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Biochemical and physiological aspects of endurance exercise in the horse

A number of biochemical and haematological changes are known to occur in horses involved in long distance riding competitions of 40- 160 km, particularly changes associated with disturbances in fluid/ electrolyte balance, catabolism of body fuel stores and alterations in the integrity of the muscle cell membrane. This study investigated these changes in more detail in 50 horses involved in competitive rides and in four horses undergoing two 80 km rides under controlled conditions. In addition, experiments were carried out on horses and ponies exposed to a hot, humid environment (41°C, 33°C wet bulb) and during intravenous adrenaline infusion, in order to study further the fluid/ electrolyte alterations associated with sweating and in particular the composition of equine sweat. Changes in plasma and urine biochemistry were also studied over 24 hours in horses at rest for comparative purposes. Significant changes were shown in 13 of the 14 plasma parameters measured in the resting horses. Most of these could be related to feeding, in particular to hay feeding which caused alterations in fluid/ electrolyte balance associated with salivary secretion. Urine composition changed very markedly during the 24 hours. Urine flow rate and creatinine and urea excretion were higher during the day and increased following drinking, as in man. Urine potassium and chloride excretion were much higher than sodium excretion and all three electrolytes (and pH, which was alkaline) showed diurnal variations markedly different from those in man. The competing endurance horses demonstrated moderate haemoconcentration, but plasma electrolyte alterations, particularly an increase in sodium concentration, were not always consistent with the production of apparently hypertonic sweat. The pattern of fuel utilisation was one of exhaustion of liver glycogen after about 40 km with extensive fat mobilisation and the use of glycerol for gluconeogenesis. Breakdown of phosphocreatine was extensive and evidence of protein catabolism was observed. Large variable increases in plasma CK and AST activities unassociated with fatigue suggested a non-pathological alteration in muscle cell membrane integrity in a number of horses. During heat exposure changes in PCV and plasma proteins were poorly related to fluid losses but changes in electrolyte concentrations were consistent with the sweat tonicity. Hypertonic chloride and potassium, and isotonic sodium concentrations (relative to plasma) were maintained in the sweat for 4.5 hours. In contrast sweat magnesium and protein concentrations were initially high but decreased exponentially with time. There was a very close correlation between these two parameters. Most of the changes in plasma parameters seen during adrenaline infusion were attributable to the adrenaline per se, but the profuse sweating induced in the horses caused some haemoconcentration. Small ponies sweated much less in response to adrenaline than Thoroughbred horses. Hypertonic sweat concentrations of chloride, sodium and potassium were maintained for 3 hours and significant differences, particularly in Na/K ratio, were found between heat and adrenalineinduced sweat. Sweat urea concentration was related to plasma urea concentration and glucose appeared in the sweat when the plasma glucose concentration exceeded 10 - 12 mmol/l. The sweat magnesium was not protein-bound and the two main electrophoretic fractions of the sweat protein were not present in serum. The possible function of this protein as a wetting agent was discussed. During the controlled 80 km rides total fluid loss was 33.5% of the total ECF volume: 78% of this was sweat and 22% respiratory evaporation. Although sweat electrolyte concentrations were again hypertonic to plasma, theoretical concentrations in total body (sweat plus respiratory) water loss were much closer to plasma concentrations - slightly hypotonic for sodium, slightly hypertonic for chloride. As a result changes in plasma electrolyte concentrations were small, an increase of 9 mmol/1 (5.7%) in sodium and a decrease of 4 mmol/l (3.5%) in chloride. Potassium appeared to move out of the intracellular fluid at the start of exercise and back in immediately afterwards and this obscured any effect of sweat losses on plasma concentration. The only urinary constituent which was conserved in the exercising horses was chloride, and the absence of any decrease in urea excretion suggested that the increase in plasma urea concentration was due to increased protein catabolism, probably from the liver. Body fuel utilisation was similar to that seen in the competing horses and plasma CK and AST activities again suggested that a non-pathological disruption of muscle cell membrane integrity was occurring in some horses which continued intermittently for several months. It was concluded that in the horse, unlike man, the thermoregulatory fluid is approximately isotonic to plasma, which minimises electrolyte imbalances and allows prolonged exercise with less need for drinking. After exercise the large caecum and colon and the sodium contained in them appear to be important in the controlled replacement of the extensive water and electrolyte losses which result.

Identiferoai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:234849
Date January 1985
CreatorsKerr, Morag Graham
PublisherUniversity of Glasgow
Source SetsEthos UK
Detected LanguageEnglish
TypeElectronic Thesis or Dissertation
Sourcehttp://theses.gla.ac.uk/3993/

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