Saccadic dysmetria and adaptation after lesions of the cerebellar cortex. (33/1215)

We studied the effects of small lesions of the oculomotor vermis of the cerebellar cortex on the ability of monkeys to execute and adapt saccadic eye movements. For saccades in one horizontal direction, the lesions led to an initial gross hypometria and a permanent abolition of the capacity for rapid adaptation. Mean saccade amplitude recovered from the initial hypometria, although variability remained high. A series of hundreds of repetitive saccades in the same direction resulted in gradual decrement of amplitude. Saccades in other directions were less strongly affected by the lesions. We suggest the following. (1) The cerebellar cortex is constantly recalibrating the saccadic system, thus compensating for rapid biomechanical changes such as might be caused by muscle fatigue. (2) A mechanism capable of slow recovery from dysmetria is revealed despite the permanent absence of rapid adaptation.  (+info)

Eccentric and concentric isokinetic moment characteristics in the quadriceps and hamstrings of the chronic isolated posterior cruciate ligament injured knee. (34/1215)

OBJECTIVE: Functional strength deficits associated with chronic isolated posterior cruciate ligament (PCL) insufficiency have received limited attention in the literature. The purpose of this study was to determine the eccentric and concentric isokinetic moment characteristics of the quadriceps and hamstrings in a sample of patients with isolated PCL injury. METHODS: Eccentric and concentric mean average and average peak moments were measured for 17 patients with a history of conservatively treated isolated PCL injury using an isokinetic dynamometer. Quadriceps and hamstring isokinetic moments were recorded from 10 degree to 90 degree of knee flexion. Strength ratios were calculated and compared with those reported in the literature for healthy subjects. RESULTS: The hamstrings of the involved side (eccentric/concentric (E/C) ratio = 1.06) were significantly weaker (p<0.05) eccentrically than those of the contralateral side (E/C ratio = 1.29). All hamstrings/quadriceps (H/Q) ratios were less than the universally accepted value of 0.60 and the eccentric H/Q ratio for the injured extremity was significantly lower than the non-injured (p<0.05). In a bilateral comparison, the injured/non-injured (I/N) ratio was less than 1.00 for concentric quadriceps, eccentric quadriceps, and hamstring isokinetic moments. Calculation of the E/C ratio showed that, for the quadriceps, it was 1.08 on the injured side and 1.07 on the non-injured extremity. CONCLUSIONS: Eccentric strengthening should be an integral part of functionally rehabilitating the quadriceps and hamstrings of athletes who suffer from the complications associated with chronic isolated PCL insufficiency.  (+info)

Influence of muscle temperature on the contractile properties of the quadriceps muscle in humans with spinal cord injury. (35/1215)

Low muscle temperature in paralysed muscles of individuals with spinal cord injury may affect the contractile properties of these muscles. The present study was therefore undertaken to assess the effects of increased muscle temperature on the isometric contractile properties of electrically stimulated paralysed quadriceps muscles. When muscle temperature at a depth of 3 cm was increased from approximately 32 degrees C to approximately 36 degrees C by ultra-short-wave application, the half-relaxation time shortened and low-frequency force responses became less fused, but the maximal rate of increase in force remained unchanged. Heating had no effect upon either force decline or slowing of relaxation during fatiguing contractions. The force-frequency relationship of the paralysed quadriceps muscle was shifted to the right after the muscle was heated. Despite this shift, however, the relationship still resembled that in muscles of non-paralysed individuals, probably due to the unexplained high twitch forces. These results indicate that reduced muscle temperature in spinal-cord-injured individuals may lead to an underestimation of the changes in contractile properties in terms of relaxation rate or the degree of fusion with low-frequency stimulation. In addition, the force-frequency relationship of paralysed muscles does not accurately reflect the magnitude of these changes, even when the muscle is heated, and should therefore be treated with caution.  (+info)

Gender differences in the fatigability of human skeletal muscle. (36/1215)

After participating in a 4-wk intervention that reduced normal usage of the elbow flexor muscles, all six women, but only one of six men, experienced a marked increase in the endurance time during a low-force fatiguing contraction. The increase in endurance time was associated with an altered pattern of muscle activation that did not involve the commonly observed progressive increase in muscle activity. Rather, the muscle activity comprised intermittent motor unit activity. In those individuals who exhibited this behavior, the novel pattern of muscle activity was only present immediately after 4 wk of limb immobilization and not before the intervention or after 4 wk of recovery. These findings suggest possible differences between women and men in the adaptations of the neuromuscular system.  (+info)

Nandrolone decanoate does not enhance training effects but increases IGF-I mRNA in rat diaphragm. (37/1215)

To examine whether concomitant anabolic steroid treatment combined with training might enhance previously observed training effects (A. Bisschop, G. Gayan-Ramirez, H. Rollier, R. Gosselink, R. Dom, V. de Bock, and M. Decramer. Am. J. Respir. Crit. Care Med. 155: 1583-1589, 1997) and whether insulin-like growth factor I (IGF-I) was involved in these changes, male and female rats were submitted to inspiratory muscle training (IMT) for 8 wk (30 min/day, 5 times/wk) and were compared with untrained controls. During the last 5 wk of training, trained rats were divided to receive weekly either low-dose (LD; 1.5 mg/kg) or high-dose (HD; 7.5 mg/kg) nandrolone decanoate or saline for the IMT and control rats. In both sexes, diaphragm muscle mass and contractile properties were unchanged with treatment. In males, HD resulted in decreased diaphragm type I cross-sectional area (-15%; P < 0.05, HD vs. IMT), whereas no changes were observed in females. Finally, an increase in IGF-I mRNA levels was present in HD male (+73%; P < 0.05, HD vs. IMT) and female treated rats [LD (+58%) and HD (+96%) vs. IMT; P < 0.001]. We conclude that administration of nandrolone decanoate did not enhance the previously observed training effects in rat diaphragm, although it increased the IGF-I mRNA expression levels.  (+info)

Effect of creatine loading on neuromuscular fatigue threshold. (38/1215)

The purpose of this investigation was to determine the effect of creatine (Cr) loading on the onset of neuromuscular fatigue by monitoring electromyographic fatigue curves from the vastus lateralis muscle using the physical working capacity at the fatigue threshold (PWC(FT)) test. Using a double-blind random design, 15 women athletes [mean age 19.0 +/- 2.0 (SD) yr] from the university crew team received a placebo (n = 8; 20 g glucose) or Cr (n = 7; 5 g Cr monohydrate + 20 g glucose) four times per day for 5 consecutive days. Analysis of covariance was used to analyze the data (covaried for presupplementation PWC(FT) values). The adjusted mean postsupplementation PWC(FT) value for the Cr group (mean = 186 W) was significantly (P < 0.05) higher than that of the placebo group (mean = 155 W). These findings suggest that Cr loading may delay the onset of neuromuscular fatigue.  (+info)

Influence of tension time on muscle fiber sarcolemmal injury in rat diaphragm. (39/1215)

We hypothesized that the amount of sarcolemmal injury is directly related to the total tension time (TT(tot)), calculated as mean tension x total stimulation time. Diaphragm strips from Sprague-Dawley rats were superfused at optimal muscle length with Krebs containing procion orange to identify sarcolemmal injury. TT(tot) was induced by stimulation with 100 Hz for 3 min at duty cycles of 0.02, 0.15, 0.3, and 0.6, or with continuous contractions at 0.2, 0.4, 0.6, and 1.0 of maximal tension. A significant positive correlation between TT(tot) and the percentage of fibers with injured sarcolemma (r(2) = 0.63, P < 0.05) is seen. Stimulation (at 100 Hz, duty cycle = 1) resulted in fast fatigue with low injury, likely caused by altered membrane conductivity. Stimulations inducing the largest injury are those showing progressive force loss and high TT(tot), where injury may be due to activation of membrane degradative enzymes. The maximal tension measured at 20 min poststimulation was inversely related to the number of fibers injured, suggesting loss of force is caused by cellular injury.  (+info)

Characteristics of phosphate-induced Ca(2+) efflux from the SR in mechanically skinned rat skeletal muscle fibers. (40/1215)

The effects of P(i) on sarcoplasmic reticulum (SR) Ca(2+) regulation were studied in mechanically skinned rat skeletal muscle fibers. Brief application of caffeine was used to assess the SR Ca(2+) content, and changes in concentration of Ca(2+) ([Ca(2+)]) within the cytosol were detected with fura 2 fluorescence. Introduction of P(i) (1-40 mM) induced a concentration-dependent Ca(2+) efflux from the SR. In solutions lacking creatine phosphate (CP), the amplitude of the P(i)-induced Ca(2+) transient approximately doubled. A similar potentiation of P(i)-induced Ca(2+) release occurred after inhibition of creatine kinase (CK) with 2,4-dinitrofluorobenzene. In the presence of ruthenium red or ryanodine, caffeine-induced Ca(2+) release was almost abolished, whereas P(i)-induced Ca(2+) release was unaffected. However, introduction of the SR Ca(2+) ATPase inhibitor cyclopiazonic acid effectively abolished P(i)-induced Ca(2+) release. These data suggest that P(i) induces Ca(2+) release from the SR by reversal of the SR Ca(2+) pump but not via the SR Ca(2+) channel under these conditions. If this occurs in intact skeletal muscle during fatigue, activation of a Ca(2+) efflux pathway by P(i) may contribute to the reported decrease in net Ca(2+) uptake and increase in resting [Ca(2+)].  (+info)