A model of open-loop control of equilibrium position and stiffness of the human elbow joint

According to the equilibrium point theory, the control of posture and movement involves the setting of equilibrium joint positions (EP) and the independent modulation of stiffness. One model of EP control, the α-model, posits that stable EPs and stiffness are set open-loop, i.e. without the aid of feedback. The purpose of the present study was to explore for the elbow joint the range over which stable EPs can be set open-loop and to investigate the effect of co-contraction on intrinsic low-frequency elbow joint stiffness (

Genetic variation and exercise-induced muscle damage: implications for athletic performance, injury and ageing.

Prolonged unaccustomed exercise involving muscle lengthening (eccentric) actions can result in ultrastructural muscle disruption, impaired excitation-contraction coupling, inflammation and muscle protein degradation. This process is associated with delayed onset muscle soreness and is referred to as exercise-induced muscle damage. Although a certain amount of muscle damage may be necessary for adaptation to occur, excessive damage or inadequate recovery from exercise-induced muscle damage can increase injury risk, particularly in older individuals, who experience more damage and require longer to recover from muscle damaging exercise than younger adults. Furthermore, it is apparent that inter-individual variation exists in the response to exercise-induced muscle damage, and there is evidence that genetic variability may play a key role. Although this area of research is in its infancy, certain gene variations, or polymorphisms have been associated with exercise-induced muscle damage (i.e. individuals with certain genotypes experience greater muscle damage, and require longer recovery, following strenuous exercise). These polymorphisms include ACTN3 (R577X, rs1815739), TNF (-308 G>A, rs1800629), IL6 (-174 G>C, rs1800795), and IGF2 (ApaI, 17200 G>A, rs680). Knowing how someone is likely to respond to a particular type of exercise could help coaches/practitioners individualise the exercise training of their athletes/patients, thus maximising recovery and adaptation, while reducing overload-associated injury risk. The purpose of this review is to provide a critical analysis of the literature concerning gene polymorphisms associated with exercise-induced muscle damage, both in young and older individuals, and to highlight the potential mechanisms underpinning these associations, thus providing a better understanding of exercise-induced muscle damage

Human skeletal muscle plasmalemma alters its structure to change its Ca2+-handling following heavy-load resistance exercise

High-force eccentric exercise results in sustained increases in cytoplasmic Ca2+ levels ([Ca2+]cyto), which can cause damage to the muscle. Here we report that a heavy-load strength training bout greatly alters the structure of the membrane network inside the fibres, the tubular (t-) system, causing the loss of its predominantly transverse organization and an increase in vacuolation of its longitudinal tubules across adjacent sarcomeres. The transverse tubules and vacuoles displayed distinct Ca2+-handling properties. Both t-system components could take up Ca2+ from the cytoplasm but only transverse tubules supported store-operated Ca2+ entry. The retention of significant amounts of Ca2+ within vacuoles provides an effective mechanism to reduce the total content of Ca2+ within the fibre cytoplasm. We propose this ability can reduce or limit resistance exercise-induced, Ca2+-dependent damage to the fibre by the reduction of [Ca2+]cyto to help maintain fibre viability during the period associated with delayed onset muscle soreness

Changes in the t-tubular system following eccentric muscle damage

Session - E33C Free Communacation/Slide Muscle InjuryPURPOSE:To examine the morphology and functional status of the T-tubular system following an eccentric contraction protocol. METHODS:Single fibers were dissected from mouse flexor digitorum brevis muscles. The fibers were stretched by 40% of their optimal length for a series of ten tetani. The T-tubules were examined using confocal microscopy and an extracellular fluorescent dye, sulforhodamine B. The time course of the dye washout was used as an estimate of the accessibility of the T-system to the extracellular space. RESULTS:Following eccentric damage, the fibers showed a reduction in force to 31 ± 2.7% of control, a shift in the peak length-tension by 1.24 ± 0.02 and a steepening of the force-frequency relation. This damage was associated with the development of vacuoles connected to the T-tubules. The rate of diffusion of the dye in and out of the T-system was significantly slowed (P < 0.01) with a half-time of 6.32 ± 2.4 min. Ouabain, a sodium pump inhibitor, inhibited the formation of vacuoles suggesting that the sodium pump is essential for their development. CONCLUSION:We propose that in eccentric contractions, T-tubules suffer shearing damage caused by sarcomere inhomogeneities. This leads to a localized increase in intracellular sodium ions. This sodium, accompanied by water, is pumped out of the cell by the sodium pump. the resulting volume load exceeds the capacity of the T-tubules and results in vacuole production