Changes in height of jump, maximal voluntary contraction force and low-frequency fatigue after 100 intermittent or continuous jumps with maximal intensity

Healthy untrained males (age 25.4 +/- 1.7 years, n=12) gave their informed consent to take part in all experiments within the study. After 100 intermittent (every 20 s) drop jumps from the height of 0. 4 m, jumps with counter-movement to 90 degrees angle in the knee and immediate maximal rebound (eccentric-concentric exercise; E-C) and 100 continuous jumps (five bouts of 20 jumps with counter-movement to 90 degrees angle in the knee with 10 s between bouts) (maximal exercise; M) with maximal intensity, the height of vertical jump decreased in a similar way, and this decrease did not depend on the performance mode of jumps. After E-C and M jumping exercises, there was a significant (P < 0.001) decrease in maximal voluntary contraction force, as well in the force generated by electrical stimulation at all stimulation frequencies, and these values were not restored to the initial level even after 24 h. After the E-C exercise, however, the muscle contraction force generated at different stimulation frequencies and, especially, at low-stimulation frequencies (1-20 Hz) decreased to a significantly (P < 0.05-0.001) greater extent than after M exercise. Twenty minutes after the end of M exercise, there was still a greater increase in low-frequency fatigue (LFF) and it was no different from the LFF registered 20 min after the end of E-C exercise. Twenty-four hours after the M exercise, however, LFF was smaller than its respective value after E-C exercise. There was no significant relationship between the values of LFF after E-C and M exercises. This may indicate that there are differences in the origin of the LFF after the E-C and M exercises.     

Prolonged remission in a patient with transitional cell carcinoma of the bladder developing brain metastases after systemic chemotherapy: a case report

We report a case of an excellent response to M-VAC chemotherapy in a patient with pulmonary metastases from transitional cell carcinoma of the bladder. He subsequently presented with acute neurological symptoms seven weeks after the completion of chemotherapy. Computed tomography of the brain revealed a solitary 24 mm x 26 mm lesion in the frontal lobe. The brain metastasis was resected. The patient was closely followed for disease progression and showed no evidence of disease up to 42 months after surgery. The presentation and treatment policy are discussed. This case suggests that long-term remission may be obtained after surgical resection of a single brain metastasis in patients with disseminated urothelial cancer who completely responded to systemic chemotherapy.     

Chronic heart failure slows late sodium current in human and canine ventricular myocytes: implications for repolarization variability

BACKGROUND: Late Na(+) current (I(NaL)) in human and dog hearts has been implicated in abnormal repolarization associated with heart failure (HF). HF slows inactivation gating of late Na(+) channels, which could contribute to these abnormalities. AIMS: To test how altered gating affects I(NaL) time course, Na(+) influx, and action potential (AP) repolarization. METHODS: I(NaL) and AP were measured by patch clamp in left ventricular cardiomyocytes from normal and failing hearts of humans and dogs. Canine HF was induced by coronary microembolization. RESULTS: I(NaL) decay was slower and I(NaL) density was greater in failing hearts than in normal hearts at 24 degrees C (human hearts: tau=659+/-16 vs. 529+/-21 ms; n=16 and 4 hearts, respectively; mean+/-SEM; p<0.002; dog hearts: 561+/-13 vs. 420+/-17 ms; and 0.307+/-0.014 vs. 0.235+/-0.019 pA/pF; n=25 and 14 hearts, respectively; p<0.005) and at 37 degrees C this difference tended to increase. These I(NaL) changes resulted in much greater (53.6%) total Na(+) influx in failing cardiomyocytes. I(NaL) was sensitive to cadmium but not to cyanide and exhibited low sensitivity to saxitoxin (IC(50)=62 nM) or tetrodotoxin (IC(50)=1.2 muM), tested in dogs. A 50% I(NaL) inhibition by toxins or passing current opposite to I(NaL), decreased beat-to-beat AP variability and eliminated early afterdepolarizations in failing cardiomyocytes. CONCLUSIONS: Chronic HF leads to larger and slower I(NaL) generated mainly by the cardiac-type Na(+) channel isoform, contributing to larger Na(+) influx and AP duration variability. Interventions designed to reduce/normalize I(NaL) represent a potential cardioprotective mechanism in HF via reduction of related Na(+) and Ca(2+) overload and improvement of repolarization.     

The Time-Course of Voluntary and Electrically Evoked Muscle Performance During and After Stretch-Shortening Exercise is Different

The aim of the study was to establish the dynamics of maximal voluntary contraction force (MVCF), height of drop jump (DJ) and electrically evoked quadriceps muscle force at different stimulation frequencies during and after 100 DJs (stretch-shortening exercise, SSE). Healthy untrained men (n = 11; age = 21.8 ± 1.7 years) participated in the study. DJs were performed with 30 s intervals between jumps from the height of 0.5 m with counter-movement to 90 degrees angle in the knee and immediate maximal rebound. The force of the quadriceps muscle, evoked by electrical stimulation at 1 Hz (Pt), 20 Hz (P20) and 100 Hz (P100) frequencies (electrically evoked performance, EEP), MVCF and height of DJ (voluntary evoked performance, VEP) were established during SSE (after 10, 50, 100 DJ) as well as at 1, 4, 8, 24, 48 and 72 h after SSE. Time-course of P20 and P100 during and after SSE was time (ANOVA: p < 0.001) and frequency dependent (ANOVA: p < 0.001) The Pt, P20 and P100 decreased significantly (p < 0.01) more than MVCF and H of DJ during SSE. At the beginning of SSE (during 1-10 DJs) P20 and P100 decreased significantly (p < 0.001) more than during 11-50 and 51-100 DJs. There was a significant (p < 0.05) increase in Pt, P20 and P100 from 8 h to 48 h, whereas height of DJ and MVCF significantly decreased at that time. In conclusion, the differences in time course of VEP and EEP are most evident at beginning of SSE, where VEP does not change as EEP decreases, and within 8-48 hours after SSE, where VEP decreases as EEP increases.

Key points

• There was no change in voluntary muscle performance while electrically evoked performance decreased significantly during first 10 drop jumps.
• There was a significant increase in electrically evoked muscle performance from 8 h to 48 h after 100 drop jumps, whereas voluntary contraction force, decreased significantly.
• The secondary decrease in the height of drop jump as well as in maximal voluntary contraction force correlated significantly with muscle soreness within 24-48 h after exercise.

Key words: Drop jump, muscle damage, electrical stimulation, low frequency fatigue     

Leg Immersion in Warm Water,Stretch-Shortening Exercise,and Exercise-Induced Muscle Damage

Context:

Whether muscle warming protects against exercise-induced muscle damage is unknown.

Objective:

To determine the effect of leg immersion in warm water before stretch-shortening exercise on the time course of indirect markers of exercise-induced muscle damage.

Design:

Crossover trial.

Setting:

Human kinetics laboratory.

Patients or Other Participants:

Eleven healthy, untrained men (age  =  21.5 ± 1.7 years).

Intervention(s):

Participants'' legs were immersed in a water bath at 44 ± 1°C for 45 minutes.

Main Outcome Measure(s):

Creatine kinase changes in the blood, muscle soreness, prolonged (within 72 hours) impairment in maximal voluntary contraction force and height of drop jump, and electrically evoked muscle force at low and high stimulation frequencies at short and long muscle lengths.

Results:

Leg immersion in warm water before stretch-shortening exercise reduced most of the indirect markers of exercise-induced muscle damage, including creatine kinase activity in the blood, muscle soreness, maximal voluntary contraction force, and jump height. The values for maximal voluntary contraction force and jump height, however, were higher during prewarming than for the control condition at 48 hours after stretch-shortening exercise, but this difference was only minor at other time points. Muscle prewarming did not bring about any changes in the dynamics of low-frequency fatigue, registered at either short or long muscle length, within 72 hours of stretch-shortening exercise.

Conclusions:

Leg immersion in warm water before stretch-shortening exercise reduced most of the indirect markers of exercise-induced muscle damage. However, the clinical application of muscle prewarming may be limited, because decreasing muscle damage did not necessarily lead to improved voluntary performance.     

Physiological comparison between non-athletes,endurance, power and team athletes

European Journal of Applied Physiology - We hypothesized that endurance athletes have lower muscle power than power athletes due to a combination of weaker and slower muscles, while their higher...     

The repeated bout effect of eccentric exercise is not associated with changes in voluntary activation

The aim of this study was to compare the possible changes in muscle activation level between a first and second bout of damaging eccentric exercise performed at 2 weeks interval (i.e. repeated bout effect). To that purpose, ten physically active males took part in this study. The eccentric exercise consisted of 10 sets of 12 maximal voluntary contractions (MVC) produced by the knee extensors during movements performed at a constant speed of 160°s⁻¹. Changes in voluntary and electrically evoked torque in concentric and/or isometric conditions were assessed at the following time points: pre-exercise, and 2 min, 1 and 24 h after each eccentric exercise. At the same time points, voluntary activation was quantified by the superimposed electrical stimulation technique. Muscle soreness and plasma CK activity were measured within 48 h after the eccentric exercise. The results showed that the decrease in eccentric peak torque was linear throughout the exercise protocol. At the end of bouts 1 and 2, torque was significantly reduced by 27.7 ± 9.1 and 23.4 ± 11.2, respectively, with no difference between bouts (P > 0.05). At 24 h post-exercise, a lower reduction (P < 0.05) in MVC (17.8 ± 5.4%) and electrically evoked (16.7 ± 4.6%) isometric torque was observed for bout 2. In contrast, no statistical difference was found in the deficit in voluntary activation between the two bouts. In conclusion, our results indicate that the repeated bout effect of eccentric exercise appears to reduce muscle damage, but does not influence the level of voluntary activation.     

Late sodium current contributes to diastolic cell Ca<Superscript>2+</Superscript> accumulation in chronic heart failure

We elucidate the role of late Na⁺ current (I_NaL) for diastolic intracellular Ca²⁺ (DCa) accumulation in chronic heart failure (HF). HF was induced in 19 dogs by multiple coronary artery microembolizations; 6 normal dogs served as control. Ca²⁺ transients were recorded in field-paced (0.25 or 1.5 Hz) fluo-4-loaded ventricular myocytes (VM). I_NaL and action potentials were recorded by patch-clamp. Failing VM, but not normal VM, exhibited (1) prolonged action potentials and Ca²⁺ transients at 0.25 Hz, (2) substantial DCa accumulation at 1.5 Hz, and (3) spontaneous Ca²⁺ releases, which occurred after 1.5 Hz stimulation trains in ~31% cases. Selective I_NaL blocker ranolazine (10 μM) or the prototypical Na⁺ channel blocker tetrodotoxin (2 μM) reversibly improved function of failing VM. The DCa accumulation and the beneficial effect of I_NaL blockade were reproduced in silico using an excitation-contraction coupling model. We conclude that I_NaL contributes to diastolic Ca²⁺ accumulation and spontaneous Ca²⁺ release in HF.     

Cardiac Contractility Modulation With the Impulse Dynamics Signal: Studies in Dogs With Chronic Heart Failure

The intravenous use of positive inotropic agents, such as sympathomimetics and phosphodiesterase inhibitors, in heart failure is limited by pro-arrhythmic and positive chronotropic effects. Chronic use of these agents, while eliciting an improvement in the quality of life of patients with advanced heart failure, has been abandoned because of marked increase in mortality when compared to placebo. Nevertheless, patients with advanced heart failure can benefit from long-term positive inotropic support if the therapy can be delivered on demand and in a manner that is both safe and effective. In this review, we will examine the use of a novel, non-stimulatory electrical signal that can acutely modulate left ventricular (LV) contractility in dogs with chronic heart failure in such a way as to elicit a positive inotropic support. Cardiac contractility modulation (CCM) with the Impulse Dynamic signal was examined in dogs with chronic heart failure produced by intracoronary microembolizations. Delivery of the CCM signal from a lead placed in the great coronary vein for periods up to 10 minutes resulted in significant improvements in cardiac output, LV peak+dP/dt, LV fractional area of shortening and LV ejection fraction measured angiographically. Discontinuation of the signal resulted in a return of all functional parameters to baseline values. In cardiomyocytes isolated from dogs with chronic heart failure, application of the CCM signal resulted in improved shortening, rate of change of shortening and rate of change of relengthening suggesting that CCM application is associated with intrinsic improvement of cardiomyocyte function. The improvement in isolated cardiomyocyte function after application of the CCM signal was accompanied by an increase in the peak and integral of the Ca²⁺ transient suggesting modulation of calcium cycling by CCM application. In a limited number of normal dogs, intermittent chronic delivery of the CCM signal for up to 7 days showed chronic maintenance of LV functional improvement. In conclusion, pre-clinical results to date with the Impulse Dynamics CCM signal indicate that this non-pharmacologic therapeutic modality can provide short-term positive inotropic support to the failing heart and as such, may be a useful adjunct in the treatment of advanced heart failure. Additional, long-term studies in dogs with heart failure are needed to establish the safety and efficacy of this therapeutic modality for the chronic treatment of this disease syndrome.     

Extension and flexion torque variability in ACL deficiency

Purpose  

To evaluate possible differences in knee extension and flexion torque variability in the anterior cruciate ligament—deficient (ACLD) leg and their dependence on muscle length and visual feedback (VF). Although a knee extension torque deficit is found in the ACLD leg, there is no evidence that variability in submaximal isometric knee extension and flexion torque is affected in the ACLD leg or that it depends on VF.