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Ten healthy sedentary male Thoroughbreds with previous race training experience were studied for 14 weeks. Horses were trained for 9 weeks, using a program designed after those used commonly in the United States. Horses were trained conventionally by slow trotting (250 m/min) for 2 weeks and galloping (390 to 450 m/min) for 4 weeks, followed by 3 weeks of galloping (440 to 480 m/min) and intermittent sprinting exercises (breezes) at distances between 600 and 1,000 m (900 to 950 m/min). The horses were then pasture rested for 5 weeks.

A standardized exercise test (set) involving an 800-m gallop at 800 m/min was administered before and after the 9-week training period and after the 5-week detraining period. Heart rate (hr) was monitored during exercise and at standardized intervals after exercise for 60 minutes. Venous blood for determination of plasma lactate concentration was obtained at 5 minutes after exercise.

Heart rate was monitored daily at rest, during exercise, and through the first 60 minutes of recovery. Venous plasma samples (for lactate determination) were obtained 5 minutes after the sprinting exercises. Horses were observed daily before exercise for signs of lameness and were not allowed to train if lame.

Differences after 9 weeks’ training were seen in the set recovery hr at 0.5 through 5 minutes after exercise (P < 0.05 to P < 0.01). Differences after detraining were seen in the set recovery hr at 40 and 60 minutes after exercise (P < 0.05 to P < 0.01). Neither training nor detraining resulted in differences in plasma lactate concentration after the set gallop.

A training-induced resting bradycardia was not observed. The mean maximal hr (hr max) during workouts was 238 ± 3.4 beats/min (n = 9). When exercise hr was expressed as a function of hr max, 22% of trotting, 89% of galloping, and 100% of sprinting workouts were performed at the ≥ 60% hr max. value characterized by the onset of blood lactate accumulation. Plasma lactate concentration further documented that all the sprinting exercises were performed with concentration above the point of onset of blood lactate accumulation. Mean postsprinting lactate concentration was not different over time and ranged from 13.4 ± 0.9 to 15.6 ± 0.6 mmol/L

As training progressed, some of the horses had days on which they were lame after exercise. Some lameness was judged sufficient to warrant phenylbutazone (pbz) administration. Retrospective analysis of the daily hr data indicated that there were no differences in hr during workouts for lame horses given pbz, compared with those not given pbz. Using analysis of variance, hr for horses that were lame during workouts was significantly higher than that for horses that were sound during workouts, during and 0.5 minutes after trotting; 0.5, 1, 2, 20, 40, and 60 minutes after galloping; and 0.5 and 20 minutes after sprinting (P < 0.05 to P < 0.01).

Free access
in American Journal of Veterinary Research


Ten healthy sedentary Thoroughbreds with previous race training experience were trained conventionally for 9 weeks. Muscle biopsy samples were obtained before and after training and after 6 weeks of detraining pasture rest. Biopsy samples were obtained from the right deltoid, triceps, vastus lateralis, middle gluteal, biceps femoris, and semitendinosus muscles.

The deep-frozen biopsy samples were analyzed for activities of succinate dehydrogenase (sdh), 3-hydroxy-acylcoenzyme A dehydrogenase (had), and phosphorylase (phos) and for glycogen concentration. The triceps and gluteal muscle samples were also serially sectioned and stained for myofibrillar actomyosin adenosine triphosphatase (ATPase) activity after alkaline (pH 10.3) and sequential acidic (pH 4.34) ATPase inactivation. Fiber types I (alkaline preincubation), IIA1, IIA2, and IIA3 (sequential acidic preincubation over 5 minutes) were identified and were evaluated for fiber-type distribution and fiber areas.

Increases in response to training were observed in deltoid and vastus muscle sdh and gluteal muscle had activities, and deltoid muscle glycogen concentration (P < 0.05 to P < 0.01). Changes in phos activity were not observed. Type-IIA1, -IIA2, and -IIA3 fiber areas in triceps muscle were increased in response to training (P < 0.05 to P < 0.01). Changes in fiber-type distribution did not occur in response to training.

Changes in muscle enzyme activities, glycogen concentration, fiber types, and fiber areas were not seen from posttraining to detraining. Further increases were observed when detraining values were compared with pretraining values in deltoid, triceps, vastus, gluteal, and biceps femoris muscle sdh activities and in gluteal muscle glycogen concentration (P < 0.05 to P < 0.01).

It was concluded that the predominant failure to detect training-induced muscle enzyme changes, along with documentation of increases in fast-twitch muscle fiber areas, indicate that conventional Thoroughbred training is principally of a sprinting nature. A greater emphasis on longer, slow endurance work early in training might add greatly to Thoroughbred horses’ abilities to withstand the rigors of sprint training.

Free access
in American Journal of Veterinary Research


OBJECTIVE To evaluate the biomechanical properties of 4 methods for fusion of the centrodistal and tarsometatarsal joints in horses and compare them among each other and with control tarsi.

SAMPLE 24 sets of paired tarsi without substantial signs of osteoarthritis harvested from equine cadavers.

PROCEDURES Test constructs (n = 6/type) were prepared from 1 tarsus from each pair to represent surgical drilling; 2 medially to laterally placed kerf-cut cylinders (MLKCs); a single large, dorsally applied kerf-cut cylinder (DKC); and a dorsomedially applied locking compression plate (DMLCP). Constructs and their contralateral control tarsi were evaluated in 4-point bending in the dorsoplantar, lateromedial, and mediolateral directions; internal and external rotation; and axial compression. Bending, torsional, and axial stiffness values were calculated.

RESULTS Mean stiffness values were consistently lower for surgical drilling constructs than for contralateral control tarsi. Over all biomechanical testing, surgical drilling significantly reduced joint stability. The MLKC constructs had superior biomechanical properties to those of control tarsi for 4-point bending but inferior properties for external and internal rotation. The DMLCP and DKC constructs were superior to control tarsi in dorsoplantar, rotational, and axial compression directions only; DMLCP constructs had no superior stiffness in lateromedial or mediolateral directions. Only the DKC constructs had greater stiffness in the mediolateral direction than did control tarsi. Over all biomechanical testing, DMLCP and DKC constructs were superior to the other constructs.

CONCLUSIONS AND CLINICAL RELEVANCE These biomechanical results suggested that a surgical drilling approach to joint fusion may reduce tarsal stability in horses without clinical osteoarthritis, compared with stability with no intervention, whereas the DMLCP and DKC approaches may significantly enhance stability.

Full access
in American Journal of Veterinary Research