LACTATE TRANSPORTERS How do these fit into Competition and Training? By Dr. Bob Treffene INTRODUCTION The human muscle has a very complicated taxi

Transcription

1 LACTATE TRANSPORTERS How do these fit into Competition and Training? By Dr. Bob Treffene INTRODUCTION The human muscle has a very complicated taxi system for transporting various things from one part to another. One of the important taxi systems is involved in the transporting of lactate from one portion of muscle to another. The working factories of muscle that produce the final working petrol or ATP are the mitochondria. If there is sufficient oxygen available to the mitochondria then the excess product of this ATP manufacture is normally carbon dioxide, which is taxied out of the red fibres, and the excess is breathed out through the lungs. If there isn t sufficient oxygen available, which is more normally the case in the white fast twitch fibres, then the end product is lactic acid. A build-up of lactic acid in the muscle fibre will eventually lower the ph within the muscle fibre to such an extent that it will cease to operate. Training for elite swimmers is normally aimed at reducing this lactic acid build-up. This paper presents a physiological model assumption indicating the role and limits of the taxi system in controlling the lactic acid. This taxi system relies mainly on two distinct components namely the MCT-3 and MCT-1 lactate transporters, which operate in separate fibre areas. The MCT-3 taxi system transports the lactic acid from the white cell mitochondria to the red cell regions. The lactic acid on reaching the red muscle cells is then is handed over to the MCT-1 system to be either transported to the aerobic mitochondria of the red cells if they have oxygen still available or directly to the blood capillary system. MITOCHONDRIA Mitochondria are small segments in the muscle with glycogen deposits near by. There are two types of mitochondria, short ones and long ones. The long ones appear to be more efficient as they have a plumbing system. Mitochondria produce ATP by the metabolism of fat, glycogen or lactic acid. Oxygen in the mitochondria is necessary for this process to proceed without lactic acid accumulation. The oxygen diffuses out of the cardiovascular system via the capillaries and is transported to the mitochondria via a specific transport system. If we increase the number of Mitochondria, we can therefore produce energy more rapidly. In order to increase the number of mitochondria, they need to be overloaded regularly at the highrequired use of competition speeds. Working at high oxygen uptake values and therefore high heart rates will accomplish this. If pressure is not put on the Mitochondria they will not increase in number or size. You need however to train INTELLIGENTLY at HIGH INTENSITY. Mitochondria increase in number by dividing. They sometimes change (adapt) periodically as a group and not individually. When they are in the transition stage they cannot take part in the aerobic energy contribution. This then puts extra strain on the remaining mitochondria and results in the heart rate increasing to supply larger concentrations of oxygen to these mitochondria. The first stage of division (mitosis) takes about three days and requires iron for the recombination during this three-day period. The following building and rehousing of the proteins take approximately 7-10 days. So for 10 days the athlete will have an oxygen utilisation problem especially if the Mitochondria are changing as a group. All muscle fibres contain mitochondria. They are therefore all able to produce ATP within these mitochondria. Some times the athlete s heart rate will increase for the same repeats. For example, assume a swimmer s average heart rate was 170 beats per minute when swimming repeat 66 seconds for 100 metres at a certain stage of his preparation. If this heart rate suddenly changed to 180 beats per minute for the same average repeat time then a mitochondrial change could be indicated as one of the possibilities. Mitochondrial changes can take place at any time during a training program. FAST & SLOW TWITCH MUSCLE FIBRES Every one is born with Red slow twitch fibres (I) Red fast twitch fibres (Iia) White fast twitch fibres (Iib) Some swimmers are born with more Fast Twitch (FT) fibres than Slow Twitch (ST) i.e. drop-dead sprinters.

2 White FT fibres (Iib) are bigger/bulkier than red FT fibres, which in turn are bigger than red ST fibres. Research has shown that the piston (myosin) sizes of the red fibres are smaller than the white fibres. Thus if the fibres change, then a major reorganisation of the pistons takes place as well as the plumbing (sarcoplasmic reticulum SR and terminal cisternae TC) and electrical pathways (T system). When a muscle cell is changing its type the chain of change is SR then T then TC followed by the contractile proteins. The mitochondria also alter at the same time. The total process takes up to 3 to 4 weeks. FIBRE CHANGE WITH TRAINING Microtears If a swimmer continues to work at too high an intensity for too long and therefore allows some of the muscles to reach excessively high values of lactate then soreness of the muscles can result. The coach will notice that the athlete looses stroke when the muscle is full of lactate. The high lactate levels results in some of the muscles closing down and being over stretched by the working fibres beside them. This produces small tears in the muscles called Microtears. This is a likely outcome at the end of a race or a very hard set. This soreness should show only infrequently in well-controlled training program. If it happens too often to an athlete the program for that athlete might be incorrect and should be revised. Fibre Changes Adaptations in muscle structure occur regularly in training seasons. This includes changes in the fibres from Red slow twitch aerobic fibres (Ia) to Red fast twitch fibres (Iia) to White fast twitch fibres (Iib) in either direction. It is now realised that these changes from slow twitch red fibres to fast twitch red fibres and then to white fast twitch fibres do occur frequently in a training muscle mass. The best way to speed up and assist these changes once they are initiated is to swim long and slow. This will have the effect of opening up the capillaries, enabling the waste products of the changes to be taken away from the muscle cell region where the mitochondria are dividing and regrowing. Opening up the capillaries also allows for the oxygen, iron and protein to be delivered to the adapting muscles. Swimming long and slow will also help the athlete to repair any muscle tears. If a swimmer complains of soreness this usually indicates the muscle has suffered tears. Swimming at slow speeds is a good massage for the tears in the internal muscle structure. These fibres can change in different ways with disproportionate training emphasis. A lot of endurance training will convert Iib fibres into Iia fibres and then Ia fibres. This involves the fibres breaking up and reforming into one of the other type of fibres. Russian research estimates that this process takes 3-4 weeks. Other research supports this. Programs with a large percentage of race speed work will change slow twitch fibres to fast twitch fibres. This sprint training will convert a large percentage of a swimmer s Iia fibres into Iiab fibres and then finally into Iib fibres. Programs with an emphasis on work in the 30bpm from maximum heart rate and speeds below this will change fast twitch fibres down the chain to slow twitch fibres. Swim coaches must be wary of changing Iib fibres of a sprinter into Ia fibres. GLYCOGEN USE IN WHITE FIBRES 70% of the swimmers program should be swum at 50-60bpm below maximum (fat metabolism) and not at speeds that utilise glycogen. This way the glycogen stores can be saved for the high intensity sets in which the muscles get an overload in the race speed requirement of force. This will give pressure on these fibres to remain as fast fibres. For proper development of the fibres each week the training program should contain enough race speed work to remind the muscle system of the need to retain the fast fibres. If a swimmer in a particular set has too much slow work at 40-30bpm below maximum then the glycogen stores in the white fibres will eventually be utilised by the red fibres. This speed approximates anaerobic threshold speed. Twenty minutes work at these 40-30bpm intensities will be enough to start the Iib fibres contributing glycogen to the ST fibres force production. The swimmer after completing consecutively two to three of these anaerobic threshold session s will not have enough fuel stored in the White FT fibres to complete successfully the sprint set in the following sessions. Ideally an athlete should train both types of fibre. For example a 200m swimmer needs to work on the speed component as well as endurance every training week of the year. THE LACTATE TRANSPORTERS White Fast Twitch Fibres

3 All muscle fibres contain mitochondria. They are therefore all able to produce ATP within these mitochondria. White fibres however have no oxygen supply to control the lactic acid produced. This control can take place in the red muscle cell in a series of reactions called the Krebs cycle. This cycle uses oxygen to eventually end up with ATP and carbon dioxide. Lactic acid leaking out as blood lactate into the cardiovascular system can also decrease the lactic acid in the red cells. To be able to understand the controlling mechanisms behind improvement of white fibres it is handy to have a picture of the white fibres. The white fibres are nestled into an infrastructure surrounded by red slow twitch and fast twitch fibres. White fibres are white because they have an almost non-existent capillary supply and therefore have no red blood permeating into their empire. White fibres work mainly anaerobically and produce lactic acid as the waste product. Any glycogen that is used by them produces lactic acid and not carbon dioxide as happens in aerobic glycogen use in the red fibres. If this lactic acid remains in the muscle tissue the acidity (as measured by the ph) will rise to very high acid levels. This results in very low ph levels. At a certain acid level the muscle will cease to operate. It is the object of training to swim at the goal race pace and to put off this critical acid value until the swim race is over. As there is no capillary network within the white fibres, they cannot get rid of this lactic acid too rapidly by oxidation. When the acid level gets too high the muscle stops working. It is important to remove lactic acid from the white fibres in order to continue to use the muscle. Transporting the Lactic Acid out of the white muscle cell does this. This transport can be improved with training. There are two main ways in which this could be done 1. By the muscle adapting by changing the type of fibre i.e. Iib to Iiab. Thus the muscle fibres grow more capillaries around them. This transition may reduce the strength of the muscle but the power of the muscle after these changes seems to be very adequate for swimming. It is a frequently reported adaptation, which results from swimming training. 2. By training the Translocation Enzymes (TAXIS) to work more efficiently. The Translocation Enzymes (MCT-1 & MCT-3) remove lactic acid from the white fibres by transporting it to the capillaries and also the other red fibres. The MCT-3 Taxi Service Wilson et al have concluded that the MCT-3 s appear to be the major MCT isoform responsible for the efflux of glycolytically derived lactic acid from the white skeletal muscle. Speeding up the transport rate requires more of the lactic acid taxis (that is MCT-3 s) to carry the lactic acid away to near tissue that can use it or disperse it to other parts of the body via the cardiovascular system. This increase in Lactic Acid taxis can only be achieved by using the taxis frequently in training. The frequent high use of these taxis puts pressure on the white fibres to expand the number of MCT-3 transporters. When the lactic acid has been taxied away from white fibre it will be carried into the red oxidative areas. Here it appears to hand its passenger over to the MCT-1 taxi system, which is the dominant lactate transporter in the red slow twitch and red fast twitch fibres. If the enzyme system involved in the increased oxidation of the lactic acid in this red fibre area has been enhanced, then much of this lactic acid will be re-utilised as a food substrate to produce ATP. MacRae et al found in the final stages of progressive exercise (after weeks of training) more than 80% of lactate was oxidised and accounted for approximately 45% of the overall carbohydrate oxidation. This combination of activities, involving the taxi service for the lactic acid from the white fibres to the red areas, and then the use of the lactic acid by the red fibres to produce ATP by oxidation, normally requires two types of training. These two types of training require 1. The overload of the taxi transporting system from the white fibres and also 2. the overload of the lactic acid oxidation system in the red fibres. The two types of sets involved are race pace sets designed to overload the lactic acid taxi system from the white fibres and heart rate sets designed to overload the lactate removal processes using the MCT-1 transporters in the red fibres. Bonen et al. has shown that the MCT-1 number increase by overloading with the appropriate training. This is training at speeds using energy at a level near maximum oxygen uptake. This can be achieved by regular well-controlled heart rate sets. OVERLOADING THE MCT-3 LACTATE TRANSPORTERS The MCT-3 overload requires training at speeds near metres racing pace. To do this requires some ingenuity from the coach. At any one time in the season the athlete might be only able to do 30

4 metres at 100m race pace at another time in the preparations the athlete might be capable of swimming 50 metres at race pace and at another time metres. Some leading coaches on observing that their athlete at a particular stage of their training can swim up to 50m at race pace for the 100m would then subdivide the repeat efforts adding up to 100 metres as follows. Swim 25 metres and then 25 metres then 50 metres with 30 seconds in between each. This constitutes 100 metres swum at race pace and therefore the taxi systems from the white fibres will be almost fully operational by the end of this first 100 metres race pace swimming. If this is now followed by metres at a fat metabolism pace the flurry of activity of the taxi system initiated by the race speed component will start off near maximum and be somewhat reduced at the end of this fat metabolism pace swim. The athlete can now be asked to do another similar subset again adding up to 100 metres. The MCT-3 taxi system will be brought into full function and again kept functioning but decreasing during another fat metabolism swim. This can be continued until the capability of the athlete at this time of the preparation has been adequately overloaded. Race Pace (RP) Training: Glycogen Limitations in White Fibres To build up the number of translocation enzymes that transport lactic acid from the white fibre tissue (MCT-3), a swimmer needs to sprint at race pace. If a coach wants to improve a 100m swimmer, then the swimmer needs to train the white fibres to work at high lactate producing levels and therefore train the translocation enzymes to remove the lactic acid. The swimmer needs to be trained regularly at the speed at which he/she will race. How many metres of this race pace work can you build up to in this type of set? It will be restricted by the amount of glycogen in the white fibres. At 100 metre pace this could be about 12 minutes (Treffene 1996) as indicated by the research of Friden et al. Therefore the advice is to restrict this set to 800 metres for mature athletes and somewhat less for younger athletes (Treffene 1995). How often could you do this 800 metre set? The restriction seems to depend on the rate of return of glycogen to the white fibre. Most current physiological information would suggest this would take only 12 hours. This information has come however from research on combinations of red and white fast twitch fibre. Experience has lead to the hypothesis that the full return of the glycogen to the white fast twitch fibres will take more likely three days. Current research is tending to suggest this also. The GLUT-4 taxi system is necessary for the return of glycogen to the white fibre muscle cells (Kishi et al). Kristiansen et al and others have indicated some problem with the GLUT-4 returning to a full operational state in the white fibre area within two days. It is the experience on the pool deck that we do need three days in between these race pace sets after they have been built up to 800 metres or slightly more. Glycogen Replacement Rate There is a definite limit of glycogen in the fast twitch fibres (Iia and Iib). This is used up at different rates depending on the speed used by the swimmer i.e. working at 50m race pace (about 200% of VO 2 max) will deplete the glycogen in the white fibres in about 8 minutes or less. If the work is done at 200m pace (106% of Vcr, 120% VO 2 max) the swimmer will obviously be able to train for longer with the same glycogen reserves. Distance swimmers are able to train race speed sets at m pace for greater than 15 minutes at m pace (e.g. 30 x 50m on 1.30 cycle). It is important to monitor the swimmers program so as to avoid full glycogen depletion and also to optimise the high intensity sets. Constant training without full glycogen stores can lead to muscle breakdown. Glycogen replacement is dependent on a number of factors. These include The type of muscle used The speed of the swim The type of exercise immediately following the fast set What is done in the following sessions? To replace the glycogen to the ST fibres takes hours and the red FT fibres take hours. The white FT fibres can take up to three days to recover and I have been lead to postulate that it may be as slow as three days to recover the glycogen fully in these fibres as opposed to a neurological recovery which should be quicker. Kristiansen has indicated that the GLUT-4 transporters that take part in the glycogen transport to the white fibres are still depleted longer than two days after exercise.

5 Experience with 800m of 100m race pace sets with mature athletes has indicated it takes three days to be able to repeat as long as no white FT work is done in between. It may take longer to replace the white fibre glycogen, as there is no capillary network directly feeding them. Distances Not Restricted by Pool Length Swimmers should rigorously and frequently train at the pace in which they are to compete to overload the races requirements and therefore initiate improvements. For example, swimmers aiming for the 200m as the main goal for the season should train at the goal time speed for the 200m. Muscle function and overload should not be limited by the length of a pool when constructing sets utilising this goal time speed. A muscle can work at a certain speed for a certain length of time. So why not design sets to those limits? With a 100m swimmer, for example, it is very rare for them to be able to swim 100m at their goal time 100m pace. Therefore, sets constructed using distances that they can swim at their race pace should be constructed. This normally means swimming distances lower than 50 metres. These race pace sub 50m swims can be introduced into a set in which the total distance of race pace work does not exceed 800 metres. Many elite coaches advocate working to a specific stroke rate (SR) at the goal speed for the event. How long can that swimmer maintain his/her ideal stroke rate and race speed? The only limitations are the individual. This is dependent on the athlete s ability and where they are presently in their programs just starting after a spell, adapting, glycogen holdings, muscle soreness, etc. To improve the performance of the swimmer it is necessary to increase the distance that swimmer can work at the ideal stroke rate (SR). Some elite coaches for example use, at the beginning of a cycle, training sets made up of 20-40m swims at the goal SR and build these up to 50-75m swims as the training cycle progresses. In order to swim 100m at Race Pace with the correct stroke rate, the swimmer could be asked to swim 1. 40m on 90sec 2. 40m on 90sec 3. 20m... and then swim off in fat metabolism (50-60bpm below max HR) with a total distance of m. They could repeat this twice early in say a six week cycle and increase to 8x100m at race speed efforts in the fifth or sixth week of the cycle. It is essential the swimmer maintain good technique. Sometimes this is not possible in the above set. This might be the case early in the season when the athlete is unfit or late in the season when the athlete is adapting. In that case it would be necessary to reduce the metres swum at race pace to something like 30m, 30m, 30m, 10m on the same cycle and/or also increase the swim down distance. This type of set is designed to increase the lactic acid in the white fibres to high levels after the 100m. This initiates the MCT-3 taxi system to transport the lactic acid away from the white cells. During each 100m subset and immediately following it during the swim down active rest the MCT-3 and MCT-1 Taxi system are very busy. The system works hard to reduce the level of lactic acid in the white fibres before the next 100m. Thus the MCT-3 Taxi system is the main system being overloaded by constant pressure to transport the lactic acid from the white fibres to the red areas. This type of thinking and set design is very important for establishing good training design for the 100, 200 and 400 events, not so important for 1500m swimmers but still needed. 1500m swimmers can normally swim their race speed work in well-designed heart rate sets and can therefore get away with a metre race pace set only once a week. The swimmer needs to swim down at speeds in the fat metabolism area with good technique and using no glycogen. This will reduce the lactic acid at two to three times faster than the reduction rate that occurs with passive rest. For the well-trained swimmers full reduction of the blood lactate has been shown to occur in 5 minutes. It is essential the swimmer learn to swim with good technique at a low heart rate. Swimmers might unconsciously alter their stroke when swimming at slow speeds (e.g. catch up). This should be corrected and avoided! Early in the program, the swimmer may only be able to do 2x100m at RP with 500m swim down between each 100m. As the swimmer gets fitter increase the pressure for adaptation by design of sets with An increase in the metres swum at RP i.e. 30 to 40 to 50m An increase in the number of repeats i.e. 200 to 400 to 800m A reduction in the swim down 500m to 300 to 200m

6 Several successful coaches have indicated their aim is build up to approximately 800m, all on the main stroke, twice a week after 4/5 weeks. This race pace training can be swum every week once or twice providing the swimmer is allowed to recover their glycogen reserves in between sessions. This means the swimmer trains mainly in the fat metabolism area apart from well-controlled high heart rate sets and these race pace training sets. Other facets of training such as distance anaerobic threshold swimming, kicking, drills and skills should be introduced into sessions so as not to threaten the glycogen reserves for the high intensity sessions. The program can be adapted to suit a squad i.e. not all swimmers will be sprinting 40m. Some will only be able to cope with 20m, etc., but all can leave on the same cycle. At the end of the subset some will have swum 100m and others 60-80m. When swimmers go into adaptations they will be able to hold shorter distances only before they lose stroke. In this case the coach should consider modifying the distances swum in each subset so that the swimmer can complete it without undue stress and be able to hold their stroke throughout. TRAINING TO INCREASE LACTATE OXIDATION: MCT-1 INCREASE The importance on the MCT-3 transporting system has been emphasised in the previous sections. We were concerned with the lactic acid being produced in the white fibres and transferred into the red fibre areas where the lactate was delivered like a passenger to a different transporting system controlled by the MCT-1 s. At this point the lactic acid has a number of alternative pathways. One of these is delivery to the blood capillary network to be transported to other parts of the body such as the liver and non-working muscle. These areas are not creating their own lactic acid. A better alternative is to transport the lactic acid to the red cell Mitochondria. If there is sufficient oxygen available the lactic acid can then be oxidized to produce ATP. One way of allowing this to happen over a prolonged period of training time is to utilise the heart rate sets. In these heart rate sets the heart rate is kept below maximum but close to maximum for up to 30 minutes. This means that the oxygen uptake is also near its maximum. The normal use of this oxygen is to be directly associated with glycogen which reacts in a controlled way called the Kreb s cycle to produce the ATP. So in effect this final bit of oxygen near the limits of that available (maximum oxygen uptake) needs to be re-trained to take part in the oxidation of lactic acid. To do this lactic acid would be required. This should be the case when the heart rate is within 20 to 10 of maximum. At this work level there will be maximal lactic acid produced in the red fibres as well as a smaller amount in the white fast twitch fibres. By swimming heart rate sets the MCT-1 transporting system will be fully utilised resulting in overload of the transporting system and improved ability for the red cells to utilise lactic acid as a food substrate for the production of ATP. This also solves the problem of excess lactic acid in the red cell areas. Thus the heart rate sets form an alliance with the race speed sets. Race pace sets increase the potential of the MCT-3 s to carry the lactic acid away from the white cells whereas the heart rate sets increase the MCT-1 transporting systems ability to respond to transferring the lactic acid to the mitochondria in the red slow and fast twitch fibres. In order to train the muscle to oxidise more lactic acid, the muscle lactate removal rate needs to be put under pressure at a speed where high lactates and near maximum oxygen utilisation are both in progress. This will have the MCT-1 taxi system fully utilised within the red fibres. (Anderson 1998) To do this a swimmer needs to train as close to his/her limits of lactate removal as possible. It has been found useful to confine the heart rate within 20 to 10 beats of maximum heart rate. This is achieved at a swimming speed illustrated at C in Figure 1. The types of set built up to 30 minutes at these speeds have popularly being referred to as heart rate sets (Treffene 1997). Work from 15 minutes to 30 minutes on 1.40 to 2min cycle is recommended for most elite swimmers. If the working muscles are fully stocked with glycogen before commencing this set then at these speeds their total quantity of glycogen will last approximately 40 minutes. This is a limiting factor in the design and weekly placement of this type of set. It has been possible to train at lactate levels of 6-8mmol at high heart rates as long as the maximum heart rate is not reached. When the heart rate is high during an intensive set but contained below its maximum for the whole of the set the lactate removal has achieved equal rates to the production rate. The nearer maximum oxygen uptake the more overload will be placed on the MCT-1 system to transport lactic acid provided by the MCT-3 transporters to the red cell mitochondria. In these high intensity sets it will take about 8 minutes for the lactate levels to reach a peak. If the training speed and turnover time are correct for the individual swimmer the lactate level will stabilise, as the production rate equals the reduction rate.

7 The maximum oxygen uptake does not have to be improved to enhance performance. It is the use of oxygen, which needs to be changed. This change of oxygen utilisation is from being directly used with glycogen for ATP production to its use in lactic acid removal by oxidation and again with ATP production. Heart Rate Sets The essentials of this type of set are 1. The oxygen uptake and therefore the heart rate must be kept near their maximum without reaching maximum until near the end of the set. 2. The set should last for no less than 15 minutes actual swimming with 30 minutes being optimal. 3. The rest period should be short but long enough to enable the set to be done with as much as possible race speed in the set. 4. The set design should structure as much race pace as possible but with sufficient critical speed work as is necessary to keep the heart rate below maximum and therefore the lactic acid levels under control. Figure 2 illustrates the different speeds. 5. Generally if the heart rate exceeds 10bpm from maximum in the first part of the set then the swimmer s speed should be decreased below critical speed or the rest time increased. 6. The last half of the set should be swum within 10bpm of maximum but only reach maximum in the last 200m of the set. Critical Speed How is it established? Critical speed is the steady state speed at which maximum heart rate is first reached (which is also when maximum oxygen uptake is first reached.). To establish the Critical Speed (Vcr) the swimmer swims a set of 5 x 200m on about 5mins ascending in speed from easy to 80% of maximum speed. From this test an estimate of critical speed (Vcr) is determined graphically. Figure 1 Blood lactate changes as time increases from commencement of the swim for several constant speed swims. A B C D E Working at just above the anaerobic threshold... the production of lactic acid = the removal. More pressure is put on the removal system, though the body is still able to remove LA at the rate of production. More pressure still but there is still available oxygen to oxidise the higher levels of lactic acid produced. (Near max VO2) LA production rate is greater than removal rate (e.g. 200m race speed) LA production rate is greater than removal rate (e.g. 100m race speed) Note however that the muscle lactic acid will not always be truly reflected by the blood lactate values due to the internal muscle synthesis of lactic acid back to glycogen.

8 This critical speed is established by extrapolation of a heart rate velocity curve to each individual s maximum heart rate (Figure 2). The correct maximum heart rate is established by testing over many high intensity sets. This critical speed although established with heart rate measurement also coincides with the steady state speed at which maximum oxygen uptake (VO 2(max)) would be first achieved. Relationship of Vcr to Competition Speeds Figure 2 shows the relationship between heart rate and the velocity of each swim. Swimming at Vcr or just below will initially increase the lactate level but then the rate of production will equal the rate of removal. At this stage, which is normally about 8-10 minutes into the event or training, the blood lactate will remain at the same level increasing or decreasing only marginally. Swimming above Vcr, the blood lactate level will continue to rise (Treffene 1980). The blood lactate level needs to be measured at critical speed and the training adjusted accordingly. 5mmol then it is possible for that athlete to train at critical speed in the set of 100 metres on say 1.30 to 2 minute cycle. 8mmol would indicate the athlete should train at a speed given on the curve 10 to 20 beats below maximum mmol would indicate that the training at Vcr should be done with care using distances between m repeats mainly with occasional m swimming slower than critical speed introduced at appropriate positions in the set. Using the model postulated by Costill et al one could indicate the difference between sprint swimmers and endurance swimmers (Treffene ). The sprint swimmers swimming at Vcr would be expected to have a greater percentage of their fast twitch fibres entrained than would an endurance swimmer. The sprinter will reach a plateau with a higher lactic acid level than the plateau achieved by an endurance swimmer at critical speed. A blood lactate test after 200 metres swum at critical speed can be used as an indicator of a trained swimmers sprint or distance potential. A high lactate level (above 10mmol) at Vcr would indicate the swimmer to be a sprinter, 6-8mmol a good swimmer and below 4mmol a good distance swimmer. These are only general rules with exceptions mainly coming from swimmers with low and very long distance backgrounds. Figure 2

9 Heart rate velocity curve extrapolated to the maximum heart rate of the athlete The lactate level of distance swimmers and sprinters differ when a swimmer trains in a short rest Heart Rate set with a total distance of m at a speed just below Vcr. The blood lactate will plateau sometime after the first 500m at a level, which is lower for the endurance swimmer relative to the sprint swimmer. With continued swimming the rate of increase for both swimmers will be small but substantially larger for the sprint swimmers. Ming has used this to compare the capacity of a swimmer to swim a maximal effort 1500m. He found that only swimmers with a blood lactate value less than 5mmol, after swimming 200m at critical speed, could swim 1500m at Vcr. It has been found that relative to critical speed the anaerobic threshold of sprinters is approximately 75% and the anaerobic threshold of endurance swimmers is 95%. The blood lactate will increase very rapidly without reaching a plateau at velocities above Vcr. Relationship of Critical Speed to Race Improvement It is possible to make predictions on swimmers capacity for events between 100m and 1500m. The rate of increase of lactic acid for the 100m event would be double that for the 200m event which takes approximately double the time. If the 100m time at critical speed is known (Tcr) and the time a swimmer has swum 100m in a previous recent race (T100), it is possible in long course swimming to calculate the approximate time for the next race 200m. This is done by using: Time for 200m = Tcr + T100. For the 400m event Lactate increase rate would be expected to one quarter of that for the 100m event. Thus knowing the 100m speed for a swimmer and the Vcr just prior to competition it is possible to predict the 400m and 200m speed (Treffene 1982). If a coach wants to use Vcr for predictions it is important to obtain the Vcr value immediately before competition (within four days) because the variations of Vcr which can be sometimes quite rapid and dramatic during training and taper periods mainly due to adaptations taking place. These adaptations should have been processed during the early taper. The majority of 800m and 1500m competitive swimmers do swim at or slightly below Vcr speed in races especially those who had less than 5mmol blood lactate after 200m test swims at Vcr. The true 800-metre competitor swims the 800 metre at critical speed and the 1500 metre at a pace close to 20bpm below maximum as determined on a extrapolated 200 metre test conducted within four days of competition. The Graph used for this extrapolation is a plot of the heart rate against the swimming velocity. The swimming velocity is calculated using the last 100 metres (foot leave) of each 200 metre in the test. MAXIMUM OXYGEN UPTAKE TRAINING Training Control Using the Vcr Model Bearing in mind that at Vcr the maximum oxygen uptake will be also achieved. To improve Vcr and lactate removal rate it is therefore important to overload the factors that are important at critical speed namely high carbohydrate turnover and high lactate removal rate and high oxygen uptake levels. The fat metabolism is not an important food substrate at Vcr speed. At critical speed the steady state blood lactate is higher than 4mmol for most swimmers and therefore is well above anaerobic threshold. When planning work routines it is important to decide that it is the overload of the oxygen uptake system, which is important, and not the overload of the fat metabolism or the need to work at low controlled levels of blood lactate as indicated by anaerobic threshold measures. The exercise should be near a speed at which VO 2 (max) will be achieved if the overload is to be appropriate. This therefore must mean that the speeds involved should be close to Vcr. This can be achieved by training at speeds for which the heart rate is within 10-20bpm of maximum. Working in this heart rate range, the 800m swimmers will predominantly use glycogen from the red ST (Ia) and FT fibres (Iia) and also some of the white FT fibres (Iib) which will then get pressure to change to red fibres. Sprinters will use a higher percentage of White FT fibres at these higher heart rates. For some swimmers, especially sprinters, this is a difficult thing to achieve without prior planning. High HR sets will fully stress 1. The lactate removal system 2. The oxygen uptake system Once a decision is made to improve lactate removal processes then overload at the present Vcr is the main ingredient of a program construction. This may mean introducing longer rests or smaller repeat distances in sets. The optimal training programs for VO 2 (max) improvement have been shown to be those lasting for longer than 10 minutes and repeated three times a week for swimmers and twice a week for

10 sprinters. These sets are now being recognised as those most important for increasing the MCT-1 population and lactate removal rate of the red muscle system. A rest period of one quarter the total work period is normal but some coaches have used 30-40% rest periods with success. If a swimmer is unable to maintain high heart rates and good stroke with one type of SET then the distance or rest period should be altered so as to attain the required high heart rates but the able to swim throughout with good stroke. If a swimmer is not able to maintain 30 minutes at high heart rates then reasons for this could include 1. The swimmer did not begin the set with enough glycogen in the red fibres. 2. Blood Lactate levels and therefore internal muscle cell lactic acid are too high (swimmers should do slower repeats or increased repeat times or more importantly lower repeat distances). 3. Adaptations are occurring in the red fast twitch fibres. Working at Vcr (VO 2 max) should be followed by a session at fat metabolism. It is important that the swimmer works so as to utilise the fat metabolism and not to swim at speeds at or above the anaerobic threshold. Swimming above the anaerobic threshold will use up the glycogen reserves and also deplete the white fibre glycogen. The total reserves of both ST and FT fibres will therefore be depleted. As a result the swimmer will not be able to do sufficient race pace work in the next two days when required. The change in blood lactate with constant speed swimming below critical speed (the speed at which maximal oxygen uptake is first obtained) is illustrated in Figure 1 (A, B & C). This peaking of the lactate at 8-10 minutes and decrease to a lower plateau has to be considered when designing sets. For sprinters it is particularly important, as their peak lactate might be so high at critical speed that some of their fast twitch fibres will cease to operate and continued swimming at the critical speed can lead to small muscle tears and subsequent soreness in the following days. For this reason it is recommended for sprinters heart rate sets that they be mainly made up of 50m efforts or even smaller distances for the drop dead type sprinter. By keeping in mind the full range of blood lactate changes that occur below and above critical speed as illustrated in Figure 1 (A to E). Also lactate will reduce by.5mmol every rest minute and at least twice as fast at speeds just below anaerobic threshold speed. Taking these points into account then suitable sets can be constructed. TESTING Using a Heart Rate Monitor The swimmers are initially tested on 5x200m ascending in speed from easy to 80% speed. This set is swum using the main stroke of each swimmer. The results are plotted onto a graph on the pool deck. The easiest way is to graph HR on the y-axis and 200m time of swim in descending time on the x-axis (see Figure 3). The coach could have prepared graph paper for each swimmer. The information from this test indicates whether the swimmer is a sprinter or endurance swimmer if the blood lactate is taken near the Vcr. This test could be done every 4-5 weeks and compared with previous results. The maximum heart rate of swimmers who remain fit does not appear to decrease with AGE. Standard Sets When athletes have obtained the skills and fitness to control pace in heart rate sets then a standard set or sets can be chosen to make weekly comparisons e.g. 10 to 20x100m for m swimmers or a 2x(50, 50, 50, 75, 75, 100) as part of a heart rate set. The latter part of which can be varied. Times and heart rates should be accurately recorded for these standard sets and compared weekly to determine when adaptations occur (Treffene 1999).

11 Figure 3 Heart rate Time for 200m submaximal constant speed swim. A heart rate after travel or adaptation 4 days B heart rate before travel or adaptation C heart rate after adaptation 14 days 190 HR 170 A MAXIMUM HEART RATE 150 B C Time for 200m Figure 4 Variations of heart rate with adaptation phases ADAPTATION If a swimmer cannot get his/her Heart Rate up and is also swimming slower on test sets then either 1. An adaptation is taking place or 2. There is a depletion of glycogen in the fibres (mainly the white fibres (Iib)). This is especially the case with sprinters who are high in White fibres. If after three days of low-level swimming the heart rates and also the swimming speeds are not high an adaptation is definitely taking place (Treffene 1999). If the swimmer is able to swim fast then a previous glycogen shortage is the possible reason. A shift in the 5x200m test to the right will indicate the adaptation is coming to an end and 2-3 weeks of good work can be expected as the athlete is aerobically fitter (Figure 4). Fibre changes display in different ways at the time the adaptations are taking place. By controlled measures of heart rate it is possible to assess the type of adaptation. Sometimes the athlete s heart rate will not be much changed at low speeds but they cannot swim at fast enough speeds to increase their heart rate to high values. This could be a lack of glycogen in the fast twitch fibres. Give the athlete two successive fat metabolism type sets. Dramatically improved speed capacity in the following session would indicate that glycogen shortage was the more likely reason. If the speed capacity of the athlete is still lacking then adaptation of the fast fibres could be a possibility. HOW THE HEART RATE RELATES TO RACE IMPROVEMENT If a test swim is swum close to a competition, then the Vcr will give an indication of 200/400/800 pace that is possible for the athlete. If the curve has shifted by 2sec per 200m to the right since a previous performance then the athlete can be expected to go approximately 1 second faster per 100m in

12 the 400m and 800m races than the previous performance. Other factors can as we are aware produce slower performances as well. ANAEROBIC THRESHOLD Working at 30-50bpm below maximum will 1. Open the capillaries 2. Put more pressure on capillaries, so capillary change will occur 3. Allow for adaptation to take place 4. Allow for repairs if the athlete has muscle microtears 5. Have the lactate production and reduction mechanisms working at a low level in the ST fibres. BUT after minutes this level of swimming starts taking glycogen from white fibres. All of the above benefits (except 5) can be gained by working in the fat metabolism area. If we reduce the amount of AT and increase the fat metabolism work, high heart rate sets can be swum 2-3 times a week. Fat Metabolism V Anaerobic Threshold One of the ways to improve efficiency or technique is to train regularly over long distances and with good technique. This training also assists the adaptation response from the high intensity sets and speeds the repair of the microtears in muscle occurring during these sets. It is better to do this type of work swimming at speeds utilising only the fat metabolism than to do too much anaerobic threshold work or faster. Too much anaerobic threshold work will eventually use glycogen from the white fibres. This then prevents sufficient high intensity work to be done satisfactorily in the week. Young swimmers often find it difficult to swim over long distances in the fat metabolism area because (a) They have not been trained to swim slowly with good technique without the use of catch up. (b) They have an undeveloped blood capillary network in the specific swimming working muscles. With the latter category of swimmers it would be unwise to swim HR sets. It probably would be more beneficial to swim them at anaerobic threshold for 1 or 2 years, working on technique, until the technique can be maintained with a low heart rate. During the fat metabolism sessions the coach could be looking and correcting technique and skills. Have a few swimmers at a time swim 15-20m to check on speed and stroke rate, fast turns timed for 7.5m in and out, etc. These are the sessions you can afford to break up in this way and not loose any of the gains that the session has for the athletes PLANNING It is important to plan the week to use specific race speed fibres and their metabolic functions but also allow for recovery time involving these fat metabolism sets. The heart rate sets need to be suitably located when the red slow and fast twitch fibres are almost fully stocked with glycogen. During recovery swimming different fibres and enzymes than those used at race pace will be mobilised but most of the blood capillary network will be open. Faster return of glycogen and quicker adaptation results. This constant pressure on the capillary network will also create extra capillary growth. The stimulus for growth is the blood pulsing in the capillaries. This planning is the topic of another paper. References Anderson O: Peak Performance 112: Dec Forget tempo workouts the way to hike your lactate threshold is by short bursts of maximum intensity. Early research strongly supports the notion that high intense training is best for boosting MCT-1 concentrations and lactate uptake rates. Bonen A. et al: Can J Appl. Physiol, 22(6): Dec Lactate transport and lactate transporters in the skeletal muscle. The primary role of this lactate transporter (MCT-1) is to take up lactate into the oxidative muscle fibres where it may be used as a fuel in mitochondrial oxidation. Increments in both MCT-1 and lactate transport with training support this role. Bonen A. et al: Am J Physiol, 274 (1 Pt 1): E Jan Short-term training increases human muscle MCT-1 and femoral venous lactate in relation to muscle lactate. Lactate extrusion from exercising muscles is increased after training, and this may be associated with the increase in skeletal muscle MCT-1. Friden J. et al: Acta Physiol Scand 135, Topographical localization of muscle glycogen: an ultrahistochemical study in the human vastus lateralis. Kishi K. et al: Diabetes, 47(4): Apr Bradykinin directly triggers GLUT-4 Translocation via an insulin independent pathway. Physical Exercise induces translocation of GLUT-4 from and intra-cellular pool to the cell surface in skeletal muscle s and increases glucose uptake via an

13 insulin independent pathway. Bradykinin is probably one of the factors responsible for exercise stimulated glucose uptake in skeletal muscle. Kristiansen S. et al: Am J Physiol, 271(2 Pt 2): R Aug Decreased muscle GLUT-4 and contraction induced glucose transport after eccentric contractions. It is concluded that the GLUT-1 and GLUT-4 protein contents in fast twitch muscle are decreased and increased, respectively, two days after eccentric contractions. The functional consequence of these changes appears to be decreased contraction induced increase in skeletal muscle glucose transport. Kristiansen S. et al Am J Physiol, 272(5 Pt 1): C May Eccentric contractions decrease glucose transporter transcription rate, mrna, and protein in skeletal muscle. We suggest that eccentric muscle contractions decrease muscle GLUT-4 transcription rate, resulting in lower GLUT-4 protein content, which in turn decreases the number of GLUT-4 transporters translocated to the sarcolemma, ultimately leading to decrease contraction induced muscle glucose transport. MacRae H.H. et al: Pflugers Arch, 430(6): Oct Effects of endurance training on lactate removal followed oxidation and gluconeogenesis during exercise. In the final stages of progressive exercise after training more than 80 percent of lactate was oxidised and accounted for approximately 45 percent of overall carbohydrate oxidation. Ming Z. Studies of the critical velocity in highly competitive swimmers. In: P. Quinlan (Ed.) Swim 86 Year Book, Australian Swimming Inc., Brisbane 1986, pp Treffene, R.J. A technique for predicting and controlling optimal performance capability of competitive swimmers based on heart rate measurements. Ph.D. thesis, University of London (1982) 251 p. Treffene R.J. The Heart Rate Lactate Connection. Proceedings XIth Annual Australian Swimming Coaches and Teachers Conference., (1991) Treffene, R.J., Dickson, R., Craven, C., Osborne, C., Woodhead, K. and Hobbs, K. Lactic acid accumulation during constant speed swimming at controlled relative intensities. J. Sports Med. Phys. Fitness., 20 (1980) Treffene R.J. Glycogen Replacement Rate & its Use in Program Design. Australian Swim Coach XI (10) (1995) Treffene R.J. Heart Rate Sets. What are they? Australian Swim Coach XIII (4) (1997) 5-6. Treffene R.J. Blood Lactates: What can they tell the swimming coach? Australian Swim Coaches Swim 85 Yearbook (1985) Treffene R.J. Effective use of Heart Rate Monitors. Australian Swimming and fitness 15 Mar/Apr (1999) Wilson M.C. et al J Biol Chem, 273(26): Jun Lactic acid efflux from the white skeletal muscle is catalyzed by the monocarboxylate transporter isoform MCT3. MCT-1 is expressed most abundantly in the oxidative fibres but is almost totally absent in the fast twitch glycolytic fibres. Thus MCT-3 appears to be the major MCT isoform responsible for efflux of glycolytically derived lactic acid from white skeletal muscle.