Electromechanical delay (EMD) is defined as the time lag between the onset of electrical activity (electromyogram, EMG) and tension development in human muscle (Zhou et al. 1995). It has been suggested that there are several components which are all linked to the generation of force in skeletal muscle. These include the conduction of the action potential along the T-tubule system, the release of sarcoplasmic reticulum, cross-bridge formation between actin and myosin filaments, the subsequent tension development in the contractile component and the stretching of the series elastic component by the contractile component (Cavanagh & Komi, 1979).
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Cavanagh and Komi (1979) suggest that one of the primary causes for the value of EMD is affected by the time necessary to stretch the series elastic component of the muscle to a point when muscle force can be detected. Chan et al (2001) therefore thought the initial length could affect the phase lag and the EMD would be expected to be shorter in a stretched position. Their results showed that the EMD of the Vastus lateralis was shortest at 90° of knee extension, compared to 150° and 175°. A study conducted by Norman and Komi (1979) was to test the hypothesis that the rate and change of length of the series elastic component of a muscle was a major contributor to variations in EMD time. They used 10 subjects with an average age of 24.6. They performed a series of horizontal forearm flexion-extensions and extension-flexions at 7 different angular velocities, over two ranges of motion. Two ranges of motion was to determine whether there were ‘muscle length’ effects on electromechanical delay. Their findings supported the hypothesis that the rate of the muscles series elastic component might be a primary cause for the value of EMD. It was supported primarily for the biceps brachii muscle, where the EMD was shorter in fast eccentric contraction that in any other condition of that muscle. An alternative explanation of a shortened EMD in biceps brachii during eccentric contraction is that in fast stretching, the slow type muscle may be capable of efficient storage of elastic energy and its utilization during the subsequent contraction phase of the stretch shortening cycle (Norman and Komi, 1979).
EMD has been found to be influenced by the type of muscle contraction (Cavanagh & Komi 1979; Norman & Komi 1979) where the biceps EMD were relatively longer in concentric contractions but shorter in eccentric exercise. Norman and Komi (1979) observed different EMD times for the triceps muscles and bicep muscles. The differences in EMD times could be explained by the differences in their fibre structures, with the shorter EMD found in muscles that recruit more fast twitch fibres than those which recruit more slow twitch motor units.
It has been discussed that reaction time and electromechanical delay can be enhanced with training (Linford et al. 2006). Linford et al. (2006) conducted a study to determine if neuromuscular training had an effect on reaction time and electromechanical delay of the peroneus longus muscle. A six week training programme was conducted on five males and eight females. The study concluded that the training significantly reduced reaction time, while slightly increasing the electromechanical delay of the muscle. Having a decreased reaction time and electromechanical delay is important for athletes for when the muscles need to activate force as rapidly as possible. Having optimal joint stability is vital during mechanical loading of a joint system, so there is not too much stress being placed on one part of the joint system, decreasing the risk of injury. The results drawn from this study are from the peroneus longus muscle so cannot be directly related to the knee joint.
Fatigue
It has been suggested that EMD measurement is crucial to have a accurate understanding of the type of central nervous system commands required for the execution of different movements, the role and coordination of muscles in a movement and the apparent anomalies between electromyographical activity (EMG) and body segment motion (Vos et al,1991; Norman & Komi, 1979).
There have been reports that EMD lengthens after a fatiguing dynamic exercise (Horita, T., & Ishiko T. 1987) where as other studies have shown no significant change in EMD after repeated dynamic or isometric contractions (Vos et al. 1991). Zhou, S. (1996) conducted a study to investigate the effects of repeated maximal isometric contractions on electromechanical delay of the quadriceps femoris muscle. Eleven subjects took part, and carried out a one leg fatiguing exercise which was 25 isometric knee extension. Each lasted 8 seconds followed by a 2 second recovery period. His results showed a significant elongation in EMD. This is in contrast to Vos et al. (1991) who did not find any significant effect on EMD after a fatigue trial was carried out on the same muscle group. The different findings could be down to the different exercise protocols or methods used to determine EMD. However in the study by Vos (1991), participants carried out the fatigue trial with a force of 50% MVC, which may be the reason for no significant effect on EMD. Whereas Zhou’s (1996) participants carried out maximal voluntary contraction. This could mean that the participants in the study by Vos (1991) may not be fully fatigued.
Minshull et al (2007) conducted a study which determined what effects an acute bout of maximal intensity static fatiguing exercise would have on voluntary and magnetically-evoked EMD in the knee flexors of males and females. Seven men and nine women participated in this study, taking part in two treatment conditions. One being an intervention condition, where the participants performed a fatigue trial of 30 second maximal static fatiguing exercise of the knee flexors. The second condition was a control, consisting of no exercise. The results showed that in both intervention and control group, males EMD performance was maintained. However the fatiguing trial elicited a 19.5% impairment in EMD performance compared to baseline levels in females.
This comes as another finding of fatigue on EMD as Zhou (1996) find a overall elongated EMD, not just specifically in females. This could be down to the different fatiguing protocols, the study by Minshull (2007) may have fatigued the participants more with a longer constant fatiguing exercise. These results may differ because of participant variation.
Chan et al (2001) examined the effects of knee joint angles and fatigue on neuromuscular performance. Fatiguing exercise caused a significant lengthening of the EMD of the vastus lateralis and medialis at 90° and 150° of knee extension. Interestingly the fatiguing protocol did not induce any significant lengthening of the EMD at 175° knee extension. This shows that knee joint position affects the neuromuscular fatigue of the vastus lateralis and vastus medialis.
b) Temperature
Cryotherapy has long been used to treat musculoskeletal soreness, with the expectation that decreased tissue temperature will result in constriction of local blood vessels thus diminishing inflammatory response and oedema associated with musculoskeletal trauma (Sellwood et al. 2009). But what effect will crotherapy and heating muscles have on neuromuscular performance.
Many studies have been conducted to examine the effects of manipulating a muscles temperature on fatigue, neuromuscular performance, delayed onset of muscle soreness and metabolic responses (Zhou et al. 1998; Nosaka et al. 2004; Bailey et al. 2007; Dae et al. 1997.) Zhou et al (1998) said that a significant increase in body temperature usually accompanies strenuous exercise. With this exercise, the muscle contractile and elastic properties would be influence due to such a change, which could have an effect on EMD values. Zhou et al (1998) conducted a study which measured Peak force, EMD values and muscle temperature before and after an intermittent isometric maximal voluntary contraction exercise, and investigated the influence of passively changed muscle temperature on EMD and peak force. The muscle temperature was manipulated by placing a plastic bag filled with hot water or cold water over the front thigh area with a intramuscular needle thermistor measuring muscle temperature.. The EMD was measured at 38, 36, 34, 32 and 30°C. They found that when the muscle temperature was 2.5°C higher than the resting level, the EMD increased by approximately 5ms. They also found that EMD was increased when muscle temperatures was either higher or lower than 36°C.
There was a trend found that showed the peak force decreased at a low temperature, however a repeated measures ANOVA did not reveal a significant difference of temperature on peak force. This supports a study conducted by Thornley, Maxwell & Cheung (2003) who examined the effects of local tissue temperatures on peak torque and muscular endurance during isometric knee extension. They found temperature has no effect on peak torque, although there was a tendency to decrease when cooled, but was found non significant. However this study did not use a intramuscular needle thermistor, they only measured the skins temperature. Their results may have differed if they used a needle thermometer, as they used heat packs of 55°C, 34°C, 22°C and -17°C, it would be interesting to see what the muscle temperatures were, to add to the knowledge to show to what extent muscle temperature has on peak force.
Nosaka et al (2004) found no change in peak eccentric force of the forearm flexors, within a microwave treatment (muscle temperature increase of 3°C (37.5°C)) and a icing treatment (muscle temperature decrease of 7°C (26.4°C)). This cannot be related to the knee flexor muscles.
Skurvydas et al (2006) conducted a study which assessed the effect of leg immersion in cold water after stretch shortening exercise (SSE) on the indirect indicators of exercise induced muscle damage. The participants muscle contractile properties were recorded before the SSE, then at 4 h, 8h, 24h and 48hours post exercise. There was a control group and a cold group. In the cold group the leg was immersed in cold water (15 ± 1°C) immediately after SSE and at 4h, 8h and 24h. The leg was immersed twice for each test for 15 minutes with an interval of 10 minutes. They found that cold water immersion reduced muscle stiffness and the amount of post exercise damage after strenuous eccentric exercise, but it had no effect on muscle force. Their results also showed that the leg muscles that had been subject to cold water immersion after SSE, significantly increased the recovery speed of maximal voluntary contraction force (MVCF). MVCF had recovered within 24 hours post SSE. However Eston and Peters (1999) observed no quick recovery of the maximal voluntary contraction force after cold water immersion. It took 48h to 72 hours post cold water immersion for their subjects MVCF to return to baseline values. This could be because in the study by Skurvydas et al (2006) cooling of the musculature was concentrated up to 24 hours, where as Eston and Peters (1999) applied cooling treatment immediately post exercise and every twelve hours there after, for a duration of three days. Another reason for the differences could be that muscle damage was applied to the leg muscles in the study by Skurvydas et al (2006) and to the elbow flexor muscles in Eston and Peters’ (1999) study.
In contrast, Skurvydas et al (2008) looked at leg immersion in warm water before SSE on the indirect markers of exercise induced muscle damage. The participants muscle contractile properties were recorded, then was sat in a 44°C water bath for 45 minutes in waist high water. The contractile properties were then recorded again and SSE took place. Contractile properties of the participant were taken at 1h, 4h, 8h, 24h, 48h and 72 hours post SSE. They found that muscle pre warming did not cause any changes in MVCF, and it took over 72 hours for MVCF to recover to pre exercise level.
The differences in the findings of these two studies may be purely be down to one study uses hot water, and one uses cold. But in the study using cold water, the participant is immersed in the water immediately after SSE and at 4h, 8h and 24 hours after SSE. But in the heat study the participants were only immersed in the water before the SSE. If the same protocol for immersion was used in the warm water study, a difference may be seen in the recovery of MVCF. A study should be conducted using the same immersion type in cold and warm water conditions, therefore showing more accurate comparisons of what effects different temperatures have on MVCF.
Bailey et al (2007) examined the influence of cold water immersion after prolonged intermittent whole body exercise. Twenty men were subjects in this study who were randomly assigned to a cryotherapy or control group. Each participant’s maximal voluntary isometric contraction of the knee extensors and flexors were recorded using an isokinetic dynamometer pre, immediately after, 1 h, 24 h, 48 h and 168 hours post exercise. Subjects completed an intermittent shuttle test and immediately after the cryotherapy group immersed their lower limbs in a cold water bath (10°C) for 10 minutes. After the cold bath or rest, subjects completed two maximal isometric repetitions of the dominant limb for 5 seconds for extension and flexion. The results showed that exercise resulted in a reduction of knee flexion peak torque at 24 and 48hours in the cryotherapy group. The control group experienced an even bigger detrimental effect in PF at 24 and 48 hours post exercise. This shows that cold water immersion improved recovery of maximal voluntary contraction of the knee flexors 24 – 48 hours post exercise. This supports the findings from Skurvydas et al (2006) suggesting that cooling the leg muscles increases recovery time of MVCF. However it takes seven days for the MVCF to return to pre exercise values. This is vastly different result compared to Skurvydas et al (2006) and Eston and Peters (1999). This may be because the exercise Bailey et al (2007) uses, is a more dynamic whole body exercise (intermittent shuttle run) as appose to a stretch shortening exercise and a bout of eccentric exercise on the elbow flexors (Skurvydas et al 2006; Eston and Peters 1999).
As well as artificially changing participants body temperature or muscle temperature with water immersion or ice / heat packs, studies have examined the effects of passively changing bodies temperature and the effect it has on neuromuscular performance. Morrison, S., Sleivert, G. G., and Cheung, S. (2004) determined if passive hyperthermia impairs maximal voluntary isometric contraction and voluntary activation. Participants quadriceps femoris muscle group was measured for neuromuscular performance, then a submaximal running pace, which was maintained for 20 – 30 minutes took place in an environmental chamber with an ambient air temperature of ~35°C. At intervals of 0.5°C, from 37.5 to 39.5°C of core temperature, subjects performed a 10 second maximal isometric knee extension, and then during skin cooling back down from 39.5 to 37.5°C of core temperature Results showed that MVC was significantly influenced by passive heating and decreased significantly to the end of passive heating. When the skin cooling was introduced there was no significant change in MVC until the end of the protocol when body core temperature had returned to normal. This shows the primary thermal input causing hyperthermia – induced fatigue, when the skin was rapidly cooled by 8°C and core temperature held stable at 39.5°C, there was no recovery of MVC.
Ranatunga et al (1987) claims isometric force properties are generally not strongly affected by lowering muscle temperature to ~25°C. Drinkwater and Behm (2007) looked at the effects of 22°C muscle temperature on voluntary and evoked muscle properties during and after high intensity exercise. Participants performed a series of isometric maximum voluntary contractions of the plantar flexors pre, 1, 5 and 10 minutes after fatigue in both hypothermic and normothermic conditions. In the hypothermic condition, a refrigerating pump circling cold (-3°C) liquid through a plastic pump was wrapped around the participants leg. Results from the normothermic condition showed a moderate decline in maximal voluntary contraction, but did not show a significant difference between 1 and 5 minutes. Maximal voluntary contraction experienced a significant decrease 1 minute after fatigue in the hypothermic condition, -12%, compared to a -15% in the normothermic condition. There was no significant difference in the recovery of MVC. This supports the findings from Morrison et al (2004) who found no recovery in MVC in a hyperthermic condition.
3 METHOD
a) Participants
Eleven males {21.4 (±1.8) years; 183.5 (±6.8) cm; 81.8 (±10.2) kg} gave their informed consent to take part in the study, and completed a health screen questionnaire. They each knew that they could cease participation at any given time without providing a reason. Participants had been told not to take part in any strenuous physical exercise 24 hours prior to the experiment taking place. Nottingham Trent University Ethics Committee gave ethical approval.
b) Experimental Design
Following one habituation session, participants were secured in a supine position in a custom built dynamometer (Gleeson et al. 1995). The experimental design comprised of three treatment conditions: (1) An ice condition that required participants to sit in an ice bath for 10 minutes; (2) a heating condition which required participants to sit in a hot bath for 10 minutes; (3) a control condition were the participant sat on a bench for 10 minutes. The conditions were presented in a random order and separated by at least three days, to prevent any carry over effects. Participants neuromuscular performance (peak force, electromechanical delay) was measured prior to and immediately after each condition, and after a fatigue trial which was performed within each condition. Participants were verbally encouraged during the periods of maximal muscle activation.
c) Participant and dynamometer orientation
Electromyographic (EMG) activity was recorded from the vastus lateralis of the participants dominant leg during maximal contractions. A standardised skin preparation technique was used (Minshull et al.2007) which included shaving of the area, light abrasion with sand paper and alcohol wiped. This yielded inter-electrode impedance of less than 5 kΩ. The mid belly of the vastus lateralis was palpated and two Bipolar surface electrodes (silver-silver, self adhesive, 10 mm diameter) were applied having a 3cm inter-electrode distance, with a reference electrode placed laterally and equidistant to the recording electrodes. The positions of the electrodes were marked on the leg by ink dots and also on a plastic sheet used to identify the exact positions for the electrodes in each test during the experimental period. Electrodes were re placed on the chosen leg once it had been fully immersed in the hot or cold conditions to prevent malfunctioning electrodes. The correct wires were then attached from the computer onto the electrodes. Participants were strapped in a supine position on the dynamometer using shoulder belts and with their dominant knee flexed passively at 25° (0.44 rad) which was held for the duration of the testing. This knee flexion angle is associated with the greatest mechanical strain on key ligaments (Beynnon and Johnson 1996). The hip extension angle was 60° and both angles were checked using a goniometer. The lever arm of the dynamometer was moved into the correct position and was attached to the participants with padded ankle cuffs and adjustable strapping. All other body parts were securely fastened with the appropriate straps.
Prior to testing, participants were asked to perform a series of warm up muscle activations, consisting of 1x 25, 50, 75 and 95% of subjectively judged maximal voluntary muscle activation (MVMA). Three 100% MVMA were then performed and recorded. Each contraction was held for 3 seconds, with a 10 second rest between each.
d) Water bathing
The cooling condition required the participants dominant leg to be fully immersed in a cold water bath at 5 ± 1° for 10 minutes. The heating condition required the participants leg to be fully immersed in 45 ± 1° water for 10 minutes. The temperature of each bath was continually measured using a thermometer, and adjusted accordingly with either added ice, or hot water to keep the water temperature consistent. The water in the bath came up to the participants iliac crest, making sure the whole of the vastus lateralis was immersed. In the control trial, the participant sat on a bench in the same position they would if they were in the bath.
e) Fatigue Trial
Once the participants exit the ice, heat bath or bench they are strapped in to the dynamometer and electrodes re placed. Three more 100% MVMA were carried out and recorded, lasting 3 seconds each with a 10 second rest between. A fatigue trial was performed, which consisted of a 30 second MVMA of the knee musculature. Finally three more 100% MVMA were carried out.
f) Maximal volitional muscle activation
Before each condition took place, the participant was required to have full musculature relaxation prior to the test. The experimenter gave a verbal indication of ‘are you ready’ and within 3 seconds, the signal for the participant to extend their knee as forcefully as possible against the immovable restraint was ‘GO’. The muscle activation lasted for 3 seconds. Verbal encouragement was given when the participant was completing the activation so maximal contraction was achieved. A verbal signal being ‘relax’ was the cue for the subject to withdraw from the force as rapidly as possible.
g) Peak Force
Peak force was defined as the highest value that the participants obtained during each of the three attempts. The mean of these maximal contractions was used as the value for peak force.
h) Electromechanical Delay
Electromyography activity was recorded from the vastus lateralis during maximal volitional contractions using bipolar surface electrodes. The onset of electrical activity was defined as the first point at which electrical signals consistently exceeded the 95% confidence limits of the isoelectric line and with the background electrical noise (Minshull et al. 2007). Electromechanical delay (EMD) was defined as the time delay between the onset of electrical activity and the onset of muscle force above 1N. The mean EMD of the three trials within each condition was recorded.
i) Statistical data
The results collected from the voluntary muscle activations showed the neuromuscular performance of the vastus lateralis. All data was presented as a group mean ± standard deviation. A fully repeated measures ANOVA was used to analyse time (pre intervention, post intervention, post fatigue) each index of performance (peak force, EMD) under three separate conditions (ice, heat, control). Statistical Packages for Social Sciences (SPSS) v.15.0. was used to analyse the data. Statistical significance was accepted at p≤0.05.
4 RESULTS
a) Peak Force
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