Fatigue of rat hindlimb motor units: Biochemical– physiological associations

Abstract

Associations between fatigability and biochemical properties within motor unit (MU) types were explored in two hindlimb muscles of the adult rat. Type FF MUs in extensor digitorum longus and type S units in soleus were subjected either to a moderate (type FF) or severe (type S) 6-min, fatigue-inducing stimulation protocol. For both MU types, the range of values for their fatigability was considerably greater than the ranges in the activity levels of three enzymes in the units' constituent muscle fibers (MFs). These enzymes represented major energy-yielding pathways: adenylokinase, for high-energy phosphate metabolism; lactate dehydrogenase, for anaerobic glycolysis; and malate dehydrogenase, for oxidative metabolism. There were also relatively weak associations between the fatigue indices of the MUs and the activity levels of the three enzymes. Thus, this work supports previous conclusions that the force decline exhibited by MUs during electrically evoked contractions depends on both MF biochemistry and other intracellular mechanisms. Electromyographic measurements suggested that these other mechanisms are distal to the intramuscular branches of the axon in type FF units, and distal to excitation-contraction coupling in type S units.

Physiological fatigue of smooth muscle contractions in rat urinary bladder

“…Characterizing the fatigue of bladder smooth muscles in terms of the decline in contractile tension during continuous stimulation for a brief period using trains of stimuli is similar to the procedure used in studies on the fatigue of skeletal muscles [2–7]. Continuing the stimulation for only 60 s in the present study, rather than stimulation for much longer periods as in the previous studies on bladder fatigue [10–13], enabled us to characterize the fatigue of bladder smooth muscles within the normal duration of voiding.…”

“…The mechanisms involved in the development of fatigue in bladder smooth muscles are not yet clear. Studies on the mechanisms of skeletal muscle fatigue indicate that a decline in contractile tension can occur due to impairment in central neural drive, failure of peripheral processes such as nerve conduction, neuromuscular transmission, muscle membrane excitation, excitation‐contraction coupling, or contractility, or exhaustion of energy resources and metabolic changes [2–7]. In the present study a preliminary attempt was made to evaluate the possible mechanisms involved in the development of bladder fatigue.…”

“…In normal human subjects voiding involves continuous contraction of the detrusor smooth muscles for 30–40 s, to empty the 300–400 mL of urine collected at maximum bladder capacity [1]. Prolonged contractile activity was shown to cause fatigue in skeletal muscles due to impairment in one or more physiological processes [2–7]. Very few studies have been undertaken to characterize the fatigue process in bladder smooth muscles.…”

Does motoneuron adaptation contribute to muscle fatigue?

“…In summary, under normal (nonpathophysiological) circumstances the literature on fatigue‐induced, axonal branch‐point, and axon‐collateral neuromuscular junction failure is quite sparse except for low‐force contractions, and that on fatigue‐induced neuromuscular transmission failure is quite controversial 33, 62. Presumably, both are task‐dependent and if they do occur, either singly or together, they are more likely to involve the higher‐threshold, more fatigable glycolytic MUs than the lower threshold, fatigue‐resistant ones 39, 62, 152…”

“…It has been known for at least a century that fatigue can be caused by an impairment of numerous physiological processes distributed throughout the central nervous system (CNS) and peripheral neuromuscular system 62. Among these processes, far more is known about those occurring external to the CNS, although much is still to be learned about them 33. The case for CNS processes is no less compelling 45, 61, 144.…”