The energy requirements for restoring normal cellular metabolite levels are represented by the additional oxygen used during recovery from exercise (Fig. 12.18). While muscle's ability to meet energy needs determines exercise duration, fatigue does not result from depletion of energy stores. Instead, the onset of fatigue is influenced by metabolic byproducts. Fatigue can potentially occur at various points involved in muscle contraction, from the brain to the muscle cells, as well as in the cardiovascular and respiratory systems responsible for maintaining energy supplies (such as fatty acids and glucose) and delivering oxygen to the exercising muscle.

Multiple factors have been implicated in muscle fatigue. During brief periods of tetany, as long as circulation is intact, the muscle receives adequate oxygen supply. However, the force/stress generated during these brief tetanic periods rapidly decays to a level sustainable for longer periods (Fig. 12.19). This decay signifies the quick and nearly complete failure of the fast motor units. The decline in force/stress corresponds to the depletion of glycogen and creatine phosphate stores and the accumulation of lactic acid. Notably, the decline in force/stress occurs when the ATP pool is not significantly reduced, preventing muscle fibers from going into rigor. On the contrary, the slow motor units can fulfill the energy demands of fibers under this condition and do not experience significant fatigue, even after extended durations. Clearly, there exists a factor associated with energy metabolism that can impede contraction, particularly in fast fibers, although this factor has not yet been clearly identified.
Fig. 12.18 are approximately equal). As indicated earlier, the additional oxygen used during recovery from exercise represents the energy requirements for restoring normal cellular metabolite levels.
The ability of muscle to meet energy needs is a major determinant of the duration of the exercise. However, fatigue is not the result of depletion of energy stores. Instead, metabolic byproducts seem to be important factors in the onset of fatigue. Fatigue may potentially occur at any of the points involved in muscle contraction, from the brain to the muscle cells, as well as in the cardiovascular and respiratory systems that maintain energy supplies (i.e., fatty acids and glucose) and oxygen delivery to the exercising muscle.
Several factors have been implicated in muscle fatigue. During brief periods of tetany, the oxygen supply to the muscle is adequate as long as the circulation is intact. However, the force/stress generated during these brief
Rate of energy expenditure •Fig. 12.18. An Oxygen Debt Is Incurred by the Exercising of Muscle When the Rate of Energy Expenditure Exceeds the Rate of Energy Production by Oxidative Metabolism. Upper panel, Energyexpenditureduringstrenuousexercise.Lower panel, Energyexpenditureduringenduranceexercise.Seetextfordetails.
tetanic periods decays rapidly to a level that can be maintained for long periods (
Fig. 12.19 ). This decay represents the rapid and almost total failure of the fast motor units. The decline in force/stress is paralleled by depletion of glycogen and creatine phosphate stores and the accumulation of lactic acid. Of importance is that the decline in force/ stress occurs when the ATP pool is not greatly reduced, so that the muscle fibers do not go into rigor. In contrast, the slow motor units are able to meet the energy demands of fibers under this condition, and they do not exhibit significant fatigue, even after many hours. Evidently, some factor associated with energy metabolism can inhibit contraction (e.g., in the fast fibers), but this factor has not been clearly identified.