Mechanisms of Exercise-Induced Muscle Fibre Injury

Abstract

Exercise for which a skeletal muscle is not adequately conditioned results in focal sites of injury distributed within and among the fibres. Exercise with eccentric contractions is particularly damaging. The injury process can be hypothesised to occur in several stages. First, an initial phase serves to inaugurate the sequence. Hypotheses for the initial event can be categorised as either physical or metabolic in nature. We argue that the initial event is physical, that stresses imposed on sarcolemma by sarcomere length inhomogeneities occurring during eccentric contractions cause disruption of the normal permeability barrier provided by the cell membrane and basal lamina. This structural disturbance allows Ca++ to enter the fibre down its electrochemical gradient, precipitating the Ca++ overload phase. If the breaks in the sarcolemma are relatively minor, the entering Ca++ may be adequately handled by ATPase pumps that sequester and extrude Ca++ from the cytoplasm ('reversible' injury). However, if the Ca++ influx overwhelms the Ca++ pumps and free cytosolic Ca++ concentration rises, the injury becomes 'irreversible'. Elevations in intracellular Ca++ levels activate a number of Ca(++)-dependent proteolytic and phospholipolytic pathways that are indigenous to the muscle fibres, which respectively degrade structural and contractile proteins and membrane phospholipids; for instance, it has been demonstrated that elevation of intracellular Ca++ levels with Ca++ ionophores results in loss of creatine kinase activity from the fibres through activation of phospholipase A2 and subsequent production of leukotrienes. This autogenetic phase occurs prior to arrival of phagocytic cells, and continues during the inflammatory period when macrophages and other phagocytic cells are active at the damage site. The phagocytic phase is in evidence by 2 to 6 hours after the injury, and proceeds for several days. The regenerative phase then restores the muscle fibre to its normal condition. Repair of the muscle fibres appears to be complete; the fibres adapt during this process so that future bouts of exercise of similar type, intensity, and duration cause less injury to the muscle.

The efficacy of manual versus local vibratory massage in promoting recovery from post-exercise muscle damage – A systematic review

“…Following muscle damage, an inflammatory reaction sets in and is associated with an invasion of neutrophils and macrophages into the damaged fibres within 6h (Armstrong et al, 1991;Peake et al, 2005). These secrete reactive oxygen and nitrogen species, cytokine factors and proteolytic enzymes that lead to initial tissue degradation (Clarkson and Sayers, 1999).…”

“…The symptoms of DOMS include a decrease in ROM and joint stiffness, reduction in muscle strength, muscle pain and tenderness. In terms of the mechanism, exercise-induced mechanical disruption of muscle cell sarcomeres and sarcolemmas, and a reduced membrane excitability (Armstrong et al, 1991;Fitts, 1994) leads, during repeated contractions, to more extensive damage and, ultimately, to necrosis of some muscle fibres. The injury triggers a local inflammatory response that is accompanied by some oedema and the breakdown products of injured tissues, sensitise nociceptors (Proske and Morgan, 2001).…”

“…The injury triggers a local inflammatory response that is accompanied by some oedema and the breakdown products of injured tissues, sensitise nociceptors (Proske and Morgan, 2001). The physiological mechanisms associated with the reduction of muscle strength post eccentric exercise are thought to be the exercise-induced mechanical disruption of muscle cell sarcomeres and sarcolemma, and a reduced membrane excitability (Armstrong et al, 1991;Fitts, 1994). In patients with exercise-induced DOMS during the first three days following unaccustomed eccentric exercise, studies have also confirmed disorganization of myofibrillar proteins, especially in and around the Z-disk (Cluett, 2010;Bubicco and Kravitz, 2010).…”

Mechanisms of exercise-induced muscle damage and fatigue: Intracellular calcium accumulation

“…Healthy resting myocytes maintain [Ca 2+ ] i under 100 nM 3) . Myocyte contraction is evoked by the transient elevation of [Ca 2+ ] i which, under normal (i.e., non-fatigued, non-damaged) conditions is almost immediately returned to basal resting levels.…”

“…Many researchers have focused on the relationship between [Ca 2+ ] i and muscle damage 3,38,45,46) . While calpain structure is now well characterized, the activation model and regulation of calpain activity are still unclear.…”