Mechanisms resisting fatigue in isometrically contracting human skeletal muscle.
Human adductor pollicis was fatigued during circulatory occlusion by supramaximal stimulation via the ulnar nerve using intermittent trains of stimuli in ascending (1, 10, 20, 50 and 100 Hz) and descending (100, 50, 20, 10 and 1 Hz) frequencies to investigate the contribution of relaxation rate slowing and post-tetanic potentiation (PTP) to fatigue resistance. At 50 and 100 Hz force was initially well maintained despite a marked loss of excitation as indicated by EMG, demonstrating the operation of a high-frequency 'safety factor' which appeared independent of the pattern of stimulation. At 10 Hz, force was initially potentiated before declining during both activity series. Potentiation was greater during the descending frequency series and the rate of decline of force, or fatigability, was reduced. The 'extra' low-frequency potentiation at 10 Hz was not simply the result of PTP of twitch force, since this declined more during the descending than during the ascending series, nor the result of maximal relaxation rate changes which were identical for both fatiguing series. It is hypothesized that the extra potentiation and reduced fatigability at low stimulation frequencies, when preceded by high frequency, is the result of increased myofibrillar Ca2+ availability and/or sensitivity. These findings may have important practical implications in relation to functional electrical stimulation techniques as used in paraplegia and in other areas of muscle research where fatigue is to be minimized.
Gibson
H
H
Department of Medicine, University of Liverpool.
Cooper
R G
RG
Stokes
M J
MJ
Edwards
R H
RH
D000200:Action Potentials; D000328:Adult; D000332:Aerobiosis; D000693:Anaerobiosis; D004558:Electric Stimulation; D005221:Fatigue / Q000503:physiopathology*; D005260:Female; D006801:Humans; D007511:Ischemia / Q000503:physiopathology; D007537:Isometric Contraction; D008297:Male; D009119:Muscle Contraction; D009126:Muscle Relaxation; D009132:Muscles / Q000098:blood supply