Plasma catecholamine responses and neural adaptation during short-term resistance training
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Published on: August 22, 2014
T Pullinen1, P Huttunen, P V Komi
1Neuromuscular Research Center, Department of Biology of Physical Activity, University of Jyväkylä, Finland. tpulline@pallo.jyu.fi
Abstract:
Low exercise-induced plasma adrenaline (A) responses have been reported in resistance-trained individuals. In the study reported here, we investigated the interaction between strength gain and neural adaptation of the muscles, and the plasma A response in eight healthy men during a short-term resistance-training period. The subjects performed 5 resistance exercises (E1-E5), consisting of 6 sets of 12 bilateral leg extensions performed at a 50% load, and with 2 days rest in between. Average electromyographic (EMG) signal amplitude was recorded before and after the exercises, from the knee extensor muscles in isometric maximal voluntary contraction (MVC) as well as during the exercises (aEMGmax and aEMGexerc, respectively). Total oxygen consumed during the exercises (VO2tot) was also measured. All of the exercises were exhaustive and caused significant decreases in MVC (34-36%, P < 0.001). As expected, the concentric one-repetition maximum (1-RM), MVC and aEMGmax were all higher before the last exercise (E5) than before the first exercise (E1; 7, 9 and 19%, respectively, P < 0.05). In addition, in E5 the aEMGexerc:load and VO2tot:load ratios were lower than in E1 (-5 and -14%, P < 0.05), indicating enhanced efficiency of the muscle contractions, However, the post-exercise plasma noradrenaline (NA) and A were not different in these two exercises [mean (SD) 10.2 (3.8) nmol x l(-1) vs 11.3 (6.0) nmol x l(-1), ns, and 1.2 (1.0) nmol x l(-1) vs 1.9 (1.1) nmol x l(-1), ns, respectively]. However, although NA increased similarly in every exercise (P < 0.01), the increase in A reached the level of statistical significance only in E1 (P < 0.05). The post-exercise A was also already lower in E2 [0.7 (0.7) nmol x l(-1), P < 0.05) than in E1, despite the higher post-exercise blood lactate concentration than in the other exercises [9.4 (1.1) mmol x l(-1), P < 0.05]. Thus, the results suggest that the observed attenuation in the A response can not be explained by reduced exercise-induced strain due to the strength gain and neural adaptation of the muscles. Correlation analysis actually revealed that those individuals who had the highest strength gain during the training period even tended to have an increased post-exercise A concentration in the last exercise as compared to first one (r = 0.76, P < 0.05).
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