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Chemotherapy is a widely used treatment for cancer, but it can also have some debilitating side effects, including muscle atrophy or wasting. Muscle atrophy is a severe condition that impairs the quality of life and worsens survival outcomes in cancer patients. While the amount of muscle mass loss varies across cancer types, between 5% and 89% of cancer patients experience low skeletal muscle mass. This article will explore the link between chemotherapy and muscle atrophy, the underlying mechanisms, and potential interventions to mitigate this adverse effect.
| Characteristics | Values |
|---|---|
| Cancer patients undergoing chemotherapy | Often experience debilitating side effects |
| Skeletal muscle mass loss | An emerging concern in oncology |
| Muscle wasting | A primary marker of poor prognosis for cancer patients |
| Chemotherapy-induced muscle wasting | Addressed through resistance and endurance exercise |
| Chemotherapy-induced weakness and fatigue | Caused by oxidative stress |
| Chemotherapy drugs | Cause toxicity and dysfunction in nontargeted tissues such as striated muscle |
| Cancer patients with low skeletal muscle mass | Have a higher risk of mortality, cancer recurrence, and reduced quality of life |
| Chemotherapy agents | Taken up by skeletal muscle cells, inducing proteolytic and oxidative damage, mitochondrial dysfunction, cellular energy depletion, and apoptotic cell death |
| Chemotherapy-induced muscle atrophy | Preceded by loss of muscle function |
| Loss of muscle function | Associated with loss of motor unit connectivity |
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What You'll Learn
Chemotherapy can cause muscle atrophy in animals
In addition, a canine model of isolated limb perfusion with doxorubicin observed a significant increase in doxorubicin concentrations in the quadriceps, along with muscle atrophy and weakness. Doxorubicin-treated animals and patients also exhibit a stress response, characterized by an increase in serum levels of inflammatory cytokines, especially TNF (tumor necrosis factor alpha). This increase in inflammatory cytokines contributes to systemic inflammation, which has been identified as a driver of skeletal muscle atrophy in cancer cachexia.
Furthermore, treadmill exercise training has been shown to attenuate the initiation and progression of cancer cachexia in mice, and both endurance and resistance exercises can modulate the inflammatory response in tumor-bearing rats. However, it is important to carefully consider factors limiting exercise capacity, such as chronic fatigue, anemia, and cardiac dysfunction, when implementing exercise programs for cancer patients.
While the mechanism by which cytotoxic chemotherapy contributes to cancer cachexia is not yet fully understood, studies have shown that chemotherapy administration produces a rapid inflammatory response, which drives the activation of the hypothalamic-pituitary-adrenal axis, increasing the circulating level of corticosterone. Additionally, chemotherapy may induce fatigue and a severe decrease in muscle strength, especially in striated muscles.
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Chemotherapy and cancer cause muscle weakness
Cancer patients undergoing chemotherapy often experience debilitating side effects, including muscle weakness. This is caused by a loss of motor unit connectivity and muscle atrophy.
Muscle weakness and atrophy can be observed in animals bearing cancer or receiving chemotherapy. For example, mice bearing C26, MC38, and HCT116 CRC tumors had reduced gastrocnemius muscle weights compared to control animals. Similarly, mice treated with chemotherapeutics like folfiri and cisplatin displayed significantly reduced gastrocnemius weights and muscle contractility.
In humans, cancer and chemotherapy-induced muscle weakness are associated with a loss of motor unit connectivity and muscle wasting. Motor units are functional units composed of a motor neuron and all the myofibers it innervates. A loss of these motor units has been linked to muscle weakness and atrophy in aging rodents, suggesting a potential mechanism for the muscle weakness observed in cancer patients.
Several chemotherapeutic agents can contribute to muscle weakness by inducing a state of oxidative stress. This occurs by decreasing antioxidant levels, impairing the cell's ability to defend against elevated oxidants. Elevated oxidant levels in skeletal muscle are known to cause muscle weakness and fatigue. Additionally, chemotherapeutic drugs can be taken up by skeletal muscle cells, leading to proteolytic and oxidative damage, mitochondrial dysfunction, cellular energy depletion, and apoptotic cell death.
The prevalence of low skeletal muscle mass in cancer patients, known as sarcopenia, is higher than in healthy individuals. This can be due to various factors, including poor nutrition, aging, and specific chemotherapeutic drugs. Sarcopenia is associated with an increased risk of mortality, cancer recurrence, and a reduced quality of life. Therefore, it is crucial for oncologists to recognize and address muscle weakness and atrophy during cancer treatment to improve patient outcomes and quality of life.
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Chemotherapy-induced muscle wasting
One of the key mechanisms proposed for chemotherapy-induced muscle wasting is the loss of motor unit connectivity. Motor units are functional units composed of a motor neuron and all the muscle fibres it innervates. Research has shown that a reduction in the number of these motor units is associated with muscle wasting and weakness caused by chemotherapy. This loss of motor unit connectivity is also linked to alterations in neuromuscular junctions (NMJs) and abnormal presynaptic morphology, indicating possible changes in innervation patterns.
In addition to the loss of motor units, chemotherapy drugs can also induce muscle atrophy through oxidative stress. Oxidative stress occurs when there is an imbalance between the production of free radicals and the body's ability to neutralise their harmful effects. Chemotherapeutic agents can either directly or indirectly induce oxidative stress, leading to toxicity and dysfunction in non-target tissues such as skeletal muscle. This results in muscle weakness and fatigue, further impairing the patient's quality of life.
Certain chemotherapeutic drugs, such as cisplatin, have been specifically implicated in muscle wasting. Studies have shown that cisplatin can regulate muscle atrophy and induce body weight loss and muscle wasting, even in healthy individuals. However, the role of protein ubiquitination and proteasome-mediated degradation in this process is still controversial and requires further investigation.
The prevalence of low skeletal muscle mass in cancer patients, often referred to as sarcopenia, is also influenced by factors such as poor nutrition, aging, and the type of cancer and chemotherapy drugs used. For example, patients with gastric cancer had a reported incidence rate of low skeletal muscle mass before chemotherapy of 47%, which may be attributed to the use of platinum-based chemotherapeutic drugs.
Overall, chemotherapy-induced muscle wasting is a complex and debilitating side effect that requires further research to develop effective treatments. While some studies suggest that antioxidants could provide relief from muscle weakness, currently, there are no approved treatments for cachexia, or muscle wasting, induced by cancer and chemotherapy.
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Chemotherapy's effect on skeletal muscle mass
Chemotherapy has been found to cause skeletal muscle atrophy and loss of skeletal muscle mass. This loss of muscle function may precede muscle wasting, and is associated with a loss of motor unit connectivity. Motor unit number estimation (MUNE) has shown that loss of motor unit number precedes loss of muscle strength and is correlated with muscle weakness and atrophy.
Studies have shown that chemotherapeutic agents are taken up by skeletal muscle cells, causing proteolytic and oxidative damage, mitochondrial dysfunction, cellular energy depletion, and apoptotic cell death. In addition, oxidative stress, mediated by cancer or chemotherapeutic agents, is an underlying mechanism of drug-induced toxicity. Striated muscle, a nontargeted tissue, is severely affected by oxidative stress during chemotherapy, leading to toxicity and dysfunction.
In mice bearing cancers or receiving chemotherapy, muscle weights were significantly reduced compared to control animals. Similarly, in vivo force assessment revealed marked reductions in skeletal muscle force with respect to the controls. In cancer patients undergoing treatment, circulating markers of oxidative stress are elevated, and these markers are a nonspecific systemic index of oxidative stress in the body.
The loss of skeletal muscle mass during chemotherapy is a poor prognostic factor in patients with advanced gastric cancer. It is associated with a higher risk of mortality, cancer recurrence, and reduced quality of life. The amount of skeletal muscle mass loss varies widely across cancer types, and between males and females, with muscle loss in males about 1.6 times higher than in females.
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Chemotherapy's impact on muscle function
Chemotherapy has been found to negatively impact muscle function in cancer patients. The loss of muscle function is a result of muscle wasting or atrophy, which is associated with a poor prognosis. Chemotherapy-induced muscle atrophy is a debilitating side effect that can drastically impair the quality of life of cancer patients and worsen survival outcomes.
Several studies have investigated the impact of chemotherapy on skeletal muscle mass and function. One study found that skeletal muscle mass decreased significantly during chemotherapy in advanced gastric cancer patients, with a median pre-chemotherapy to post-chemotherapy skeletal muscle index (SMI) decrease of -4.5 cm2/m2 (-11.3%). Another study reported that cancer patients with low skeletal muscle mass during treatment had a higher risk of mortality, cancer recurrence, and reduced quality of life.
The mechanism behind chemotherapy-induced muscle atrophy involves oxidative stress, which can lead to toxicity and dysfunction in nontargeted tissues such as striated muscle. Chemotherapeutic agents can also be taken up by skeletal muscle cells, inducing proteolytic and oxidative damage, mitochondrial dysfunction, cellular energy depletion, and apoptotic cell death. Additionally, the loss of motor unit connectivity has been implicated in muscle weakness and atrophy. Motor units are functional units composed of a motor neuron and all the myofibers it innervates. Loss of motor unit number has been shown to precede loss of muscle strength and is correlated with muscle atrophy.
Certain chemotherapeutic agents, such as cisplatin and doxorubicin, have been specifically linked to muscle atrophy and weakness. In animal models, cisplatin was found to regulate muscle atrophy and induce body weight loss and muscle wasting. Doxorubicin has been shown to have negative effects on skeletal muscle function, causing skeletal muscle toxicity and catabolic responses leading to muscle loss.
To mitigate the impact of chemotherapy on muscle function, resistance and endurance exercises have been suggested as an integral part of supportive care for cancer patients undergoing chemotherapy. Additionally, omega-3 fatty acids have been shown to reduce muscle loss associated with cisplatin chemotherapy. Further research into antioxidants and other interventions may provide relief from muscle weakness and improve the quality of life for cancer patients.
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Frequently asked questions
Yes, chemotherapy has been shown to cause muscle atrophy in mice bearing C26, MC38 and HCT116 CRC tumors. Chemotherapy drugs can cause muscle atrophy by disrupting striated muscle function through oxidative stress.
Muscle wasting is a primary marker of poor prognosis for cancer patients and negatively affects their quality of life. Patients with low skeletal muscle mass during cancer treatment have been reported to have a higher risk of mortality, cancer recurrence, and reduced quality of life.
There are currently no approved treatments for cachexia (muscle wasting and weakness caused by cancer and its treatments). However, resistance and endurance exercises are recommended as an integral part of supportive care for cancer patients undergoing chemotherapy. Additionally, omega 3 fatty acids have been shown to reduce the muscle loss associated with cisplatin chemotherapy.
