Energetics of Exercise and Fatigue

Catabolism of ATP, creatine phosphate, and glycogen is the anaerobic source of energy during high-intensity exercise. Such exercise at an individual animal's highest attainable speed cannot be maintained for >30–40 sec. Thereafter, fatigue occurs and the animal slows down.

In general, when energy is supplied by aerobic energy sources, the onset of fatigue is delayed because of limited lactic acid production and efficient use of available substrates (glucose or fatty acids). The relative contribution of aerobic or anaerobic energy pathways during exercise depends greatly on the duration and energy demands of the event. All exercise has some contribution from aerobic and anaerobic energy sources. Short, intense exercise lasting 20–30 sec (eg, Quarter horse races, some Greyhound races) has >90% of energy demands supplied by anaerobic sources; other events last many hours (eg, endurance races for horses, camels, and dogs), with >90% of energy demands met by aerobic sources. During intense exercise at maximal speeds lasting 1–3 min, as in Standardbred and Thoroughbred horse races, it has been estimated that energy supply is >60% aerobic. Intramuscular stores of ATP decrease by 20–50% in racehorses after such exercise. The loss in ATP content may vary considerably; in some muscle fibers it may be negligible, while in others, especially Type II fibers, it may be substantial. Similarly, after intense exercise, muscle glycogen concentration decreases by ~30% after a single exercise bout, and by as much as 50% with repeated bouts of intense exercise. Again, depletion varies between fibers, with greater depletion observed in Type IIB muscle fibers. Superior racing performance in Thoroughbreds and Standardbreds has been correlated with high rates of oxygen transport and low rates of accumulation of lactate in the blood during submaximal exercise tests. This indicates a high ability to utilize aerobic energy pathways during exercise, preserving the limited anaerobic energy sources.

Muscular Fatigue

Fatigue during intense exercise is attributed to depletion of stores of creatine phosphate and glycogen, accumulation of ADP and inorganic phosphate, and accumulation of lactate anions and protons in active muscle cells.

Ionic imbalances, including changes in the ratio of intracellular to extracellular potassium occurring across the sarcolemma, alter the resting membrane potential and contribute to decreased sarcolemmal excitability and the ability to generate an action potential. This reduced excitability contributes to a reduction in calcium release by the sarcoplasmic reticulum (a process that requires ATP) and a consequent decrease in the force of muscle contraction. During intense exercise water moves into muscle cells, and intracellular concentrations of potassium decrease. It has been suggested that accumulation of calcium and depletion of ATP in muscle cells during exercise induces more rapid potassium efflux from muscle cells, and potassium ions accumulate in the extracellular fluid. This may inactivate the sarcolemma and t-tubule membranes and prevent tension development.

Intracellular acidosis as a result of lactate accumulation has been blamed for this decrease in efficiency or force of muscle contraction. However, in vitro research has demonstrated the protective effect of lactic acidosis and hydrogen ions in maintaining sarcolemmal function and muscle force production in the face of potassium shifts associated with intense exercise.

The decline in intramuscular ATP is correlated with the accumulation of lactate and the appearance of ammonia in the muscle. It has been postulated that ammonia accumulation in plasma may also contribute to fatigue. Increased ADP concentration also results in accumulation of AMP, inosine monophosphate, allantoin, ammonia, and uric acid in horses. In treadmill studies, the decrease in muscle ATP during intense exercise is correlated with the increase in plasma uric acid concentration 30 min after exercise. Running time during the treadmill tests is correlated with uric acid concentrations after exercise. Significant but low correlations have also been found between racing performance of Standardbred pacers and uric acid concentrations after the race. Infusion with ammonium acetate during a treadmill exercise to fatigue did not significantly affect the time to fatigue in horses, suggesting that plasma ammonia levels do not have a role in fatigue during intense exercise.

Thermoregulation and Fatigue

Fatigue during intense exercise is influenced by environmental conditions. Intense exercise in hot conditions is associated with earlier onset of fatigue, due to increased blood flow to the skin for thermoregulation at the expense of cardiac output and hence oxygen delivery to the exercising muscle. There is also a central effect of high temperatures, resulting from high brain temperatures. Earlier onset of fatigue in hot conditions could be a protective response to avoid heat stroke.

In contrast, thermoregulatory fatigue during prolonged, lower intensity exercise originates mainly from central factors, because the decreased cardiac output is offset by increased oxygen dissociation. The cerebral perfusion is reduced, but oxygen delivery to the brain does not appear to be critically low during laboratory experiments. Rather, the high brain temperature in itself seems to be the main factor affecting motor activation.

Last full review/revision July 2011 by Catherine McGowan, BVSc, MACVSc, DEIM, DECEIM, PhD, FHEA, MRCVS