Effects of caffeine on mouse skeletal muscle power output during recovery from fatigue

2004 ◽  
Vol 96 (2) ◽  
pp. 545-552 ◽  
Author(s):  
Rob. S. James ◽  
Robbie S. Wilson ◽  
Graham N. Askew
Keyword(s):  
Skeletal Muscle ◽  
Power Output ◽  
Muscle Power ◽  
Plasma Concentrations ◽  
Muscle Stiffness ◽  
Muscle Performance ◽  
Work Output ◽  
Work Input ◽  
Net Power Output

The effects of 10 mM (high) and 70 μM (physiologically relevant) caffeine on force, work output, and power output of isolated mouse extensor digitorum longus (EDL) and soleus muscles were investigated in vitro during recovery from fatigue at 35°C. To monitor muscle performance during recovery from fatigue, we regularly subjected the muscle to a series of cyclical work loops. Force, work, and power output during shortening were significantly higher after treatment with 10 mM caffeine, probably as a result of increased Ca2+ release from the sarcoplasmic reticulum. However, the work required to relengthen the muscle also increased in the presence of 10 mM caffeine. This was due to a slowing of relaxation and an increase in muscle stiffness. The combination of increased work output during shortening and increased work input during lengthening had different effects on the two muscles. Net power output of mouse soleus muscle decreased as a result of 10 mM caffeine exposure, whereas net power output of the EDL muscle showed a transient, significant increase. Treatment with 70 μM caffeine had no significant effect on force, work, or power output of EDL or soleus muscles, suggesting that the plasma concentrations found when caffeine is used to enhance performance in human athletes might not directly affect the contractile performance of fatigued skeletal muscle.

Sprint training increases human skeletal muscle Na(+)-K(+)-ATPase concentration and improves K+ regulation

1993 ◽  
Vol 75 (1) ◽  
pp. 173-180 ◽  
Author(s):  
M. J. McKenna ◽  
T. A. Schmidt ◽  
M. Hargreaves ◽  
L. Cameron ◽  
S. L. Skinner ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Binding Site ◽  
Intermittent Exercise ◽  
Recovery Period ◽  
Muscle Performance ◽  
Vastus Lateralis Muscle ◽  
Work Output ◽  
Sprint Training ◽  
Ouabain Binding ◽  
Before And After

This study investigated the effects of sprint training on muscle Na(+)-K(+)-adenosinetriphosphatase (ATPase) concentration, plasma [K+] regulation, muscle performance, and fatigue during severe intermittent exercise. Six untrained male subjects underwent intensive cycle-sprint training for 7 wk. Muscle biopsies were taken at rest from the vastus lateralis muscle before and after 7 wk of training and were assayed for Na(+)-K(+)-ATPase concentration using vanadate-facilitated [3H]ouabain binding to intact samples. Before and after the training period, subjects performed four maximal 30-s exercise bouts (EB) on a cycle ergometer, each separated by a 4-min recovery. Arterialized venous blood samples were drawn immediately before and after each sprint bout and were analyzed for plasma [K+]. The work output was significantly elevated (11%) across all four EBs after training. The muscle [3H]ouabain binding site concentration was significantly increased (16%) from 333 +/- 19 to 387 +/- 15 (SE) pmol/g wet wt after training but was unchanged in muscle obtained from three control subjects. Plasma [K+] rose by 1–2 mmol/l with each EB and declined rapidly by the end of each recovery period. The increases in plasma [K+] resulting from each EB were significantly lower (19%) after training. The ratios of rise in plasma [K+] relative to work output during each EB were also significantly lower (27%) after training. The increased muscle [3H]ouabain binding site concentration and the reduced ratio of rise in [K+] relative to work output with exercise are both consistent with improved plasma and skeletal muscle K+ regulation after sprint training.

Early effects of ageing on the mechanical performance of isolated locomotory (EDL) and respiratory (diaphragm) skeletal muscle using the work-loop technique

2014 ◽  
Vol 307 (6) ◽  
pp. R670-R684 ◽  
Author(s):  
Jason Tallis ◽  
Rob S. James ◽  
Alexander G. Little ◽  
Val M. Cox ◽  
Michael J. Duncan ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Power Output ◽  
Muscle Performance ◽  
Maximal Power ◽  
Maximal Power Output ◽  
Age Related ◽  
Loop Technique ◽  
Edl Muscle ◽  
Work Loop

Previous isolated muscle studies examining the effects of ageing on contractility have used isometric protocols, which have been shown to have poor relevance to dynamic muscle performance in vivo. The present study uniquely uses the work-loop technique for a more realistic estimation of in vivo muscle function to examine changes in mammalian skeletal muscle mechanical properties with age. Measurements of maximal isometric stress, activation and relaxation time, maximal power output, and sustained power output during repetitive activation and recovery are compared in locomotory extensor digitorum longus (EDL) and core diaphragm muscle isolated from 3-, 10-, 30-, and 50-wk-old female mice to examine the early onset of ageing. A progressive age-related reduction in maximal isometric stress that was of greater magnitude than the decrease in maximal power output occurred in both muscles. Maximal force and power developed earlier in diaphragm than EDL muscle but demonstrated a greater age-related decline. The present study indicates that ability to sustain skeletal muscle power output through repetitive contraction is age- and muscle-dependent, which may help rationalize previously reported equivocal results from examination of the effect of age on muscular endurance. The age-related decline in EDL muscle performance is prevalent without a significant reduction in muscle mass, and biochemical analysis of key marker enzymes suggests that although there is some evidence of a more oxidative fiber type, this is not the primary contributor to the early age-related reduction in muscle contractility.

Glutamine Metabolism in Skeletal Muscle of Glucocorticoid-Treated Rats

1990 ◽  
Vol 79 (2) ◽  
pp. 139-147 ◽  
Author(s):  
M. Salleh M. Ardawi ◽  
Yasir S. Jamal
Keyword(s):  
Skeletal Muscle ◽  
Exchange Rates ◽  
Skeletal Muscles ◽  
Plasma Concentrations ◽  
Maximal Activity ◽  
Glutamine Metabolism ◽  
Dexamethasone Treatment ◽  
Concentration Difference

1. The effect of dexamethasone (30 μg day−-1 100 g−-1 body weight) on the regulation of glutamine metabolism was studied in skeletal muscles of rats after 9 days of treatment. 2. Dexamethasone resulted in negative nitrogen balance, and produced increases in the plasma concentrations of alanine (23.4%) and insulin (158%) but a decrease in the plasma concentration of glutamine (28.7%). 3. Dexamethasone treatment increased the rate of glutamine production in muscle, skin and adipose tissue preparations, with muscle production accounting for over 90% of total glutamine produced by the hindlimb. 4. Blood flow and arteriovenous concentration difference measurements across the hindlimb showed an increase in the net exchange rates of glutamine (25.3%) and alanine (90.5%) in dexamethasone-treated rats compared with corresponding controls. 5. Dexamethasone treatment produced significant decreases in the concentrations of skeletal muscle glutamine (51.8%) and 2-oxoglutarate (50.8%). The concentrations of alanine (16.2%), pyruvate (45.9%), ammonia (43.3%) and inosine 5′-phosphate (141.8%) were increased. 6. The maximal activity of glutamine synthetase was increased (21–34%), but there was no change in that of glutaminase, in muscles of dexamethasone-treated rats. 7. It is concluded that glucocorticoid administration enhances the rates of release of both glutamine and alanine from skeletal muscle of rats (both in vitro and in vivo). This may be due to changes in efflux and/or increased intracellular formation of glutamine and alanine.

scholarly journals Trimetazidine attenuates dexamethasone-induced muscle atrophy via inhibiting NLRP3/GSDMD pathway-mediated pyroptosis

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Li Wang ◽  
Xin-Feng Jiao ◽  
Cheng Wu ◽  
Xiao-Qing Li ◽  
Hui-Xian Sun ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Muscle Performance ◽  
Skeletal Muscle Atrophy ◽  
C2c12 Myotubes ◽  
High Dose ◽  
Protective Effects ◽  
Akt Inhibitor ◽  
Caspase 1

AbstractSkeletal muscle atrophy is one of the major side effects of high dose or sustained usage of glucocorticoids. Pyroptosis is a novel form of pro-inflammatory programmed cell death that may contribute to skeletal muscle injury. Trimetazidine, a well-known anti-anginal agent, can improve skeletal muscle performance both in humans and mice. We here showed that dexamethasone-induced atrophy, as evidenced by the increase of muscle atrophy F-box (Atrogin-1) and muscle ring finger 1 (MuRF1) expression, and the decrease of myotube diameter in C2C12 myotubes. Dexamethasone also induced pyroptosis, indicated by upregulated pyroptosis-related protein NLR family pyrin domain containing 3 (NLRP3), Caspase-1, and gasdermin-D (GSDMD). Knockdown of NLRP3 or GSDMD attenuated dexamethasone-induced myotube pyroptosis and atrophy. Trimetazidine treatment ameliorated dexamethasone-induced muscle pyroptosis and atrophy both in vivo and in vitro. Activation of NLRP3 using LPS and ATP not only increased the cleavage and activation of Caspase-1 and GSDMD, but also increased the expression levels of atrophy markers MuRF1 and Atrogin-1 in trimetazidine-treated C2C12 myotubes. Mechanically, dexamethasone inhibited the phosphorylation of PI3K/AKT/FoxO3a, which could be attenuated by trimetazidine. Conversely, co-treatment with a PI3K/AKT inhibitor, picropodophyllin, remarkably increased the expression of NLRP3 and reversed the protective effects of trimetazidine against dexamethasone-induced C2C12 myotube pyroptosis and atrophy. Taken together, our study suggests that NLRP3/GSDMD-mediated pyroptosis might be a novel mechanism for dexamethasone-induced skeletal muscle atrophy. Trimetazidine might be developed as a potential therapeutic agent for the treatment of dexamethasone-induced muscle atrophy.

scholarly journals The Aerob and Anaerob Performance Beta-Alanine Supplement and Ergogenic Aid Using to the Power Output Variables in Cyclists: A Cohort Studies Random Model Effect

2021 ◽  
Author(s):  
Yeliz Kahraman
Keyword(s):  
Cohort Studies ◽  
Power Output ◽  
Muscle Power ◽  
Aerobic Power ◽  
Anaerobic Power ◽  
The Body ◽  
Muscle Performance ◽  
P Value ◽  
Value Analysis ◽  
Beta Alanine

: Supplement the use of ergogenic aids in cyclist’s directly have been improved the body metabolism and hemodynamic factors that are micro supplement in chancing reactions on the body muscle mass and limb muscle. Mostly knowing that, muscle power development progressive fast glycolytic and short time oxidative systems reactions. Sport competition intervals, therefore, during periods has been used specific drinks supported to cyclists. But, be obtained during should be long race times. Athletes directly needed some drug and fluid intake to prevented from metabolic breakdown rapidly the dynamic physiologic performance factors. Beta-alanine supplementation can be direct muscle performance development affects the anaerobic metabolism and capacity. It should be de-termined how the cyclists will use the competitive and training period intervals can increase the cyclists specific sprint and endurance race performance. Science cyclist International Road doses will be created in which, intervals can random effectively the investigate. This study random a cohort studies is examined the effects of beta-alanine supplementation on aerobic and anaerobic power output in specific cyclists. Therefore, we have been databases PubMed, Scopus and Medline initial search 10 August 2020 were created prospective effect the quality of bias work concluded effect size (ES) 95% confidence interval (CI) were used in participant. Participations (N=66) have age range 25 to 38 of the using beta-alanine in training periods to endurance muscle performance, aerobic power, anaerobic power, and sprint time trials. As a result of beta-alanine improved an-aerobic and aerobic power output on 4-week time-dependent trial performance condition. Signifi-cant values are obtained level factor alpha <0.05 and p-value analysis pre-post interactive stand-ardization.

scholarly journals Improved Tetanic Force and Mitochondrial Calcium Homeostasis by Astaxanthin Treatment in Mouse Skeletal Muscle

Antioxidants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 98 ◽  
Author(s):  
Sztretye ◽  
Singlár ◽  
Szabó ◽  
Angyal ◽  
Balogh ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Calcium Homeostasis ◽  
Inhibitory Effect ◽  
Calcium Transients ◽  
Muscle Performance ◽  
Control Group ◽  
Mitochondrial Calcium ◽  
Tetanic Force

Background: Astaxanthin (AX) a marine carotenoid is a powerful natural antioxidant which protects against oxidative stress and improves muscle performance. Retinol and its derivatives were described to affect lipid and energy metabolism. Up to date, the effects of AX and retinol on excitation-contraction coupling (ECC) in skeletal muscle are poorly described. Methods: 18 C57Bl6 mice were divided into two groups: Control and AX supplemented in rodent chow for 4 weeks (AstaReal A1010). In vivo and in vitro force and intracellular calcium homeostasis was studied. In some experiments acute treatment with retinol was employed. Results: The voltage activation of calcium transients (V50) were investigated in single flexor digitorum brevis isolated fibers under patch clamp and no significant changes were found following AX supplementation. Retinol shifted V50 towards more positive values and decreased the peak F/F0 of the calcium transients. The amplitude of tetani in the extensor digitorum longus was significantly higher in AX than in control group. Lastly, the mitochondrial calcium uptake was found to be less prominent in AX. Conclusion: AX supplementation increases in vitro tetanic force without affecting ECC and exerts a protecting effect on the mitochondria. Retinol treatment has an inhibitory effect on ECC in skeletal muscle.

The mechanical power output of the pectoralis muscle of blue-breasted quail (Coturnix chinensis): thein vivolength cycle and its implications for muscle performance

2001 ◽  
Vol 204 (21) ◽  
pp. 3587-3600 ◽  
Author(s):  
Graham N. Askew ◽  
Richard L. Marsh
Keyword(s):  
Power Output ◽  
Muscle Performance ◽  
Emg Activity ◽  
Pectoralis Muscle ◽  
Shortening Velocity ◽  
Mechanical Power Output ◽  
Strain Trajectory ◽  
The Mean ◽  
Net Power Output

SUMMARYSonomicrometry and electromyographic (EMG) recordings were made for the pectoralis muscle of blue-breasted quail (Coturnix chinensis) during take-off and horizontal flight. In both modes of flight, the pectoralis strain trajectory was asymmetrical, with 70 % of the total cycle time spent shortening. EMG activity was found to start just before mid-upstroke and continued into the downstroke. The wingbeat frequency was 23 Hz, and the total strain was 23 % of the mean resting length.Bundles of fibres were dissected from the pectoralis and subjected in vitro to the in vivo length and activity patterns, whilst measuring force. The net power output was only 80 W kg–1 because of a large artefact in the force record during lengthening. For more realistic estimates of the pectoralis power output, we ignored the power absorbed by the muscle bundles during lengthening. The net power output during shortening averaged over the entire cycle was approximately 350 W kg–1, and in several preparations over 400 W kg–1. Sawtooth cycles were also examined for comparison with the simulation cycles, which were identical in all respects apart from the velocity profile. The power output during these cycles was found to be 14 % lower than during the in vivo strain trajectory. This difference was due to a higher velocity of stretch, which resulted in greater activation and higher power output throughout the later part of shortening, and the increase in shortening velocity towards the end of shortening, which facilitated deactivation.The muscle was found to operate at a mean length shorter than the plateau of the length/force relationship, which resulted in the isometric stress measured at the mean resting length being lower than is typically reported for striated muscle.

In situ measurements of skeletal muscle power output using new capacitive strain gauge

1999 ◽  
Vol 37 (4) ◽  
pp. 451-455
Author(s):  
P. G. Cooper ◽  
G. J. Wilson ◽  
D. T. A. Hardman ◽  
O. Kawaguchi ◽  
Y. -F. Huang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Strain Gauge ◽  
Power Output ◽  
Muscle Power ◽  
In Situ Measurements ◽  
Capacitive Strain ◽  
Muscle Power Output

Effect of stimulation frequency on force, net power output, and fatigue in mouse soleus muscle in vitro

2009 ◽  
Vol 87 (3) ◽  
pp. 203-210 ◽  
Author(s):  
George Vassilakos ◽  
Rob. S. James ◽  
Valerie M. Cox
Keyword(s):  
Electrical Stimulation ◽  
Fatigue Test ◽  
Soleus Muscle ◽  
Power Output ◽  
Fatigue Tests ◽  
Stimulation Frequency ◽  
Force Generation ◽  
Net Power Output ◽  
Work Loop

The effects of electrical stimulation frequency on force, work loop power output, and fatigue of mouse soleus muscle were investigated in vitro at 35 °C. Increasing stimulation frequency did not significantly affect maximal isometric tetanic stress (overall mean ± SD, 205 ± 16.6 kN·m–2 between 70 and 160 Hz) but did significantly increase the rate of force generation. The maximal net power output during work loops significantly increased with stimulation frequency: 18.2 ± 3.7, 22.5 ± 3.3, 26.8 ± 3.7, and 28.6 ± 3.4 W·kg–1 at 70, 100, 130, and 160 Hz, respectively. The stimulation frequency that was used affected the pattern of fatigue observed during work loop studies. At stimulation frequencies of 100 and 130 Hz, there were periods of mean net negative work during the fatigue tests due to a slowing of relaxation rate. In contrast, mean net work remained positive throughout the fatigue test when stimulation frequencies of 70 and 160 Hz were used. The highest cumulative work during the fatigue test was performed at 70 and 160 Hz, followed by 130 Hz, then 100 Hz. Therefore, stimulation frequency affects power output and the pattern of fatigue in mouse soleus muscle.

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