Explosive neuromuscular performance refers to the ability to rapidly increase force in response to neuromuscular activation. The lower explosive force production of the hamstrings relative to the quadriceps could compromise knee joint stability and increase the risk of anterior cruciate ligament injury. However, the time course of the rise in explosive force of the hamstrings and quadriceps from their initial activation, and thus the explosive hamstrings-to-quadriceps (H/Q) force ratio, has not been documented.
The neuromuscular performance of 20 untrained males was assessed during a series of isometric knee flexion and extension contractions, with force and surface EMG of the hamstrings and quadriceps recorded during explosive and maximum voluntary contractions. Hamstrings force was expressed relative to quadriceps force to produce hamstring-to-quadriceps ratios of explosive H/Q force and H/Q maximum voluntary force. For the explosive contractions, agonist electromechanical delay (EMD), agonist and antagonist neural activation were assessed.
The quadriceps was 79% stronger than the hamstrings, but quadriceps explosive force was up to 480% greater than the hamstrings from 25 to 50 ms after first activation. Consequently, the explosive H/Q force ratio was very low at 25 and 50 ms (0%–17%) and significantly different from H/Q maximum voluntary force ratio (56%). Hamstrings EMD was 95% greater than quadriceps EMD (44.0 vs 22.6 ms), resulting in a 21-ms later onset of force in the hamstrings that appeared to explain the low explosive H/Q force ratio in the early phase of activation.
Prolonged hamstrings EMD appears to impair early phase (0–50 ms) explosive force production relative to the quadriceps and may render the knee unstable and prone to anterior cruciate ligament injury during this period.
1Sport, Health and Performance Enhancement (SHAPE) Research Group, School of Science and Technology, Nottingham Trent University, Nottingham, UNITED KINGDOM; 2Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, London, UNITED KINGDOM; 3School of Health and Life Sciences, Glasgow Caledonian University, Glasgow, UNITED KINGDOM; and 4School of Sport, Exercise and Health Sciences, Loughborough University, Loughborough, UNITED KINGDOM
Address for correspondence: Ricci Hannah, Ph.D., Institute of Neurology, University College London, Box 146, Queen Square, London WC1 3BG, United Kingdom; E-mail: email@example.com.
Submitted for publication March 2013.
Accepted for publication October 2013.