Hyperbaric Oxygen Therapy for Musculoskeletal System Diseases
2026-05-04
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Tip 1 Discomfort Symptoms of the Musculoskeletal System After Viral Infection
- Fatigue
- Joint pain
- Muscle pain
- Muscle weakness
Tip 2 Causes of Musculoskeletal Impairment After Viral Infection
- Direct viral attack on joints and muscles, causing damage to these tissues.
- Inflammatory cytokine storm leading to skeletal myositis and rhabdomyolysis syndrome.
- Lactic acid accumulation due to high fever causing muscle soreness.
- Skeletal and muscle damage induced by glucocorticoid use.
Tip 3 Clinical Improvement of Musculoskeletal Diseases by Hyperbaric Oxygen Therapy
- Alleviate fatigue and lassitude.
- Reduce pain caused by skeletal myositis due to inflammatory cytokine storm.
- Mitigate bone destruction caused by glucocorticoids.
- Relieve joint pain.
Section 1 Musculoskeletal Symptoms After Viral Infection
1. Musculoskeletal Pain
Muscle and joint pain is a common symptom during both the acute and recovery phases of viral infection, with low back pain, hip pain, and thigh pain being most prominent, severely affecting ambulation in severe cases. Most pain is myogenic, with a small portion being neurogenic.
Some studies suggest that viruses bind to specific receptors (ACE-2 receptors) in musculoskeletal tissues, triggering persistent pain, or activate specific immune responses leading to autologous muscle injury and lysis; however, the exact mechanism remains unclear. Such pain may involve the shoulder, hip, knee, spine, and other joints.
A 2021 cohort study of 1,276 patients reported that a small number of individuals experienced chronic pain after recovery, most commonly joint and muscle pain.
2. Muscle Weakness
Foreign studies show that patients with severe viral infection experience significant loss of muscle mass and strength during hospitalization. One study found that the cross-sectional area of the rectus femoris (a major thigh muscle) decreased by 30% in critically ill patients with viral pneumonia after 10 days of hospitalization, indicating obvious muscle atrophy.
Another study reported that 7%–85% of patients recovering from viral infection developed weakness in the quadriceps femoris (thigh) and forearm flexors. This weakness may persist for 4–7 months after recovery from viral pneumonia and is significantly correlated with disease severity and length of hospital stay: longer hospitalization and more severe illness correlate with worse muscle weakness.
3. Decreased Exercise Tolerance
Decreased exercise tolerance manifests as easy fatigability, shortness of breath during walking, stair climbing, or other physical activities. Studies show that patients recovering from viral pneumonia still exhibit impaired pulmonary oxygen uptake 3 months after discharge.
Compared with healthy individuals, grip strength and 6-minute walking test performance decreased by 32% and 13%, respectively, in recovered patients. Some scholars hypothesize that decreased exercise tolerance is related to damage to mitochondria (the “powerhouses” of cells), though this has not been fully confirmed.
Section 2 Causes of Musculoskeletal Pain After Viral Infection
Virus infection-related pain refers to a series of pain symptoms caused by viral infection, including headache, abdominal pain, arthralgia, myalgia, ostealgia, or neuropathic pain during or after infection.
Invasion of the central nervous system, peripheral nerve cells, and skeletal muscle cells by viruses can cause severe pain described as “waist-breaking” or “leg-breaking.”
1. Direct Viral Attack on Musculoskeletal Tissues
The structural spike of SARS-CoV-2 binds to ACE2 receptors on human cells, which are also expressed in the peripheral nervous system and skeletal muscle. The virus can replicate in skeletal muscle cells and destroy muscle tissue.
2. Inflammatory Cytokine Storm
The inflammatory response induced by SARS-CoV-2 infection adversely affects musculoskeletal tissues. After pulmonary infection with SARS-CoV-2, the immune system releases massive cytokines, triggering an exaggerated inflammatory response (cytokine storm) that promotes multiple organ injury.
Inflammatory cytokines such as IL-6, IL-1β, IL-8, IFN-γ, IP-10 (CXCL10), and TNF-α induce myofibrillar proteolysis, reduce protein synthesis, interfere with myogenesis, and disrupt homeostasis.
Uncontrolled systemic inflammation activates multiple inflammatory pathways, leading to musculoskeletal manifestations such as fatigue and myalgia, and even skeletal myositis and rhabdomyolysis syndrome.
3. Anaerobic Respiration
Skeletal muscle is the primary source of heat production during high fever and chills. Anaerobic respiration in skeletal muscle produces excessive lactic acid and metabolites; their accumulation stimulates nociceptors and causes muscle soreness.
4. Excessive Glucocorticoid Use
Excessive glucocorticoid administration can cause osteonecrosis and osteoporosis, which may contribute to chronic pain after recovery.
Section 3 Home Management of Virus-Related Musculoskeletal Pain
- Lifestyle modification: Increase water intake; maintain a balanced diet rich in vitamin C and vitamin E to accelerate lactic acid metabolism; ensure adequate sleep. Listen to soothing music and maintain a positive mood.
- Physical therapy: Local warm towel compresses to improve blood circulation, accelerate metabolism, and partially relieve pain and discomfort.
- Analgesic medication: Consult a doctor before use; do not self-medicate.
Section 4 Analgesic Selection for Virus-Related Musculoskeletal Pain
Viral infection is associated with myalgia, arthralgia, abdominal pain, headache, chest pain, and other pain symptoms. Analgesic options include opioids, antidepressants, anticonvulsants, ketamine, nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, and muscle relaxants.
- For muscle pain, joint pain, and low back pain: Selective cyclooxygenase-2 (COX-2) inhibitors such as celecoxib are recommended, especially for elderly patients, to minimize gastrointestinal adverse effects. The Expert Consensus on Chronic Musculoskeletal Pain Management identifies NSAIDs as the most evidence-based and widely prescribed analgesic class, with selective COX-2 inhibitors having better gastrointestinal safety than non-selective NSAIDs.
- For neuropathic pain (presenting as stabbing, burning, cutting, or throbbing pain): Pregabalin extended-release tablets, gabapentin, and other neuropathic pain relievers are first-line options; combination with NSAIDs may be used if needed.
- Long-term or high-dose antipyretic analgesics carry a risk of peptic ulcer. High-risk groups (elderly patients, those on antiplatelet/anticoagulant therapy, or with a history of gastrointestinal ulcer) must use medications under medical supervision.
- Do not take multiple antipyretic analgesics simultaneously, as this may cause liver and kidney damage, even multiple organ failure. Dosage tolerance varies individually; seek medical attention if pain persists for dose adjustment.
- For patients with impaired liver or kidney function or those taking other hepatotoxic/nephrotoxic drugs, adjust the dosage under physician guidance, monitor liver and kidney function regularly, and seek immediate medical care for nausea, jaundice, or decreased urine output.
Section 5 Application of Hyperbaric Oxygen Therapy in the Musculoskeletal System
1. Hyperbaric Oxygen Improves Lassitude
Muscle soreness and fatigue are usually caused by muscle tissue hypoxia. Hyperbaric oxygen exerts beneficial effects on mitochondrial function, a key determinant of muscle performance.
Hyperbaric oxygen increases the number of proliferating and differentiating satellite cells and regenerating muscle fibers, promoting muscle strength. It elevates maximal oxygen uptake by 34% and lactate threshold by 16.9%, significantly alleviating lassitude.
2. Hyperbaric Oxygen Relieves Fatigue
Fatigue is a common post-viral infection symptom, reported in 77% of patients. Hyperbaric oxygen therapy significantly reduces fatigue in patients with viral pneumonia.
Fatigue in viral pneumonia overlaps considerably with chronic fatigue syndrome (CFS). Shared symptoms include fatigue, pain, neurocognitive/psychiatric symptoms, reduced daily activity, and post-exertional malaise. Studies confirm that hyperbaric oxygen therapy effectively reduces symptom severity and improves quality of life in CFS patients.
3. Hyperbaric Oxygen Alleviates Musculoskeletal Pain
Muscle and joint pain after viral infection resembles central sensitization syndromes such as fibromyalgia. Clinical studies show that hyperbaric oxygen therapy improves pain and quality of life in fibromyalgia patients, with increased regional blood perfusion and effective pain relief after treatment.
Section 6 Application of Oxygen Therapy in the Musculoskeletal System
Oxygen therapy is one of the most widely used respiratory therapies in clinical practice, applied in the treatment and resuscitation of various diseases via physical, chemical, biological, and physiological mechanisms of oxygen.
Hypoxia-inducible factor-1α (HIF-1α), an oxygen-sensitive transcription factor, regulates the expression of numerous downstream target genes including vascular endothelial growth factor (VEGF), matrix metalloproteinase-2 (MMP-2), and erythropoietin (EPO). It participates in hypoxia adaptation, angiogenesis, immune response, apoptosis, and other processes, and is closely associated with diabetes, chronic obstructive pulmonary disease, tumors, oral diseases, etc.
HIF-1α is involved in the differentiation of bone marrow mesenchymal stem cells and repair of calvarial defects. Oxygen inhalation may regulate bone metabolism signaling pathways related to VEGF, MMP-2, EPO, and other downstream genes by modulating HIF-1α expression, thereby promoting osteogenesis and angiogenesis, improving sleep quality, and preventing osteoporosis.
Exploring optimal long-term home oxygen therapy regimens for osteoporosis prevention is a key research direction.
The hypoxia/HIF-1α pathway critically regulates the coupling between osteoblasts and osteoclasts to maintain bone metabolic balance. HIF-1α accelerates bone resorption by enhancing glycolysis and acid production in osteoclasts.
HIF-1α and VEGF play important physiological adaptive roles in bone marrow and cardiac tissue under high-altitude hypoxia. Studies indicate that HIF-1α modulates the chondrogenic and osteogenic differentiation of stem cells induced by bone morphogenetic protein 2 (BMP-2), regulating bone metabolism.
Hypoxia treatment affects proliferation, apoptosis, and necrosis of rat bone marrow mesenchymal stem cells, with HIF-1α playing a vital role in regulating their proliferation and differentiation.
References
[1] Laith KH, Brittney D, Aryan H, et al. Effects of COVID-19 on the Musculoskeletal System: Clinician's Guide. Orthopedic Research and Reviews [J]. 2021, 13: 141
[2] Nathaniel PD, Andrea J, Martin MS, et al. Musculoskeletal Consequences of COVID-19. J Bone Joint Surg Am [J]. 2020, 102: 1197-1204.
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