Anaerobic Capacity Training For A 400m Runner Physical Education Essay

The client is a 23 year old, county standard 400 meter runner. Upon arrival to the laboratory the athlete was measured and weighed on a standard stadiometer (Harpenden, Cambridge, UK) to the nearest 0.1 cm and 0.1 kg. Athlete height and weight was 176.8cm and 87.1kg respectively. The athlete was then seated on an mechanically braked Monark cycle ergometer (Model 894e Cranlea, Birmingham, UK) and began a 10 minute warm up corresponding to 2watts/kg at 70rpm (Palmer et al., 2008). Following the warm up, the athlete was instructed to increase the cadence to 100rpm. A 3 second countdown was given, and on 0 a fixed resistance of 0.075 kg/kilo of body mass was applied to the flywheel. On 0 the athlete was expected to be at a maximal sprinting pace (McArdle, Katch and Katch, 2006). The client was instructed to maintain maximal effort throughout the test. Immeidiantly after the test a capillary blood sample was taken from the right index finger and analysed for blood lactate (Lactate Pro, HAB Direct, UK). Peak power output (PPO) and mean power output (MPO) were 861Watts and 725Watts, or 9.88W/kg and 8.3W/kg when normalised for body weight, and a final blood lactate value of 7.8mmols.

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A 400 meter event will last anywhere between Ì´43 seconds to 2 minutes depending on ability. This event places a heavy reliance on both aerobic and anaerobic metabolism for energy production. This event requires maximal or near maximal utilization of the anaerobic glycolytic and phosphorylative pathways, as well as the provision of considerable aerobic energy is also required to perform these sustained high-intensity efforts (Duffield et al., 2005). Estimates of energy system contribution have typically been carried out using laboratory based test procedures, such as the accumulated oxygen deficit (AOD) and/or measures of glycolytic activity from blood lactate concentrations to estimate anaerobic contribution. This has lead to a relatively large range of values being reported, with values estimated at 36-72% anaerobic contribution (Duffield et al., 2005). Duffield et al., 2005 conducted a track based study utilizing both AOD and blood lactate data to estimate energy system contribution to 400 meter running, reporting the anaerobic contribution for each of these measures to be 59 and 65% respectively. This agrees with previous reports (Hill, 1999; Spencer and Gastin, 2001).
Intramuscular stores of PCr have been reported to be between 75-85.kg dry wt-1., with a maximal turnover rate of 7-9.kg dry wt-1.s-1 (Gaitanos, et al., 1993; Hultman & Sjoholm, 1983; Parolin, et al., 1999), enough to fuel approximately 5 seconds of maximal effort (Newsholme, et al., 1986). However, the contribution from anaerobic glycolysis and aerobic metabolism to the total ATP supply during maximal short duration efforts means that PCr stores are not usually depleted during this time (Spencer, et al., 2005). PCr stores are reduced by 60-80% of resting values following 30 seconds of maximal exercise (Medbo, et al., 1999; Boobis, et al., 1982; Cheetham, et al., 1986; Bogdanis, et al., 1995), which is similar to those reported in track sprinting (Spencer and Gastin, 2001).
Many other studies have investigated the energy system contribution during maximal sprint exercise of varying durations. Medbo, et al., (1999) assessed changes in muscle metabolites and ATP turnover, reporting the relative contributions from aerobic processes, anaerobic glycolysis and alactic anaerobic (ATP-PCr breakdown) processes during 30 seconds of maximal sprint cycling to be 38, 45, and 17% respectively. Other studies have also reported the contribution of aerobic sources to be between 28-40% during 30s of sprint cycling (Medbo & Tabata, 1989; Withers, et al., 1991). Sprint exercise of 10-30 seconds duration has been shown to be dependent on anaerobic glycolysis, with this energy system providing more than twice as much ATP as PCr degradation (47% to 22%) in one study (Medbo, et al., 1999).
These studies utilizing sprint cycling display slightly divergent energy system contributions compared to track based 400 meter running. This could be explained by the smaller active muscle mass compared to that of running (Medbo et al., 1999). It is also likely that the different muscle recruitment patterns that are observed during cycling compared to running lead to these differing results. However, the Wingate anaerobic power test provides a quick and convenient way to assess an athlete’s anaerobic power, which has been demonstrated to supply over half the ATP required for 400 meter running (Hill, 1999; Duffield, 2005).
Current training status of the athlete
The results displayed by the current athlete place him in the top 90% of physically active young adults for both peak and average power output. However when the data is normalised for body weight, the athletes PPO of 9.88w/k and MPO of 8.3W/kg place him within the 60th and 80th percentile respectively (McArdle Katch and Katch, 2005). When looking at sprint athletes these values become even more modest. Indeed, elite track sprint cyclists would be expected to produce a peak power >1700W during the kilo time trial. (Craig and Norton, 2001).
A study by Amusa and Toriola (2003) assessed the anaerobic power of elite national level track sprinters trained in 100, 200 and 400m running. The athletes assessed in this study produced PPO of 972W at 13.3 W/kg. The average power output for these athletes was lower than the client (624.6W), however there was a large range reported for this variable (264-624W) which may have skewed the results. It is likely that the 100meter runners would have produced a high initial power output during the initial 10 seconds of the test, dropping off dramatically from 10 – 30 seconds, due to the shorted nature of the 100m event.
The results discussed indicate that the athlete discussed here is some way of national standard levels, with 4W/kg a lot to have to make up. His high mean peak power value of 725W would indicate he can maintain a good pace throughout the race, but that his initial speed could be improved through a specific training programme. The results would also indicate that the client has a large body type for 400m sprinting. Typically 400m runners have a BMI of Ì´ 21kg/m2 (Amusa and Toriola, 2003; Duffield et al., 2005), however the clients BMI of 27.9 kg/m2 show that he could lose some body fat, which would increase his power to weight ratio and decrease his race times.
The client’s peak lactate value of 7.9mmol is also substantially lower compared to those observed at the end of 400m running. Duffield et al., (2005) reported blood lactate values of 13.9mmols immediately following a 400m race. Typically post Wingate lactate levels of 12mmols have also been reported (Gaitanos et al., 1993). The low blood lactate level achieved by the client may indicate that he derives a greater percentage of ATP from aerobic sources during the Wingate test, and potentially during 400m running If this is the case it may be that the client has a lower than optimal percentage of Type IIx muscle fibres, limiting his ability to produce energy anaerobically. The following section will discuss training processes that could be used to increase the client’s aerobic base and peak power output.
Training anaerob
ic capacity
Overall speed, or peak power output, is influenced by many things, such as heredity, reaction time, external resistance, technique (often where large improvements can be made)and muscle elasticity, and there are many methods that can be used to develop speed. Both the intensity and duration of the stimulus need to be optimally designed to achieve the greatest improvement. The intensity should range between sunmaximum and supermaximum. Furthermore the duration of the training stimuli is the time required to accelerate to maximum velocity. If this is too short then the client will not reach maximum speed. For sprinters the suggested duration is 5-20 seconds, with longer efforts enhancing anaerobic endurance (Bompa, 1999). The intervention described below utilises supermaximal intensities at a duration of 30 seconds.
As both aerobic and anaerobic sources are required for 400 meter running it is important to train both of these parameters. The client’s data would seem to indicate he needs to improve both his peak power output, and aerobic base in order to further reduce 400 meter running time. In order to achieve these aims high intensity sprint interval training could be used. This is a form of recurring sessions of brief, repeated bouts of very hard, and intense exercise, and has been demonstrated repeatedly to lead to rapid remodelling of skeletal muscle (Ross and Leveritt, 2001). This therefore could be an efficient and time saving strategy. By design, this type of training schedule, and time commitment, with a weekly exercise time of around 10 minutes.
A sprinter typically reaches maximal speed after 30meters, and maintains it for 80 meters (Harre, 1982). Athletes in sprint events improve further by improving power, speed endurance, and power endurance. SIT training rapidly improves speed endurance as discussed below.
The proposed training regime consists of repeated Wingate maximal sprint tests, interspersed with 4 minutes of light rest and recovery. This programme is carried out over a 2 week period and has been shown to increase a range of oxidative enzyme activities and increase cycle time trial performance. A training programme should theoretically adhere to the principles of training, namely, overload, progression, specificity, and recovery in order to produce the desired outcome. The client;s training status will only be improved by gradually increasing the load that his body is subjected to. The following training programme sufficiently stresses the client’s physiological systems by gradually increasing the required workload from 4 to 6 Wingate tests. This therefore increases the intensity and volume of the session. This resembles a form of step loading, which allows the training load to increase with a phase of unloading (rest and recovery) during which the client would adapt and regenerate (Bompa, 1999). It is known that one training session in insufficient to promote physiological adaptation and that it is necessary to repeat the same session several times. The proposed 2 week microcycle achieves this by including duplicate sessions before a step up in training load (table 1).
A continuation of this principle is that of progression. As the body’s physiological mechanisms adapt to the training stimulus being applied, there is a need for the training to be advanced. Otherwise the client will remain in a training plateau and will not respond to further training efforts (Brewer, 2005). This 2 week cycle clearly demonstrates a progression in the training load through increases in the number of Wingate’s performed.
A problem with the proposed training cycle relates to that of specificity. All training regimes need to (or should be) tailored to the specific demands of that sport, in this case 400m running. This maximises the benefits of competitive performance. When devising a training programme factors such as the bioenergetics of metabolism (i.e. the energy demand of the event/sport) and mechanical factors (musculo-skeletal requirements, i.e. similar movement patterns) involved in the specific movements of the sport need to be taken into account. Whilst cycling bears little resemblance to 400 m running, the use of repeated Wingate tests as a training stimulus will likely still lead to beneficial bioenergetic improvements that are the specific focus of this intervention (i.e. aerobic and anaerobic power). As the client will eventually need to work on power development to improve overall speed, the rapid adaptations and remodelling that will occur as a result of the Wingate training will likely aid this future process. The increases that will occur to muscle oxidative capacity, muscle buffering capacity, and decreases in net muscle glycongenesis and lactate accumulation. These factors are related to exercise tolerance, and thus may contribute to enhancing the ability of the client to train and compete at a high intensity (Hawley, 2002).
Finally, one of, if not the most important factors to consider are the length of recovery between training sessions. The act of training provides the stimulus for development, however the recovery period , when the body returns to normal homeostasis, are when these alterations in muscle physiology occur. An insufficient length of recovery will lead to overtraining, poor performance, and increased risk of injury (Brewer, 2005). Furthermore, if the recovery period is overlong, then the training effect will be lost. As this form of intense training will likely reduce the client’s net ATP stores, a sufficient recovery week afterwards must be employed. Training also depletes energy releasing fuels such as intramuscular glycogen, whilst waste products build up. Restoring these fuels and removing the metabolites requires a certain amount of time depending on the energy system used during the training session (Bompa, 1999).
This training outlined below will require the client to restore their phosphate and intramuscular glycogen stores, and remove the excess build up of lactate. During the 30 second period of the Wingate test it is likely that approximately 50% of the clients PCr stores will be depleted. The rest and recovery period during the protocol (4 minutes) allows ample time for the resynthesis of ATP-PCr. Phosphates are 50 – 70% restored after approximately 20-30 seconds of recovery, the remainder restored following a period of 3minutes. The 4 minutes of recovery leads to a 90% restoration of these stores, allowing the client to complete repeated maximal efforts, leading to the greatest overload and supercompensation (Bompa, 1999). At the end of the training bout it is likely that the client will have high blood lactate levels. Clearing these is important to ensure full recovery. This occurs in 2 phases: removing it from the muscle, and removing it from the blood. Passive rest and recovery removes lactate after approximately 2 hours. However active recovery consisting of light jogging, or walking removes this metabolite much quicker (1 hour) and would be recommended.
The next stage of recovery entails replacing the depleted glycogen store. The extent of depletion again depends on the length and intensity of the exercise bout. Indeed, several factors affect the rate and amount of recovery of glycogen stores following training. The manipulation of dietary carbohydrates leads to a positive effect on intramuscular CHO storage (Bompa, 1999). The 24 hour recovery period the client would receive would allow him to consume a large quantity of CHO in his diet, allowing full muscle glycogen restoration. A low CHO diet following this form of training will only allow a partial recovery of muscle glycogen and affect subsequent training performance. Recent research has shown that a high CHO diet following SIT training maintains performance in subsequent sessions (Burke et al., 2006). Balsom et al., (1999) examined the effects of a high or low CHO diet on intermittent sprint performance (6s bouts at 30s intervals), finding muscle glycogen was reduced by 50% in the low glycogen trial, leading to reductions in work output. Further support was also provided by Nevill et al., (1993). This group studied the effects of different CHO diets on 24 hour recovery. They reported the low CHO group to have a compromised work output in the subsequent training bout, whereas the high CHO group displayed only slight reductions in performance. Bangsbo et al., (1996) examined the effects of pre exercise CHO levels on intermittent running performance in footballers. The group of athletes studied were placed on either a high or normal CHO diet for 48 prior to completing an intermittent running protocol. The group of footballers that received a high CHO diet significantly increased their intermittent running time to fatigue by 1km. These studies show that higher pre exercise glycogen stores enhance ones capacity to undertake repeated bouts if high intensity exercise (Burke et al., 2006).
This clearly demonstrates the necessity of good nutrition following SIT type training, and the importance of recovery. The 24 and 48 hour recovery bouts suggested for the client should allow for adequate recovery during this training cycle, allowing him to complete each session at near maximal capacity.
Short term sprint interval training (SIT)
When developing a training programme for middle sprint athletes it is important to consider the aerobic and anaerobic contributions to overall performance. As previously discussed, during the 400meters, aerobic energy provision supplies approximately 40% of the ATP demand during the race, with anaerobic glycolysis and the PCr system accounting for the other 60%. The beginning of the sprint training program should build on the aerobic foundation on which the speed training has to rely (Bompa, 1999). Table 1 shows an intensive 2 week schedule designed to improve muscle oxidative capacity (Gibala et al., 2006). As the athlete approaches a competition phase the focus of training would emphasise maximum velocity, progressing from 10 to 15 to 30 to 60 meters.
Table 1. 2 week Training programme outline.
Week
Monday
Tuesday
Wednesday
Thursday
Friday
Saturday
Sunday
1
4 x 30s wingate, 4 mins recovery between reps
Rest
4 x 30s wingate, 4 mins recovery between reps
Rest
5 x 30s wingate, 4 mins recovery between reps
Rest
Rest
2
5 x 30s wingate, 4 mins recovery between reps
Rest
6 x 30s wingate, 4 mins recovery between reps
Rest
6 x 30s wingate, 4 mins recovery between reps
Rest
Rest
The training programme would consist of repeated 30s maximal Wingate test efforts, interspersed with 4 minute recovery or rest at 30W. The training load is progressed by increasing the number of repetitions from 4 to 6 over the 2 week period, as described by Gibala and co workers (2005, 2006, 2007, 2008). It is anticipated that following such a programme would enhance the client’s aerobic potential, laying the foundations for future improvements in speed.
Physiological adaptation to anaerobic training
Sprint interval training, characterized by recurring sessions of brief repeated bouts of very intense exercise, has been shown to be a potent stimulus for inducing metabolic adaptations in human skeletal muscle (Burgomaster et al., 2006). SIT has been shown to increases the maximal activities of mitochondrial enzymes (Salin et al., 1976), reduce glycogen utilization and lactate accumulation during matched work exercise (Burgomaster et al., 2006). Important for 400m performance, this form of training has also been shown to improve muscle buffering capacity (Edge et al., 2006). This may allow increased duration of maximal efforts due to an increased time until muscle homeostasis becomes disrupted, and maximal contraction rates begin to slow (Noakes et al, 2004).
The outlined training protocol has been consistently shown to lead to training induced increases in maximal activity of cytochrome c oxidase (COX) and the protein contents of COX subunits II and IV. This protocol was also found to lead to increases in skeletal muscle buffering capacity (Burgomaster et al., 2006, 2008). This form of training has also been shown to decrease net muscle glycongenesis and lactate accumulation via an increased capacity for pyruvate oxidation (Burgomaster et al., 2006). It is also possible that SIT may enhance the maximum capacity to oxidize pyruvate due to greater PDHa during exercise, leading to a slower rate of pyruvate presentation, allowing a greater proportion of it to be oxidized (Harmer et al., 2000). This form of intense training does however lead to decreased muscle ATP content (Ì´ 20%). During SIT type exercise AMP produced from ATP hydrolysis can be deaminated from by AMP deaminase, resulting in the formation of IMP and ammonia, possibly leading to further breakdown of IMP to inosine, and hypoxanthine, resulting in a net loss of adenine nucleotides from the muscle (Burgomaster et al., 2008) Replacing the purine nucleotides is a slow process, so a longer recovery and transition period at the end of such training would be necessary in order to achieve the full supercompensation.
However, these adaptations in skeletal muscle oxidative capacity over a short period of training also lead to significant improvements in power output and cycle time trial performance by approximately 9-10%. Continuing this programme for a longer period of time does not lead to a significantly greater increase in citrate sythase or COX , suggesting that most of the increases in mitochondrial enzyme activity and content occurs in the first few sessions of such activity (Burgomaster et al., 2008). This form of training could form a useful part of a 400m runners programme, allowing quick increases in aerobic ability, whilst maintaining the high intensity work required for the event.