Electromagnetic stimulation blocks isometric twitch contraction in the frog sciatic nerve-gastrocnemius muscle preparation

The effect of electromagnetic stimulation (EMS) on nerve conduction and muscle twitch contraction was studied in isolated sciatic nerve-gastrocnemius muscle of the frog. Electrical stimulation (ES) of the sciatic nerve produced twitch contractions in the gastrocnemius muscle and these responses were reduced and eventually blocked by EMS, applied to the nerve simultaneously with ES, from a d.c. source at a certain frequency and duration of the induced current. The EMS-induced inhibition of the twitch contractions was reversible, and this depended on the induced current and its duration. The possibility that other factors may have contributed to the inhibition of twitch contractions, such as a rise in temperature, was also investigated. It was concluded that EMS inhibited indirectly-elicited twitch contractions produced by ES in the frog nerve-muscle preparation.     

Diaphragmatic fatigue in the rat

We studied fatigue of rat diaphragm in response to repetitive brief and prolonged electrical stimulation of the phrenic nerve, at 0.2, 1-100 Hz. Low and high frequency of stimulation produced twitch and tetanic contractions in the rat diaphragm. A mean maximum twitch tension of 1.4 +/- 0.1 g was produced at 1 Hz, and a mean maximum tetanic tension of 5.6 +/- 0.3 g was obtained at 100 Hz (means +/- S.E., n = 8). Twitch and tetanic fatigue was produced at all frequencies of stimulations, but with different time scale, or duration, and with different number of stimuli delivered to the muscle. At low rates of stimulation, e.g. 10 Hz, fewer stimuli were needed to fatigue the muscle (3000 in 5 min), whereas at high rates of stimulation, e.g. 50 Hz, more stimuli were needed to fatigue the muscle (6600 in 2.2 min). The amplitude of the tetanic tensions elicited at 10 and 50 Hz, at the end of 5 or 2 min fatiguing stimulation, was 39 +/- 2.7% and 80 +/- 3.1% of their respective control tensions (2.8 +/- 0 2 g and 5.3 +/- 0.5 g, n = 8, P 0.001). It was concluded that fatigue in the rat diaphragm depended on the frequency and duration of stimulation as well as on the number of stimuli delivered to the muscle. Various mechanisms of muscle fatigue are described in the discussion to explain the observations made in the present investigation.     

Effects of exhaustive incremental treadmill exercise on diaphragm and quadriceps motor potentials evoked by transcranial magnetic stimulation.

It is unknown whether changes in corticomotor excitability follow exercise in healthy humans. We hypothesized that a fall in the diaphragm and quadriceps motor-evoked potential (MEP) amplitude elicited by transcranial magnetic stimulation of the motor cortex would occur after an incremental exercise task. In 11 healthy subjects, we measured transdiaphragmatic pressure and isometric quadriceps tension in response to supramaximal peripheral magnetic nerve stimulation. MEPs were recorded from these muscles in response to transcranial magnetic stimulation. After baseline measurements, subjects performed a period of submaximal exercise (gentle walking). Measurements were repeated 5 and 20 min after this. The subjects then exercised on a treadmill with an incremental protocol to exhaustion. Transcranial magnetic stimulation was performed at baseline and at 5, 20, 40, and 60 min after exhaustive exercise, and force measurements were obtained at baseline, 20 min, and 60 min. Mean exercise duration was 18 +/- 4 min, and mean maximum heart rate was 172 +/- 10 beats/min. Twitch transdiaphragmatic pressure and twitch isometric quadriceps tension were not different from baseline after exercise, but a significant decrease was observed in diaphragm MEP amplitude 5 and 20 min after exercise (60 +/- 38 and 45 +/- 24%, respectively, of baseline, P = 0.0001). At the same times, the mean quadriceps MEPs were 59 +/- 39 and 74 +/- 32% of baseline (P < 0.0001 and P < 0.01, respectively). Studies using paired stimuli confirmed a likely intracortical mechanism for this depression. Our data confirm significant depression of both diaphragm and quadriceps MEPs after incremental treadmill exercise.     

A strong constant magnetic field affects muscle tension development in bullfrog neuromuscular preparations

Effects of a constant magnetic field (CMF) of 0.65 T on muscle tension over 9 h were studied in the neuromuscular preparation of the bullfrog sartorius muscle. Tension was developed every 30 min by stimulation of the sciatic nerve (nerve stimulation) or of the sartorius muscle itself (muscle stimulation). In sciatic nerve stimulation, tension decreased rapidly for the first 3-4 h at a similar rate in both test (exposed to CMF) and control muscles. However, the rate of decrease became smaller and almost leveled off after 3-4 h in the test muscles, whereas tension continued to decrease monotonically in control muscles. The slope of the decrease for these later periods was significantly different between the test and the control conditions. Accordingly, tension was larger in test than in control muscles. In muscle stimulation, tension decreased monotonically from the start of experiments in control muscles, while tension in test muscles maintained their initial values for almost 3 h. Thereafter they started to decrease with a similar rate to the control. Hence, tension was always larger in test than in control muscles. A similar pattern of temporal change was observed for the rate of rise of the maximum tension for nerve or muscle stimulation. However, a significant difference was detected only in the case of muscle stimulation. The present results showed that a strong CMF of 0.65 T had biological effects on tension development of the bullfrog sartorius muscle by stimulation of the sciatic nerve as well as by stimulation of muscle itself. The presence of a small AC magnetic field component leaves open the possibility of an AC, rather than a CMF effect.     

Tetrodotoxin blocks mechanical response in mammalian muscle in the presence of tetrodotoxin-resistant action potentials

The effect of tetrodotoxin (TTX) (10(-5)-10(-6)M) on the mechanical activity and on the action potential of innervated and denervated muscle of the rat was studied. The twitch tension was reduced to 10 % of the control values within 20 min of TTX 10(-6) introduction. This effect was reversible. The mean twitch tension in the presence of 10(-6)M TTX expressed as a percentage of control was 9.3 +/- 2.4 (SEM) for innervated muscle and 10.9 +/- 2.5 for denervated muscle. The dose-effect twitch relation for denervated muscles was not significantly different from that observed in control innervated muscles in the 10(-3)-10(-6) TTX range. Action potentials of innervated muscles could not be elicited in 10(-6)M TTX. In the presence of this (TTX) fibers of chronically denervated muscles consistently responded to stimulation with action potentials which were slower and smaller but still with overshoot, contrasting with fibrillation potentials that had been described to be blocked by TTX.     

Failure of oxygen radical scavengers to modify fatigue in electrically stimulated muscle.

We used in situ gastrocnemius muscle of anaesthetized dogs to test the hypothesis that O2 radical production during muscle contraction contributes to fatigue. Muscle tension was measured with a force transducer and blood flow was monitored with an electromagnetic flow probe. Muscle contractions were produced by stimulating the nerve for 15 min at 20 Hz, 12 trains/min, and a duty cycle of 0.25. Three groups of seven animals were given an infusion of 0.2 mL.min-1 of either saline, low-dose oxygen radical scavengers (250 IU.mL-1 superoxide dismutase, 640 IU.mL-1 polyethylene glycol (PEG)-catalase, 0.25 mg.mL-1 deferoxamine, and 0.1 mg.mL-1 oxypurinol), or high-dose oxygen radical scavengers (3300 IU.mL-1 superoxide dismutase, 6600 IU.mL-1 PEG-catalase, 2.5 mg.mL-1 deferoxamine, and 0.1 mg.mL-1 oxypurinol). Blood flow and vascular resistance of the gastrocnemius muscle during stimulation did not differ among groups. After 15 min of stimulation, the developed tension (represented as a percentage of initial tension developed) was 66 +/- 7% in the saline treated group, 70 +/- 6% in the low-dose group, and 70 +/- 4% in the high-dose group. The change in tension during recovery was not significant in the control or low-dose groups. However, there was partial recovery in the high-dose group. In conclusion, in this preparation, oxygen radical scavengers did not delay the development of decreased muscle tension.     

Effects of Ca2+ withdrawal on diaphragmatic fiber tension generation

The effects of extracellular Ca2+ withdrawal were studied on isolated diaphragmatic muscle fibers and compared with the effects on the papillary, soleus, and extensor digitorum longus (EDL) contractility, using the same in vitro model. Diaphragmatic fibers were obtained from 15 rats, and papillary muscles, soleus, and EDL were obtained from 10 animals. Isometric force generated in response to 1-Hz supramaximal electrical stimulation was measured with a highly sensitive photoelectric transducer. After control measurements, perfusion with a Krebs solution depleted of calcium (0 Ca2+) was started while the fibers were continuously stimulated (4 times/min) and twitches recorded. For the papillary fibers, perfusion with zero Ca2+ was followed by an immediate decrease in twitch tension, complete twitch abolition occurring within 3 +/- 1 min after zero-Ca2+ exposure. Diaphragmatic fibers behaved similarly, although twitch abolition was delayed (10 +/- 3 min after 0-Ca2+ exposure). For the soleus fibers, the twitch amplitude amounted to 38 +/- 10% of control (62% decrease on the average) after 30 min of zero-Ca2+ exposure, no twitch abolition being noted even after 1 h of Ca2+-free exposure. The twitch amplitude of the EDL fibers amounted to 75 +/- 7% of control (25% decrease) after 30 min of zero-Ca2+ exposure. The recovery kinetics for the four fiber types after reexposure to Ca2+-containing solution were also different, with papillary and diaphragmatic fibers recovering completely within 2.5 +/- 0.5 and 4 +/- 0.5 min, respectively. By contrast, neither the soleus nor the EDL showed complete recovery after 30 min.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of twitch potentiation in the gastrocnemius of young and elderly men

The capacity for twitch potentiation in the gastrocnemius muscle was determined following maximal voluntary contractions (MVC) in 11 elderly (means +/- SD; 66.9 +/- 5.3 years) and 12 young (25.7 +/- 3.8 years) men. Potentiation was observed by applying selective stimulation to the muscle belly, 2 s after a 5 s MVC. With this procedure, both groups showed significant (P less than 0.05) increases in twitch tension in the gastrocnemius (ratios of potentiated twitch to baseline were means = 1.68 +/- 0.40 for young vs means = 1.40 +/- 0.20 for the elderly, P less than 0.001). Time to peak tension of the twitch decreased from means = 101.5 +/- 17.9 ms to means = 88.0 +/- 15.8 ms in the young men following potentiation; the respective values for the older men were 136.7 +/- 17.9 ms and 133.1 +/- 28.6 ms. These changes resulted in a greater rate of tension development in the potentiated state. The elderly gastrocnemius thus showed qualitatively similar changes in the isometric twitch following potentiation, but reduced and prolonged responses in comparison to young adults. Slowed muscle contraction and reduced capacity for potentiation may be physiological correlates of the reported morphological changes in aged skeletal muscle.     

Optimal electrode placement for noninvasive electrical stimulation of human abdominal muscles.

Abdominal muscles are the most important expiratory muscles for coughing. Spinal cord-injured patients have respiratory complications because of abdominal muscle weakness and paralysis and impaired ability to cough. We aimed to determine the optimal positioning of stimulating electrodes on the trunk for the noninvasive electrical activation of the abdominal muscles. In six healthy subjects, we compared twitch pressures produced by a single electrical pulse through surface electrodes placed either posterolaterally or anteriorly on the trunk with twitch pressures produced by magnetic stimulation of nerve roots at the T(10) level. A gastroesophageal catheter measured gastric pressure (Pga) and esophageal pressure (Pes). Twitches were recorded at increasing stimulus intensities at functional residual capacity (FRC) in the seated posture. The maximal intensity used was also delivered at total lung capacity (TLC). At FRC, twitch pressures were greatest with electrical stimulation posterolaterally and magnetic stimulation at T(10) and smallest at the anterior site (Pga, 30 +/- 3 and 33 +/- 6 cm H(2)O vs. 12 +/- 3 cm H(2)O; Pes 8 +/- 2 and 11 +/- 3 cm H(2)O vs. 5 +/- 1 cm H(2)O; means +/- SE). At TLC, twitch pressures were larger. The values for posterolateral electrical stimulation were comparable to those evoked by thoracic magnetic stimulation. The posterolateral stimulation site is the optimal site for generating gastric and esophageal twitch pressures with electrical stimulation.     

Spike-triggered average torque and muscle fiber conduction velocity of low-threshold motor units following submaximal endurance contractions.

The motor unit twitch torque is modified by sustained contraction, but the association to changes in muscle fiber electrophysiological properties is not fully known. Thus twitch torque, muscle fiber conduction velocity, and action potential properties of single motor units were assessed in 11 subjects following an isometric submaximal contraction of the tibialis anterior muscle until endurance. The volunteers activated a target motor unit at the minimum discharge rate in eight 3-min-long contractions, three before and five after an isometric contraction at 40% of the maximal torque, sustained until endurance. Multichannel surface electromyogram signals and joint torque were averaged with the target motor unit potential as trigger. Discharge rate (mean +/- SE, 6.6 +/- 0.2 pulses/s) and interpulse interval variability (33.3 +/- 7.0%) were not different in the eight contractions. Peak twitch torque and recruitment threshold increased significantly (93 +/- 29 and 12 +/- 5%, P <0.05) in the contraction immediately after the endurance task with respect to the preendurance values (0.94 +/- 0.26 mN.m and 3.7 +/- 0.5% of the maximal torque), whereas time to peak of the twitch torque did not change (74.4 +/- 10.1 ms). Muscle fiber conduction velocity decreased and action potential duration increased in the contraction after the endurance (6.3 +/- 1.8 and 9.8 +/- 1.8%, respectively, P <0.05; preendurance values, 3.9 +/- 0.2 m/s and 11.1 +/- 0.8 ms), whereas the surface potential peak-to-peak amplitude did not change (27.1 +/- 3.1 microV). There was no significant correlation between the relative changes in muscle fiber conduction velocity or surface potential duration and in peak twitch torque (R2= 0.04 and 0.10, respectively). In conclusion, modifications in peak twitch torque of low-threshold motor units with sustained contraction are mainly determined by mechanisms not related to changes in action potential shape and in its propagation velocity.     

Immunohistochemical localization of substance P, vasoactive intestinal polypeptide and gastrin-releasing peptide in vas deferens and seminal vesicle, and the effect of these and eight other neuropeptides on resting tension and neurally evoked contractile activity

Immunohistochemical studies of the vas deferens and seminal vesicle of mouse, guinea-pig, and rabbit showed the presence of nerve fibres containing vasoactive intestinal polypeptide (VIP), substance P (SP), and gastrin-releasing peptide (GRP) supplying the smooth muscle layers as well as blood vessels. The nerve supply was better developed in the seminal vesicle than in the vas deferens. The motor activity of the vas deferens and seminal vesicle of the guinea-pig was studied in vitro. The vas deferens responded to transmural electrical stimulation with a twitch followed by a slow contraction. The twitch was blocked by guanethidine and tetrodotoxin, but not by atropine, propranolol, phenoxybenzamine, or fluphenazine. The slow contraction exhibited features of an alpha-receptor-mediated response. SP, physalaemin and eledoisin contracted the smooth muscle and also potentiated the twitch response to electrical nerve stimulation in a concentration-dependent manner. The SP blocking agent, (D-Pro2,D-Trp7,9)-SP, affected neither the resting tension nor the response to electrical stimulation. It is therefore suggested that the SP fibres act mainly prejunctionally. VIP, Leu-enkephalin, cholecystokinin octapeptide (CCK-8), angiotensin II, vasopressin, neurotensin, bombesin, and GRP had no effect on either the resting tension or the response to electrical nerve stimulation. The seminal vesicle responded to electrical stimulation with a contraction which was unimpaired by atropine, propranolol, phenoxybenzamine, and guanethidine, but abolished by tetrodotoxin. Hence, this contraction is mediated by a non-adrenergic, non-cholinergic neurotransmitter. Bombesin, GRP, SP, physalaemin and eledoisin contracted the smooth muscle and potentiated the response to electrical stimulation. VIP, Leu-enkephalin, CCK-8, angiotensin II, vasopressin, and neurotensin had no effect on the resting tension or on the response to transmural electrical stimulation. The SP antagonist abolished the contraction elicited by SP but did not influence the response to nerve stimulation. The results suggest that the SP and GRP nerves may have prejunctional and facilitating postjunctional effects in the seminal vesicle.     

Exercise-induced abdominal muscle fatigue in healthy humans.

The abdominal muscles have been shown to fatigue in response to voluntary isocapnic hyperpnea using direct nerve stimulation techniques. We investigated whether the abdominal muscles fatigue in response to dynamic lower limb exercise using such techniques. Eleven male subjects [peak oxygen uptake (VO2 peak) = 50.0 +/- 1.9 (SE) ml.kg(-1).min(-1)] cycled at >90% VO2 peak to exhaustion (14.2 +/- 4.2 min). Abdominal muscle function was assessed before and up to 30 min after exercise by measuring the changes in gastric pressure (Pga) after the nerve roots supplying the abdominal muscles were magnetically stimulated at 1-25 Hz. Immediately after exercise there was a decrease in Pga at all stimulation frequencies (mean -25 +/- 4%; P < 0.001) that persisted up to 30 min postexercise (-12 +/- 4%; P = 0.001). These reductions were unlikely due to changes in membrane excitability because amplitude, duration, and area of the rectus abdominis M wave were unaffected. Declines in the Pga response to maximal voluntary expiratory efforts occurred after exercise (158 +/- 13 before vs. 145 +/- 10 cmH2O after exercise; P = 0.005). Voluntary activation, assessed using twitch interpolation, did not change (67 +/- 6 before vs. 64 +/- 2% after exercise; P = 0.20), and electromyographic activity of the rectus abdominis and external oblique increased during these volitional maneuvers. These data provide new evidence that the abdominal muscles fatigue after sustained, high-intensity exercise and that the fatigue is primarily due to peripheral mechanisms.     

Force-frequency relationship and potentiation in mammalian skeletal muscle.

Repetitive activation of a skeletal muscle results in potentiation of the twitch contractile response. Incompletely fused tetanic contractions similar to those evoked by voluntary activation may also be potentiated by prior activity. We aimed to investigate the role of stimulation frequency on the enhancement of unfused isometric contractions in rat medial gastrocnemius muscles in situ. Muscles set at optimal length were stimulated via the sciatic nerve with 50-micros duration supramaximal pulses. Trials consisted of 8 s of repetitive trains [5 pulses (quintuplets) 2 times per second or 2 pulses (doublets) 5 times per second] at 20, 40, 50, 60, 70, and 80 Hz. These stimulation frequencies represent a range over which voluntary activation would be expected to occur. When the frequency of stimulation was 20, 50, or 70 Hz, the peak active force (highest tension during a contraction - rest tension) of doublet contractions increased from 2.2 +/- 0.2, 4.1 +/- 0.4, and 4.3 +/- 0.5 to 3.1 +/- 0.3, 5.6 +/- 0.4, and 6.1 +/- 0.7 N, respectively. Corresponding measurements for quintuplet contractions increased from 2.2 +/- 0.2, 6.1 +/- 0.5, and 8.7 +/- 0.7 to 3.2 +/- 0.3, 7.3 +/- 0.6, and 9.0 +/- 0.7 N, respectively. Initial peak active force values were 27 +/- 1 and 61.5 +/- 5% of the maximal (tetanic) force for doublet and quintuplet contractions, respectively, at 80 Hz. With doublets, peak active force increased at all stimulation frequencies. With quintuplets, peak active force increased significantly for frequencies up to 60 Hz. Twitch enhancement at the end of the 8 s of repetitive stimulation was the same regardless of the pattern of stimulation during the 8 s, and twitch peak active force returned to prestimulation values by 5 min. These experiments confirm that activity-dependent potentiation is evident during repeated, incompletely fused tetanic contractions over a broad range of frequencies. This observation suggests that, during voluntary motor unit recruitment, derecruitment or decreased firing frequency would be necessary to achieve a fixed (submaximal) target force during repeated isometric contractions over this time period.     

Effects of ascorbic acid on lead induced alterations of synaptic transmission and contractile features in murine dorsiflexor muscle

Lead is a common environmental toxin that affects neuromuscular junction and potentially might cause muscle weakness. Antioxidants like ascorbic acid may protect against lead induced myopathy. The present study measured isometric twitch tensions (evoked either directly by muscle stimulation or indirectly by nerve stimulation) to study effects of ascorbic acid on lead induced alterations at murine dorsiflexor skeletal muscle. Resting membrane potentials (RMPs), endplate potentials (EPPs) and miniature endplate potentials (MEPPs) were also recorded. Forty animals were divided into four groups of n = 10 each. (10 control, 10 lead alone, 10 ascorbic acid alone, 10 lead treated plus ascorbic acid). Lead (1 mg/kg) i.p, was administered daily for 2 weeks before the recording day and ascorbic acid (200 mg/kg, i.p) was given daily for 3 weeks prior to the experiment day. Lead treatment reduced twitch tension significantly (from 4.3 +/- 0.5 g to 2.7 +/- 0.2 g) and delayed half time of decay compared to the control. Similarly MEPPs frequencies were reduced following lead treatment. Application of ascorbic acid prevented twitch tension reduction in lead treated mice (3.3 +/- 0.3 g) and reversed lead induced delay in half time of decay. The negative actions of lead treatment on MEPPs frequencies were also modified with ascorbic acid. It appears that ascorbic acid exerts a protective role against lead induced peripheral nerve and muscle dysfunction. This effect of ascorbic acid on lead induced neuromyopathy is probably mediated via a free radical scavenging mechanism or modification of Ca(2+) homeostasis.     

Effect of phencyclidine on post-tetanic twitch tension of the mouse diaphragm preparation

The effects of phencyclidine(PCP) on the post-tetanic potentiation(PTP) of twitch tension were studied on the isolated mouse phrenic nerve diaphragm preparation. Phencyclidine increased directly elicited twitch tension while it decreased post-tetanic potentiation of the indirectly elicited twitch tension. The maximal depression effect of the PTP was found after higher frequencies and longer durations of stimulation. After repetitive stimulation, the amplitude of endplate potential was potentiated. Phencyclidine decreased the post-tetanic potentiation of the amplitude of endplate potential while the quantal content of the endplate potential was not affected. 4-Aminopyridine increased both directly and indirectly elicited twitch tension while it did not inhibit the post-tetanic potentiation of the twitch tension. It is concluded that phencyclidine suppressed the post-tetanic potentiation of the indirectly elicited twitch tension. The depressant effect may be mainly due to its effect on the acetylcholine receptor-ionic channel complex of the motor endplate.     

Inspiratory muscle work in acute hypoxia influences locomotor muscle fatigue and exercise performance of healthy humans

Our aim was to isolate the independent effects of 1) inspiratory muscle work (W(b)) and 2) arterial hypoxemia during heavy-intensity exercise in acute hypoxia on locomotor muscle fatigue. Eight cyclists exercised to exhaustion in hypoxia [inspired O(2) fraction (Fi(O(2))) = 0.15, arterial hemoglobin saturation (Sa(O(2))) = 81 +/- 1%; 8.6 +/- 0.5 min, 273 +/- 6 W; Hypoxia-control (Ctrl)] and at the same work rate and duration in normoxia (Sa(O(2)) = 95 +/- 1%; Normoxia-Ctrl). These trials were repeated, but with a 35-80% reduction in W(b) achieved via proportional assist ventilation (PAV). Quadriceps twitch force was assessed via magnetic femoral nerve stimulation before and 2 min after exercise. The isolated effects of W(b) in hypoxia on quadriceps fatigue, independent of reductions in Sa(O(2)), were revealed by comparing Hypoxia-Ctrl and Hypoxia-PAV at equal levels of Sa(O(2)) (P = 0.10). Immediately after hypoxic exercise potentiated twitch force of the quadriceps (Q(tw,pot)) decreased by 30 +/- 3% below preexercise baseline, and this reduction was attenuated by about one-third after PAV exercise (21 +/- 4%; P = 0.0007). This effect of W(b) on quadriceps fatigue occurred at exercise work rates during which, in normoxia, reducing W(b) had no significant effect on fatigue. The isolated effects of reduced Sa(O(2)) on quadriceps fatigue, independent of changes in W(b), were revealed by comparing Hypoxia-PAV and Normoxia-PAV at equal levels of W(b). Q(tw,pot) decreased by 15 +/- 2% below preexercise baseline after Normoxia-PAV, and this reduction was exacerbated by about one-third after Hypoxia-PAV (-22 +/- 3%; P = 0.034). We conclude that both arterial hypoxemia and W(b) contribute significantly to the rate of development of locomotor muscle fatigue during exercise in acute hypoxia; this occurs at work rates during which, in normoxia, W(b) has no effect on peripheral fatigue.     

Effect of acute hypercapnia on limb muscle contractility in humans

The effect of acute hypercapnia on skeletal muscle contractility and relaxation rate was investigated. The contractile force of fresh and fatigued quadriceps femoris (QF) and adductor pollicis (AP) was studied in normal humans by use of electrical stimulation. Maximum relaxation rate from stimulated contractions was measured for both muscles. Acute hypercapnia led to a rapid substantial reduction of contraction force. The respiratory acidosis after 9% CO2 was breathed for 20 min [mean venous blood pH 7.26 and end-tidal PCO2 (PETCO2) 65.1 Torr] reduced 20- and 100-Hz stimulated contractions of QF to 72.8 +/- 4.4 and 80.0 +/- 5.1% of control values, respectively. After 8 and 9% CO2 were breathed for 12 min, AP forces at 20- and 50-Hz stimulation were also reduced. Twitch tension of AP was reduced by a mean of 25.5% when subjects breathed 9% CO2 for 12 min [mean arterialized venous blood pH (pHav) 7.25 and PETCO2 66 Torr]. Over the range of 5% (pHav 7.38 and PETCO2 47 Torr) to 9% CO2, there was a linear relationship between twitch tension loss and pHav, arterialized venous blood PCO2, and PETCO2. Acute respiratory acidosis (mean PETCO2 61 Torr) increased the severity of low-frequency fatigue after intermittent voluntary contractions of AP. At 20 min of recovery, twitch tension was 63.2 +/- 13.4 and 46.8 +/- 16.4% of control value after exercise breathing air and 8% CO2, respectively. Acute hypercapnia (mean PETCO2 65.1 and 60.5 Torr) did not alter the maximum relaxation rate from tetanic contractions of fresh QF and from twitch tensions of AP.     

甲状腺功能亢进大鼠比目鱼肌肌浆网Ca2+-ATP酶活性增高可加速强直收缩疲劳

甲状腺功能亢进(甲亢)时甲状腺素分泌增加,不仅使具有神经支配的慢缩型肌纤维向快缩型转化,而且改变骨骼肌的强直收缩功能.因此,甲亢性肌病的肌肉乏力可能与骨骼肌强直收缩易发生疲劳有关.本实验在离体条件下,观测甲亢4周引起的大鼠慢缩肌--比目鱼肌(soleus, SOL)单收缩与间断强直收缩功能的变化.结果显示,甲亢4周大鼠体重明显低于同步对照组[(292±13)g vs (354±10)g],但SOL湿重没有明显改变[(107.3±8.6)mg vs (115.1±6.9)mg].甲亢大鼠SOL单收缩张力达到峰值的时间(time to peak tension, TPT)、从峰值降至75%舒张时间(time from peak tension to 75% relaxation, TR75)均明显缩短;强直收缩的TR75也明显缩短[(102.8±4.1)ms vs (178.8±15.8)ms];强直收缩的最适频率从对照组的100Hz增加到140Hz;间断强直收缩期间容易发生疲劳.甲亢大鼠SOL肌浆网Ca2 -ATP酶(sarcoplasmic-reticulum Ca2 -ATPase, SERCA)活性增高.采用SERCA特异性抑制剂CPA (1.0μmol/L)处理后,对照组与甲亢大鼠SOL间断强直收缩的TR75均延长,同时不易出现疲劳.5.0μmol/L CPA灌流虽可进一步抵抗甲亢大鼠SOL间断强直收缩引起的疲劳,但强直收缩期间的静息张力却明显升高.将CPA浓度增至10.0μmol/L,甲亢大鼠SOL间断强直收缩又趋向易发生疲劳.这些结果提示,与心肌相同,骨骼肌肌纤维SERCA活性亦可影响单收缩与强直收缩的舒张时间,SERCA活性升高可加速间断强直收缩发生疲劳.     

Isometric contractile properties and instantaneous stiffness of amphibian skeletal muscle in the temperature range from 0 to 20 degrees C

The isometric contractile properties of frog (Rana pipiens) and toad (Bufo bufo) sartorii have been studied over the temperature range from 0 to 20 degrees C. The isometric twitch tension was found to vary considerably between these two species and between muscles in the same species. Between 0 and 4 degrees C there was very little change in maximum isometric twitch tension. Between 4 and 12 degrees C several muscles from frog or toad showed a potentiation of twitch tension whereas others showed a decline. Over this temperature range the toad sartorii consistently demonstrated a greater potentiation. By 12 degrees C a steady decline in twitch tension in both muscles was seen as the temperature range the toad sartorii consistently demonstrated a greater potentiation. By 12 degrees C a steady decline in twitch tension in both muscles was seen as the temperature approached 20 degrees C. The maximum isometric tetanic tension recorded between 18 and 20 degrees C increased fractionally to an average of 1.504 +/- 0.029 (n = 4) for frog sartorii and to 1.377 +/- 0.008 (n = 5) for toad sartorii. The time to peak twitch tension and the half-relaxation time decreased markedly with an increase in temperature. Moreover, the half-relaxation time was reduced by a greater proportion than the time to peak twitch tension. Measurements of instantaneous stiffness by controlled velocity releases from the plateau of isometric tetani revealed that the large increase in isometric tetanus tension as the muscle was warmed was not accompanied by a corresponding increase in the total number of active cross-bridges. The possibility that a decreased availability of intracellular Ca2+ ions at the contractile sites contributing to the fall of isometric twitch tension at elevated temperatures is discussed. The possibility exists that at elevated temperatures a change inthe intrinsic contractile ability of the muscle occurs which produces an increased tension per cross-bridge.     

Fatigue from high- and low-frequency muscle stimulation: contractile and biochemical alterations

This study examined the effect of high- (75 Hz, 1 min) and low- (5 Hz, 1.5 min) frequency stimulation on contractile and biochemical properties of the diaphragm. Tension was reduced to 21 +/- 1 and 54 +/- 2% (SE) of the initial value after high- and low-frequency stimulation, respectively. After 0, 0.25, 1, and 2 min of recovery from high-frequency stimulation, 5 Hz elicited more force (expressed as % of initial tension) than 75-Hz stimulation. Time 0 recovery values were 21 +/- 1 and 78 +/- 6% of the initial force for 75- and 5-Hz stimulation, respectively. By 1 min of recovery, force elicited by 5-Hz stimulation had returned to the prefatigue value. In contrast, force production with 75-Hz stimulation did not full recover until 10-15 min. After fatigue produced by low-frequency stimulation, force production with 5-Hz stimulation was reduced to 54 +/- 2% of the initial tension, a value significantly lower than the 71 +/- 2% of initial force elicited by 75-Hz stimulation. Force production with 5-Hz stimulation increased rapidly in the first 15 s of recovery (54 +/- 2% at 0 and 70 +/- 2% at 15 s) and by 5 min was significantly greater than the force elicited by 75-Hz stimulation (100 +/- 3 vs. 93 +/- 1%). As before, force production at 75-Hz stimulation did not fully recover until 10-15 min. Both fatigue protocols produced a significant prolongation in isometric twitch contraction and one-half relaxation times. Creatine phosphate (CP) concentration was reduced and muscle lactate increased by both fatigue protocols.(ABSTRACT TRUNCATED AT 250 WORDS)