Understanding the Complex Interplay of Immobilization on Muscles

 

 

Collagen Alterations Impacting the Stress-Strain Reaction

Immobilization's effects

Reduced stiffness is the result of collagen turnover brought on by immobilization and weak bonding between the newly formed, unstressed fibers. Adhesion formation is also caused by increased cross-linking between disordered collagen fibers and a reduction in the ground substance's ability to keep space and lubricate between the fibers. For immobilized tissue, the pace of restoration to normal tensile strength is sluggish. In monkeys, for instance, the anterior cruciate ligament failed at 61% of maximum load after 8 weeks of immobilization; it failed at 79% after 5 months of reconditioning; and it failed after 12 months of reconditioning. In addition, there was a drop in energy absorbed and a reduction in stiffness just before failure after immobilization.

Consequences of Inactivity (Reduction in Regular Activity)

Collagen fibers shrink in size and quantity when inactive, weakening the tissue as a result. Tissue compliance increases as the percentage of elastin fibers increases proportionately to the decrease in collagen. It takes roughly five months of consistent cyclic stress to recover from these alterations. Engaging in physical activity positively impacts connective tissue strength. Age's Effects As we age, our tissues lose some of their maximal tensile strength and stiffness, and we respond to loads at a slower rate. Stretching-related tears, exhaustion failures, and overuse symptoms are more common.

Corticosteroid Effects

Tensile strength decreases as a result of a long-lasting negative impact corticosteroid use has on collagen's mechanical characteristics. Reduced collagen production and organization, necrosis, and an elevated ratio of type III to type 1 collagen are among the side effects of corticosteroid injections. Near the injection site, there is fibrocyte death, and it can take up to 15 weeks for the cells to return.

Impact of Injury

Damaged tissue heals in a predictable way, with the injury site being bridged by newly produced type III collagen. In terms of structure, this collagen is not as strong as mature type 1 collagen. Type 1 collagen ultimately matures as remodeling continues.. Remodeling typically starts three weeks after the damage and lasts for many months to a year, depending on the extent of the rupture and the size of the connective tissue structure.

Additional Conditions That Impact Collagen

Dialysis, hormonal abnormalities, and nutritional deficits can make connective tissue more vulnerable to damage at lower loading levels than usual.

Muscle Tissue's Physiological and Mechanical Characteristics

Both contractile and noncontractile connective tissues make up muscle. Muscle has the qualities of contractility and irritability due to its contractile components. The noncontractile connective tissues that surround and comprise muscles share all connective tissue's characteristics, such as their resistance to deforming pressures. The endomysium, the deepest layer that divides individual muscle fibers and myofibrils, the perimysium, which encloses fiber bundles, and the epimysium, the fascial sheath enclosing the entire muscle, are the noncontractile connective tissue structures of muscle. The main factor preventing a muscle from passively elongating is its connective tissue architecture. Joint contracture may arise from tissue adhesions that resist and restrict movement inside and between the collagen fibers of these structural tissues."

Muscle's Contractile Elements

Numerous muscle fibers arranged in parallel make up each individual muscle. Numerous myofibrils make up a single muscle fiber.. Sarcomeres, which are even smaller structures that are arranged end to end within a myofibril, make up each individual myofibril. Actin and myosin protein myofilaments overlap to form the sarcomere, the contractile unit of the myofibril. Muscle may contract and relax thanks to sarcomeres. Actin-myosin filaments create cross-bridges, slide in relation to one another, and actively shorten the muscle when a motor unit initiates a contraction. Myofilaments in muscles slip apart slightly during relaxation, allowing the muscle to lengthen back to its resting length.

Contractile Unit's Mechanical Reaction to Stretch and Immobilization

Over time, alterations can arise in the anatomical structure and physiological function of sarcomeres. These alterations may be brought about by a stretch made during an exercise or by prolonged immobility followed by remobilization. A muscle's reaction to stretching and immobility is also influenced by the noncontractile components located within and surrounding it.

Reaction to Stretch

The endomysium and perimysium transfer the stretch force to the muscle fibers when a muscle is stretched and elongates. It is postulated that molecular interactions facilitate this force transduction by connecting these noncontractile components to the sarcomere."Muscle transduction happens both longitudinally (in series) and laterally (in parallel) during a passive stretch. Tension in the series elastic component increases dramatically during early lengthening. Sarcomere give, or the abrupt lengthening of the sarcomeres, is caused by the mechanical disruption of the cross-bridges caused by the myofilaments sliding apart with continuing extending. The individual sarcomeres revert to their resting length upon relaxation of the stretch force. Elasticity, as previously mentioned, is the characteristic of a muscle that facilitates its return to its resting length following a brief stretch. In order for length increases to be more permanent or longer-lasting (plastic or viscoelastic), the stretch force needs to be sustained for a considerable amount of time.

Reaction to Immobilization and Reemergence morphological modifications

When a muscle remains immobilized for an extended period of time, it is not utilized for functional tasks and the physical strain on it is significantly reduced.. This leads to a decrease in the number of myofibrils, intramuscular capillary density, and muscle fiber diameter in the immobilized muscle, as well as a breakdown of contractile protein. This process results in weakening and atrophy of the muscles. There is an increase in fibrous and fatty tissue in the muscle when the immobile muscle atrophies. Muscle's reaction to immobilization depends on its composition; in tonic (slow-twitch) postural muscle fibers, atrophy occurs more rapidly and extensively than in phasic (fast-twitch) fibers. The degree of atrophy and weakening is also influenced by the length of immobilization and its position; a longer period of immobilization results in a larger trophy and a loss of functional strength. In as little as a few days to a week, atrophy can start. With atrophy, there is a corresponding reduction in the cross-sectional area of muscle fibers, but electromyographic (El G) activity indicates a much more severe decline in motor unit recruitment. The ability of the muscle to produce force is compromised by both of these conditions.

Immobility in a Slouched Posture

Sarcomere absorption causes a decrease in muscle length, the number of muscle fibers, and the number of sarcomeres in series inside myofibrils when a muscle is immobilized in a shortened position for several weeks in animal studies. This absorption happens more quickly than the muscle's capacity to produce new sarcomeres in an effort to repair itself. Muscle atrophy and weakening are the results of this reduction in the total length of the muscle and the number of sarcomeres. Additionally, it has been proposed that compared to a muscle immobilized in an extended state, a muscle immobilized in a shorter position atrophies and weakens more quickly.

Effects of Immobilization on Muscle Mechanics

Muscle shortening brought on by immobilization causes a change in the length-tension curve to the left, reducing the amount of tension that can be produced when the muscle contracts at its typical resting length. As the muscle is stretched, the reduction in muscle length also causes passive tension to start earlier. This mechanical change is associated with the lengthening of the muscles and the rise in the ratio of connective tissue to muscle tissue that occurs as a result of immobilization. Crucially, when the muscle is extended, the increase in connective tissue and early initiation of passive tension also work to shield the weaker and shorter muscle.

Immobilization while Stretched out

A muscle may occasionally become immobile in a stretched posture for an extended amount of time. Certain surgical treatments can cause this, including limb lengthening, the use of dynamic orthoses to increase range of motion and stretch long-standing contractures, or the administration of a series of positional casts, also known as serial casts. Myofibrillogenesis, the process by which a muscle that has been stretched for a prolonged period of time adjusts by growing the number of sarcomeres in series, is supported by a small body of research on animals but not much on human skeletal muscle. Sarcomere addition is thought to preserve the ideal functional overlap between actin and myosin filaments in the muscle and could be reasonably durable provided the newly acquired length is regularly used in stretched, functional activities. It is unknown how long it takes for an extended muscle (fiber) to get longer by the addition of sarcomeres in series.

Sarcomere Adaptation: Lengthening Muscle in Humans

In animal experiments, sarcomere number addition resulting in increased muscle length necessitated weeks of continuous immobilization in an extended position. It is hypothesized that the same mechanism, either directly through increases in Joint OM or indirectly through the use of serial casts, dynamic or otherwise, and possibly as a consequence of stretching activities, leads to increases in muscle length. Remarkably, direct proof of sarcomere adaptation in human skeletal muscle was recently documented after a patient underwent continuous, long-term limb distraction to lengthen their femur.

Adjustment

If the muscle returns to its pre-immobilization use and degree of lengthening for functional activities, the adaptation of the contractile units of the muscle (an increase or decrease in the number of sarcomeres) to prolonged positioning in either lengthened or shortened positions is temporary, lasting only 3 to 5 weeks. This emphasizes the necessity for patients to perform full-range motions during a range of functional activities in clinical practice in order to sustain the stretch-induced improvements in muscle, extensibility, and joint range of motion.