Sepsis is a medical emergency defined as the body’s overwhelming and life-threatening response to an infection. Instead of fighting the invading pathogen locally, the immune system’s reaction becomes dysregulated and begins to injure the body’s own tissues and organs. Severe muscle pain, known medically as myalgia, is a frequent symptom reported by patients with severe sepsis or septic shock. The mechanisms behind this pain are complex, involving systemic inflammation, cellular breakdown, and circulatory failure.
Sepsis and the Global Inflammatory Cascade
The initial systemic reaction to an infection involves the body’s defensive cells releasing signaling molecules. These chemical messengers, which include pro-inflammatory cytokines such as Tumor Necrosis Factor-alpha (TNF-α), Interleukin-6 (IL-6), and Interleukin-1 beta (IL-1β), are distributed throughout the bloodstream. This surge of circulating molecules is often described as a “cytokine storm” and is intended to coordinate the immune response against the pathogen.
When uncontrolled, these potent agents travel beyond the original infection site. They move into distant tissues, including skeletal muscle, where they initiate a widespread inflammatory state. This systemic inflammation is the primary trigger for tissue damage and organ dysfunction seen in sepsis, contributing directly to the experience of pain.
Direct Myocyte Breakdown and Protein Loss
The inflammatory cascade directly attacks the functional units of muscle tissue, the myocytes. This systemic assault triggers accelerated catabolism. The body begins to degrade its own muscle proteins, specifically the contractile filaments actin and myosin, to provide amino acids. These released amino acids are then diverted to the liver and immune cells to fuel the body’s heightened metabolic and defensive needs.
This destructive muscle protein loss is primarily executed through the activation of specialized cellular machinery, notably the ubiquitin–proteasome system. As structural proteins break down, muscle fibers shrink, leading to a myopathy characterized by reduced muscle mass and strength. This cellular destruction and wasting contributes significantly to the myalgia experienced during the septic state.
Another element in muscle cell dysfunction is the loss of energy production. Sepsis causes significant mitochondrial dysfunction within the muscle cells. Mitochondria generate adenosine triphosphate (ATP), the primary energy currency of the cell. When these organelles fail due to oxidative damage, the muscle cells become starved of ATP, impairing their function and leading to severe muscle weakness and pain.
Muscle Ischemia Caused by Reduced Perfusion
Beyond the direct cellular attack, a circulatory problem in sepsis compromises muscle tissue health. Sepsis frequently progresses to septic shock, characterized by a drop in blood pressure (hypotension). This drop occurs because inflammatory mediators cause widespread dilation of the blood vessels.
This loss of vascular tone means the circulatory system cannot deliver blood effectively to the skeletal muscles. The resulting reduced blood flow, known as tissue hypoperfusion, starves the muscle tissue of oxygen and nutrients. This state of oxygen deprivation, or ischemia, is intensely painful because the muscle cells are unable to sustain normal aerobic metabolism.
How Metabolic Byproducts Trigger Pain Signals
The tissue hypoperfusion and resulting oxygen starvation force the muscle cells to switch to an emergency energy production method called anaerobic respiration. This process does not require oxygen but is highly inefficient and produces an acidic waste product. The most significant byproduct of this shift is the buildup of lactic acid.
When blood flow is severely reduced, the body cannot clear this lactic acid from the muscle tissue quickly enough. The high concentration of these acidic byproducts leads to a condition known as lactic acidosis. This acidic environment directly stimulates local pain receptors, called nociceptors, embedded in the muscle and surrounding tissue. This stimulation sends a strong pain signal to the brain, translating metabolic distress directly into myalgia.