Paraplegia is a form of paralysis resulting from a spinal cord injury (SCI), which causes the impairment or loss of motor and sensory function in the lower half of the body. Following this neurological trauma, a rapid decrease in leg muscle mass, known as muscle atrophy, is a universal consequence. Muscle atrophy describes the wasting or thinning of muscle tissue, where the muscle fibers decrease in size and strength. This dramatic change in the lower limbs results from three interconnected biological processes that begin immediately after the spinal cord is damaged.
Atrophy Caused by Physical Inactivity
The most immediate cause of muscle loss is the sudden cessation of mechanical loading, often termed disuse atrophy. Skeletal muscles require constant tension and contraction to maintain their mass and structural integrity. When a spinal cord injury prevents standing or walking, the large muscles of the legs are no longer subjected to the forces of gravity and body weight.
This lack of mechanical stimulus signals that the muscle is metabolically expensive and no longer needed for movement or posture. The body responds by shifting the balance between muscle protein synthesis and muscle protein breakdown. Protein synthesis, which builds new muscle tissue, is significantly reduced, while catabolic pathways that break down muscle protein are activated.
The muscle fibers begin to shrink rapidly as the body seeks to conserve energy by dismantling unused tissue. This process is distinct from nerve damage, as simple prolonged bed rest also causes disuse atrophy. However, in paraplegia, this effect is compounded by other factors, making the atrophy far more severe and difficult to reverse than simple inactivity alone.
The Role of Lost Neural Signaling
A second mechanism is denervation atrophy, the direct result of the severed connection between the spinal cord and the lower limb muscles. Motor neurons carry signals from the spinal cord to the muscle, providing not only the impulse for voluntary contraction but also a continuous, low-level chemical influence known as trophic support. When the nerve supply is disrupted, the muscle fibers lose this constant stream of electrical and chemical signals.
The loss of these trophic factors causes muscle fibers to shrink dramatically, often leading to a loss of 80% to 90% of muscle mass within a few months of injury. This atrophy is neurogenic, meaning it originates from the damaged nerve, and can occur even if the limb were passively moved. The muscles become disconnected from the central nervous system, which is a major signal for their survival and maintenance.
Denervation also causes muscle fibers to change their physical properties, a phenomenon called fiber type conversion. The fatigue-resistant, slow-twitch fibers (Type I), abundant in leg muscles for endurance activities, begin to convert into fast-twitch, highly fatigable fibers (Type II). This transition impairs the muscle’s ability to use oxygen for energy, accelerating its metabolic decline. The severity of the resulting atrophy relates closely to the extent of nerve damage and whether the SCI is complete or incomplete.
Systemic Metabolic Changes After Spinal Cord Injury
Beyond disuse and denervation, the spinal cord injury triggers systemic metabolic changes that contribute to leg atrophy. The trauma alters the body’s hormonal and inflammatory environment, impairing the muscle’s ability to maintain itself. This widespread disruption means muscle loss is a systemic condition, not solely a problem of the legs.
One significant change is the development of chronic, low-grade inflammation throughout the body. Circulating inflammatory molecules accelerate protein breakdown in muscle tissue and inhibit signaling pathways that promote muscle growth. This inflammatory state acts as a constant catabolic signal, pushing the body toward muscle wasting.
Another factor is the disruption of glucose metabolism, leading to insulin resistance. Insulin is a hormone that helps transport nutrients, including glucose and amino acids, into muscle cells for energy and repair. With insulin resistance, muscle cells become less responsive, impairing the muscle’s ability to take up the necessary building blocks for maintenance.
The injury also leads to alterations in circulating anabolic hormones, such as growth hormone and testosterone, which stimulate muscle protein synthesis. The decrease in these hormones, combined with increased fat deposition and chronic inflammation, creates a hostile internal environment for muscle preservation. This combination of systemic factors works alongside disuse and denervation, contributing to the rapid loss of lean mass observed in the legs following paraplegia.