Institute of Sport Sciences, University of Lausanne, Lausanne, Switzerland.
Med Sci Sports Exerc. 2013 Jul;45(7):1252-60. doi: 10.1249/MSS.0b013e318284706a.
The effects of β(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 β(2)-agonists. This study investigated central and peripheral neuromuscular adjustments induced by β(2)-agonist terbutaline on a predominantly slow human muscle, the soleus.
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.
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).
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.
β（2）-激动剂对人类骨骼肌收缩特性的影响，特别是对慢肌纤维的影响尚不清楚。此外，β（2）-激动剂是否能在自愿收缩期间改变中枢运动驱动（CMD），以抵消β（2）-激动剂引起的潜在收缩改变，这一点仍有待确定。本研究调查了β（2）-激动剂特布他林对主要为慢肌的比目鱼肌引起的中枢和外周神经肌肉调整。
10 名休闲活跃的男性以随机双盲的方式（两个实验疗程）摄入 8mg 特布他林或安慰剂的单剂量。在单刺激和强直（10 和 100Hz）刺激以及亚最大和最大自愿收缩（MVC）期间测量等距足底屈肌扭矩。计算抽搐峰值扭矩和半松弛时间。通过在大约 50%MVC 的自愿收缩期间获得的比目鱼肌肌电图记录来估计 CMD。
特布他林对 MVC 和抽搐峰值扭矩没有影响。与安慰剂相比，特布他林给药后抽搐半松弛时间缩短了 28%（P<0.001）。强直 10 和 100Hz 的扭矩在特布他林摄入后明显低于安慰剂（分别降低了-40%和-24%，P<0.001）。尽管在两种情况下的亚最大自愿收缩的扭矩相当，但特布他林摄入后的 CMD 比安慰剂高 7%（P<0.01）。
这些结果提供了证据表明特布他林调节慢比目鱼肌的收缩性，并表明在亚最大收缩期间增加的 CMD 可以被视为中枢神经系统的补偿调整，以抵消特布他林对慢肌纤维收缩功能的削弱作用。
