Morphology of immobilized skeletal muscle and the effects of a pre- and postimmobilization training program

The hind limbs of mice were immobilized with plaster cast for different periods of time, and the atrophy of the anterior tibial muscle was examined by measuring fiber cross sections. In a second series of experiments, mice were trained on a treadmill before and after immobilization. The most pronounced decrease in fiber diameters was observed during the 1st week; during prolonged immobilization, only a moderate atrophy occurred. Red fibers were found to be more susceptible to immobilization atrophy than white fibers. The ultrastructural observations extended to loss and fragmentation of myofibrils, mitochondria, and the sarcotubular system. Some fibers split and appeared to undergo segmental necrosis, which was followed by invasion of leucocytes into the muscle. Still while immobilized, the muscles exhibited a regenerative capacity; satellite cells differentiated to myoblasts, which fused to myotubes, being the precursors of new muscle fibers. This was already observed during the 1st week of immobilization. The effect of training after immobilization was documented by an increase of fiber diameters. The ultrastructural alterations, however, in these muscles were severe; it was concluded that a postimmobilization training has to be undertaken very carefully. When the muscles were trained before immobilization, the atrophy was almost negligible. A preimmobilization training can probably prevent the muscle from developing severe atrophy.     

Effects of immobilization and subsequent lowand high-intensity exercise on morphology of rat calf muscles

After a cast immobilization of 3 weeks, the effects of 4-week remobilization by free cage activity or treadmill running on the morphology of the rat soleus and gastrocnemius muscles were studied. The studied morphometric parameters were: percentage volume of intramuscular connective tissue, capillary density, muscle fiber size, number of fibers with a pathological structural alteration, and fiber type distribution.
In both muscles, immobilization of 3 weeks produced a significant increase in the connective tissue volume and number of fibers with pathological alterations, with a similar decrease in the capillary number and fiber size. At the same time, the relative amount of type I fibers decreased and type IIA fibers increased. Free remobilization and especially intensified remobilization by treadmill running significantly restored these values towards controls.
These findings indicate that in rat soleus and gastrocnemius muscles immobilization-induced accumulation of intramuscular connective tissue, capillary loss, reduction in fiber size, accumulation of fibers with pathological structural alterations, and changes in fiber type distribution are to a great extent reversible phenomena, especially if remobilization is intensified by physical training. In clinical practice, this suggests that in patients with musculoskeletal injuries the postimmobilization rehabilitation should be early and effective.     

Skeletal muscle HSP expression in response to immobilization and remobilization

Heat shock proteins play an important regulatory role in the cellular defence. Oxidative stress is one of the factors inducing heat shock protein expression. This study tested the effects of 4 weeks of immobilization and subsequent remobilization on heat shock protein expression and oxidative stress in the lateral gastrocnemius and plantaris muscles of the rat. Active mobilization or free mobilization protocols were used for remobilization. In active mobilization, strenuous uphill treadmill running, twice a day, was started immediately after the immobilization and lasted for six days. Rats in the free mobilization group moved freely in their cages immediately after the immobilization. Expression of heat shock proteins was upregulated during the recovery from immobilization, especially in the lateral gastrocnemius muscle in the active mobilization group. However, markers of oxidative stress, such as protein carbonyls and 4-hydroxynonenal protein adducts, or activities of the antioxidant enzymes glutathione peroxidase and glutathione reductase, did not change after the immobilization and subsequent recovery. In summary, following immobilization, both intensive and spontaneous exercise upregulated the heat shock protein expressions in the lateral gastrocnemius muscle and partly in the plantaris muscle, which may contribute to the recovery from immobilization atrophy.     

The effects of training, immobilization and remobilization on musculoskeletal tissue

The effects of different types of training and immobilization on muscle tissue have been studied intensively and have been well established. At the beginning of strength or power training, 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 inhibitory inputs to the active alpha motor neurons. After 6 to 8 weeks, further progress is due to gradual muscular hypertrophy, that is, a true increase in size of pre-existing fibres. Today, the theory of muscular hyperplasia (new fibre formation by a splitting of existing fibres) is not supported in critical reviews. With endurance training, there is an increased concentration and volume density of muscle mitochondria with corresponding biochemical adaptation, allowing the muscle to produce more mechanical power output aero-bicalry and to be activated for longer periods of time without being fatigued. Immobilization, in turn, atrophies the muscle very quickly, significantly 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 intramuscular connective 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 tensile strength, elastic stiffness and total weight of a tendon or ligament have increased due to training (collagen fibre thickening) and decreased due to immobilization (fibre splitting and disorientation). These changes can be explained by an exercise (immobilization-induced increase (decrease) in synthesis of collagen and proteogrycan-water matrix due to increased (decreased) fibroblast activity. The effects of training on the myotendinous junction or proprioceptors (muscle spindles and Golgj tendon organs) are largely unknown. Our recent studies showed that immobilization is very detrimental to these organs morphologically as well as biochemically. Slowly progressing physical exercise causes meaningful adaptive changes in the articular cartilage: the cells and nuclei of chondrocytes enlarge and the proteoglycan content and cartilage thickness increase. However, if training is too strenuous or biomechanically misloading, a degeneration process of the cartilage may begin, which is also the case in an immobilized joint Bone tissue adapts to weight-bearing 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 occur. The achieved bone mass is also dependent on genetic, nutritional and hormonal factors. Immobilization, on the other hand, causes exactly the reverse effects on bone tissue and may finally (that is, after 5 to 6 months) lead to irreversible osteoporosis.     

被动运动对制动后兔膝关节软骨和关节囊超微结构变化的影响

本文通过对30只兔左侧膝关节屈曲位石膏固定,观察制动、制动后的不同运动形式对关节软骨和关节囊组织超微结构的影响,发现制动4周后,软骨细胞出现退行性变,而成纤维细胞呈代谢活跃;制动9周后,软骨细胞退行性变迸一步加重,成纤维细胞同样出现退行性变。去制动后自行活动9周,软骨细胞和成纤维细胞退行性变尚未恢复。去制动后如给予早期被动运动,与同期自行活动相比,软骨细胞和成纤维细胞退行性变的恢复明显加快。     

Incomplete restoration of immobilization induced softening of young beagle knee articular cartilage after 50-week remobilization

The aim of this study was to characterize the biomechanical and structural changes in canine knee cartilage after an initial 11-week immobilization and subsequent remobilization period of 50 weeks. Cartilage from the immobilized and remobilized knee was compared with the tissue from age-matched control animals. Compressive stiffness, in the form of instant shear modulus (ISM) and equilibrium shear modulus (ESM) of articular cartilage, was investigated using an in situ indentation creep technique. The local variations in cartilage of glycosaminoglycan (GAG) concentration were measured with a microspectrophotometer after safranin O staining of histological sections. Using a computer-based quantitative polarized light microscopy method, collagen-related optical retardation, gamma, of cartilage zones were performed to investigate the collagen network of cartilage. Macroscopically, cartilage surfaces of the knee joint remained intact both after immobilization and remobilization periods. Immobilization caused significant softening of the lateral femoral and tibial cartilages, as expressed by ESM (up to 30%, p < 0.05). Remobilization restored the biomechanical properties of cartilage in the lateral condyle of tibia, but in the lateral condyle of femur ESM remained 15% below the control level (p = 0.05). The instant shear modulus was not changed either after immobilization or remobilization. The GAG content of the cartilage was slightly decreased after immobilization, especially in the superficial zone of cartilage, but the change was not statistically significant. After remobilization the intensity of safranin O content rose to control level. Neither immobilization nor remobilization had any effect on the gamma value of collagen fibril network either in the superficial or the deep zone at any of the test points. The changes of ESM were positively correlated with the alterations in GAG content of the superficial and deep zones after immobilization and remobilization. This confirms the key role of protoglycans in the regulation of the equilibrium stiffness of articular cartilage. As a conclusion, immobilization of the joint of a young individual may cause long-term, if not permanent, alterations of cartilage biomechanical properties. This may predispose joint to degenerative changes later in life.     

Muscular atrophy following immobilisation. A review

Muscular atrophy regularly occurs as a consequence of immobilisation or disuse after sports injuries. Several experimental models deal with muscle atrophy and are suitable for investigations of the underlying mechanisms of muscle atrophy. Strength loss is the most evident response to atrophy. Muscle strength decreases most dramatically during the first week of immobilisation; little further weakening occurs later on. This is reflected in changes in the EMG of disused muscles and can also be observed in muscle weight and size of muscle fibres. Slow muscles with predominantly oxidative metabolism are most susceptible to atrophy as indicated by various findings: slow muscle fibers show greater atrophy than fast fibres; their relative and probably absolute number is decreased in atrophic muscles; in addition, the oxidative enzyme content is most severely affected by disuse. Atrophic muscle is characterised by a catabolic metabolism. The rate of protein synthesis is reduced and that of protein breakdown increased. Autophagic activities probably play an important role in early stages of muscular atrophy. The oxygen supply to disused muscle may be impaired, although myoglobin content is increased in atrophic muscle. The complete loss of mitochondrial function during the first days of disuse may be of aetiological importance. The amount of connective tissue is increased in atrophic muscle and surrounding periarticular tissue which may lead into a vicious circle of musculoskeletal degeneration. An almost complete recovery from atrophy is possible, yet often the recovery phase is much longer than the total immobilisation period.     

Benefits of aerobic exercise for the paraplegic: a brief review

The importance of exercise for the general population is emphasized widely; therefore, it must be even more important for paralegics who are already threatened with poor health due to the sedentary nature of their lifestyle. The effects of functional degeneration are vast and greatly reduce the overall health of paraplegics, particularly within the musculoskeletal and cardiovascular systems, thereby increasing their risk for cardiovascular disease. Recent investigations suggest that this process may be reversible through exercise training and that paraplegics respond to exercise training in essentially the same manner as the non-handicapped individual. In addition, exercise training has been reported to decrease the resorptive process of the skeleton by decreasing bone and collagen catabolism and possibly aiding in new bone formation. This review attempts to summarize the available literature on the effects of exercise on the paraplegic and will hopefully provide some direction not only for further research but also recommendations for practitioners working in the field.     

制动对兔膝关节韧带力学特性和形态学的影响

本文通过对兔膝关节制动前后股骨—内侧副韧带—胫骨复合装置抗张强度的测定,以及对外侧副韧带和韧带附着骨端的形态学观察,研究制动及制动后进行被动运。动对骨—韧带—骨复合装置抗张强度的影响并探讨其机制。结果表明,制动可导致股骨—内侧副韧带—胫骨复合装置的最大载荷、能量吸收明显下降。这种改变可能与韧带附着胫骨端破骨细胞增多,骨膜下骨吸收增加,导致韧带附着力减弱,以及韧带组织中胶原纤维束减少有关。去制动后,由于韧带附着胫骨端的形态结构恢复较慢,韧带—骨复合装置抗张强度的完全恢复需较长的时间。制动后的早期被动运动对韧带—骨复合装置抗张强度的恢复及韧带组织结构的恢复有一定促进作用。     

Different frequency treadmill running in immobilization-induced muscle atrophy and ankle joint contracture of rats

We investigated the effects of different frequencies of treadmill running on immobilization-induced soleus and gastrocnemius muscle atrophy and ankle joint contracture in rats using morphology and histochemistry. The right ankle joint of rat was immobilized for 2 weeks. Thereafter, the rats were randomly assigned to four groups for 6 weeks of exercise under different conditions: free cage activity and free remobilization (FR), once-a-week treadmill running (low-frequency running program (LFR)), three-time-a-week running (middle-frequency running program (MFR)), and six-time-a-week running (high-frequency running program (HFR)) groups. Two weeks of immobilization significantly reduced the cross-sectional area of soleus type I (62%, P<0.05) and type II muscle fibers (66%, P<0.05), gastrocnemius type I (78%, P<0.05) and type II muscle fibers (68%, P<0.05), and the range of ankle joint movement (46%, P<0.05). Immobilization also increased the ratio of type II to total fiber numbers in the soleus (P<0.05), and gastrocnemius (P<0.05), and induced pathological changes in muscle fibers. Some of these changes could not be corrected by free remobilization; however, the LFR, MFR, and HFR groups clearly recovered toward normal levels with exercise frequency, the effect on muscle recovery being more beneficial in the MFR and HFR groups. In addition, the range of ankle joint contracture was improved in LFR, MFR, and HFR groups in comparison with that in the FR group. These findings indicate that treadmill running exercise improved the immobilization-induced muscle fiber histochemical alterations and the range of the ankle motion in rats. Running three times and six times a week was more beneficial for recovery of immobilization-induced muscle atrophy and joint contracture compared with no running or once-a-week running.     

The role of apoptosis in age-related skeletal muscle atrophy

Skeletal myocyte atrophy and death contribute to sarcopenia, a condition associated with normal aging. By 80 years of age, it is estimated that humans generally lose 30-40% of skeletal muscle fibres. The mechanism for this loss is unknown; however, it may involve apoptosis. Mitochondrial dysfunction and sarcoplasmic reticulum (SR) stress that occurs with age may be possible stimuli inducing apoptosis. Hence, mitochondria and SR may be important organelles within skeletal myocytes responsible for apoptosis signalling. The activation of apoptosis may be partly responsible for the initiation of muscle protein degradation, loss of muscle nuclei associated with local atrophy, and cell death of the myocyte. Exercise training and caloric restriction are two interventions known to enhance skeletal muscle function. The effects of these interventions on apoptosis are discussed.     

Collagen fibre arrangement and functional crimping pattern of the medial collateral ligament in the rat knee

Ligaments have been described as multifascicular structures with collagen fibres cross-connecting to each other or running straight and parallel also showing a waviness or crimping pattern playing as a shock absorber/recoiling system during joint motions. A particular collagen array and crimping pattern in different ligaments may reflect different biomechanical roles and properties. The aim of the study was to relate the 3D collagen arrangement in the crimping pattern of the medial collateral ligament (MCL) to its functional role. The MCL is one of the most injured ligaments during sports activities and an experimental model to understand the rate, quality and composition of ligaments healing. A deep knowledge of structure–function relationship of collagen fibres array will improve the development of rehabilitation protocols and more appropriate exercises for recovery of functional activity. The rat MCL was analysed by polarized light microscopy, confocal laser microscopy and scanning electron microscopy (SEM). Histomorphometric analysis demonstrated that MCL crimps have a smaller base length versus other tendons. SEM observations demonstrated that collagen fibres showing few crimps were composed of fibrils intertwining and crossing one another in the outer region. Confocal laser analyses excluded a helical array of collagen fibres. By contrast, in the core portion, densely packed straight collagen fibres ran parallel to the main axis of the ligament being interrupted both by planar crimps, similar to tendon crimps, and by newly described right-handed twisted crimps. It is concluded that planar crimps could oppose or respond exclusively to tensional forces parallel to the main ligament axis, whereas the right-handed twisted crimps could better resist/respond to a complex of tensional/rotational forces within the ligament thus opposing to an external rotation of tibia.     

Effects of remobilization on rat femur are dose-dependent

Seventy 9 to 11-week-old Sprague-Dawley male rats were divided into seven groups [baseline, 3-week, 11-week control groups; a group with a left limb immobilization for 3 weeks; and three groups with a similar immobilization and subsequent 8-week free (FR), low-intensity running (LR) or high-intensity running (HR) remobilization] to determine the site-specific effects of decreased mechanical loading and subsequent increased activity on rat femur. Bone mineral content of the proximal femur (PBMC), femoral midshaft (SBMC) and distal femur (DBMC) and the histomorphometry of the distal femur were used as outcome variables. The 3-week immobilization period resulted in significant bone loss in the proximal and distal ends of the immobilized left limb, the deficit being -5.9% in PBMC and -14.7% in DBMC. Immobilization also led to marked microarchitectural changes in the distal femur, the left-side deficit in trabecular bone volume (BV/TV) being -23.9%. After remobilization, there was a clear indication for dose-dependent response; i.e., immobilization-induced left-to-right side differences in BV/TV persisted in the FR animals (-23.8%), while these left limb deficits were significantly reduced in the LR group (-15.0%) and virtually absent in the HR group (-3.1%). The left limb deficit in PBMC was still significant in all groups after the 8-week period of remobilization [-9.6% in the FR group; -13.4% in the LR group; and -7.2% in the HR group]. The left-limb deficit in SBMC was significant in the HR11 group only (-7.2%), and, contrary to histomorphometric data, virtually absent in DBMC in all remobilization groups. As compared with the age-matched control data, the weight-adjusted BMCs of both limbs of the LR and HR groups were comparable or even higher (right limbs) than those of the controls. In conclusion, this study indicates that remobilization-induced bone recovery depends on the intensity of the remobilization so that during the 8-week period of remobilization, high-intensity running results in better recovery than low-intensity running, both of which are more efficient than free-cage activity only. Immobilization-induced changes in rat femur are also restored in a site-specific fashion, the most trabecular distal region of the femur showing more complete recovery than the more cortical proximal and midshaft regions.     

Cross education and immobilisation: Mechanisms and implications for injury rehabilitation

ObjectivesUnilateral strength training produces an increase in strength of the contralateral homologous muscle group. This process of strength transfer, known as cross education, is generally attributed to neural adaptations. It has been suggested that unilateral strength training of the free limb may assist in maintaining the functional capacity of an immobilised limb via cross education of strength, potentially enhancing recovery outcomes following injury. Therefore, the purpose of this review is to examine the impact of immobilisation, the mechanisms that may contribute to cross education, and possible implications for the application of unilateral training to maintain strength during immobilisation.DesignCritical review of literature.MethodsSearch of online databases.ResultsImmobilisation is well known for its detrimental effects on muscular function. Early reductions in strength outweigh atrophy, suggesting a neural contribution to strength loss, however direct evidence for the role of the central nervous system in this process is limited. Similarly, the precise neural mechanisms responsible for cross education strength transfer remain somewhat unknown. Two recent studies demonstrated that unilateral training of the free limb successfully maintained strength in the contralateral immobilised limb, although the role of the nervous system in this process was not quantified.ConclusionsCross education provides a unique opportunity for enhancing rehabilitation following injury. By gaining an understanding of the neural adaptations occurring during immobilisation and cross education, future research can utilise the application of unilateral training in clinical musculoskeletal injury rehabilitation.     

Fiber-type discrimination in disuse and glucocorticoid-induced atrophy

Data are presented which demonstrate that phasic/glycolytic muscles atrophy more than tonic/oxidative muscles in response to exogenously introduced glucocorticoids. Data are also presented demonstrating that immobilization makes a muscle unusually sensitive to glucocorticoid-induced atrophy and that remobilization of a previously immobilized muscle protects a muscle from glucocorticoid-induced atrophy. These observations are discussed within the context of the role of mechanical activity in the acquisition and maintenance of fiber-type characteristics. In addition, the available data on the glucocorticoid receptor population in skeletal muscles of various types and circumstance are reviewed within the context of the recent observations concerning the glucocorticoid induction of the enzyme glutamine synthetase in skeletal muscle. It is proposed here that atrophy is not necessarily the response of skeletal muscle to glucocorticoids. Rather, atrophy is a possible consequence of the glucocorticoid-induced increase in export of amino acid carbon from the muscle. Whether such export causes a muscle to atrophy or perhaps even hypertrophy will depend on the capacity of the muscle to sustain its free amino acid pools. Mechanical activity greatly promotes the uptake of free amino acids in skeletal muscle. Such promotion takes the form of both contraction-induced uptake and increased insulin sensitivity. Within this perspective, it is suggested that tonic muscles and remobilized muscles are protected from atrophy by exogenous glucocorticoids because their high level of mechanical activity allows them to maintain their free amino acid pools.     

Imaging features of therapeutic drug-induced musculoskeletal abnormalities

Increasing use of a wide variety of therapeutic drugs with known musculoskeletal side-effect profiles necessitates a rigorous understanding and approach when evaluating imaging features suggestive of drug-induced musculoskeletal abnormalities. The etiology of such abnormalities is diverse, and the clinical and imaging manifestations may be nonspecific. The recognition of adverse effects depends, first, on the physician's vigilant review of clinical information for relevant drug history and indicative signs, and second, on the radiologist's ability to detect musculoskeletal changes consistent with known potential effects of specific drugs. Musculoskeletal abnormalities induced by therapeutic drugs may be broadly categorized as embryopathic, juvenile, or postmaturation. Embryopathic skeletal abnormalities result from the teratogenic effects of drugs administered to pregnant women (eg, thalidomide, anticonvulsants). Other therapeutic agents characteristically lead to abnormalities during postnatal skeletal maturation (eg, high-dose vitamins or prostaglandin) either because they are used exclusively in children or because they have idiosyncratic effects on immature musculoskeletal structures. Many drugs (eg, statins) may have musculoskeletal side effects that, although independent of the stage of skeletal maturation, are most often seen in adults or elderly people because they are commonly prescribed for people in these age groups. Drug-induced musculoskeletal abnormalities may be further characterized according to the predominant skeletal manifestations as osteomalacic, proliferative, or osteoporotic and according to the involvement of soft tissues as musculotendinous or chondral.     

The effects of immobilization on the quality of Achilles tendon in rats

Immobilization of an Achilles tendon in a shortened position for 1 and 3 weeks did not change pyridinoline and mature collagen concentrations. Although a significant decrease in the biosynthesis of collagen was observed simultaneously in the soleus muscle of the same hindlimb, these results suggest that the stability of collagen provided by the nonreducible cross-link, pyridinoline, is not altered during this type of immobilization. The significance of stable cross-links for the known decrease in tensile strength during immobilization remains open.     

Eccentric rehabilitation exercise increases peritendinous type I collagen synthesis in humans with Achilles tendinosis

It has been shown that 12 weeks of eccentric heavy resistance training can reduce pain in runners suffering from chronic Achilles tendinosis, but the mechanism behind the effectiveness of this treatment is unknown. The present study investigates the local effect of an eccentric training regime on elite soccer players suffering from chronic Achilles tendinosis on the turnover of the peritendinous connective tissue. Twelve elite male soccer players, of whom six suffered from unilateral tendinosis and six were healthy controls, participated in this study. All participants performed 12 weeks of heavy-resistance eccentric training apart from their regular training and soccer activity. Before and after the training period the tissue concentration of indicators of collagen turnover was measured by the use of the microdialysis technique. After training, collagen synthesis was increased in the initially injured tendon (n=6; carboxyterminal propeptide of type I collagen (PICP): pre 3.9+/-2.5 microg/L to post 19.7+/-5.4 microg/L, P<0.05). The collagen synthesis was unchanged in healthy tendons in response to training (n=6; PICP: pre 8.3+/-5.2 microg/L to post 11.5+/-5.0 microg/L, P>0.05). Collagen degradation, measured as carboxyterminal telopeptide region of type I collagen (ICTP), was not affected by training neither in the injured nor in the healthy tendons. The clinical effect of the 12 weeks of eccentric training was determined by using a standardized loading procedure of the Achilles tendons showing a decrease in pain in all the chronic injured tendons (VAS before 44+/-9, after 13+/-9; P<0.05), and all subjects were back playing soccer following the eccentric training regime. The present study demonstrates that chronically injured Achilles tendons respond to 12 weeks of eccentric training by increasing collagen synthesis rate. In contrast, the collagen metabolism in healthy control tendons seems not to be affected by eccentric training. These findings could indicate a relation between collagen metabolism and recovery from injury in human tendons.     

Nerve supply of anterior cruciate ligaments and of cryopreserved anterior cruciate ligament allografts: a new method for the differentiation of the nervous tissues

We investigated the nerve supply of anterior cruciate ligaments ((ACLs) and of cryopreserved bone-ACL-bone allografts in a rabbit model with immunohistochemical methods to establish the distribution pattern of the nervous tissues and to determine the reinnervation rate of ACL allografts. The ACL is innervated by three different classes of nerve fibre: (1) fibres of large diameter, characterized by neurofilament immunoreactivity, which are fast-conducting mechanoreceptive sensory afferents; (2) fibres of small diameter, characterized by substance Pimmunoreactivity, which are slow-conducting nociceptive sensory afferents; and (3) sympathetic efferent vasomotor fibres, characterized by their immunoreactivity to the ratelimiting enzyme of noradrenaline synthesis, tyrosine hydroxylase. The ACLs showed numerous fibres of all three nerve classes; as specialised sensory nerve endings only Ruffini corpuscles were observed. All nerve fibres were located subsynovially, none within the collagen core of the ligament itself. No nerve fibres were detected in the ACL allografts at 3 and 6 weeks. Sparse fibres were detected at 12 weeks, while the 24-, 36-and 52-week specimens showed plenty of all three fibre types. No mechanoreceptors were found in the ACL allografts. To our knowledge, this method for the first time allows a differentiation of the nerve fibres of ACLs and ACL allografts into three different nerve fibre classes with known neurophysiological functions.     

Overuse injuries in athletes: a perspective

Injuries secondary to sporting activities have increased significantly in the past decade. Traditional treatment programs for these maladies have frequently failed to meet the physiological expectations of the athlete. Forced rest or immobilization result in predictable musculoskeletal atrophy with impaired function. Furthermore, the rehabilitation process has commonly focused on the management of the acute problem with minor attention to the etiology and pathomechanics of the injury (preventive medicine). Many sports injuries, as a result of overuse, can be avoided by scientific coaching and contemporary sports medicine.