Getting the balance: overtraining or undertraining for peak performance - Veterinary Practice
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Getting the balance: overtraining or undertraining for peak performance

Marion McCullagh continues her reports from the 2016 BEVA congress with an account of some of the presentations on sports injuries and the importance to horses of the pattern of training

THE SESSION ON “SPORTS INJURIES” at this year’s congress of the British Equine Veterinary Association was sponsored by the Horserace Betting Levy Board (HBLB) and moderated by Dr Evita Busschers of the Bristol veterinary school.

Stefan Witte of Tierklinik Schoenbuehl, Switzerland, gave his views on the “Approach to poor performance”. When the owner presents the horse with a problem of poor performance, the veterinarian needs to take a thorough history.

Firstly, is the horse fit for purpose? Owner expectations may be unrealistic; a chunky cob which is presented with a bad back may not be suitable for the collection required for dressage or he may not be a very good jumper.

Temperament and mental attitude play a big part in how a horse performs in competitive events. This cob may be stubborn and inquisitive but not good material to fulfil the owner’s ambition.

The presenting poor performance needs to be compared with the horse’s recorded achievements. Extrinsic factors such as the pattern of training and day-to-day management, nutrition, tack and rider all need to be considered. The horse can be overtrained or undertrained; exercise testing and clinical pathology can help achieve a diagnosis. The veterinarian needs to have a sound knowledge of whatever branch of sport the horse is undertaking so that the contribution of the training pattern can be evaluated.

Poor riding or ill-fitting tack can lead to musculo-skeletal lameness. Inappropriate nutrition can limit performance or contribute to episodes of exertional rhabdomyolysis.

Having sorted out the extrinsic factors, it is time to see the horse moving.

There is even a horse-mounted smartphone that allows objective lameness data acquisition and dynamic endoscopes are widely used in investigating poor performance.

It all depends on how the oxygen gets into the cells that need it. Problems can be in the nostril, the pharynx or larynx or the lower airways where broncho-alveolar lavage can contribute useful information. Cardiac arrhythmias may not always be significant.

Better training?

The oxygen theme surfaced again in Ulrich Hartmann’s paper, “Could we train horses better?”

Ulrich, from the University of Leipzig in Germany specialises in human sports science. He said that with horses, training is concentrated on increasing efficiency of the skeleton and the cardiovascular system. With humans the focus has shifted to looking at energy metabolism and muscular adaptation.

Historically, horse performance has not altered radically where human peak performance has improved by 1% over four years. In the race, the initial acceleration from start to running speed takes a huge burst of energy; there is a steep increase in oxygen uptake which then levels out to a maximum oxygen uptake which continues through the race.

It is the mitochondrial mass in the muscle cell which determines performance. It takes more than 10 years of training for a marathon runner to achieve peak ability, with six to eight years for a track athlete. Thanks to computer modelling and the attention of sports scientists and physiologists, humans now train for longer periods than before but at lower intensity, where horses are trained more at high intensity, most of their training being near maximum load.

All benefit is lost if training stops for three months; it is difficult to get an athlete back to peak performance after injury, both psychologically and physically.

Most human high-level athletes do most of their training in the effort level that is free from lactate accumulation. In fact, the lactic capacity is not altered by training. Traditionally, athletic training looked at the various tasks that were to be performed and trained for each specifically. Better results have come when more biology has been employed, looking at the metabolic background.

Athletic performance improves when oxidative capacity increases: it is all down to the mitochondria. Glycolysis has its own feedback mechanism, when it increases to a certain point, phospho-fructo-kinase blocks the anaerobic lactic energy supply system so that acidity does not destroy the proteins and mitochondria of the muscle cells.

So to gain in staying power, we need to improve the oxidative processes and utilise the lactate pathway as late as possible. Computer modelling has helped in gaining this insight, which has been applied to achieve a dramatic improvement in peak human athletic performance.

SDFT lesions

Professor Roger Smith of the RVC asked, “Did the superficial digital flexor tendon lesions just happen?” Looking at the evidence of this most common racecourse injury, the question is, is this an acute injury to normal tissue or is it the end-point of a gradual degenerative process?

Superficial digital flexor tendon (SDFT) takes a peak load of about one tonne and operates very close to breaking point. Loading tendon before the horse achieves skeletal maturity has been found to develop strong tendons whereas “training”, stressing the mature tendon tissue, does not help in resistance to injury. This holds good for both horses and humans.

There is a positive correlation between increasing age and tendon breakdown. Genetics and conformation come into play: some horses have stronger tendons than others. Factors such as the speed of the race, high impact, hard ground, fatigue, inco-ordination, the weight of the horse and shoeing all contribute.

The tendon undergoes hyperthermia when subjected to repetitive cyclical loading or the cause of the degeneration may be cytokines released from the resident cells which induce proteolytic enzymes which damage the matrix. In either case, probing the degeneration of tendon tissue has reached the molecular level.

In contrast to tendon, bone remodels in response to stress and training results in increased bone density. Six weeks’ rest leads to bone resorption so that any extra strength is lost and exercise needs to be started slowly when the horse comes back to work to allow bone remodelling to take place. Each individual adapts in its own time and its own way.

Overtraining leads to micro-cracking of the bone. The age of the horse is significant: the horse is at the highest risk of fracture in its first year of racing and the risk increases again after five years of age. As with tendons, early training is protective.

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