Muscle fatigue is the decrease in the force-generating ability of a muscle resulting from recent activation.5
Fatigue exhibits task dependency and its evolution and extent depend on the conditions at which the muscle operates. In the late 1960s, Aljure and Borrero1
used the influence of muscle length as a model to determine whether fatigue in isolated toad sartorius muscle was due either to failure of the contractile machinery resulting from metabolic activity or to impairments in excitation–contraction coupling. More recently, Fitch and McComas15
conducted a similar study using human ankle dorsiflexor muscles. The premise of both of these studies was that if the amount of fatigue observed was independent of muscle length, then fatigue could be attributed to impairments in excitation–contraction coupling. Conversely, if fatigue resulted from metabolic events associated with crossbridge interactions, then greater fatigue should be observed at optimal length because crossbridge interactions would be maximal. Both studies found less fatigue if the muscles were fatigued at a short suboptimal length and evaluated at a long length than if the muscles were fatigued and evaluated at a long length.1,15
Thus, both groups concluded that the metabolic consequences of contractile activity were the primary mechanism for muscle fatigue and that reduced contractile activity when the muscle was held in the shortened length resulted in the decrease in fatigue. Aljure and Borrero1
also noted, however, that muscles that were both fatigued and tested at the short length demonstrated greater fatigue than if fatigued and tested at the optimal length.
Sacco et al.28
studied human dorsiflexor muscles and also found contradictory findings, depending on the muscle length at which fatigue was evaluated. These investigators concluded that their data supported both metabolic factors and impairments in excitation–contraction coupling as mechanisms for fatigue. Sacco and colleagues concluded that diminished fatigue observed when the muscle was fatigued at the short length and then tested at the optimum length was due to movement of the leg, which attenuated the fatigue. This conclusion supports the theory that impairment in excitation–contraction coupling is the mechanism for fatigue, resulting from T-tubule action potential propagation failure.
They postulated that greater narrowing or compression of the T-tubule may occur at short muscle lengths and that excitation–contraction coupling failure, due to localized ionic imbalances that impair action potential propagation in the transverse tubules, may have created relatively quiescent regions of muscle fibers during stimulation. Moving the muscle to a longer length would account for the unexpected force recovery if the previously quiescent fibers now contributed to force development. These studies raise important concerns for understanding the mechanisms underlying fatigue.
In spite of several studies on the human ankle doriflexor muscles,15,28
this model presents various methodological difficulties. Fitch and McComas were unable to monitor changes in dorsiflexion torque when fatiguing the muscles at short lengths. Additionally, Sacco and colleagues did not discuss the contribution of changes in the effective lever arm of the dorsiflexors and its potential effect on myofilament overlap and torque production about the ankle. Thus, the relative contribution that changes in muscle length and lever arm make to the observed decline in force is not known. To overcome these difficulties, we chose to study the human quadriceps femoris muscle.
The purpose of this study was to examine the effects of muscle length on fatigue resulting from repetitive activation with short-duration stimulation trains. Because a previous study in our laboratory showed surprising fatigue resistance at short muscle lengths,22
we hypothesized that less muscle fatigue would occur at short than long muscle lengths. The quadriceps femoris was activated at both the same absolute and relative forces at the two muscle lengths to control for the level of force produced at each muscle length. On a subpopulation of subjects, responses to high- and low-frequency trains of stimulation were used to examine excitation–contraction coupling failure at each muscle length. Additionally, because of our laboratory’s long-standing interest in using the catchlike property of skeletal muscle to augment muscle forces,6–9,23
stimulation trains that elicit a catchlike response were also used to evaluate muscle performance for each fatigue condition. Preliminary results have been presented elsewhere.22