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Muscle breakdown, also known as muscle atrophy, can occur due to various factors, including disuse, nerve damage, malnutrition, age, genetics, and underlying medical conditions. Disuse atrophy happens when muscles are not contracted or used regularly, leading to a decrease in size and strength. On the other hand, neurogenic atrophy is caused by nerve problems or diseases that affect the stimulation of muscle activity. Additionally, certain conditions, such as rhabdomyolysis, can lead to rapid muscle breakdown, often due to high-intensity exercise, crush injuries, or medical conditions. Rhabdomyolysis is a serious condition that can result in muscle pain and weakness and potentially life-threatening complications like renal failure if left untreated. Understanding the causes and treatment options for muscle breakdown is crucial for maintaining overall health and well-being.
| Characteristics | Values |
|---|---|
| Muscle breakdown due to | Muscle atrophy, rhabdomyolysis |
| Muscle atrophy caused by | Disuse, nerve problems or diseases |
| Disuse atrophy caused by | Sedentary lifestyle, malnutrition, lack of exercise, desk job, bed rest, genetic disorders, stroke, age-related atrophy |
| Neurogenic atrophy caused by | Injury, nerve diseases |
| Rhabdomyolysis caused by | Muscle injury, extreme muscle strain, medications, substance use, metabolic disorders, muscle disease, infections, electrical injury, heat stroke, immobilization, lack of blood flow, snake bites, intense or prolonged exercise, high temperatures |
| Symptoms of rhabdomyolysis | Muscle pain, muscle weakness, muscle stiffness, change in urine colour, vomiting, confusion, irregular heartbeat, swelling of muscles, kidney failure |
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What You'll Learn
Muscle disuse
The process of muscle atrophy due to disuse can begin within two to three weeks of muscle inactivity. The extent of muscle atrophy depends on various factors, including age, fitness level, and the underlying cause of the atrophy. It is important to note that muscle disuse atrophy can be reversed through exercise and a healthy diet. Resistance exercises, in particular, have been shown to promote recovery and regrowth of muscle mass following disuse atrophy.
The molecular mechanisms underlying muscle disuse atrophy involve declines in muscle protein synthesis and a potential increase in muscle protein breakdown. This results in a significant loss of muscle mass and force production. Additionally, disuse atrophy has been associated with increased inflammatory cytokines and glucocorticoids, as well as malnutrition, all of which contribute to muscle wasting.
While there are currently no effective therapies or pharmaceutical interventions to prevent or treat disuse-induced muscle atrophy, early rehabilitation and nutritional strategies may play a crucial role in mitigating muscle loss. For example, manipulating protein intake through dietary protein or amino acid supplementation has been shown to diminish muscle atrophy and preserve muscle function in experimental models of disuse. Furthermore, neuromuscular electrical stimulation and stem cell therapy have been proposed as potential therapeutic approaches to combat muscle disuse atrophy in humans.
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Neurogenic conditions
Muscle atrophy, or muscle wasting, can be caused by neurogenic conditions. Neurogenic atrophy 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 can no longer trigger the muscle contractions that are needed to stimulate muscle activity. This results in muscles weakening and wasting away.
Neurogenic atrophy is the most severe type of muscle atrophy. It can be caused by an injury to, or disease of, a nerve that connects to the muscle. Examples of diseases affecting the nerves that control muscles include amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), carpal tunnel syndrome, Guillain-Barre syndrome, and spinal muscular atrophy.
Neuromuscular disorders are conditions that affect the nerve, muscle, or neuromuscular junction (where the nerve communicates with the muscle). Nerve cells (neurons) send and receive electrical messages to and from the body to help control voluntary muscles. When the neurons become unhealthy or die, communication between the nervous system and muscles breaks down, resulting in muscle atrophy. Many neuromuscular disorders have symptoms that begin in infancy, while others may appear in childhood or even adulthood. Symptoms depend on the type of neuromuscular disorder and the areas of the body that are affected.
Treatment for neurogenic atrophy depends on the degree of muscle loss and any underlying medical conditions. Treating the underlying condition may help slow the progression of muscle loss. As some causes of neurogenic atrophy are incurable, some treatments may aim to reduce symptoms. Physical therapy involves performing specific stretches and exercises to prevent immobility. Surgery may also be an option in some cases.
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Rhabdomyolysis
The symptoms of rhabdomyolysis include muscle pain, muscle weakness, muscle stiffness, vomiting, confusion, and a change in urine colour. This change in urine colour is due to the presence of myoglobin, a component of broken-down muscle, in the urine. Myoglobinuria, or the presence of myoglobin in the urine, occurs when the level in plasma exceeds 0.5-1.5 mg/dL. Once plasma levels reach 100 mg/dL, the urine becomes visibly discoloured and corresponds with the destruction of about 200 grams of muscle.
Diagnosis of rhabdomyolysis involves a physical examination, asking about recent physical activity, prescription medications, and substance use, urine tests to check myoglobin levels, and blood tests to measure creatine kinase (CK) levels. Treatment for rhabdomyolysis focuses on managing the airway, breathing, and circulation, as well as preserving renal function through vigorous rehydration. In some cases, surgery may be required to ease tension or pressure and prevent muscle death or nerve damage.
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Genetic disorders
Muscular dystrophy (MD) is a group of more than 30 inherited genetic conditions that cause progressive weakness and degeneration of skeletal muscles. The condition is caused by mutations in the genes responsible for the structure and functioning of a person's muscles. These mutations are often inherited from a person's parents. MD grows worse over time as muscles progressively degenerate and weaken, leading to an increasing level of disability. Many people with MD eventually lose the ability to walk and may develop swallowing disorders. Some types of MD also affect the heart, lungs, gastrointestinal system, endocrine glands, spine, eyes, brain, or other organs.
There are several types of MD, including Duchenne muscular dystrophy, which is the most common form, Becker muscular dystrophy, myotonic dystrophy, facioscapulohumeral dystrophy, Emery-Dreifuss dystrophy, limb-girdle dystrophy, oculopharyngeal muscular dystrophy, and congenital dystrophies. Duchenne muscular dystrophy is the most severe form, while Becker muscular dystrophy has a later onset and causes milder symptoms. Myotonic dystrophy is characterised by the inability of muscles to relax at will. Facioscapulohumeral dystrophy causes muscle weakness that often starts in the face, shoulders, and upper arms. Emery-Dreifuss dystrophy causes stiffness in certain joints, and muscle wasting and weakening in the shoulders, upper arms, and calves. Congenital muscular dystrophy refers to a group of muscular dystrophies that are either present at birth or become evident before the age of 2. It is characterised by diminished muscle tone and delayed motor function and muscle control.
MD is typically diagnosed through genetic testing, muscle biopsies, blood and urine tests, exercise tests, diagnostic imaging, and neurological and muscle exams. While there is currently no cure for MD, treatments such as medicines, steroids, physical therapy, and occupational therapy can help manage symptoms and slow the progression of the disease.
In addition to MD, other genetic muscle disorders include distal arthrogryposes (DAs), which are inherited disorders characterised by contractures in two or more distal limb joints without neurological issues. Up to 40% of patients with DA have mutations in genes that encode sarcomeric proteins, including myosin heavy chains, troponins, tropomyosin, and myosin binding protein-C (MYBPC).
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Age and lifestyle factors
Several factors contribute to age-related muscle breakdown. One key factor is the reduction in nerve cells responsible for transmitting signals from the brain to the muscles, initiating movement. This leads to a decrease in muscle function and performance. Additionally, ageing is associated with lower levels of certain hormones, including growth hormone, testosterone, and insulin-like growth factor. These hormonal changes can further accelerate muscle loss.
Lifestyle choices also influence muscle breakdown. Physical inactivity or a sedentary lifestyle is a significant risk factor for muscle loss and can severely reduce muscle mass and strength, even in younger individuals. In addition, dietary choices play a role, particularly a reduction in dietary protein intake. Older adults may experience anabolic resistance, which impairs their body's ability to break down and synthesise protein efficiently. This can lead to a decline in muscle mass and strength.
Chronic inflammation is another factor that contributes to muscle breakdown. Hospitalisations and illnesses can accelerate muscle loss, and the associated increase in pro-inflammatory agents and cortisol can exacerbate the condition. Furthermore, specific health conditions, such as chronic obstructive pulmonary disease (COPD), kidney disease, diabetes, cancer, and HIV, can further increase the risk of muscle breakdown.
The effects of age and lifestyle factors on muscle breakdown can be mitigated to some extent. Strength training and resistance exercises have been shown to improve muscle mass, strength, and overall health. Additionally, a well-balanced diet that includes sufficient high-quality protein can help maximise muscle growth and improve recovery. While ageing is a natural process, adopting healthy lifestyle habits can help slow muscle breakdown and improve overall physical function.
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Frequently asked questions
Muscles can break down due to several reasons, including lack of physical activity, nerve problems, nerve diseases, malnutrition, age, genetics, or certain medical conditions.
Muscle atrophy is the wasting or thinning of muscle mass. It occurs when muscles are not used enough or due to neurogenic conditions. It can be reversed with exercise and a healthy diet.
Rhabdomyolysis is a rare but serious condition where damaged skeletal muscles break down rapidly due to high-intensity exercise, muscle injury, medications, substance use, or other reasons. It can lead to life-threatening complications such as renal (kidney) failure if left untreated.
Common symptoms of rhabdomyolysis include muscle pain, weakness, stiffness, vomiting, confusion, and a change in urine colour (tea-coloured urine). However, some people with rhabdomyolysis may not experience any muscle-related symptoms.
Rhabdomyolysis is diagnosed through physical examination, blood tests for creatine kinase (CK), and urine tests for myoglobin. Treatment involves managing airway, breathing, and circulation, as well as preserving renal function to prevent kidney damage.
