Interaction between clenbuterol and run training: effects on exercise performance and MLC isoform content

1996 ◽  
Vol 80 (3) ◽  
pp. 795-801 ◽  
Author(s):  
C. P. Ingalls ◽  
W. S. Barnes ◽  
S. B. Smith
Keyword(s):  
Skeletal Muscle ◽  
Exercise Performance ◽  
Myosin Light Chain ◽  
Polyacrylamide Gel Electrophoresis ◽  
Interval Training ◽  
Myofibrillar Protein ◽  
Total Work ◽  
Treadmill Test ◽  
Running Performance ◽  
Treatment Groups

The purpose of this study was to determine the separate and combined effects of clenbuterol (CB) administration and interval training on running performance and myosin light-chain (MLC) isoform expression in mouse skeletal muscle. Mice were randomly assigned to one of four treatment groups: 1) control (Con), 2) exercise (Ex), 3) drug (CB), or 4) exercise + drug (Ex + CB). CB and Ex + CB mice were given CB (1.6 mg/kg) orally 4 days/wk. Ex and Ex + CB mice were trained 4 days/wk on a motorized treadmill (3 sets of 3 min, 36-40 m/min, 10-17% grade, 30-s recovery). After 8 wk of treatment, exercise conditioning increased total work performed 58% in the Ex group during a run-to-exhaustion treadmill test, whereas CB decreased total work by 25% in the CB group; in combination with exercise training, CB treatment eliminated the Ex-induced increase in work. Polyacrylamide gel electrophoresis indicated that run training, CB treatment, or a combination did not (P = 0.01) promote changes in fast and slow MLC isoforms in the soleus, gastrocnemius, or tibialis anterior muscles. Although not different from each other after 8 wk, CB and Ex + CB treatments produced significantly greater values than Con and Ex for the following variables: muscle mass (17-46%), total protein (22-50%), and myofibrillar protein (19-53%). It was concluded that CB decreases exercise performance and that the combination of Ex and CB have antagonistic effects on running performance; the two treatments do not interact to diminish the anabolic effects of CB on skeletal muscle and do not alter MLC isoform profiles.

Calmodulin Binding Proteins In Platelet Actomypsin

1981 ◽  
Author(s):  
L Muszbek ◽  
J Harsfalvi
Keyword(s):  
Skeletal Muscle ◽  
Light Chain ◽  
Myosin Light Chain ◽  
Binding Proteins ◽  
Troponin I ◽  
Polyacrylamide Gel Electrophoresis ◽  
Regulatory System ◽  
Inhibitory Protein ◽  
Calmodulin Binding ◽  
Actomyosin Complex

Platelet actomyosin (thrombosthenin) possesses a myosin-linked Ca2+ regulation and Ca2+ sensitivity is conferred to it by calmodulin through myosin light chain kinase. Calmodulin binding proteins if they are present in the actomyosin complex may have an important regulatory role in the contractile mechanism of platelet activation. To test this possibility an aceton powder was made from platelet actomyosin and extracted with an 8 M urea containing buffer. The extract was examined for the presence of calmodulin binding proteins by alkaline urea polyacrylamide gel electrophoresis. It was shown by this technique that some proteins in the actomyosin complex can form a Ca2+ dependent complex with both calmodulin and skeletal muscle troponin C (TNC is closely related to calmodulin) even in the presence of 8 M urea. Calmodulin binding proteins could be isolated from the extract by affinity chromatography in 8 M urea on TNC-Agarose column. 3 major proteins of 270 K, 6l K and 23 K molecular weight were eluted by EGTA and each of them was able to bind to calmodulin or TNC if Ca2+was present. At least one of these calmodulin binding proteins exerted a troponin I like effect when tested on reconstituted skeletal muscle actomyosin and the 23 K protein showed a close similarity to troponin I. the inhibitory protein of the actin linked Ca2+ regulatory system in skeletal muscle. It is presumed that calmodulin binding proteins may have a dual role in the regulation of platelet actomyosin. They can inhibit the Ca2+ dependent phosphorylation of myosin light chain and one or more of them may also exert an actin linked inhibitory effect.

Effect of estradiol on tissue glycogen metabolism in exercised oophorectomized rats

1987 ◽  
Vol 63 (2) ◽  
pp. 492-496 ◽  
Author(s):  
Z. V. Kendrick ◽  
C. A. Steffen ◽  
W. L. Rumsey ◽  
D. I. Goldberg
Keyword(s):  
Skeletal Muscle ◽  
Exercise Performance ◽  
Sunflower Oil ◽  
Glycogen Content ◽  
Vastus Lateralis ◽  
Glycogen Metabolism ◽  
Submaximal Exercise ◽  
Total Work ◽  
Glycogen Utilization ◽  
Glycogen Sparing

The effect of both physiological and pharmacological doses of estradiol on exercise performance and tissue glycogen utilization was determined in oophorectomized estradiol-replaced (ER) rats. Doses of beta-estradiol 3-benzoate (0.02, 0.04, 0.1, 0.2, 1, 2, 4, or 10 micrograms.0.1 ml of sunflower oil-1.100 g body wt-1) were injected 5 days/wk for 4 wk. Controls were sham injected (SI). After treatment, the animals were run to exhaustion on a motorized treadmill. ER animals receiving the 0.02-microgram dose ran significantly longer and completed more total work than the SI group. ER animals receiving doses of greater than or equal to 0.04 microgram ran longer and performed more work than the 0.02-microgram group. At exhaustion, myocardial glycogen content was significantly decreased in animals that were ER with less than or equal to 0.1 microgram, whereas those replaced with doses greater than 0.1 microgram utilized significantly less glycogen. With the 10-micrograms dose no significant decrease in heart glycogen content was observed at exhaustion. A submaximal 2-h run significantly reduced glycogen content in heart, red and white portions of the vastus lateralis, and the livers of SI animals. The latter effect was attenuated in skeletal muscle and liver, and there was no effect in the hearts of the ER animals receiving 2 micrograms. These data indicate that estradiol replacement in oophorectomized rats influenced myocardial glycogen utilization during exhaustive exercise and spared tissue glycogen during submaximal exercise. These glycogen sparing effects may have contributed to the significant improvements in exercise performance observed in this study.

Improvements in exercise performance with high-intensity interval training coincide with an increase in skeletal muscle mitochondrial content and function

2013 ◽  
Vol 115 (6) ◽  
pp. 785-793 ◽  
Author(s):  
Robert Acton Jacobs ◽  
Daniela Flück ◽  
Thomas Christian Bonne ◽  
Simon Bürgi ◽  
Peter Møller Christensen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Capacity ◽  
Exercise Performance ◽  
High Intensity ◽  
Interval Training ◽  
Peripheral Fatigue ◽  
High Intensity Interval Training ◽  
Mitochondrial Content ◽  
Respiratory Capacity ◽  
High Intensity Interval

Six sessions of high-intensity interval training (HIT) are sufficient to improve exercise capacity. The mechanisms explaining such improvements are unclear. Accordingly, the aim of this study was to perform a comprehensive evaluation of physiologically relevant adaptations occurring after six sessions of HIT to determine the mechanisms explaining improvements in exercise performance. Sixteen untrained (43 ± 6 ml·kg−1·min−1) subjects completed six sessions of repeated ( 8 – 12 ) 60 s intervals of high-intensity cycling (100% peak power output elicited during incremental maximal exercise test) intermixed with 75 s of recovery cycling at a low intensity (30 W) over a 2-wk period. Potential training-induced alterations in skeletal muscle respiratory capacity, mitochondrial content, skeletal muscle oxygenation, cardiac capacity, blood volumes, and peripheral fatigue resistance were all assessed prior to and again following training. Maximal measures of oxygen uptake (V̇o2peak; ∼8%; P = 0.026) and cycling time to complete a set amount of work (∼5%; P = 0.008) improved. Skeletal muscle respiratory capacities increased, most likely as a result of an expansion of skeletal muscle mitochondria (∼20%, P = 0.026), as assessed by cytochrome c oxidase activity. Skeletal muscle deoxygenation also increased while maximal cardiac output, total hemoglobin, plasma volume, total blood volume, and relative measures of peripheral fatigue resistance were all unaltered with training. These results suggest that increases in mitochondrial content following six HIT sessions may facilitate improvements in respiratory capacity and oxygen extraction, and ultimately are responsible for the improvements in maximal whole body exercise capacity and endurance performance in previously untrained individuals.

β-Alanine Supplementation Does Not Augment the Skeletal Muscle Adaptive Response to 6 Weeks of Sprint Interval Training

2015 ◽  
Vol 25 (6) ◽  
pp. 541-549 ◽  
Author(s):  
Andrew J.R. Cochran ◽  
Michael E. Percival ◽  
Sara Thompson ◽  
Jenna B. Gillen ◽  
Martin J. MacInnis ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Performance ◽  
Training Stimulus ◽  
Training Session ◽  
Time Trial ◽  
Interval Training ◽  
Work Capacity ◽  
Oxidative Capacity ◽  
Sprint Interval Training ◽  
Repeated Sprint

Sprint interval training (SIT), repeated bouts of high-intensity exercise, improves skeletal muscle oxidative capacity and exercise performance. β-alanine (β-ALA) supplementation has been shown to enhance exercise performance, which led us to hypothesize that chronic β-ALA supplementation would augment work capacity during SIT and augment training-induced adaptations in skeletal muscle and performance. Twenty-four active but untrained men (23 ± 2 yr; VO2peak = 50 ± 6 mL·kg−1·min−1) ingested 3.2 g/day of β-ALA or a placebo (PLA) for a total of 10 weeks (n = 12 per group). Following 4 weeks of baseline supplementation, participants completed a 6-week SIT intervention. Each of 3 weekly sessions consisted of 4–6 Wingate tests, i.e., 30-s bouts of maximal cycling, interspersed with 4 min of recovery. Before and after the 6-week SIT program, participants completed a 250-kJ time trial and a repeated sprint test. Biopsies (v. lateralis) revealed that skeletal muscle carnosine content increased by 33% and 52%, respectively, after 4 and 10 weeks of β-ALA supplementation, but was unchanged in PLA. Total work performed during each training session was similar across treatments. SIT increased markers of mitochondrial content, including cytochome c oxidase (40%) and β-hydroxyacyl-CoA dehydrogenase maximal activities (19%), as well as VO2peak (9%), repeated-sprint capacity (5%), and 250-kJ time trial performance (13%), but there were no differences between treatments for any measure (p < .01, main effects for time; p > .05, interaction effects). The training stimulus may have overwhelmed any potential influence of β-ALA, or the supplementation protocol was insufficient to alter the variables to a detectable extent.

Sign in / Sign up

Export Citation Format

Share Document