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Chemotherapy is a treatment option for cancer that involves the use of medications to target and kill cancer cells. While chemotherapy can be effective in treating cancer, it is also associated with a range of side effects, one of which is muscle weakness. Muscle weakness can be a debilitating complication of chemotherapy, affecting patients' quality of life and increasing the risk of falls and fractures. This issue has sparked investigations into the underlying mechanisms and potential treatments.
| Characteristics | Values |
|---|---|
| Cancer type | Colorectal cancer, breast cancer, lymphoma, leukemia |
| Chemotherapy type | Doxorubicin, folfiri, cisplatin, paclitaxel, interferon, aldesleukin, filgrastim |
| Side effects | Muscle weakness, fatigue, muscle wasting, weight loss, depletion of fat, increased mortality, muscle aches, joint pain, anaemia |
| Treatments | NSAIDs, Tylenol, steroids, erythropoietic agents, physical therapy, occupational therapy, blood transfusion, relaxation techniques |
| Research | Dr David Waning's research at Penn State College of Medicine focuses on the study of cancer and chemotherapy-induced muscle weakness and cachexia |
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What You'll Learn
Doxorubicin-based chemotherapy and muscle weakness
Chemotherapy is often associated with muscle weakness and fatigue. This is due to the oxidative stress that chemotherapeutic agents can induce, which results in elevated levels of oxidants in the skeletal muscle.
Doxorubicin is a chemotherapeutic agent prescribed for a variety of tumors. It is known to cause muscle weakness and fatigue, with patients experiencing debilitating fatigue and a decline in functional ability. This is evident even years after doxorubicin exposure.
Doxorubicin-induced muscle weakness has been observed in both human and animal studies. In a study by Pfieffer and associates, a canine model of isolated limb perfusion with doxorubicin showed increased muscle atrophy and weakness. Similarly, rodent models of systemic doxorubicin treatment have consistently revealed negative effects on skeletal muscle function, including muscle loss and edema.
Doxorubicin is also associated with diaphragm weakness, as observed in murine models. This weakness is caused by increased DCFH oxidation and elevated levels of nitrotyrosine and 4-hydroxynonenal (HNE) residues on myofibrillar proteins.
Supplementing the diet with creatine has been suggested as a potential intervention for managing doxorubicin-induced skeletal muscle weakness. Studies have shown that creatine pretreatment can mitigate skeletal muscle dysfunction, extending the time to fatigue and decreasing force production at baseline.
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Chemotherapy-induced peripheral neuropathy
CIPN is caused by damage to peripheral sensory, motor, and autonomic neurons due to the use of certain substance groups as a part of chemotherapy. These groups include platinum-based antineoplastic agents (such as oxaliplatin, cisplatin, and carboplatin), vinca alkaloids, epothilones (ixabepilone), taxanes, proteasome inhibitors (bortezomib), and immunomodulatory drugs (thalidomide).
Platinum-based drugs, in particular, induce CIPN by activating glial cells, which then activate and attract immune cells. This process leads to the release and elevation of pro-inflammatory cytokines, resulting in nociceptor sensitization and peripheral neuron hyperexcitability. Additionally, platinum-based drugs increase the production of reactive oxygen species (ROS), causing enzyme, protein, and lipid damage within neurons and disrupting calcium homeostasis. This, in turn, induces apoptotic changes in peripheral nerves and DRG cells. These drugs also alter the activity of Na+, K+, and TRP ion channels, further contributing to peripheral neuron hyperexcitability.
The impact of CIPN can be severe, affecting both the hands and feet simultaneously and causing predominant pain. It can significantly reduce the quality of life for cancer patients and survivors, as well as pose challenges for their healthcare providers. Unfortunately, there is currently no single effective method of preventing or treating CIPN, and the possibilities for managing this syndrome are very limited. However, some therapies, such as cold therapy (cryotherapy) and compression therapy, have been explored to prevent or limit the effects of CIPN, but more research is needed to prove their effectiveness.
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Chemotherapy and muscle wasting
Muscle wasting and weakness are common side effects of chemotherapy. This condition is called cachexia, which is characterised by weight loss, depletion of fat and muscle, increased fatigue, reduced quality of life, and high mortality. Chemotherapy-induced cachexia is associated with mitochondrial depletion and the activation of certain enzymes.
Cachexia drastically impairs the quality of life of cancer patients and worsens survival outcomes. Currently, there are no approved treatments for cachexia, although researchers are investigating its causes. Studies have been conducted on mice bearing cancers and those administered with chemotherapeutics to understand the loss of motor unit function and muscle wasting.
Chemotherapy can cause muscle weakness by decreasing antioxidant levels, crippling the cell's defences against elevated oxidants. This results in oxidative stress, which is known to cause muscle weakness and accelerate fatigue. Doxorubicin, a chemotherapeutic agent, decreases GSH content, a vital antioxidant in striated muscles. This can lead to cardiac contractile impairment and left ventricular dysfunction.
In addition to doxorubicin, other chemotherapeutic agents such as paclitaxel, interferon, aldesleukin, and filgrastim have been associated with muscle aches and joint pain. These side effects usually resolve when the medication is discontinued. Patients undergoing chemotherapy may also experience muscle weakness due to anemia, a condition where the body does not produce enough red blood cells, resulting in decreased circulating oxygen.
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Chemotherapy's impact on bone and muscle
Chemotherapy can have a significant impact on bone and muscle health, leading to various issues, including muscle weakness, bone loss, and fatigue.
Muscle Weakness
Chemotherapy-induced muscle weakness is a common side effect of cancer treatment. Doxorubicin-based chemotherapy, for instance, has been associated with lower extremity muscle weakness and a decline in functional ability. This weakness can persist for months or years after treatment, causing problems such as fatigue and falls, which can lead to fractures and increased mortality. Existing studies in both rodents and humans show the negative effects of doxorubicin on skeletal muscle function, including muscle atrophy and necrosis. Chemotherapy can also cause muscle aches, known as myalgias, which can be a deep, constant dull ache or a sharp, sporadic pain. These aches usually resolve when the medication is no longer taken.
Bone Loss
Chemotherapy has been linked to bone loss and changes in bone health. Dr. David Waning and his team are researching the role of chemotherapy in bone alterations and how it affects the overall musculoskeletal system. Their studies indicate that chemotherapy may contribute to muscle weakness by disrupting the normal calcium cycle needed for muscle contraction. This disruption involves the release of excessive TGFβ from the bone, with TGFβ, Nox4, and RyR1 being identified as potential drug targets for cancer-associated muscle weakness.
Fatigue
Chemotherapy-induced muscle weakness is closely associated with fatigue. Doxorubicin-based chemotherapy, for example, has resulted in reports of debilitating fatigue in patients. This fatigue can be moderate to severe and persist for an extended period. Fatigue can also be a side effect of pain medications, such as narcotics, which are often used to manage pain during chemotherapy.
The impact of chemotherapy on bone and muscle can significantly affect a patient's quality of life and survival outcomes. Further research and understanding of these effects are crucial for developing treatments and improving patient care.
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Chemotherapy and anaemia
Chemotherapy-induced anaemia (CIA) is a common side effect of chemotherapy. It occurs when the chemicals in chemotherapy drugs that target rapidly dividing cancer cells also damage other healthy cells in the body, including those in the bone marrow that produce red blood cells. As a result, the body does not produce enough red blood cells or haemoglobin to carry oxygen to the cells throughout the body, leading to symptoms of anaemia.
Anaemia can cause a range of symptoms, including fatigue, dizziness, shortness of breath, lightheadedness, headaches, a fast heartbeat, and pale skin. These symptoms can significantly impact a person's quality of life, making everyday tasks difficult and potentially delaying or reducing cancer treatment.
The duration and severity of CIA can vary depending on the type of chemotherapy drugs, dosage, and the person's overall health. It is estimated that about 70% of people who receive chemotherapy develop anaemia. CIA is particularly common in people with low haemoglobin levels before treatment and those receiving platinum-based chemotherapy medications.
Treatment for CIA aims to manage symptoms and may include medications, blood transfusions, and prescribing vitamins and minerals. Doctors may recommend erythropoietin-stimulating agents (ESAs) to stimulate red blood cell production. However, it is best to avoid ESAs when the goal is to cure cancer, as they increase the risk of thromboembolic events. The symptoms of CIA usually improve within 2-4 weeks after completing chemotherapy, and anaemia typically resolves once chemotherapy stops.
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Frequently asked questions
Yes, chemotherapy can cause muscle weakness and bone loss. This can be caused by oxidative stress in the muscle, which can be induced by certain chemotherapeutic agents.
Muscle weakness caused by chemotherapy can result in fatigue, falls, and fractures. It can also cause muscle wasting and loss of motor unit function.
Muscle weakness can persist for months or years after chemotherapy treatment.
There are currently no approved treatments for chemo-induced muscle weakness. However, physical therapy and occupational therapy may help improve mobility and reduce the risk of falls.
