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Причем говорят это стандарт, рост после кастрации
Желтка в 2 с копейками почикали - нифига не вырос )
Причем говорят это стандарт, рост после кастрации
, вот и я об чем...In neither young animals nor humans is the amount of ‘natural’ exercise that is ideal for musculo-skeletal function in later life known, and is one reason why forced exercise during growth is contentious.
The first study, into the effect of exercise on tendon, lasted 18 months and compared 2-year-old trained horses (galloped on a treadmill three times weekly, trotted on a mechanical horse walker three times weekly, and walked for 40 min 6 days per week) with control horses exercised at the walk only for 40 min daily for 6 days per week. The third carpal bone of trained horses had a thicker cortical shell, and thickening of trabeculae, resulting in an increased bone mass and mineral density as assessed by dual X-ray absorptiometry (Firth et al. 1999b), associated with local forces passing through the dorsal load path of the carpus. In a second study, using a similar exercise regimen for only 18 weeks, the third carpal bone responded in a similar way, and the difference between trained and controls was similar to that of the 18-month study (Firth et al. 1999c).
In the distal Mc3 epiphysis, the adaptive anatomical change may lead to excess stiffening within the condyles owing to extensive new bone formation, and this may lead to a patho-anatomical change, namely concentration of strain at the condylar grooves, which is a common site of fracture (Riggs & Boyde, 1999).
There was greater thickening of trabeculae and lower porosity on histomorphometric examination in PSB of horses trained for 5 months and a cumulative distance of 152 km on less compliant tracks (dirt) than on wood-chip tracks (Young et al. 1991a). Thoroughbred horses aged 2 or 3 years that had raced or been in race training had greater area fraction and stiffness (determined biomechanically by indentation) in the dorsal aspect of the radial facet of the third carpal bone than did untrained horses. Area fraction and stiffness were closely related, and were significantly greater in horses with patho-anatomical change than without (Young et al. 1991b).
Аналогичные результаты были и на других дорожках (в смысле, травяной, песочной).Horses exercised on a treadmill 5 days per week for 6 months had greater volumes of higher bone density on computed tomography and were significantly more lame than horses given only slow exercise at hand (Kawcak et al. 2000). This was possibly due to the greater distance cantered when compared with the 18-month study referred to above. Radionuclide uptake in the metacarpal condyles, but not in the carpal joints, was greater in exercised horses than in control horses. Exercised horses also had a higher subchondral bone density in the metacarpal condyles than control horses, but such differences were not detected in the carpal bones.
In the Mc3 diaphyseal shaft of these animals (Firth et al. 2005), bone density, as assessed by peripheral quantitative computed tomography, was greater in horses that had been trained at high speed, but density did not contribute to bone strength as much as increase in the CSA. Confocal fluorescence laser microscopy showed that active osteons, defined as Haversian systems containing calcein label, were fewer, of smaller diameter at the time of calcein injection and had a greater bone apposition rate in trained than in untrained horses. Horses that had cantered but not galloped had similar bone density to those that had galloped, presumably due to the alteration in remodelling associated with cantering. But horses that had cantered but not galloped had bone CSA, mineral content, periosteal circumference and bone strength similar to control (untrained) horses, indicating that the Mc3 had not grown in response to the cantering exercise. Caution is required because the number of horses examined was small, but the observation was consistent with previous studies in which metacarpal enlargement occurred in treadmill-trained horses (McCarthy & Jeffcott, 1992), increased duration of training was associated with greater dorso-palmar bone diameter and higher cross-sectional moment of inertia (Sherman et al. 1995), and gait velocity of > 12 m s−1 was required for significant stimulation of Mc3 dorsal cortex (Davies et al. 1999). Most training involves lower velocities, which may inadequately adapt the bone for forces sustained in competitive racing (Verheyen & Wood, 2004), and patho-anatomical change in the form of metacarpal periostitis may occur less in horses that do more galloping during training (Nunamaker, 2002). All of these underline the concept that bone tissue will adapt if the forces acting upon it cause the deformation (strain) sustained by the bone to exceed certain values, but if that strain value is not exceeded then the bone will not respond to increase its resistance to the deforming forces (Frost et al. 2002).
The implication of fast exercise in terms of adaptive change in functional anatomy is that doubling the minimum second moment of inertia (induced by mechanical means) resulted in > 100-fold increase in fatigue resistance, thus reducing the likelihood of stress fractures (Warden et al. 2005). Of course, such massive increase in size is not desirable in the horse in evolution or in training, as larger bones are heavier, with an associated functional disadvantage. However, suitable exercise programmes to enhance skeletal structural properties, introduced during early growth or early training, would seem to be the most effective approach to attempting to reduce stress fracture incidence, which is one of the main categories of bone injury affecting equine athletes (Verheyen & Wood, 2004).
The effect of exercise on tendon development was studied in the three groups of foals referred to above, experiencing stall rest, sprint exercise superimposed on stall rest, and pasture exercise to 5 months of age, and then all having access to paddock exercise from 6 to 11 months of age (Cherdchutham et al. 1999, 2001). By 5 months of age there were more small-diameter fibrils in the peripheral and central regions of the SDFT of foals that had been exercised compared with those confined to a large box stall; pasture exercise induced more change than did the artificial sprinting exercise. Such development of small-diameter fibres did not occur in the confined foals until after they had been permitted pasture exercise from 6 to 11 months of age. Previous exercise regimen influenced collagen restructuring, as development in the two confined groups lagged behind the pastured group at 11 months of age. The previous sprinting exercise superimposed upon stall confinement may have had negative effects on tenocyte metabolism in the longer term.
Treadmill training of 2-year-old horses for 18 months, but not for 18 weeks, resulted in a decrease in collagen fibril mass average diameter in the SDFT (Patterson-Kane et al. 1997d) and change in crimp morphology (Patterson-Kane et al. 1998a) compared with age cohorts which were not exercised at high speed. This effect was not found in the CDET of the same horses, underlining the functionally distinct nature of these two tendons resulting in fundamentally different responses to high-speed exercise. It was subsequently shown that the SDFT is a stiffer structure than the CDET, and differences in the matrix molecular composition, including water and total sulfated glycosaminoglycan content, allow it to remain more elastic as a material, permitting its energy-storing function (Batson et al. 2003). Presumably such differences in function and structure resulted in less change in the collagen fibril diameter distribution in the DDFT and SL after 18 months of exercise (Patterson-Kane et al. 1998b).
In Dutch Warmblood horses housed except for 2–4 h of pasture exercise six times per week and exercise at various gaits on a walker one, three or five times per week from the age of 3 months, the CSA of the SDFT was not significantly affected by exercise at 14 months of age whereas all the other tendons and ligaments did show adaptive change (van den Belt, 1995). In early race training of thoroughbreds, an increase in size of the SDFT was ultrasonographically detected, although the fact that some horses developed clinical signs means that more than adaptive structural change was probably occurring (Gillis et al. 1993). Training of 2-year-old thoroughbreds for 13 weeks on sand and grass was associated with an ultrasonographically determined increase in mean CSA of the SDFT (Perkins et al. 2004), which was substantiated by tissue examination of the tendons. The CSA, weight and volume of the SDFT and CDET were greater in the trained than in control group, and the lack of clinical or histological abnormality led to the presumption that this change was adaptive to the training (Firth et al. 2004b).
In a more recent study (Kasashima et al. 2002), a control and an exercise group of thoroughbreds received 4 h of pasture exercise from 2 to 15 months of age and the exercise group had an additional short period of treadmill exercise daily. The exercise programme resulted in a significantly larger tendon CSA in the exercise group at several, but not all, time points, which may be attributed to levels of variance. A significantly greater rate of increase in tendon CSA with time in the exercised compared with the control group suggested that tendon development can possibly be modulated by exercise during growth. However, the type and timing of the exercise regimen is likely to be critical, as the mean CSA of the SDFT of a large group of pastured foals exercised from 10 days to 18 months of age for 1030 m 5 days per week at velocities of 4.2–12 m s−1 was not significantly different from that of a matched group receiving only pasture exercise (Moffat, 2004).
И ещеNo effect of exercise on the water or DNA content was found. GAG content was greater in exercised foals at 5 months, but differences had disappeared after 6 months of access to pasture. Moderate exercise had no apparent effect on any of the collagen parameters but had a beneficial, but reversible, effect on the GAG component.
Differences in heterogeneity between the two sites were present for GAG, DNA, collagen and hydroxylysine in exercised foals aged 5 months but only for GAG and DNA in confined foals. For some collagen-related parameters, the delay in attainment of heterogeneity was not compensated for after the additional 6-month period of moderate exercise (Brama et al. 2002). Short bouts of heavy exercise superimposed on a confinement regimen appear to have adverse effects on long-term viability of the tissues and may lead to an impaired resistance to injury (Van De Lest et al. 2002; Billinghurst et al. 2003). The exercise regimen that is ideal for cartilage adaptive change remains unknown.
Conditioning exercise for 1030 m at a velocity up to 12.5 m s−1 for 5 days per week on a grass and sand track up to 18 months of age did not markedly affect articular cartilage structure or function. There was marked site-associated variation, with sites medial and lateral to the sagittal ridge of Mc3 showing signs of early degeneration, with low indentation stiffness and collagen content, and relatively high water content (Nugent et al. 2004), compared with the control group undertaking spontaneous exercise at pasture only. This concurs with more viable chondrocytes in the metacarpo-phalangeal joint of foals in the conditioned than control group, and in the palmar than dorsal sites of the same joint (Dykgraaf, 2003).
In 2-year-old horses undergoing 19 weeks of high-intensity treadmill training or low-intensity exercise, cartilage from the dorsal aspect of the carpal bones was less permeable, thinner and had loss of chondrocyte alignment compared with palmar cartilage. Cartilage of strenuously trained animals was significantly less stiff, had reduced superficial toluidine blue staining, showed more fibrillation and chondrocyte clusters than that from gently exercised animals (Murray et al. 1999a), and had greater fibronectin staining (Murray et al. 2000) and interterritorial cartilage oligomeric matrix protein distribution (Murray et al. 2001).
In the dorsal sites sampled, trained horses had thicker calcified (but not hyaline) cartilage than did control horses, pooled hyaline cartilage thickness in trained and control horses was not significantly different, and hyaline cartilage thickness from dorsal sites was not significantly different from that in palmar sites (Murray et al. 1999b). By contrast, after 13 weeks of training on sand and grass tracks of 2-year-old horses that had been raised at pasture (Firth et al. 2004a), third carpal bone articular cartilage was thicker in dorsal than palmar sites (although many more sites sampled in Murray's study may have reduced the significance of difference). At the sites of thickest cartilage, mean hyaline cartilage thickness in trained horses was significantly greater than in untrained horses (Firth & Rogers, 2005). In this first evidence that the amount of hyaline cartilage is responsive to exercise in the horse, histological examination of the sites showed that staining of the hyaline matrix was more basophilic, chondrocytes were more numerous adjacent to the tidemark, and chondrocyte palisades and chromatin were more obvious through their increased basophilic staining. No patho-anatomical change was evident, and thus the thickness difference was presumed to be adaptive to the forces associated with exercise. This concurs with recent work showing that in childhood, strenuous activity promoted development of knee cartilage, without pain and significant injury, and children who had had no vigorous activity had 22–25% less cartilage than even mildly active children (Jones et al. 2003). It also concurs with the significant effect of exercise on newly synthesized proteoglycan in the third carpal bone of horses exercised for 6 weeks compared with horses that had been boxed for the same period (Palmer et al. 1995), with the difference in rate of proteoglycan synthesis in metacarpo-phalangeal joint cartilage of 2-year-old horses trained on a treadmill for 19 weeks compared with that of control horses (Bird et al. 2000), and with the increase in cartilage thickness after moderate (Kiviranta et al. 1988) but not strenuous running (Kiviranta et al. 1992) in dogs.
In early osteoarthritis, study of the patho-anatomical and biochemical changes in articular cartilage or subchondral bone (Radin, 1999) has dominated the investigation of response of articular calcified cartilage (ACC). In areas of high stress on the articular cartilage, the ACC may or may not alter its thickness (Murray et al. 1999a; Norrdin et al. 1999; Firth & Rogers, 2005). In 18-month-old horses at pasture, the mean linear accretion rate was 0.89 µm day−1 with much higher rates in some regions (Doube et al. 2005). In addition, the suggested concentration of strain at the condylar grooves may lead to cracking, beginning in the ACC and propagating into the subchondral bone (Riggs & Boyde, 1999; Boyde et al. 2001; Boyde, 2003). In random source horses, race training exercise has been associated with macroscopically visible cracks at the sites of condylar fractures (Radtke et al. 2003), in contrast to horses without such an exercise history, although the involvement of ACC, as opposed to that of subchondral bone, was not indicated (Stepnik et al. 2004). High-stress sites of the joint had thinner, more irregular ACC, indicating that subchondral remodelling involves the ACC layer (Norrdin et al. 1998) and in overload arthrosis, breaks in ACC appeared to lead to collapse and cartilage infolding (Norrdin et al. 1999). ACC may be implicated even earlier in the pathogenesis of osteoarthritis if the higher stiffness, hypermineralization and abrasive role of ACC (Ferguson et al. 2003) are confirmed in the horse.
Clearly, ACC is highly responsive to exercise, and shows a wide range of morphology and patho-anatomical change. Microcracks in ACC have been detected in many sites in racehorses in training, and can be filled with calcified material in an apparently reparative response to overload exercise regimens (Boyde, 2003). A recent new finding in 2-year-old horses is the presence of canals through ACC, mainly in a site which is relatively less loaded than other sites, on the sagittal ridge of Mc3. The canals appear to result from osteoclastic resorption (cutting cones) penetrating from bone through to the non-mineralized hyaline articular cartilage, possibly connecting the extracellular fluid of bone and cartilage (Boyde & Firth, 2004).
The effect of withdrawal of a particular exercise regimen (which is a different effect than that of confinement) has not yet been investigated directly, but has been suggested to be of importance because return to racing after spelling from earlier racing was strongly associated with humeral fracture risk in horses (Carrier et al. 1998).
Эх, как знакомо... И не родственники ж кони. И никто никого не кусал, чтобы этим "заразить"....(В целом, как там - на колу мочало...?... Снова - Машка не двигается, Чапа не гнется, Вог не тормозится