The Veterinary Journal The Veterinary Journal 170 (2005) 184–192 www.elsevier.com/locate/tvjl
Review
Mechanical and functional properties of the equine superficial digital flexor tendon B.A. Dowling, A.J. Dart
*
University Veterinary Centre Camden, Faculty of Veterinary Science, University of Sydney, Werombi Road, Camden, NSW 2570, Australia Accepted 29 March 2004
Abstract The in vitro and in vivo mechanical properties of the superficial digital flexor tendon have been described. To date the focus has been on single load to failure testing, however refined in vivo methods may prove useful to evaluate the effects of treatment and exercise on tendons. During maximal exercise, the adult superficial digital flexor tendon operates close to its functional limits with a narrow biomechanical safety margin. This combined with exercise and age associated microdamage, and a limited adaptive ability may increase the risk of fatigue failure. Studies evaluating treatment regimens for tendonitis have focused on repair and regeneration and yielded varying results. It would appear that the superficial digital flexor tendon has a limited ability if any to adapt positively to exercise after maturity. In contrast, the foalÕs superficial digital flexor tendon may have a greater adaptive ability and may respond to an appropriate exercise regimen to produce a more functionally adapted tendon. Recent studies have shown that foals allowed free pasture exercise develop a larger, stronger, more elastic tendon compared to foals that were confined or subjected to a training program. Effects on the non-collagenous matrix appear to be responsible for these differences. In contrast, training or excess exercise may have permanent detrimental effects on the biomechanical and functional properties of the superficial digital flexor tendon in the foal. The implication is that the determination of optimum exercise intensity and timing, and the role of the non-collagenous matrix in tendon physiology in the young horse may hold the key to developing tendons more capable of resisting injury. Ó 2004 Elsevier Ltd. All rights reserved. Keywords: Equine; Horse; Tendon; Superficial flexor tendon; Tendonitis
1. Introduction Evolution and domestic selection of equine athletes have resulted in a streamlined distal limb with strong ligaments and tendons that contribute to the efficiency of locomotion through their elastic properties (Biewener, 1998). It is apparent, however, that during maximal exercise the superficial digital flexor tendon (SDFT) operates close to its physiological limits with a narrow biomechanical safety margin (Riemersma and Scham*
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[email protected] (A.J. Dart).
1090-0233/$ - see front matter Ó 2004 Elsevier Ltd. All rights reserved. doi:10.1016/j.tvjl.2004.03.021
hardt, 1985; Stephens et al., 1989; Wilson and Goodship, 1990). This coupled with early maturation of the SDFT, limited adaptive ability after maturation, and cellular and biochemical alterations suggestive of progressive degeneration is likely to be responsible for the high incidence of clinical tendonitis (Riemersma and Schamhardt, 1985; Stephens et al., 1989; Wilson and Goodship, 1990; Genovese, 1993; Goodship, 1993; Wilson et al., 1996; Patterson-Kane et al., 1997a,b). Despite significant recent scientific advances, our understanding of tendon homeostasis, effects of maturation, exercise and training, and the pathophysiology of SDFT injury and healing is incomplete. Consequently
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it is not surprising that the efficacy of proposed treatment regimens is equivocal and the results of clinical trials vary substantially (Dowling et al., 2000). It would appear treatment and rehabilitation of horses with SDFT injury is problematic and prevention of tendon injury may be a more realistic goal. Modulation of tendon physiology prior to maturation may hold the key (Cherdchutham et al., 2001a; Smith et al., 2002a). The purpose of this article is to review current literature on the biomechanical properties of the SDFT and the effects of maturation, exercise and treatment methods.
2. Biomechanical testing (in vitro) Mathematical models assume that the mechanical properties of tendon are related to elasticity, viscosity, plasticity, internal friction and strain history, and that the stress–strain curve represents the instantaneous response of tendon (Viidik, 1968; Woo, 1986; Johnson et al., 1996). The error associated with these assumptions is reduced by the fact that tendon stiffness is strain-rate dependent (VanBroklin and Ellis, 1965; Johnson et al., 1996). Increasing the strain rate shifts the stress–strain curve to the left as the tendon exhibits a stiffer response. Under cyclical loading the curve shifts to the right until it reaches a steady state. This is likely related to packing of collagen fibrils and redistribution or elimination of water from the extra-collagenous matrix (Rigby, 1964; Gelberman et al., 1987). Hysteresis is a measure of energy loss, primarily as heat, during cyclical loading. Under a fixed sub-maximal load, tendon creep occurs leading to stress relaxation such that the measured load initially increases then decreases and levels out (Graf et al., 1994). The time-dependant effect of preconditioning (static or cyclical) is relatively short lived with no apparent effect on maximal load (Woo, 1982; OÕBrien et al., 1989; Graf et al., 1994). Measurement of the in vivo biomechanical properties of tendon using strain gauges, ground reaction force (kinetic), and motion analysis (kinematic) data has been reported (Lochner et al., 1980; Silver et al., 1983; Riemersma et al., 1988a,b; Stephens et al., 1989; Platt et al., 1991; Clayton et al., 1998; Takahashi et al., 2001; Meershoek et al., 2001a,2001b). Disadvantages include surgical intervention, bending and damage to tendon fibres, interference from adjacent structures, site-specific data, extrapolation from measured in vitro data and required correction of inherent errors in kinetic measurements (Stephens et al., 1989; Clayton et al., 1998; Meershoek et al., 2001a,b). Despite inherent errors, in vitro testing methods have been described and shown to provide objective and repeatable data on the biomechanical properties of tendons and the response to treatment (Woo, 1982; Riemersma and De Bruyn, 1986; Gelberman et al., 1987;
Fig. 1. Simplified stress–strain curve for the SDFT (from Goodship et al., 1994). Key: 1, toe region; 2, linear deformation; 3, yield; 4, rupture.
Woo et al., 1987; Wilson and Goodship, 1990; Crevier et al., 1996; Smith et al., 1999; Dowling, 1999; Dowling et al., 2002a,b). The in vitro mechanical properties of equine flexor tendons approximate a sigmoidal curve (Fig. 1) when stress is plotted against strain (Evans and Barbenel, 1975; Goodship et al., 1994; Crevier et al., 1996; Dowling et al., 2002a). The initial lax phase or ‘‘toe’’ region extends to 3–4% strain and represents progressive loading of individual fibres and elimination of the collagen fibre ‘‘crimp’’ (Evans and Barbenel, 1975; Woo, 1982; Cribb and Scott, 1995). As stress increases tensile force is transferred as shear stress to adjacent overlapping fibrils and the tendon exhibits a stiffer, near linear response (Birk et al., 1991). Further increases in load leads to collagen deformation through molecular stretching and slippage, fibrillar stretching and slippage, defibrillation and rupture (Pins et al., 1997; Kotha and Guzelsu, 2003). A number of variables can be measured directly or indirectly depending on the mechanical testing apparatus and method of data expression. Maximal load (N) is the peak load at the point of specimen rupture. Ultimate tensile strain (%) is the percentage elongation of the test specimen at the point of rupture. Ultimate tensile stress (N mm 2 or MPa) is maximal load per unit cross-sectional area of the test specimen at the point of rupture. Values for yield load, yield strain and yield stress are obtained at the point of deviation from linear elastic behaviour. Measures of tendon elasticity including modulus of elasticity or Emax (MPa), and tendon stiffness (N mm 1) are calculated from the slope of the linear region of the stress–strain or load–displacement curve.
3. Biomechanical properties of the equine SDFT (in vitro) Linear deformation of normal adult fore limb SDFT under static loads occurs between 3.6% and 10.6% strain and 2.0–8.4 kN load (Wilson and Goodship, 1990).
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Table 1 In vitro biomechanical properties for normal adult forelimb SDFT (mean ± SEM) Authors
Maximal load (kN)
Ultimate strain (%)
Ultimate stress (MPa)
Stiffness (N mm-1)
Modulus (MPa)
Yield load (kN)
Yield strain (%)
Yield stress (MPa)
Crevier et al. (1996) Dowling et al. (2002a)
12.4 ± 1.3 7.5 ± 0.9
12.5 ± 1.7 17.3 ± 1.2
109.4 ± 8.4 65 ± 4.1
na 1075.6 ± 92.8
1189 ± 63 na
5.5 ± 0.8 6.7 ± 2.3
4.85 ± 0.6 12.6 ± 3.5
48 ± 4.6 57.2 ± 5.9
Table 2 In vitro biomechanical properties for normal foal forelimb SDFT (mean range ± SEM) Foal age (months)
Maximal load (kN)
Ultimate strain (%)
Ultimate stress (MPa)
5 11
7.4 ± 0.8–9.3 ± 1.3 11.5 ± 1.1–12.4 ± 1.3
11 ± 1–12 ± 2 11 ± 1–12 ± 2
99 ± 11–119 ± 8 100 ± 10–116 ± 8
Mean values for maximal load, ultimate strain, ultimate stress, stiffness, modulus of elasticity, yield load, yield stress and yield strain of normal adult metacarpal SDFT have been reported (Table 1) (Wilson and Goodship, 1990; Crevier et al., 1996; Dowling et al., 2002a). In vitro mechanical properties of foal SDFT have also been evaluated (Table 2), and it would appear that by 11 months of age the in vitro biomechanical properties of forelimb SDFT approximate those of adults (Cherdchutham et al., 2001a). The metacarpal region of the SDFT is reportedly stiffer than the sesamoido-digital region and reportedly has a higher modulus, higher yield stress, and lower yield strain and yield load (Crevier et al., 1996; CrevierDenoix and Pourcelot, 1997). These findings were suggested as evidence of non-homogenous strain characteristics along the SDFT. Increased stiffness, smaller CSA and lower yield strain suggested a relative weakness of the metacarpal region compared to the sesamoido-digital region that may partly explain the higher incidence of injury at this site (Crevier et al., 1996; Crevier-Denoix and Pourcelot, 1997). SDFT with naturally occurring tendonitis had significantly increased mean cross-sectional area (CSA) and lower ultimate tensile stress, and tended to have higher maximal loads and lower ultimate tensile strain compared to normal SDFT (Crevier-Denoix et al., 1997). These findings suggest that the healing response in injured tendons results in an increase in CSA leading to reduced stress, lower stiffness and lower strain. There was a tendency for failure to occur adjacent to the junction of normal and abnormal tendon, suggesting a relative overstress and or overstrain within these regions.
4. Biomechanical properties of the equine SDFT (in vivo) The forelimb SDFT is loaded preferentially and maximally during the early part of the stance phase at the walk and trot on a flat surface, however load patterns change when exercised on a slope (Silver et al., 1983;
Stephens et al., 1989; Platt et al., 1991; Riemersma et al., 1996b; Liduin et al., 2001; Takahashi et al., 2001). Reported values for tendon strain at the walk range from 2.2% to 4.6% with peak loads of 844.8 N to one-third body weight (Silver et al., 1983; Stephens et al., 1989; Platt et al., 1991; Riemersma et al., 1996b). At the walk the hind limb SDFT experiences a maximal load early in the stance phase of 4.1 N kg 1 and ultimate strain of 2.3% (Riemersma et al., 1988a; Riemersma et al., 1988b). No differences were reported in strain at the walk on either brick pavement or sand, however strain increased significantly from 2.5% to 3.2% with a rider (Riemersma et al., 1996b). At the walk no significant difference was detected in SDFT maximal strains between flat, egg bar, raised heel or toe extension shoes (Lochner et al., 1980; Riemersma et al., 1996a). However, at the trot heel elevation increases strain in normal SDFT, and load in injured SDFT (Stephens et al., 1989; Meershoek et al., 2002). At the trot a peak load of 6.9 kN was recorded using kinematic and kinetic data (Liduin et al., 2001), and values for strain ranged from 4.15% (unridden) to 10.1% (ridden) at maximal weight bearing (Riemersma et al., 1996b; Stephens et al., 1989). In vivo SDFT strain at the gallop ranges from 11.5% to 16.6%, which is in close agreement with measured in vitro ultimate strains of 12–21% (Riemersma and Schamhardt, 1985; Stephens et al., 1989; Wilson and Goodship, 1990; Crevier et al., 1996; Dowling et al., 2002a). Calculated in vivo strain rates at the gallop of 200% per second, are in agreement with predicted in vitro strain rates of 150–200% per second (Herrick et al., 1978; Lochner et al., 1980; Stephens et al., 1989). Reported mean in vitro yield stress for forelimb SDFT of 57.2 ± 5.9 MPa, is similar to in vivo stresses of 40–50 MPa for forelimb flexor tendons at the gallop (Biewener, 1998; Dowling et al., 2002a). A tendon safety factor of between 1.1 and 3.0 has been estimated for large ungulates (Biewener, 1998). The magnitudes of in vivo strains at the gallop suggest site-specific strain that is largest in the metacarpal region and that variation in tendon morphology is responsible for the strain differences (Stephens
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et al., 1989). These findings suggest that at maximal exercise the SDFT operates close to its physiological limits with a relatively narrow safety margin.
5. Factors effecting the biomechanical properties of tendons 5.1. Tendon cross-sectional area and collagen content A direct biomechanical relationship exists between specimen CSA and stress. It is generally accepted that the mechanical strength of a tissue is proportional to its CSA. However, in adult hind limb SDFT, CSA is inversely proportional to total collagen content, dry weight of collagen and the percentage of collagen fibres (Riemersma and De Bruyn, 1986). These results suggest variations in CSA are related to differences in non-collagenous components and that CSA does not necessarily represent tendon strength. The metacarpal region has the smallest CSA and greater collagen content yet has lower mean values for yield stress, yield strain and yield load compared to metacarpophalangeal region, which has a larger CSA and higher concentrations of larger proteoglycans (Smith and Webbon, 1996; Crevier et al., 1996; Crevier-Denoix and Pourcelot, 1997; Micklethwaite, 1997). This most likely reflects metabolic and functional adaptations of different regions of the SDFT. It has been suggested that by two years of age the SDFT has reached an adequate cross-sectional area in order to withstand certain physiological loads (Gillis et al., 1995c,b). In 19-month-old horses high intensity treadmill exercise increased CSA of common digital extensor tendon (CDE) however, not SDFT (Birch et al., 1999). From this it was proposed that the SDFT was not capable of an adaptive response to exercise in this age group of horses. However, in a previous study SDFT CSA increased and mean echogenicity decreased in response to ridden exercise (Gillis et al., 1993). These authors suggested an effect of rider weight and subclinical tendonitis. In foals however, SDFT CSA significantly increased in response to exercise yet collagen content (% dry weight) was higher in non-exercised foals at five months. Based on current information increases in CSA likely reflect alterations in the non-collagenous matrix (Cherdchutham et al., 1999; Cherdchutham et al., 2001a; Kasashima et al., 2002). Results of the studies to date suggest an adaptive response to exercise in tendons in young horses that decreases as horses reach maturity. However, it remains unclear if development of a larger tendon is protective later in life. 5.2. Effects of maturation and ageing The rate of collagen synthesis apparently declines with age, whereas cross-link formation increases with
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age and may be related to environmental stimuli and tissue function (Ruiz-Torres, 1978; Davison, 1978; Gelberman et al., 1987). Collagen fibrils have an approximately circular cross-sectional area and as fibril diameter increases there is a concomitant increase in tensile strength and the number of intra-fibrillar covalent cross-links (Parry et al., 1978; Goodship and Birch, 1996). Collagen fibril diameter is typically bi-modal and is influenced by age and exercise (Goodship and Birch, 1996; PattersonKane et al., 1997d; Cherdchutham et al., 2001b). Recent investigations have suggested that the equine SDFT attains maturity at 2–3 years of age. Similarly collagen fibril diameter, mature collagen cross-links, and crimp morphology have stabilised by two years (PattersonKane et al., 1997a,b). Increased stiffness of tendons in horses over two years age is likely related to increasing numbers of non-reducible cross-links, decreasing fascicle size and selective reduction in collagen crimp angle and length within the central core region of SDFT (Parry et al., 1978; Wilmink et al., 1991a,b; Reiser, 1994; Gillis et al., 1995b; Gillis et al., 1997; Patterson-Kane et al., 1997a). Tendons with a smaller crimp angle and length may reach the end of the toe region sooner and experience lower values for ultimate stress and strain (Patterson-Kane et al., 1997a). Three cell types have been identified within equine tendon: type I, type II and type III tenocytes (Webbon, 1978; Goodship et al., 1994; Smith and Webbon, 1996). Type II cells predominate in foetal tendon, are thought to be metabolically more active and responsible for matrix maintenance (Webbon, 1978; Smith and Webbon, 1996). With increasing age, cell populations change such that type I cells predominate and cell numbers decline within the core region of the metacarpal SDFT (Webbon, 1978). An age-associated decline in cellular metabolic activity occurs in tensional (metacarpal) regions of bovine tendon (Perez-Castro and Vogel, 1998). Reduced cell metabolism may account for age associated extracellular matrix alterations although these changes require substantially more study. Concentrations of cartilage oligomeric matrix protein (COMP) within the metacarpal region of the SDFT are low in neonates, increase with growth and decline after maturation (Smith et al., 1997a,b). In contrast, COMP concentrations within the metacarpophalangeal region increase with maturation and level of, probably reflecting differences in cellular metabolic activity and function between regions (Perez-Castro and Vogel, 1998; Smith et al., 1999). COMP concentrations are influenced by weight bearing and correlate with SDFT mechanical properties in young horses (Smith et al., 2002a). Tenocytes from immature tendons synthesise more COMP compared to tenocytes from mature tendons suggesting impaired metabolic activity after maturity (Smith et al., 1998b, 2002b). These studies suggest that the tendon matrix contributes significantly to the biomechanical
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properties and has the ability to adapt in response to loading but this ability decreases with maturity and age. 5.3. Effect of exercise on the biomechanical properties Preferential reductions in collagen fibril crimp angle and length, and mass average diameter occur in response to exercise within central regions of SDFT (Patterson-Kane et al., 1997a,c,d, 1998). Central fibrils develop a lower toe limit strain than peripheral fibrils that leads to selective loading and earlier failure (Wilmink et al., 1991a,b; Patterson-Kane et al., 1997a, 1998). Conversely the peripheral region from exercised horses was shown to exhibit a significant increase in crimp angle. This was suggested as being evidence of an adaptive response to exercise that may reduce the susceptibility of this region to exercise induced damage (Patterson-Kane et al., 1998). It was postulated that microdamage secondary to peak biomechanical and thermal effects within the central region accounts for the relatively high incidence of SDFT ‘‘core’’ lesions. More recently, the effect of different exercise regimens on SDFT properties was evaluated in three groups of foals (Cherdchutham et al., 1999, 2001a,b). One group was confined, a second group allowed free pasture exercise and a third subject to a training program from two to five months of age. From 5 to 11 months of age all foals were allowed the same level of free exercise. Exercise resulted in increased numbers of thin fibrils within the periphery before the central core region of the SDFT at 5 months (Cherdchutham et al., 2001b). This was attributed to synthesis of new fibrils due to the young age of the foals. This effect was retarded in foals that were confined from 2 to 5 months of age, but partly reversible if then allowed exercise from 5 to 11 months of age suggesting an adaptive ability (Cherdchutham et al., 2001b). SDFT from pastured foals at five months of age were stronger, more elastic and had larger CSA compared to non-exercised and trained foals (Cherdchutham et al., 2001a). An increase in smaller diameter fibrils may add to the surface area for interfibrillar cross-linking and interaction with the non-collagenous matrix and reduce tendon stiffness (Cherdchutham et al., 2001a). Exercise also resulted in a trend towards increased hydroxylysine and hydroxypyridoline cross-links suggesting increased biomechanical properties in foals aged five months (Cherdchutham et al., 1999). These findings may partly explain why SDFT from pastured foals were stronger and more elastic. By 11 months there were no significant differences in force at rupture or CSA suggesting a compensatory increase in the mechanical properties of SDFT from the previously non-exercised group. However, stress at rupture and at 4% strain was still lowest in the previously pastured foals indicating a persistent effect of free pasture exercise on tendon elasticity.
Cellularity, PSGAG, HA and COMP concentrations were highest in foals allowed free pasture exercise at 5 months of age (Cherdchutham et al., 1999). At 11 months of age, after all foals were allowed the same level of exercise, cellularity and PSGAG concentrations were significantly lower in the previously trained group compared to other groups suggesting a lasting negative effect of training (Cherdchutham et al., 1999). Smaller proteoglycans, decorin, fibromodulin and biglycan are thought to influence tenocyte functions, collagen fibrillogenesis, and the spatial organisation of fibres thereby influencing tendon strength and transmission of stress (Scott, 1992; Hedbom and Heinegard, 1993; Svensson et al., 1995; Gu and Wada, 1996; Smith and Webbon, 1996). The purpose of proteoglycan interactions with collagen fibrils and their effect on load transmission and or resistance has been investigated, however little is known about their precise role in modulating the biomechanical properties of tendons (Cribb and Scott, 1995). Long-term, high-intensity exercise results in a reduction in COMP concentration within the central region of the SDFT (Smith et al., 1998a, 1999). COMP concentrations were lower in SDFT from foals subjected to a training program compared to those at pasture or box confined (Cherdchutham et al., 1999). COMP concentrations were found to correlate with ultimate tensile stress, modulus of elasticity and tendon stiffness in tendons from horses aged 2 years ± 2 months (Smith et al., 2002a). No correlation was found in tendons from older horses suggesting age and exercise induced loss of COMP influences mechanical properties of tendons in mature horses. These results suggest that relative over exercise at a young age may pre-dispose horses to SDFT injury later in life. 5.4. Effects of growth factors The mechanisms of age related alterations in the composition and behaviour of musculoskeletal tissues are diverse and complex, however the role of declining circulating levels of growth factors has been investigated (Buckwalter et al., 1993; Rudman et al., 1990; Smith et al., 1998b; Molloy et al., 2003). Several growth factors are involved in repair and regeneration of musculoskeletal soft tissues including growth hormone, insulin-like growth factor I (IGF-I) and transforming growth factor b-1 (TGF b-1) (Molloy et al., 2003; Dowling et al., 2002a,b). TGF b-1 supplementation of equine tenocyte explants in vitro resulted in stimulation of COMP production and tenocyte replication (Smith et al., 1998b). Intramuscular administration of recombinant equine growth hormone (rEGH) failed to alter the in vitro biomechanical properties of normal SDFT in adult horses (Dowling et al., 2002a). A significant increase in CSA, and decrease in stress and stiffness was observed in healing SDFT in re-
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sponse to treatment with rEGH (Dowling et al., 2002b). IGF-I significantly increased collagen content and cellularity, and reduced lesion size in healing SDFT yet no significant effects on biomechanical properties were detected (Dahlgren et al., 2002). Intralesional IGF-I was found to have an anti-inflammatory effect and improved functional properties in healing rat tendons but no effect on stiffness or maximal load (Kurtz et al., 1999). However, further investigations evaluating the pharmacological, biomechanical, histological, and functional aspects of IGF-I and its role in soft tissue regeneration and repair must be performed before its clinical applicability can be established (Kurtz et al., 1999; Molloy et al., 2003). Disappointing results following use of growth factors may be related to inappropriate dose rates and routes, reduced cellularity and down-regulation of cellular metabolic activity in mature tendons.
6. Conclusions Tendon failure may occur as a single over strain event or as cumulative fatigue failure as a result of cyclical loading. To date much of the focus of in vitro mechanical testing has been on single-static loads to failure. While ultimate strength is important, it may not necessarily mean a stronger tendon is less likely to fail. Fatigue failure under cyclical loads may be a more important indicator of tendon strength and future techniques may be developed to evaluate this. Previous investigations have focused on repair and regeneration of injured adult tendon often with disappointing results (Genovese, 1992; Reef et al., 1996; Reef et al., 1997; Dowling et al., 2002a,b; Dahlgren et al., 2002). An alternative approach aimed at prevention of fatigue failure suggests equilibrium between microdamage and healing. In the adult equine SDFT, exercise and age associated microdamage combined with a limited adaptive ability and narrow safety margin may mean fatigue failure is inevitable. However, foal SDFT appears to be able to adapt to an appropriate exercise regimen. The effect may be to produce a more functionally adapted tendon, increase the safety margin and reduce the incidence of exercise associated injury. Despite a smaller CSA, foal SDFT has values similar to adult SDFT for maximal load and ultimate strain, suggesting ultimate strength may not be the most important factor in preventing tendon injury. Based on current information it would appear that foals allowed free pasture exercise develop SDFT that are larger, stronger and more elastic. It is likely that changes in the non-collagenous matrix are responsible for these differences. In contrast it appears that training or Ôover-exerciseÕ has lasting detrimental effects on the biomechanical and functional properties of SDFT in the foal that may pre-dispose these horses to SDFT in-
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jury later in life. The type of exercise appears to be important in determining the tendonÕs response (Buchanan and Marsh, 2002). The total number of muscle contractions (i.e. cycles) rather than absolute force applied may be more important in modifying biomechanical properties (Simonsen et al., 1995). Determining optimum exercise intensity and timing, and the role of the non-collagenous matrix in tendon physiology in the young horse may help to develop more adapted tendons and hold the key to prevention of SDFT injury in horses.
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