A spontaneous rupture of a tendon may be definied as a rupture that occurs during movement and activity, that should not and usually does not damage the involved musculotendinous units (1). Spontaneous tendon ruptures were uncommon before the 1950s. Böhler found only 25 Achilles tendon ruptures in Wien between 1925 and 1948 (2). Mösender & Klatnek treated 20 Achilles tendon ruptures between 1953 and 1956, but 105 ruptures between 1964 and 1967 (3). Lawrence et al. found only 31 Achilles tendon ruptures in Boston during a period of 55 years (1900‐1954) (4). During the recent decades tendon ruptures have, however, become relatively common in developed countries, especially in Europe and North America. A high incidence of tendon ruptures has been reported in Austria, Denmark, Finland, Germany, Hungary, Sweden, Switzerland and the USA; somewhat lower incidences have been reported in Canada, France, Great Britain and Spain. On the other hand, Greece, Japan, the Netherlands and Portugal have reported a clearly lower incidence. Interestingly, Achilles tendon ruptures are a rarity in developing countries, ecpecially in Africa and East‐Asia (5). In many developed countries, the increases in the rupture incidence have been dramatic. In the National Institute of Traumatology in Budapest, Hungary, the number of patients with an Achilles tendon rupture increased 285% in men and 500% in women between two successive 7‐year periods, 1972‐1978 and 1979–1985(5).

Since a tendon is a living tissue, it is not a surprise that tendon shows the capacity to adapt its structure and mechanical properties to the functional demands of the entire muscle‐tendon unit. However, compared with muscle, the experimental knowledge of the effects of strength or endurance‐type training on tendon tissue is scarce and clinical human experiments are completely lacking (1). Research should, however, be able to improve the true understanding of the biomechanical, functional, morphological and biochemical changes that occur in tendons due to training and physical activity, since understanding of the basic physiology of a tissue is the key to understanding its pathological processes (1,2). Compared with muscle tissue, the metabolic turnover of tendon tissue is many times slower due to poorer vascularity and circulation (1, 3). The adaptive responses of tendons to training are therefore also slower than those in muscles, but they may finally be considerable if the time frame is long enough (3, 4).

The three-dimensional ultrastructure of human tendons has been studied. Epitenon and peritenon consis of a dense network of longitudinal, oblique and transversal collagen fibrils crossing the tendon fibres. The interna structure of tendon fibres is also complex. The collagen fibrils are oriented not only longitudinally but also transversel· and horizontally. The longitudinal fibrils do not run only parallel but also cross each other forming spirals (plaits) These fibril bundles are bound together by a three-dimensional collagen fibril network of endotenon. In the myotendi nous junction the surface of the muscle cells form processes. A network of tendineal collagen fibrils fills the recesses between the muscle cell processes penetrating the basement membrane of these processes. This complex ultrastructur < of human tendons most likely offers a good buffer system against longitudinal, transversal, horizontal as well as rotational forces during movement and activity.

During the last few decades, the incidence of tendon ruptures has increased in civilized countries. Our material comprises 749 patients who had 832 tendon ruptures treated surgically between 1972 and 1985. There were no competitive athletes among the patients studied. There were 292 single ruptures of the Achilles tendon, 274 of the proximal biceps brachii, 113 of the extensor pollicis longus, and 70 of other tendons. Forty-eight patients had multiple ruptures and 35 patients had reruptures. Achilles tendon ruptures often occurred in recreational sports activities (59%), in contrast to other tendon ruptures (2%; P less than 0.001). The mean age for patients who had Achilles tendon rupture was 35.2 years and for patients with other ruptures, 50.7 years (P less than 0.001). There was a connection between the high incidence of blood group O and tendon ruptures (P less than 0.001). In cases of multiple ruptures and reruptures, the frequency of blood group O was 71%. Sixty-two point three percent of the patients with Achilles tendon rupture were professionals or white collar workers, which is markedly more than in the Hungarian population (12.7%; P less than 0.001). Two hundred and six Achilles tendon ruptures were studied histologically, and all cases displayed pathological alterations. The results indicate that complete rupture of the Achilles tendon is usually a sequel to a sedentary life-style and participation in sports activities.

The effects of tmkhg, immobilization and remobilization on musculoskeletal tissue. 1. ?f.aining and immobilization. Scand J Med Sci Sports W 2 10048.The effects of Merent types of training and immobilization on muscle tissue have been studied intensively and have been well established. At the beginning of strength or power train@, the increase in muscular performance can be explained by neural and psychological adaptation; that is, recruitment of more motor units per time unit, learning of more effective and economical usage of the active motor units and reduction of the inhiiitoIy inputs to the active alpha motor neurons. A€ter 6 to 8 weeks, further progress is due to gradual muscular hypertrophy; that is, a true increase in size of pre-existing fibres. =y, the theoxy of muscular hyperplasia (new fibre formation by a splitting of existing fibres) is not supported in uitid reviews. With endurance training there is an increased concentration and volume density of muscle mitochondria with correspond& biochemical adaptation, allowing the muscle to produce more mechanical power output aerobically and to be activated for longer periods of time without being fatigued. Immobilization, in turn, atrophies the muscle veq quickly, signiticantly already after one week. The most striking morphological findings are reduction in fibre size and diameter, reduction in the capillary density and a simultaneous increase in intramconnective tissue. At the same time, many harmful functional and biochemical effects also occur. Compared with muscle tissue, the knowledge of the effects of training and immobilization on tendon or ligament tissue is scarce and research has not been systematic.In animal experiments the tenaile strength, elastic stitbess and total weight of a tendon or ligament have increased due to training (collagen fibre thickening) and decreased due to immobilization (fibre splittiug and disorientation). These changes can be explained by an exercise (immobktion)-in-' duced increase (decrease) in synthesis of collagen and protmglycan-water matrix due to increased (decreased) fibroblast activity. The effects of training on the mptendinous junction or proprioceptom (muscle spmdles and Go@ tendon organs) are largely unknown. Our recent studies s h d that immobili-I zation is very detrkntal to these organs morphologicauy as well as biochemicthe articular cartilage: the cells and nuclei of chondrocytes enlarge and the proteoglycan content and cartilage thickurn increase. However, if training is too strenuous or biornechanically misloading, a degeneration process of the cartilage may begin, which is also the case in an immobilized joint. Bone tissue adapts to weight-krhg and muscular work well by increasing bone mass and density, most probably through osteoblast stimulation. The remodelling cycle of bone tissue is, however, a slow process, taking at least several months to OCCUT. The achieved bone mass is also dependent on genetic, nutritional and hormonal factors. Immobilization, on the other hand, causes exactly the reverse e...