出版社：Japan Society of Physical Education, Health and Sport Sciences
摘要：The factors involving muscle fatigue of the first dorsal interosseous (FDI) muscle were studied during 5-min isometric maximal voluntary contractions (MVC). Measurement of the MVC force, integrated electromyogram (IEMG) and the force induced by tetanic electrical stimulation (50 Hz, 2 s in duration) , recording of M wave from two subjects, and measurement of whole blood K^+ concentration were performed during the fatiguing exercise and recovery period of 1O min. k^+ concentration in the draining vein increased significantly from 3.4 ± 0.5 m Eq/l to 5.0 ± 1.1 m Eq/l and the area of the M wave obtained from two subjects decreased by 5-10% of the control value. These facts suggest that the resting membrane potential declined, leading to the loss of contraction force. The declining rate of the MVC force was bigger than that of the IEMG during the fatiguing exercise and at the early stage of the recovery period. While whole blood K^+ concentration recovered to its normal level quickly, there was a marked delay in the recovery of MVC force. These results suggest that the electrical excitation was not efficiently converted to muscle contraction. The MVC force declined in parallel to the 50Hz stimulation force, indicating that the central nervous system (CNS) failure was not involved in this experiments. Thus, we conclude that the failure in muscle membrane excitation and in excitation/contraction coupling are involved in the deteriorating force generating capacity of the FDI during the 5-min MVC.
其他摘要：The factors involving muscle fatigue of the first dorsal interosseous (FDI) muscle were studied during 5-min isometric maximal voluntary contractions (MVC). Measurement of the MVC force, integrated electromyogram (IEMG) and the force induced by tetanic electrical stimulation (50 Hz, 2 s in duration) , recording of M wave from two subjects, and measurement of whole blood K^+ concentration were performed during the fatiguing exercise and recovery period of 1O min. k^+ concentration in the draining vein increased significantly from 3.4 ± 0.5 m Eq/l to 5.0 ± 1.1 m Eq/l and the area of the M wave obtained from two subjects decreased by 5-10% of the control value. These facts suggest that the resting membrane potential declined, leading to the loss of contraction force. The declining rate of the MVC force was bigger than that of the IEMG during the fatiguing exercise and at the early stage of the recovery period. While whole blood K^+ concentration recovered to its normal level quickly, there was a marked delay in the recovery of MVC force. These results suggest that the electrical excitation was not efficiently converted to muscle contraction. The MVC force declined in parallel to the 50Hz stimulation force, indicating that the central nervous system (CNS) failure was not involved in this experiments. Thus, we conclude that the failure in muscle membrane excitation and in excitation/contraction coupling are involved in the deteriorating force generating capacity of the FDI during the 5-min MVC.
