Example of Systemic Dysfunction
Hypothesis

Persistent Impaired Muscle Relaxation

THE CARCO STRESS MODEL: Carbon Monoxide Exposure → Peroxynitrite Formation in Capillaries → Fibrin Amyloid Formation → Microvascular Obstruction → Reduced Mitochondrial Oxygen Availability → Aerobic Energy Production Failure → Systemic Dysfunctions

Reduced oxygen delivery → reduced aerobic ATP production → impaired calcium removal + increasing acidity → incomplete muscle relaxation and persistent pain

Unrecognized State of Muscle Contraction

Many people experience persistent leg tightness, heavy aching, stiffness, or restricted movement without understanding why. Standard laboratory tests, imaging, and physical fitness evaluations frequently return completely normal results, offering no clear medical explanation for the pain.

Persistent muscle pain and tightness often occur because muscles lack the energy required to relax.

When everyday movements cause enduring discomfort, the muscle tissue may simply be trapped in a prolonged, partial state of contraction. Rather than an inflammatory injury, structural damage, or poor physical conditioning, this persistent tension can indicate that local cells lack the cellular energy needed to return the muscle to a fully relaxed resting state.

Normal Muscle Relaxation Requires ATP

Muscle contraction is controlled by calcium ions (Ca²⁺). When a muscle is activated, calcium is released inside the muscle cell and allows the contractile proteins to produce force. For the muscle to relax again, calcium must be removed from the active contractile area and returned to its intracellular storage.

This process is not passive. The SERCA pump uses ATP to actively pump Ca²⁺ back into the sarcoplasmic reticulum after every contraction. Normal muscle function therefore requires energy not only to produce movement, but also to stop the contraction and restore the muscle to its resting state.

Muscle relaxation requires ATP because calcium must be actively pumped back into storage after contraction.

Reduced Oxygen Slows Calcium Removal

When Fibrin amyloids restrict oxygen delivery, mitochondria cannot maintain normal aerobic ATP production. When ATP availability becomes insufficient, the ATP-dependent SERCA pump cannot restore calcium balance as efficiently. Ca²⁺ therefore remains elevated in the cytoplasm for longer after contraction, allowing the contractile machinery to remain activated longer than it normally would.

Reduced oxygen → reduced aerobic ATP production → reduced ATP availability → slower SERCA activity → prolonged Ca²⁺ elevation → delayed muscle relaxation

The muscle may therefore remain partially contracted even after the activity has stopped. This can produce persistent tightness, stiffness, tension, heaviness, or the sensation that the muscle never completely “lets go.”

Hydrogen Ions Add Pain and Further Disrupt Muscle Function

When ATP demand exceeds aerobic capacity, hydrogen ions (H⁺) can accumulate faster than they are buffered and removed. Increasing H⁺ concentration lowers intracellular and tissue pH, creating a more acidic environment.

This acidity affects muscle proteins, enzymes and calcium regulation and activates acid-sensitive pain receptors. The resulting pain can feel like the burning or deep aching normally associated with strenuous exercise, even when the activity itself has been minor.

Ca²⁺ contributes to incomplete relaxation, while increasing H⁺ and falling pH contribute to pain and can further disturb normal calcium regulation.

Persistent pain is caused by increased acidity

During normal exercise, temporary oxygen shortage and acidity resolve during recovery. Blood flow supplies oxygen, ATP production returns toward baseline, calcium is restored to intracellular storage, excess H⁺ is buffered and removed, and the muscle relaxes.

If microvascular obstruction continues to restrict oxygen delivery, this recovery may remain incomplete. Normal everyday activity then begins before the muscle has fully restored its ATP supply, calcium balance and pH from the previous demand. Increasing acidity affects cellular function and activates acid-sensitive pain receptors, producing a distinctly burning or overloaded sensation.

Reduced oxygen delivery → increased reliance on glycolysis → H⁺ accumulation → lower pH → pain receptor activation

Walking, standing, climbing stairs, carrying groceries or maintaining posture can repeatedly add new energy demand to muscle that is already functioning below its normal baseline.

Persistent pain can therefore develop when the muscle repeatedly uses energy faster than oxygen-dependent recovery can restore normal ATP, calcium and pH balance.

What Persistent Muscle Dysfunction Can Feel Like

The symptoms can resemble the sensation following very strenuous exercise, but instead of resolving normally after rest, they persist or return rapidly with new activity.

People may experience:

• burning or deep aching pain
• persistent muscle tightness
• stiffness or tension
• muscles that feel permanently overloaded
• intense heaviness
• difficulty sustaining muscle activity
• rapid recurrence of pain with movement
• poor recovery after exertion
• muscles that never seem to relax completely

The severity depends on how much oxygen delivery and aerobic energy production remain available relative to the energy required by the muscle.

The Role of Magnesium

Magnesium is involved in normal muscle and calcium regulation. Calcium promotes contraction, while normal relaxation requires controlled removal and storage of Ca²⁺ inside the muscle cell.

Adequate magnesium availability supports normal ATP-dependent cellular processes and calcium handling. Magnesium therefore may influence muscle tightness, cramping and relaxation, but it does not correct an underlying shortage of oxygen or restore aerobic ATP production if oxygen delivery remains impaired.

Magnesium should therefore be viewed as supporting the muscle’s normal regulatory mechanisms rather than removing the underlying cause of persistent energy and calcium imbalance.

The Central Mechanism

Persistent fibrin amyloids obstruction can reduce oxygen delivery to muscle. Reduced oxygen limits mitochondrial aerobic ATP production, leaving less energy available for the ATP-dependent SERCA pumps that restore calcium after contraction. At the same time, increasing reliance on anaerobic energy production and rapid ATP turnover can increase H⁺ concentration and lower pH.

The result is a muscle that produces too little aerobic energy, removes calcium too slowly, becomes increasingly acidic, and cannot return efficiently to its normal resting state between activities.

Fibrin amyloids
→ reduced muscle oxygen delivery
→ reduced aerobic ATP production
→ slower SERCA-dependent Ca²⁺ removal
→ incomplete muscle relaxation

combined with:

Reduced oxygen availability
→ increased reliance on anaerobic energy production
→ H⁺ accumulation and lower pH
→ pain and further disruption of muscle function

Sources