Expert Opinion


David R. Hodgson, Pullman, Washington

Current Therapy in Equine Medicine, ed. N. R. Robinson Vol. II

Muscular fatigue can be defined as the inability to maintain a given exercise intensity. The process of fatigue appears to be task specific and its causes multifactorial. In humans, both central (within the central nervous system) and peripheral (within the muscles themselves) causes of fatigue have been described. Although central fatigue is likely to occur in the horse, assessment and description of the particular factors involved is not possible. In contrast, many factors causing peripheral fatigue have been described. These include impairment of excitation-contraction coupling, impairment of energy production, and limitations in fuel supply. The particular processes that result in the production of fatigue are related to the type or intensity of work the horse is required to perform. Therefore, given the large number of tasks equine athletes are asked to undertake, it is most useful to characterize the causes of fatigue in relation to the imposed work load.


A number of mechanisms have been postulated to explain fatigue during extremely heavy exercise in which muscular force can only be maintained for a maximum of several minutes. One view ascribes fatigue to a reduction in the efficiency of muscular excitation at the neuromuscular junction. An alternative hypothesis suggests that the fatigue results from events at or beyond the muscle t-tubular system. Although fatigue at the level of the neuromuscular junction has not been demonstrated in the horse, several of the changes occurring within the muscle cell itself, known to be associated with the production of fatigue, have been described.

Of these intracellular events, depletion of the phosphagen pool, which is composed of adenosine triphosphate (ATP) and creatine phosphate (CP), and the accumulation of lactate appear to be important processes contributing to fatigue. Although cellular homeostatic mechanisms are designed to maintain the levels of ATP within working muscle, short-term exhaustive exercise produces initial depletion of CP stores, with subsequent reduction in intramuscular ATP levels. There is a resultant diminution of the force-producing potential of the working muscle. Accumulation of lactate within working muscle reduces intracellular pH to 6.3 or lower, from a resting value of 7.0 to 7.1. Such changes in pH probably exert their effects in several ways. Protons may displace calcium ions from troponin, interfering with the actmyosin contractile machinery. Additionally, as intracellular pH falls, several of the key enzymes within the major metabolic pathways are progressively inhibited. The net result of these processes is a reduced availability or production of ATP for muscular contraction, with a subsequent decrease in the ability to perform muscular work. Progressive lactate accumulation in the working muscle of horses usually occurs at or above speeds of approximately 600 meters per minute. Decreases in the concentration of intramuscular ATP per se have only been reported following short-term exhaustive exercise (speeds greater than 800 meters per minute). Therefore it is important to realize that the accumulation of lactate, even at somewhat slower speeds, ultimately undermines the force-producing capacity of muscle.


Many factors  including disturbance in thermoregulation, hydration, and ionic balance, and depletion of muscle glycogen stores  have been implicated, both singularly and collectively, as causes of fatigue during prolonged submaximal exercise.

The energy that allows continued muscular contraction is provided by the enzymic degradation of substrates within the muscles themselves. One of the consequences of these metabolic processes is the liberation of large amounts of heat. To dissipate this heat and avoid hyperthermia, horses are endowed with a finely controlled thermoregulatory system, based primarily on the evaporation of sweat. However, as ambient temperature increases, the efficiency of this mechanism is reduced, potentially resulting in hyperthermia and a decreased capacity to perform endurance exercise. Increases in heart rate and cardiac output are necessary to increase peripheral blood flow for heat dissipation. It is likely that a similar sequence of events occurs in the horse in response to heat stress. As sweating is the most important mechanism for heat dissipation in the horse during prolonged submaximal exercise, large volumes of fluid may be lost via this route. In humans, dehydration equivalent to approximately 5 percent body weight is associated with a marked reduction in the capacity to perform endurance exercise. As the state of dehydration increases, this diminution in exercise capacity becomes more pronounced. This relationship between alterations in fluid balance and fatigue would also appear to be critical for the horse.

Horse sweat is hypertonic, and the potential exists for dramatic electrolyte losses during prolonged exercise. Sodium and chloride are the major ionic constituents of sweat, and sodium loss appears to have the most pronounced effects on body function. Due to the central role of sodium in fluid homeostasis, the major signs resulting from the loss of sodium and associated fluid are those of decreased circulatory function and poor organ profusion. Such alterations in homeostatic mechanisms could be intimately related to reductions in athletic performance.

During exercise, potassium is liberated from working muscle. This potassium enters the circulation with some being liberated in sweat. However, most of the potassium is taken up by nonworking muscle. Studies in humans have demonstrated that if exercise of moderate to high intensity in continued to exhaustion, decreases in the intracellular potassium concentration of working muscle, from resting values of approximately 160 mEq/L to as low as 130 mEq/L, are possible. Such alterations in potassium concentration have been related to decreases in the force-producing potential of the muscle and would therefore contribute to fatigue. This effect is relatively transient, as on cessation of exercise there is rapid repletion of the potassium deficits within the working muscle.

Calcium ions (Ca 2+) have been reported to increase in the mitochondria of working muscle during prolonged submaximal exercise. These ions are liberated from the sarcoplasmic reticulum during excitation  contraction coupling and some may be sequestered by the mitochondria. This process requires the consumption of oxygen and therefore may reduce the potential of mitochondria to phosphorlyate adensosine diphosphate (ADP) to ATP, which in turn may result in fatigue.

Regardless of the causes of fatigue just described, there does appear to be one common element associated with fatigue during prolonged exercise of moderate to high intensity. This is closely related to a depletion of the intramuscular glycogen store. It occurs in a selective manner in given muscle fibers (fiber types) as a function of the intensity or duration or both of the exercise. Depletion of glycogen from within muscle fibers is associated with a decreased force-producing capacity of the fibers. Although muscle fibers are selectively recruited during submaximal exercise, with new ones being added as others become exhausted, eventually many fibers are depleted of their glycogen stores and the overall force-producing capacity of the muscle is reduced. The depletion of glycogen, despite the fact that fats are the major substitute for muscular work during this type of exercise, indicates that glycogen is vital if exercise is to continue. When horses undergo endurance training, one of the major metabolic adaptations is to further increase the ability of working muscle to utilize fats during submaximal exercise. This has the effect of reducing the rate of glycogen utilization and therefore delays the onset of fatigue.

In summary, the inability to maintain a given exercise intensity depends on several factors, including the nature of the exercise, the physiologic or training status of the horse, the environmental conditions, and other (poorly defined) psychologic considerations. At times, the inability to continue exercise at a given intensity depends on the availability of a key metabolite within a particular tissue. Under other conditions abnormal or inadequate interaction of several individual systems may result in the onset of fatigue. However, as physiologic systems are often matched in their capacities, it may be extremely difficult to identify precisely the factor or factors that result in a decrease in exercise capacity.

Return to
Expert Opinion