Proceedings of The Physiological Society

King's College London (2009) Proc Physiol Soc 14, PC25

Poster Communications

Strength training affects the agonist-antagonist but not the force-agonist activation relationship

N. A. Tillin1, M. T. Pain1, J. P. Folland1

1. School of Sport and Exercise Science, Loughborough University, Loughborough, United Kingdom.

There is conflicting evidence for enhanced neuromuscular activation after strength training (Folland and Williams, 2007). Few studies have normalised agonist electromyography (EMG) to maximal M-wave (Mmax), which is recommended to improve reliability (Gandevia 2001), or measured antagonist activation relative to agonist activation. This study investigated the effects of unilateral isometric strength training of the knee extensors on agonist and antagonist neural activation in the trained and untrained leg. Nine previously untrained males, sat in a strength testing chair with knee and hip angles at 85° and 100°, respectively, and completed 4 sets of 10 isometric knee extensions at 75% of maximum voluntary force (MVF), 4 times a week for 4 weeks. The same apparatus was used for measurement trials pre and post training, which involved a series of involuntary and voluntary isometric contractions of the knee extensors. Force was measured with a strain gauge perpendicular to the tibia, and EMG was collected from the agonist (rectus femoris, vastus lateralis, and vastus medialis) and antagonist (bicep femoris) muscles (Bagnoli-4, Delsys, USA). The Mmax of each agonist muscle was established by supramaximal stimulation of the femoral nerve with single square pulses (100 µs; DS7AH, Digitimer Ltd, UK). MVF was determined as the peak force of four, 3-s maximal voluntary contractions. EMG root mean square (RMS) during a 200 ms epoch was measured at MVF and during a stable segment of voluntary contractions performed at 20, 40, 60 and 80% of MVF. Agonist and antagonist EMG was normalised to Mmax and maximal EMG during isometric knee flexions, respectively. MVF increased in both the trained (+20%; P = 0.001) and untrained leg (+8%; P = 0.007). There was no change in absolute agonist EMG at MVF in either leg, but agonist EMG normalised to Mmax increased in the trained leg (+26%; P = 0.046). There was no change in the quadratic relationship between normalised agonist EMG and absolute force for either leg. Despite a trend for antagonist neural activation to increase at MVF in the trained leg (+8%; P = 0.056), there was a downward shift in the linear relationship between agonist and antagonist neural activation (P = 0.014). This indicates that antagonist activation was lower for any given level of agonist activation post-training. In conclusion, strength and agonist activation increased by a similar magnitude after short term strength training, as reflected by no change in the entire agonist EMG-force relationship. Increased antagonist activation at MVF appears to be a response to greater force and agonist activation, as antagonist activation was lower for any given level of agonist activation post-training.

Where applicable, experiments conform with Society ethical requirements