4.6 Article

Actions of β2-Adrenoceptor Agonist Drug on Human Soleus Muscle Contraction

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MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
卷 45, 期 7, 页码 1252-1260

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LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1249/MSS.0b013e318284706a

关键词

beta(2)-AGONISTS; MUSCLE CONTRACTILITY; ELECTRICAL STIMULATION; ELECTROMYOGRAPHY

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Purpose: The effects of beta(2)-agonists on human skeletal muscle contractile properties, particularly on slow fibers, are unclear. Moreover, it remains to be ascertained whether central motor drive (CMD) during voluntary contractions could counter for eventual contractile alterations induced by beta(2)-agonists. This study investigated central and peripheral neuromuscular adjustments induced by beta(2)-agonist terbutaline on a predominantly slow human muscle, the soleus. Methods: Ten recreationally active men ingested either a single dose of 8 mg of terbutaline or placebo in a randomized double-blind order (two experimental sessions). Isometric plantarflexion torque was measured during single and tetanic (10 and 100 Hz) stimulations as well as during submaximal and maximal voluntary contractions (MVC). Twitch peak torque and half-relaxation time were calculated. CMD was estimated via soleus electromyographic recordings obtained during voluntary contractions performed at approximately 50% MVC. Results: MVC and twitch peak torque were not modified by terbutaline. Twitch half-relaxation time was 28% shorter after terbutaline administration compared with placebo (P < 0.001). Tetanic torques at 10 and 100 Hz were significantly lower after terbutaline intake compared with placebo (-40% and -24% respectively, P < 0.001). Despite comparable torque of submaximal voluntary contractions in the two conditions, CMD was 7% higher after terbutaline ingestion compared with placebo (P < 0.01). Conclusion: These results provide evidence that terbutaline modulates the contractility of the slow soleus muscle and suggest that the increased CMD during submaximal contractions may be viewed as a compensatory adjustment of the central nervous system to counter the weakening action induced by terbutaline on the contractile function of slow muscle fibers.

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