Training for superior fitness and fatigue resistance

Preparation of racehorses for racing necessitates gradual increases in the speed of exercise. It is only at exercise intensities near maximal that improvements in anaerobic capacity and anaerobic power can be expected. Lactic dehydrogenase (LDH) concentration in skeletal muscle has been used as a marker of anaerobic enzyme activity. Interval training at high speeds on a treadmill resulted in increased concentration of LDH in skeletal muscle, but conventional training does not have the same effect (9). Likewise, training at a moderate intensity (80% of VO2max) for 6 weeks does not result in increases in skeletal muscle (gluteus medius) LDH concentration, although that training did increase the muscle buffering capacity by 8% and increase the ratio of fast twitch highly oxidative fibres to fast twitch fibres (FTH/FT) (10). These adaptations to training did not occur in a group of horses trained concurrently at a lower intensity of 40% VO2max. Intensity of training is therefore an important factor in determining the degree of local adaptations in skeletal muscle.

There is some evidence that prolonged periods of endurance training stimulate continued adaptation of skeletal muscle. The activities of two enzymes, used as markers of oxidative capacity of muscle, continued to increase throughout a nine-month training program in endurance horses (11).

A study of effects of training and detraining on muscle physiology also confirmed the importance of prolonged training, and avoidance of prolonged detraining unless absolutely essential (12). Twenty-four 4-year-old Andalusian (Spanish breed) stallions were used to examine the plasticity of myosin heavy chain (MHC) phenotype and the metabolic profile in horse skeletal muscle with 8 months endurance-exercise training and 3 months of detraining in a paddock. Long-term changes with training were an increase of slow MHC-I, increases of high-oxidative fibres, capillary density, activities of aerobic enzymes and endogenous glycogen. Intramuscular lipid deposits also increased after 8 months of training, whereas the activities of anaerobic enzymes declined. Most of the exercise-induced alterations reverted after 3 months of detraining. The results also found a dose-response relationship between the duration of training and the magnitude of muscle adaptations. As training duration increased, so did the adaptations in the muscle. The results also infer that the capacity for anaerobic metabolism of muscle cells is reduced by prolonged, low intensity training. This response could reduce a horse's ability to accelerate, and reduce maximal speed and jumping ability. Such a response is of little relevance to an endurance horse, but in horses racing over 800-32000 metres, and in eventers, specific additional training should be used to promote anaerobic and buffering capacities of skeletal muscle.

These key references illustrate the importance of designing training programs that help trainers use appropriate training intensities, and which help trainers keep their horses in training to maximise the long term responses. Appropriate blood lactate and heart rate measurements are the measurements that can provide the necessary guidance.


 

9. Lovell DK, Rose RJ: Changes in skeletal muscle composition in response to interval and high intensity training. In Persson SGB, Lindholm A, Jeffcott LB, eds.: Equine Exercise Physiology 3, Davis: ICEEP Publications, 1991, p. 215.

10. Sinha AK, Ray SP, Rose RJ: Skeletal muscle adaptions to different training intensities and to detraining in different hindlimb muscles in thoroughbred horses. In Persson SGB, Lindholm A, Jeffcott LB, eds.: Equine Exercise Physiology 3, Davis: ICEEP Publications, 1991, p. 223.

11. Hodgson DR, Rose RJ: Effects of a nine month endurance training program on skeletal muscle composition in the horse. Vet Record 121:271, 1987.

12. Serrano AL, Quiroz-Rothe E, Rivero JLL: Early and long-term changes of equine skeletal muscle in response to endurance training and detraining. Eur. J. Physiol. 441:263, 2000.

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