Eccentric Contractions: Extension to Eccentric Exercise

Disruption

The observations of eccentric exercise all indicate a cummulative effect of stretches. If popping sarcomeres are to explain these effects, some mechanism for this accummulation must be postulated. The postulate is based on the suggestion that a small number of popped sarcomeres fail to return to return to the normal pattern of interdigitating myofibrils after each contraction. This could be simply due to "scrunching" of the filament brushes, or due to damage or other changes to passive structures such as titin, or possibly to tearing and resealing of transverse tubules, leaving myofibrils that cannot be activated in some sarcomeres. It is postulated to occur randomly among the popped sarcomeres.

The number of disrupted sarcomeres should increase with the number of contractions. The relation is likely to show some saturation, as disrupted sarcomeres absorb more of the stretch, and less sarcomeres are required to pop in subsequent contractions. These disrupted sarcomeres are the conversion of active to passive tissue responsible for the shift in optimum length and accompanying events seen by Katz. Furthermore, they have greater significance as the mechanical indicator of the first step in the process that leads to damage.

Damage.

During a subsequent stretch this disrupted half-sarcomeres will be stretched as soon as tension is generated. Through structural connections between myofibrils, this will place extra load on the same sarcomere in neighbouring myofibrils, making it more likely that they will reach their yield point and pop during that stretch. They will then be more likely to become disrupted, in turn straining their neighbours. Hence successive stretches can produce an accummulation of disrupted sarcomeres, rather similar to the production of a fatigue crack in a solid.

A mechanism can also be postulated for spread of a disrupted region along a sarcomeres as follows. When a sarcomere pops, it will tend to do so at constant volume, due simply to viscous resistance to the flow of myoplasm into it. This implies that popping will be associated by a reduction in cross-section, at least momentarily. The continuity of structures along the myofibril will lead to a reduction in cross-section of neighbouring sarcomeres along the myofibril, and by constant volume, an increase in length. This in turn leads to a reduction in filament overlap, reduction of isometric capability, and increased probability of popping, and so of becoming disrupted.

At some point, the disrupted area will become so large that the membranes of the cell will be unable to stretch around it and will tear. Possible candidate mebranes include transverse tubules, sarcoplasmic reticulum, and sarcolemma. At this point control of the intracellular calcium ion concentration is lost, calcium concentration rises, the myofibril goes into an uncontrolled contraction, or contracture, damaging more membranes and releasing more calcium.

This progression from disruption to damage will depend on the initial pattern on sarcomere non-uniformites. If the weakest sarcomeres are all close together, then many of the popped sarcomeres will be adjacent, and progression to damage will be rapid. If the weakest sarcomeres are widely scattered through the fibre, then so will be the popped sarcomeres. Isolated popped sarcomeres are less likely to strain membranes to breaking point, so that damage will be less likely. This could explain some of the variability in response between muscles, and also such reports as fibres from hibernating frogs being more easily damaged by stretch. Note that the degree of non-uniformity is not important to the process, but the pattern of non-uniformity is.

Training.

A further postulate is that the rapid training effect of eccentric exercise, whereby even a singl bout of eccentric training produces significant protection from damage, arises from the growth of extra sarcomeres in series in the muscle fibres. This will cause the sarcomeres to operate at a shorter sarcomere lengths for the same muscle length, so that eccentric contractions that previously extended onto the descending limb of the length-tension curve will be confined to the ascending limb. This will avoid the instability, the non-uniformity, and ultimately the damage. It is planned to test this by looking at athletes who undertake eccentric actions in the course of their sport. eg softball catchers squatting.