* This is the Veterinary Version. *
Fatigue during Prolonged Exercise
Fatigue as a result of prolonged exercise depends on the duration and intensity of the activity, liver glycogen stores, the ambient temperature, and mechanisms of central fatigue. Prolonged exercise mainly depends on aerobic metabolism. Fatigue during prolonged exercise has been associated with depletion of glycogen stores in muscle and liver, and with hypoglycemia. Intramuscular glycogen provides 50% of the energy during the first 30 min of submaximal exercise but drops to <20% after 1 hr. Blood glucose makes a smaller contribution, providing only 10% of total energy utilized. Although circulating fatty acids may provide an energy source during prolonged exercise, fatigue will set in before these fat stores are completely exhausted.
In prolonged exercise, the heat generated during aerobic ATP resynthesis imposes a high thermoregulatory demand on the animal. Only 25% of the total energy produced by the muscles is converted to mechanical energy, leaving 75%–80% of that energy that must be removed as heat. Physiologic responses to heat production include sweating and/or panting to remove excess heat from the body. Complications from these compensatory mechanisms include dehydration, acid base and electrolyte disturbances (which are implicated as causes of fatigue), exhaustion, and even death (which can occur after prolonged exercise).
Horses occasionally develop severe clinical signs of fatigue at endurance events, despite current preventive practices, including evaluation of recovery at rest stops. Horses that compete in sports that include 3-day eventing, endurance rides, or combined driving are at risk of presenting with life-threatening exhaustion. In hot conditions, horses may lose body fluids at a rate of 10–15 L/hr through sweat during prolonged exercise. Urgent treatment of fluid and electrolyte deficits and hyperthermia (rectal temperatures >40.5°C [104.9°F]) may be required. Exhausted horses may lose up to 10% of their body weight in water, with some having body fluid deficits of up to 40 L, depending on their size. Water lost as sweat is mainly lost from the extracellular fluid and circulating plasma. Decreased blood volume reduces perfusion to vital organs and hampers thermoregulation. In severe cases, cardiovascular compromise may result in multiorgan failure, including damage to the kidneys, GI mucosa, and lamina of the hoof.
Sweating is associated with the loss of electrolytes, mainly sodium, potassium and chloride, as well as calcium and magnesium. Alterations in muscle electrolytes can contribute directly to signs of fatigue. The most common acid-base alteration resulting from electrolyte imbalances is metabolic alkalosis. Aerobic energy metabolism of endurance events produces minimal amounts of lactic acid; therefore, alkalosis caused by alterations in strong ions (hypochloremia and hypokalemia) predominates. Depletion of magnesium and calcium may contribute further to neuromuscular dysfunction, causing ileus, cardiac arrhythmias, and synchronous diaphragmatic flutter. Unlike endurance riding, anaerobic metabolism predominates in 3-day eventing and combined driving, resulting in metabolic acidosis during the event. After recovery, which can range from 30 min to 2 hr after the event, lactate is oxidized and the acidosis resolves. Metabolic alkalosis will then predominate.
Horses affected by exhausted horse syndrome demonstrate a range of symptoms, from changes in attitude and gait inconsistencies to colic, laminitis, clinical signs of myopathies (hard muscle bellies, pain on palpation), depression, ataxia, and eventually recumbency. Persistent tachycardia and tachypnea are noted despite rest, and rectal temperature may be ≥42°C (107.6° F). Perfusion abnormalities and signs of dehydration may be seen. Sweating may be inappropriate or absent.
Treatment involves cooling the horse and providing fluid therapy to restore circulating volumes. Hyperthermic horses should be moved to shade and treated with cool or cold water sponge baths, cold hosing, or misting fans. Water should be scraped off the haircoat and reapplied repeatedly, to prevent an insulating layer of water from forming. Application of ice water should be avoided, as well as alcohol baths or direct ice application, to prevent tissue damage. Cool-water enemas, or peritoneal and gastric lavage, may help to reduce body temperature in severe cases.
Isotonic balanced electrolyte solutions may be provided for dehydration by nasogastric intubation if the horse has normal borborygmi. Horses may be given up to 8 L initially, with subsequent administration of 4–8 L every 1–2 hr, as needed. Commercial electrolyte mixtures for horses are suitable, but hypertonic, hypotonic, and alkaline solutions should not be used. In severe cases, IV fluid therapy is preferred. A shock dose of a balanced electrolyte solution should be provided initially (20–40 mL/kg bolus) with addition of 100 mL 23% calcium gluconate per 5 L, and 5% dextrose. Additional fluids and additives should be based on reevaluation of serum chemistries and hydration status.
Additional treatments may include NSAIDs for muscle pain and colic, administered simultaneously with fluid therapy to prevent renal injury, and phenothiazines for anxiety caused by myopathies. Anticonvulsant medications may be required, and dexamethasone may help reduce cerebral edema. DMSO may be useful to further reduce inflammation, and low-molecular-weight heparin can be administered to treat coagulopathies.
Environmental temperature and humidity have a major impact on the severity of disturbance of the horse's fluid balance during prolonged exercise. It is important to ensure adequate hydration before an event, especially after long trailer rides to the competition, and to provide access to fluids during and after exercise to reduce the likelihood of dehydration. Administration of supplementary fluids, electrolytes, and glucose before and during competition, when allowed by doping regulations, may reduce the incidence of exhausted horse syndrome.
Highly intense exercise training over many weeks can result in a form of chronic fatigue referred to as overtraining syndrome. Racehorse trainers have long used the terms “overtraining,” “staleness,” or “sourness” to describe a syndrome of poor performance, failure to recover from exercise, and prolonged fatigue that does not resolve for weeks or months. By definition, signs of overtraining syndrome should persist after >2 wk of rest or reduced physical activity. A less severe form of overtraining syndrome is termed “overreaching,” which is also a syndrome of poor performance and fatigue, but athletic recovery in overreaching typically occurs from a few days to 2 wk after a reduced workload.
Overtraining syndrome was first reported in Swedish Standardbred trotters based on observations of horses with signs of fatigue and poor performance combined with weight loss, inappetence, and signs of stress, including tachycardia, nervousness, muscle tremors, sweating, and diarrhea. The severity of clinical signs of overtraining was associated with the degree of red cell hypervolemia, and horses exhibited adrenal exhaustion that may be similar to parasympathetic overtraining reported in people.
In experimental studies, a milder form of overtraining has been reproduced, without any evidence of red cell hypervolemia, inappetance, or adrenal gland exhaustion. However, this syndrome was associated with a decrease in the plasma cortisol response to intense exercise, suggesting that overtraining is associated with dysfunction of the hypothalamic-pituitary-adrenal axis. Recent research has shown that overtrained horses have altered growth hormone activities, with an increase in the normal pulsatile growth hormone activity overnight, in addition to altered glucose metabolism. Biomarkers of skeletal muscle metabolism are currently being investigated as a means to identify overtraining syndrome but require invasive muscle biopsies for measurement.
Overtraining syndrome should be suspected in horses with evidence of sustained decreased performance in association with one or more physiologic or behavioral signs. While no single physiologic marker is able to identify the syndrome, clinical signs in horses may include decreased body weight, increased heart rate during exercise, decreased plasma cortisol response to exercise, and increased plasma concentrations of muscle enzymes or gamma glutamyl transferase. Behavioral signs are a consistent and early marker of overtraining syndrome, and development of a behavioral score to assist in early detection of overtraining syndrome in horses is warranted.
* This is the Veterinary Version. *