age of 30 onwards. The loss can become more noticeable from the age of 60, with studies suggesting that between 11% and 50% of people aged over 80 have sarcopenia. Sarcopenia can be diagnosed when a patient has muscle mass that is at least two standard deviations below the relevant population mean and has a slow walking speed. An early indicator of the onset of sarcopenia can be a significant loss of muscle mass in the anterior thigh and abdominal muscles.
There are several proposed causes of sarcopenia, including changes in hormones, immobility, age-related muscle changes, nutrition, and neurodegenerative changes. One of the molecular mechanisms believed to cause sarcopenia is the loss of proteostasis, which affects muscle tissue regulation. Another is mitochondrial dysfunction, which can lead to skeletal muscle atrophy. An accumulation of mitochondrial DNA mutations has been observed in sarcopenic muscle, with a deficiency of BNIP3 leading to muscle inflammation and atrophy.
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Mitochondrial dysfunction affects muscle tissue regulation
Muscle atrophy, or muscle wasting, is the thinning or loss of muscle tissue. It can be caused by various factors, including age, nutrition issues, genetics, injury, illness, or inactivity. Mitochondria play a crucial role in maintaining muscle health by generating energy for cells. Mitochondrial dysfunction occurs when mitochondria do not function properly due to another disease or condition. This dysfunction can directly affect skeletal muscle regulation and lead to muscle atrophy.
Mitochondria are the key organelles that regulate the metabolic state of skeletal muscle. They produce most of the chemical energy that powers cells, making them essential for maintaining cellular homeostasis and skeletal muscle health. When mitochondria are damaged or dysfunctional, it can trigger catabolic signaling pathways that promote the expression of muscle atrophy genes. This results in skeletal muscle atrophy, which is characterized by a shortening of muscle fibers and a loss of overall muscle mass.
The molecular mechanism of mitochondrial dysfunction leading to skeletal muscle atrophy is complex and involves various signaling pathways. These pathways include AMPK-SIRT1-PGC-1α, IGF-1-PI3K-Akt-mTOR, FoxOs, JAK-STAT3, TGF-β-Smad2/3, and NF-κB. Understanding these regulatory pathways is crucial for developing targeted treatments for skeletal muscle atrophy.
Targeted mitochondrial therapy has emerged as a promising strategy to directly regulate mitochondria and improve treatment outcomes in skeletal muscle atrophy. This approach includes mitochondria-targeted drug therapy, exercise and diet therapy, and mitochondria-targeted gene therapy. By improving mitochondrial function, we can delay muscle atrophy and enhance treatment efficiency.
Additionally, mitochondrial dysfunction can affect muscle tissue regulation by impacting the immune system and inflammation. HSP60, a mitochondrial chaperone protein, interacts with the immune system and plays a role in skeletal muscle adaptation during exercise and tissue regeneration. Overexpression of HSP60 can improve muscle performance and reduce cachexia, highlighting its potential therapeutic benefits.
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Frequently asked questions
Muscle atrophy is the wasting (thinning) or loss of muscle tissue and muscle strength.
Muscle atrophy can be caused by a lack of physical activity, ageing, malnutrition, medications, or a wide range of injuries or diseases that impact the musculoskeletal or nervous system.
Treatment for muscle atrophy depends on the type and underlying cause. Physiologic atrophy can be treated with regular exercise and better nutrition. Neurogenic atrophy, caused by physical damage to nerves, is harder to treat and may require a special kind of physical therapy called electrical stimulation.
