coach education. But a more challenging question to answer is why a worker who has performed the same job for years without symptoms now starts to report symptoms consistent with overuse. In some cases at least, an answer might be found in age-related changes in tissues and slower tissue healing and remodeling rates, so that tissues can no longer repair and remodel tissue quickly enough. Let us now examine some of the known injury mechanisms in the tissues of interest.
Contraction-induced injury is defined as morphological damage to small focal groups of sarcomeres as a result of mechanical disruption of the interdigitation of the thick and thin filament arrays or of the Z-lines of single sarcomeres (Faulkner & Brooks, 1995). The injury initiates a cascade of events that produce a more severe secondary injury after two or three days. This involves an inflammatory response, free radical damage, appearance of cytosolic enzymes in the serum, and phagacytosis of elements within the cytosol of damaged sarcomeres (Faulkner & Brooks, 1995) Human beings report pain associated with this phase as delayed onset muscle soreness. Striated muscle is rarely injured when active in isometric, or shortening contractions, but injuries are known to occur when muscle is activated and forcibly stretched (Brooks, Zerba, & Faulkner, 1995) in a so-called 'plyometric' contraction. That stretch can be caused by impact of a body segment with an external surface or object, as well as during certain self-initiated movements such as jumping up onto something. Depending upon the severity of the injury, 1-4 weeks is required for complete recovery of muscle structure and function (Brooks & Faulkner, 1990).
Stretch-related injuries in striated muscle can also be caused by a rapid movement associated with a recovery from loss of balance, a slip, trip, throw, catch, landing, or other rapid movement. Over the past fifteen years research in man, as well as in situ and in vitro animal studies, has indicated that stretch-related injuries in striated muscle are caused by a mechanical-mediated event rather than a chemical or metabolic event. Generally, this involves a single rapid stretch to actively contracting muscle (Lieber & Friden, 1993) or a series of repetitive plyometric contractions (Friden, Sjostrom, & Ekblom, 1983) (Newham, Jones, & Edwards, 1983a) (McCulley & Faulkner, 1985). At present, in animal experiments the muscle injury is best characterized by the resulting deficit in maximum force developed by the muscle, rather than by ultrastructural measures ((Newham, McPhail, Mills, & Edwards, 1983b) cited by (Brooks & Faulkner, 1996)). For single stretches the threshold for injury in mice has been estimated as a work input of 150 J/Kg muscle, corresponding to stretches in excess of 20% L0 (optimal muscle length) strain, say, at a rate of 2Lf/s (muscle fiber lengths per second). Experiments in rodents suggest that one of the factors best predicting the injury is the combination of the muscle strain and average force, or work input to the muscle, and its