Repeated contractions of skeletal muscle cause fatigue, as manifested by a reduced ability to produce force and slowed contraction. During studies of muscle fatigue, a phenomenon known as low-frequency fatigue (LFF) was observed in human skeletal muscles. It is characterized by a greater loss of force in response to low- versus high-frequency muscle stimulation and a long period of time for full recovery. This force deficit is most likely to be owing to disturbances in sarcoplasmic reticulum (SR) Ca²⁺ release and/or reductions in myofibrillar Ca²⁺ sensitivity. Studies on metabolites have implied that inorganic phosphate and Mg²⁺ might have some role in reduced SR Ca²⁺ release that occurs immediately after fatiguing contraction. In addition, recent experiments have shown that impaired myofibril function may relate to increased nitric oxide and hydroxyl radical production, whereas deterioration of SR function may be attributable to increased superoxide production, elevation of cytoplasmic Ca²⁺ concentration and/or decreased muscle glycogen. Finally, we will discuss possible proteins which are affected and contribute to the development of LFF.

We investigated the effects of strength training a muscle fiber conduction velocity in biceps brachii of 7 male students. The subjects were trained to exhaustion by 60% of maximum isotonic voluntary contraction with 3 sets/day, 3 days/week for 16 weeks. The muscle fiber conduction velocity was measured with a surface electorode array placed along the muscle fibers, and calculated from the time delay between 2 myoelectric signals recorded during a maximal voluntary contraction. Upper arm girth significantly increased (p<0.01), from 29.2±1.4 cm (means±S. D.) to 30.6±1.5 cm. On the other hand, training induced no significant changes in upper arm skinfold. A significant difference between pre- and post-training was found in maximum isotonic strength (p<0.01) . Although maximum isometric strength showed no significant changes with training, there was a tendency for an increase in maximum isometric strength. Muscle fiber conduction velocity increased by 3.5% during training period, but this was not significant. These results suggest no effects of strength training on muscle fiber conduction velocity.

To investigate whether muscle fiber conduction velocity reflects muscle fiber type, we studied the extensor digitorum longus (EDL) and soleus (SOL) muscle in 7 male rats aged 12 weeks. Muscle fiber conduction velocity was measured with a surface electrode array during stimulated contraction and calculated from the delay between two action potentials along muscle fibers for a given inter-electrode distance. Conduction velocity in the EDL (2.71±0.50 m/s) was significantly higher (p<0.05) than that in the SOL (2.14±0.34 m/s) . Fiber type, fiber area and fiber diameter were determinated by myosin ATPase staining and NADH-tetrazolium reductase staining. Muscle fiber composition of the EDL and SOL was 94.6±1.8 and 14.8±4.3% FT fibers, respectively, and mean muscle fiber diameter was 62.7±6.2 pm and 79.2±7.8pm, respectively, that of the EDL being significantly smaller (p<0.01) than that of the SOL. It was suggested that individual differences in conduction velocity were caused by differences in muscle fiber composition rather than differences in muscle diameter.

Objective: In the management of drug information, pharmacists are required to appropriately transmit information to the corresponding medical staff.  However, it is unclear whether the transmitted information is received and utilized effectively.  In this study, we assessed the effectiveness of drug safety information transmitted to doctors by pharmacists and investigated the requirements of doctors for the transmitted drug safety information in Okayama University Hospital.
Design and Methods: We performed the assessment via questionnaire from doctors who had been sent drug safety information by electronic mail (e-mail) from January to October 2010.  The return rate and responses for the questionnaire were investigated.
Results: For the study time period, 15 cases of e-mail drug safety information transmissions occurred.  The questionnaire was sent to 204 doctors, and the recovery rate of the questionnaire was 46.1%.  Seventy-six percent of doctors who responded to the questionnaire answered that the e-mail information was useful for the clinical practice.  Among the comments, it was noted that an improvement in the content of e-mail information would allow doctors to access the required information more conveniently.
Conclusion: In this study, it was demonstrated that the majority of doctors were satisfied with the transmission of drug safety information using e-mail, although some improvement was needed.  Furthermore, it was considered that the feedback assessment and re-construction of information transmittal system were important to improve usability and availability of the drug information service.

To investigate the influences of high-intensity training and/or a single bout of exercise on in vitro Ca²⁺-sequestering function of the sarcoplasmic reticulum (SR), the rats were subjected to 8 weeks of an interval running program (final training : 2.5-min running×4 sets per day, 50 m/min at 10% incline). Following training, both trained and untrained rats were run at a 10% incline, 50 m/min for 2.5 min or to exhaustion. SR Ca²⁺-ATPase activity, SR Ca²⁺-uptake rate and carbonyl group contents comprised in SR Ca²⁺-ATPase activity were examined in the superficial portions of the gastrocnemius and vastus lateralis muscles. For rested muscles, a 12.7% elevation in the SR Ca²⁺-uptake rate was induced by training. Training led to improved running performance (avg time to exhaustion : untrained-191.1 vs trained-270.9 sec ; P<0.01). Regardless of training status, a single bout of exercise caused progressive reductions in SR Ca²⁺-ATPase activity and SR Ca²⁺-uptake rate. Increases in carbonyl content only occurred after exhaustive exercise (P<0.05). At both point of 2.5-min and exhaustion, no differences existed in SR Ca²⁺-sequestering capacity and carbonyl content between untrained and trained muscles. These findings confirm the previous findings that oxidative modifications may account, at least partly, for exercise-induced deterioration in SR Ca²⁺-sequestering function ; and raise the possibility that in the final phase of acute exercise, high-intensity training could delay the progression of protein oxidation of SR Ca²⁺-ATPase.

Cardiac surgery for very-low-birth-weight infants is rarely reported, especially for a triplet. We herein report the successful staged repair of a premature triplet accompanied with transposition of the great arteries. During pregnancy, the fetuses were diagnosed as dichorionic diamniotic triplets, and the mother entered a hospital for maternal protection and health care from 25 weeks' gestation. The triplets were delivered by Caesarean section at 33 weeks and 5 days of gestation because of intrauterine growth retardation. One of the infants, weighing 1,336 g, was diagnosed with transposition of the great arteries (type II). Since he was deemed unable to endure an intracardiac repair, he received balloon atrial septostomy on the 27th day of life and then bilateral pulmonary artery banding on the 29th day of life. However, further balloon atrial septostomy on day 69 and left pulmonary arterial de-banding on day 73 post-birth were needed because of the progression of hypoxia. He received prolonged intubation and inotropic support after temporary cardiopulmonary stability, and we ultimately decided to perform arterial switch operation on day 110, when he weighed 1,838 g. The patient showed a good recovery. In the field of pediatric cardiac surgery, we occasionally select staged strategies for patients who cannot undergo radical operations all at once because of their general condition or low body weight. However, there are no established guidelines concerning the timing of palliative or radical operations in low-birth-weight infants. At present, we select medical strategies ourselves, on a case-by-case basis. In the present case, although our medical strategy had to be adapted, we still obtained a good recovery for this triplet with extremely low birth weight. We herein report this case with some references from the literature.

This study examined the impact of acute high-intensity exercise on the rate of Ca²⁺uptake and release and Ca²⁺-stimulated adenosine triphosphatase (ATPase) activity of the sarcoplasmic reticulum (SR) in the soleus muscle (SOL) and the superficial region of the vastus lateralis muscle (VS) of rats. The animals were run on a 10% grade at 50 m/min of a motorized treadmill until fatigued (The average time to exhaustion was 306 sec.) . At exhaustion, glycogen concentrations were 65% and 85% less in the SOL and VS, respectively. The rate of Ca²⁺release induced by 4-chloro-m-cresol was un-changed in fatigued SOL and VS. The rate of Ca²⁺uptake stimulated by adenosine triphosphate (ATP) was significantly lower following exercise in VS but not in SOL. This lower rate observed in VS was paralleled by decreased catalytic activity of SR Ca²⁺-ATPase. The rate of Ca2+ uptake measured using adenosine diphosphate and phosphocreatine, as substrate was lower than that of ATP in fatigued VS. These findings suggest that, in fast-twitch muscles, high-intensity exercise not only reduces SR Ca²⁺-ATPase activity but also elicits a decrease in creatine kinase activity, probably resulting from nitric oxide that is produced during exercise.

We tested the hypothesis that a force reduction in soleus muscles from hyperthyroid rats would be associated with oxidative modification of myofibrillar proteins. Daily injection of thyroid hormone [3, 5, 3’-triiodo-_L-thyronine (T₃)] for 21 days depressed isometric forces in whole soleus muscle across a range of stimulus frequencies (1, 10, 20, 40, 75 and 100 Hz) (P<0.05). In fiber bundles, hyperthyroidism also led to pronounced reductions (P<0.05) in both K⁺- and 4-chloro-m-cresol-induced contracture forces. The degrees of the reductions were similar between these two contractures. These reductions in force production were accompanied by a remarkable increment (103% ; P<0.05) in carbonyl groups comprised in myofibrillar proteins. In additional experiments, we have also tested the efficacy of carvedilol, a non-selective β₁-β₂-blocker that possesses anti-oxidative properties. Treatment with carvedilol prevented T₃-induced oxidation of myofibrillar proteins. However, carvedilol did not improve the hyperthyroid-induced reductions in force production. These data suggest that oxidative modification of myofibrillar proteins may not account for the reductions in force production of hyperthyroid rat soleus muscle.

The purpose of this study was to examine the effects of eccentric contractions (Ecc) on cation (i.e., K⁺, Na⁺ and Ca²⁺) regulation in skeletal muscle. The left anterior crural muscles of male Wistar rats were subjected in vivo to either Ecc or isometric contrations (Iso) for 200 cycles. The extensor digitorum longus and tibialis anterior muscles were removed immediately after and 2, 4 and 6 days following contractions and used for measures of force output and biochemical analyses, respectively. Ecc led to a 75% decrease in maximal tetanic force. Decreased force output did not revert to pre-exercise levels during 6 days of recovery. Sarcoplasmic reticulum (SR) Ca²⁺-ATPase activity was reduced by 52 and 60% 4 and 6 days after Ecc, respectively. The reduction in catalytic activity after 6 days was accompanied by a 63% decrease in SR Ca²⁺-ATPase protein and an approximately 3.5-fold increase in calpain activity. Na⁺-K⁺-ATPase acticity was decreased by 23% immediately after Ecc and restored during 2 days of recovery. These alterations were specific for Ecc and not observed for Iso. These results suggest that disturbances in cation regulation may account, at least partly, for Ecc-induced decreases in force and power which can take a number of days to recover and that the decrease in SR Ca²⁺-ATPase activity would result from the degradation of the enzyme.