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#1
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Lactic acid is good? need more mitochondria?
There's been some news articles in the last month or so saying that lactic
acid is actually a very effective fuel for muscles during endurance performance, and that many previous beliefs that lactic acid is just a waste product, or even a poison, are mistaken. (try a Web search on "lactic acid waste product" or "lactic acid poison") It's tricky for me to sort out, because some of the new biochemistry findings sound a lot like well-established old findings. And because the researchers say that training approaches used by good coaches were on the right track and effective even though though they were based on incorrect biochemistry. So any help I can get in sorting out my confusion is much appreciated. Here's some ideas and claims I'm trying to make sense of -- are they true, or half-true, or misunderstood? (a) The recent biochemical finding seems to be that there is a specific path for the mitochondria in a cell to aerobically "burn" lactic acid -- even if the lactic acid was originally produced by anaerobic respiration elsewhere outside the mitochondria. (My initial response is, "I should hope so. The chemical reactions are well-described in lots of textbooks: Seems like it would be a stupid design if our mitochondria were _not_ able to execute the process using either glucose or lactic acid as a starting point." -- or is there something trickier here that I'm missing?) (b) The key limiting factor on most endurance performance is not oxygen uptake or transport -- it's the amount and effectiveness of mitochondria. So the critical primary goal of athletic training for endurance performance is to build mitochondria. (? presumably then increases in oxygen uptake or transport will soon follow as those increased mitochondria start to demand more oxygen ?) (c) Sometimes even if muscle cells are getting more than enough oxygen, they still use anaerobic respiration and produce lactic acid -- because it puts little or no burden on the limited amount of mitochondria available -- and it's quicker. (? if the lactic acid can be transported away quickly, it could be "burned" aerobicially by other less-critical muscles that have currently under-utillized mitochondria available ?) (d) Short intense interval workouts are helpful stress mainly because they stimulate the muscles to develop more mitochondria. (not because they directly increase oxygen uptake or central cardio-vascular capacity) (e) Lactic acid does not "cause" pain in any simple way. This should be obvious, since lactic acid is cleared quickly after exercise is complete, but the pain and fatigue-feeling often endures much longer. (Unfortunately I have not heard anyone say what else _does_ cause the short-term and long-term pains associated with intense exercise). Thanks for any help in sorting out the confusion. Ken |
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Ken
I have studied and read a lot about this issue for years. I will attach a recent artcile that reviewed current literature. It seems to me that the scientist are saying that something on the order of 85% of the limitation of VO2max is central. I tend to beliee based on the research I have read the peripheral limitations are of greater importance, than may currently be recogonized. Likewise I am not sure the research upholds your statement that short intense exercise develops more mithochondria, and enzymes. -Statement of the Topic The Limitation to Vo2 Max Is Central! Introduction Maximal oxygen uptake (VO2max) is defined as the highest rate of oxygen, which can be taken up and utilized by the body during severe exercise (Basset and Howley 2000). It is frequently used as an indicator of an individual's cardiorespiratory fitness as oxygen consumption is linearly related to energy expenditure (Basset and Howley 2000). VO2max is commonly used in scientific literature to evaluate changes in maximal ability to work aerobically and in exercise prescription (Basset and Howley 2000). To determine VO2max, incremental exercise testing is used. It is taken as the point at which oxygen uptake peaks with additional power failing to produce VO2 gains (Lindstedt et al 1988). Secondary criteria to verify VO2 max include: 1. expiratory exchange ratio 1.15 2. blood lactate level 8-9 mM (Duncan 1997) It is generally expressed in ml.kg - 1.min - 1 There has been longstanding interest in identifying physiological factors that control VO2 max and especially debate over whether the limitation is centrally or peripherally regulated. Background Knowledge In order to examine VO2max limitation an understanding of those factors affecting O2 transport from the atmosphere to mitochondria of the muscle must be examined. The O2 delivery system can be viewed as including the pulmonary and cardiovascular systems. Central physiological factors, which may affect VO2 max limitation include: 1. pulmonary diffusing capacity, 2. maximal cardiac output, 3. O2 carrying capacity of the blood. Peripheral skeletal muscle limitations include: 1. peripheral diffusion gradients, 2. mitochondrial enzyme levels, 3. capillary density. Centrally Limited VO2max - Traditional View Hill who postulated that developed the concept of maximal oxygen uptake: 1. Oxygen uptake had an upper limit; 2. VO2 max was limited by the rate at which the cardiorespiratory system could transport O2 to the muscles (Bassett and Howley 2000) The majority of the following research supports the concept that VO2max is limited by the rate of oxygen delivery (central factors) not the ability of the muscles to take up O2 (peripheral factors). Pulmonary System The ability of the pulmonary system to maintain arterial oxygen level (% SaO2) in healthy subjects remains high even during maximal work. Richardson et al (2000) examined whether the quadriceps are O2 supply dependant at maximal exercise. The VO2max of the muscle group was measured during altered inspired O2 levels (hypoxia 12%; normoxia 21% and hyperoxia 100%). It was found VO2 max increased with increased O2 delivery. It was concluded therefore that in normal conditions of isolated knee extension, VO2 max of trained subjects was limited not by peripheral factors but centrally by O2 supply. A similar study examining the effects of breathing hyperoxic gas on the VO2max of trained athletes again demonstrated an increase in VO2max (Powers 1989). The rationale for the increase in VO2 max while breathing hypoxic gas is thought to be due to an expended arterial-venous O2 difference (a-v O2 difference). Small increases in hemoglobin (Hb) saturation and in O2 dissolved in plasma produce an increased O2 supply. Such an increase in arterial PO2 can produce a 10% improvement in VO2max (McArdle1986). Daniels and Oldridge (1970) likewise found that the reduced oxygen levels at altitude compared to sea level reduced maximal aerobic power in elite athletes. These research studies demonstrate that a central pulmonary limitation to maximal exercise capacity indeed exists. Maximal Cardiac Output Cardiac output (CO) is determined by heart rate and the quantity of blood ejected with each stroke (stroke volume). Hill identified maximal cardiac output as the principle factor for individual differences in VO2 max. As maximal heart rates do not show considerate variation in those of a similar age, differences in VO2max have been closely related to maximal stroke volumes (Basset and Howley 2000, Bergh et al 2000). McArdle et al (1986) conducted a study which compared maximal heart rate, stroke volume, cardiac output and VO2max among three groups; athletes, sedentary subjects and subjects with mitral valve stenosis. While maximal heart rates were similar, CO was considerably higher in the athletes due to larger stroke volumes. Those with mitral stenosis had the lowest stroke volumes. Athletes had a 62.5% higher VO2 max than sedatory subjects, which paralleled a 60% higher stroke volume. Similar results were found in a study in which sedatory students put on an 8 week aerobic training program demonstrated a 35% increase in stroke volume and a similar increase in cardiac output (McArdle et al 1986). Such research suggests a linear relationship between oxygen consumption and cardiac output over a wide range of submaximal exercise (McArdle et al 1986). Saltin and Strange (1992) again in comparing subjects post bed rest and training found the higher VO2 max post training to be due to differences in cardiac output. Since there is little O2 left to be extracted from venous blood in maximal exercise the main mechanism to increase VO2 max with training is due to increased CO. An estimated 70-85% of the limitation to VO2 max is centrally linked to maximal cardiac output (Basset and Howley 2000). Oxygen Carrying Capacity The hemoglobin concentration in blood alters its O2 carrying capacity. There is again evidence to show that by manipulating this part of the O2 delivery system, VO2max is affected. One example occurs in a low Hb environment, such as anaemia. In this situation there is a linear fall in VO2 max as a function of lower Hb (Lindstedt 1988). The practice of blood doping involves artificially increasing the Hb level by removing, storing and later infusing total red blood cells. This can increase Hb levels by 8-20%. This increases O2 carrying capacity and produces an increase in cardiac output, by increased blood volume. A review of well-designed double blind experiments on blood doping reported VO2 max improvements of 4-9% (McArdle et al 1986, Bassett and Howley 2000). This again strengthens the evidence that increasing O2 delivery improves VO2 max. Periphally Limited VO2max Skeletal Muscle Limitation While the large body evidence presented so far would suggest a central limitation to VO2 max there is research to suggest peripheral factors may also play a role. These mechanisms include peripheral diffusion gradients, mitochondrial enzyme levels and capillary density (Cain 1995, Basset and Howley 2000). Peripheral Diffusion Gradient Some researchers would suggest that while central mechanisms are altered to meet the needs of the peripheral system, it is the peripheral diffusion gradient, which may be the limiting factor. The main resistance to O2 diffusion is at the capillary sarcolemma interface. A study which used canine muscle to examine the effect of experimentally manipulating the peripheral O2 perfusion gradient found a low intracellular PO2 was required relative to blood PO2 to maintain differsion and enhance conductance. When comparing the VO2max in hyperoxic breathing alone and in with the presence of a drug, which enhanced peripheral O2, diffusion found no significant difference between the two. The conclusion drawn was again that it is not the supply of O2 to the muscle rather than the ability of the muscle to conduct O2 that limits VO2max (Grassi 2000). A study by Salin et al (Basset and Howley 2000) compared VO2 max and cycle training. When comparing a trained leg, control leg and 2 legged bicycling VO2 max was found to be 23% higher in the trained compared to the control. They concluded peripheral factors limited VO2 max. They later demonstrated that this experiment was limited in using only small muscle mass as the blood flow to quadriceps was 2.3 times higher than in whole body exercise. The final conclusion drawn was that it was the increased blood flow and resultant O2 delivery which constrained VO2 max and not O2 consumption by the muscle. Richardson (2000) also suggests maximal metabolic rate may be set not by the mitochondrial enzyme rate but by the convective/diffusive components of O2. It was found PO2 was a determination of VO2 max as increased inspired oxygen levels increased intracellular PO2. In hyperoxia the intracellular PO2 was now in excess of mitochondrial capacity indicating cellular metabolism, which was moving towards a change between O2 supply and O2 demand as the VO2 max limiting factor. The previous study by Grassi (2000) would indicate these findings to be due to the increased O2 supply rather than a peripheral one. Mitochondrial Enzyme levels Mitochondria are located within muscle fibres and are the sites of O2 consumption via the electron transport chain. Much research has been performed to examine whether mitochondrial enzyme levels are a limiting factor for VO2 max. Under normal circumstances oxygen uptake is matched by the demand of the mitochondria (Lindstedt et al 1988). Aerobic training causes mitochondria to enlarge and increase in number. Enhanced concentration of rate limiting enzymes also occurs, which improve the muscles capacity for aerobic production of ATP (McArdle et al, 1986). Saltin and Strange (1992) found that even a 220% increase in mitochondrial enzymes only demonstrated a modest VO2 max increase (20-40%). It is argued that the increased mitochondrial enzymes produced by aerobic training have a metabolic role in fat oxidation and to produce less lactate. Therefore the increased enzyme activity appears to be to improve endurance performance rather than increase VO2 max. Capillary Density Training produces an increase in capillary density and this increases the capillary to muscle fibre ratio and improves O2 extraction. This is represented as the difference between the oxygen content of arterial and venous blood (a - v O2 difference). At rest only 5 ml of O2 in blood is extracted from each 20 ml in 100 ml of blood, leaving 75% still bound to haemoglobin. McArdle (1986) found following 8 weeks of training subjects a-v O2 difference was increased by 11% with 85% of O2 extracted from blood during exercise. Saltin and Strange (1992) also show a strong relationship between capillary fibre ratio in vastus lateralis and VO2 max during cycling. It could be suggested this represented improved peripheral factors previously limiting VO2max. It is suggested however that this training effect improves O2 delivery by enhancing mean transit time to maintain or expand O2 extraction (a-v O2 difference) even at high blood flow rates. This again suggests a central O2 delivery limitation not a peripheral one. Conclusion There is undeniable scientific evidence to support the conclusion that it is the ability of the cardiorespiratory system to deliver O2 to the muscles and not the ability of the mitochondria to consume O2 that is the limitation to VO2 max. This relates to healthy subjects performing maximal, large muscle mass exercise (Saltin and Strange 1992; Basset and Howley 2000; Richardson 2000). Basset and Howley (2000) identify maximal cardiac output as the major factor limiting VO2 max during bicycling and running tests. There is no single central limiting factor to VO2 max. Just as O2 delivery involves an integrated pathway, any factor which reduces the delivery of O2 to the mitochondria, will limit VO2 max (Basset and Howley 2000; Richardson 2000). Clinical Implications If indeed the limitation to VO2 max is in the delivery of O2 how can this knowledge be utilised to increase an individual's capacity for aerobic work? It should be noted that endurance is not only limited by VO2 max but also by factors such as lactate threshold and the efficient use of the three energy systems. Aerobic Training Aerobic training was found to improve O2 delivery by increasing stroke volume and thus cardiac output by 50-60% above resting in trained athletes. Improved a-v O2 difference is achieved by an increased mitochondria size and number, increased rate limiting enzymes and capillary density (Basset and Howley 2000). An 8 week training program using large muscle mass could produce a 35% increase in VO2max (McArdle et al 1986) O2 inhalation There was not found to be any ergonomic value in breathing O2 pre or post exercise with regard to improving VO2 max or in increased removal of blood lactate (McArdle et al 1986). Anaemia As Hb levels affect O2 carrying capacity an anaemic state can significantly affect the aerobic capacity of an individual. Early detection and correction is therefore vital. Blood Doping An endurance athlete who won gold at 1976 Montreal Olympics was alleged to have used this illegal technique. While there is conflicting evidence blood doping while generally thought to increase VO2 max by 5-13%, reduced sub maximal HR and blood lactate levels for standard tasks and improved endurance performance at altitude and at sea level. It poses serious side effects however including venous thrombosis and pulmonary embolism via increased platelet viscosity. (McArdle et al 1986) Respiratory and Cardiac Disease Both respiratory and cardiac disease alter O2 supply to working muscle and will alter an individuals ability to work aerobically. Such conditions and those taking medication, which may alter cardiac or respiratory function, must be identified by those prescribing exercise programmes. References Bassett DR and Howley ET (2000) Limiting factors for maximum oxygen uptake and determinants of endurance performance. Medicine and Science in Sports and Exercise 32:70-84. Bergh U, Ekblom B, Astrand P (2000) Maximal oxygen uptake "classical" versus "contemporary" viewpoints. Medicine and Science in Sports and Exercise 32:85-88 Cain SM (1995) Mechanisms which control VO2 near VO2max: an overview. Medicine and Science in Sports and Exercise 27 (1):60-64. Daniels J and Oldridge N (1970) The effects of alternate exposure to altitude and sea level on world class and middle distance runners. Medicine and Science in Sports and Exercise 2:107-112. Grassi B (2000) Skeletal muscle VO2 on-kinetics: set by O2 delivery or by O2 utilization? New insights into an old issue. Medicine and Science in Sports and Exercise 32:108-115. Lindstedt SL, Wells DL, Jones JH, Hopprter H and Thronson HA (1988) Limitations to aerobic performance in mammals: interaction of structure and demand. International Journal of Sports and Medicine 9:210-217. McArdle WD, Katch FI and Katch VL (1986) Exercise Physiology. (2nd ed.). Philadelphia: Lea and Febiger. Powers SK, Lawler J, Dempsey JA, Dodd S and Landry G (1989) Effects of incomplete gas exchange on VO2max. Journal of Applied Physiology 66:2491-2495. Richardson RS (2000) What governs skeletal muscle VO2max? New evidence. Medicine and Science in Sports and Exercise 32:100-107. Richardson RS, Harms CR, Grassi B and Hepple RT (2000) Medicine and Science in Sports and Exercise 32:89-93 Saltin B and Strange S (1992) Maximal oxygen uptake: "old" and "new" arguments for a cardiovascular limitation. Medicine and Science in Sports and Exercise 24:30-37. Wagner PD (1995) Muscle O2 transport and O2 Dependent control of metabolism. Medicine and Science in Sports and Exercise 27 (1):47-53. |
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Jim:
Wow. Nice review article, but where did it come from? Pretty well covers the coventional wisdom. Ken: Yes, we've known that lactate is a great fuel for the muscles, but ya gotta have the oxygen to use it. Remember, it's only produced (in quantity) when the muscle is called upon to produce more work than it can "aerobicaly" with the oxygen supply available. It's all about oxygen delivery. And no, lactate isn't "cleared" rapidly after the cessation of exersize. This was proven to me with lactate testing at a ski clinic. We measured resting lactate, then did a 10K (skiing) time trial, and measured lactate again. (High, as you might guess) We then ate lunch and rested an hour or two, and then rechecked lactate. The lactate was higher than the original resting level. We then went out for a very easy ski, about 40 minutes while keeping our heart rates about 15 BPM less than our "lactate balance point", or lactate threshold. (We knew this from testing days earlier.) We then rechecked lactates, which were lower than before the easy ski. The explaination is that we still had lactate sitting in our cells and in our blood from the all-out time trial, even after resting, and that it was burned more efficiently with our easy ski, making sure that lots of oxygen was available for the muscles to use to burn it. Makes sense? Randy |
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Ken Roberts wrote: There's been some news articles in the last month or so saying that lactic acid is actually a very effective fuel for muscles during endurance performance, and that many previous beliefs that lactic acid is just a waste product, or even a poison, are mistaken. (try a Web search on "lactic acid waste product" or "lactic acid poison") It's tricky for me to sort out, because some of the new biochemistry findings sound a lot like well-established old findings. And because the researchers say that training approaches used by good coaches were on the right track and effective even though though they were based on incorrect biochemistry. So any help I can get in sorting out my confusion is much appreciated. Here's some ideas and claims I'm trying to make sense of -- are they true, or half-true, or misunderstood? (a) The recent biochemical finding seems to be that there is a specific path for the mitochondria in a cell to aerobically "burn" lactic acid -- even if the lactic acid was originally produced by anaerobic respiration elsewhere outside the mitochondria. (My initial response is, "I should hope so. The chemical reactions are well-described in lots of textbooks: Seems like it would be a stupid design if our mitochondria were _not_ able to execute the process using either glucose or lactic acid as a starting point." -- or is there something trickier here that I'm missing?) (b) The key limiting factor on most endurance performance is not oxygen uptake or transport -- it's the amount and effectiveness of mitochondria. So the critical primary goal of athletic training for endurance performance is to build mitochondria. (? presumably then increases in oxygen uptake or transport will soon follow as those increased mitochondria start to demand more oxygen ?) (c) Sometimes even if muscle cells are getting more than enough oxygen, they still use anaerobic respiration and produce lactic acid -- because it puts little or no burden on the limited amount of mitochondria available -- and it's quicker. (? if the lactic acid can be transported away quickly, it could be "burned" aerobicially by other less-critical muscles that have currently under-utillized mitochondria available ?) (d) Short intense interval workouts are helpful stress mainly because they stimulate the muscles to develop more mitochondria. (not because they directly increase oxygen uptake or central cardio-vascular capacity) (e) Lactic acid does not "cause" pain in any simple way. This should be obvious, since lactic acid is cleared quickly after exercise is complete, but the pain and fatigue-feeling often endures much longer. (Unfortunately I have not heard anyone say what else _does_ cause the short-term and long-term pains associated with intense exercise). Thanks for any help in sorting out the confusion. Ken Hi Ken, I just became aware of these articles a few days ago, and after reading a few, my carefully crafted bubble-world of understanding how LT relates to sustainable pace has been shattered. I am busy trying to determine what this information means for me in practice. For bicycle time-trials I have been using my measured LT of 163 HR to pace myself. However, in group start races I often have my HR way above that and even feel good for extended periods at 173 or so. and I se short bursts of 185. Sort of like this second wind some of the articles mentioned. I am very confused. If lactic acid is in the bloodstream and is available for mitochondria to use, is this so that less stressed muscles can use it thus "saving" oxygen for the muscles doing the real work? Is it possible that my apparent increase in tolerance of lactic acid while on a bike between last year and this year is from increased mitochondria in my upper body from skiing? As I understand things, LSD type training encourages mitochondria development. Is this the case? So a training program would include LSD to develop mitochondria for the purpose of being able to make use of lactic acid, and intervals would be for the purpose of increasign the pump-volume, and long above LT intervals would be for th epurpose of accostoming the body to using lactic acid. Doe sthis make sense? Joseph |
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Joseph wrote
If lactic acid is in the bloodstream and is available for mitochondria to use, is this so that less stressed muscles can use it thus "saving" oxygen for the muscles doing the real work? I think that's part of the debate. It gets more complicated because different types of muscle fibers are specialized for more or less emphasis on mitochondria. So the recent 3rd edition of Bicycling Science by D.G.Wilson speculates on page 61 that one purpose of short bursts of standing pedaling on a bicycle might help by mobilizing stored glycogen in FG ("fast-twitch") fibers and send the resulting lactic acid to fuel glycogen-depleted SO ("slow-twitch") fibers. The new thinking is that one of the positive advantages of lactic acid as fuel is that it's easy to move it around (unlike glycogen). a training program would include LSD to develop mitochondria for the purpose of being able to make use of lactic acid, ... I think everybody agrees that Long Slow Distance is good for building mitochondria (and other critical peripherial infrastructure). ... and intervals would be for the purpose of increasing the pump-volume That sounds like the old-school interpretation of short-interval workouts. An emerging interpretation is that the short intervals _also_ build mitochondria. But I think both the old and new schools agree that short-interval workouts for peaking are good (provided your body is prepared to handle them without damage). I think the new school is saying something like: "short-interval training works because it builds up mitochondria, and the oxygen demand from those increased mitochondria stimulates central cardio-vascular adaptations like increased stroke volume." So it's partly an argument about whether the Central adaptation is primary + direct versus secondary + indirect. As long as you do the workout, does it matter which theory is correct? To me it matters, because if I believed only the old-school theory, I would not do any short-interval workouts (like 4 minutes and less) -- because I don't have any skiing or bicycling goals that require for sprints or peak-VO2max performance. Ken |
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Lots of helpful findings in that article Jim posted titled "The Limitation
to VO2max is Central". But my main concern is not with VO2max, it's with endurance performance. The article seems to be aware of the difference, and even says, "the increased [mitochondrial] enzyme activity appears to be to improve endurance performance rather than increase VO2max". Sounds like agreement with the "new school" interpretation of endurance performance. Jim wrote I am not sure the research upholds your statement that short intense exercise develops more mithochondria It's not my statement. I just found it at the end of a May 16 article on www.nytimes.com. I was actually surprised by the claim by a biochemist that short-interval workouts for "peak" training would result in additional increase in my mitochondria mass. Maybe it depends on what is meant by "short intense exercise". I was thinking of work intervals of less than 4 minutes. Like some coaches advocate doing 4 hard work intervals of 3:00 minutes each. Or I've seen suggested for deleveloping Central CV capacity doing short work intervals in the range of 40 to 80 seconds, with shorter rests in between. If those are not effective for longer endurance performance like a 50km ski race, please let me know, and I'll stop doing them. Ken |
#7
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Ken Roberts wrote: Joseph wrote If lactic acid is in the bloodstream and is available for mitochondria to use, is this so that less stressed muscles can use it thus "saving" oxygen for the muscles doing the real work? I think that's part of the debate. It gets more complicated because different types of muscle fibers are specialized for more or less emphasis on mitochondria. So the recent 3rd edition of Bicycling Science by D.G.Wilson speculates on page 61 that one purpose of short bursts of standing pedaling on a bicycle might help by mobilizing stored glycogen in FG ("fast-twitch") fibers and send the resulting lactic acid to fuel glycogen-depleted SO ("slow-twitch") fibers. The new thinking is that one= of the positive advantages of lactic acid as fuel is that it's easy to move = it around (unlike glycogen). That is a very interesting theory. If true, it may help me a great deal. Often when I am struggling to not get dropped on a hill (on a bike or skis) I concentrate all my effort on as smooth and "regular" as possible power transmission. Remain seated (cycling) and try to be as efficient as possible in the hopes that I won't loose contact before the crest. But maybe what I should do is a last-ditch effort monster standing stomp to get the juices flowing, which I do not do now for fear of blowing up. ... and intervals would be for the purpose of increasing the pump-volume That sounds like the old-school interpretation of short-interval workouts. An emerging interpretation is that the short intervals _also_ build mitochondria. But I think both the old and new schools agree that short-interval workou= ts for peaking are good (provided your body is prepared to handle them witho= ut damage). I think the new school is saying something like: "short-interval training works because it builds up mitochondria, and the oxygen demand from those increased mitochondria stimulates central cardio-vascular adaptations like increased stroke volume." So it's partly= an argument about whether the Central adaptation is primary + direct versus secondary + indirect. As long as you do the workout, does it matter which theory is correct? To me it matters, because if I believed only the old-school theory, I wou= ld not do any short-interval workouts (like 4 minutes and less) -- because I don't have any skiing or bicycling goals that require for sprints or peak-VO2max performance. Knowing which theory it is matters for me too for precisely the same reason. 99% of my interest is in raising my sustainable sub-maximal power output. While I do enjoy sprinting, I have no plans to train specifically for doing so. My body is by nature suited to sprinting such that I am automatically pretty good and only people who train specifically for sprints are able to (occasionaly) beat me (speaking of course about people with a similar level of conditioning). But what really interests me is things like Birkebeinerrennet, Vassal=F8pet, and similar yet longer cycling events. An ideal training plan for me in terms of what would be fun and doable would be 80% LSD at 75% of LT and 20% at 105% of LT. Dropping structured intervals would be nice. Not because I want to avoid the discomfort, but more because it is a hassle to deal wth the logistsics of finding a suitable place, timing the intervals, timing the recovery, etc. When I ride or ski, I just want to get into a groove. Joseph |
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Joseph wrote
when I am struggling to not get dropped on a hill I concentrate all my effort on as smooth and "regular" as possible power transmission. Remain seated (cycling) ... I think the real lesson here is the biochemistry and physical transport is so complicated, and there's so many strategy mixes available to our body, that there's little point in trying to calculate some optimal theory of how to climb hills. Better to actually try out some personal time trials using different mixes of techniques and turnover frequencies and see which mixes are obviously better or obviously worse in objective timing results. try to be as efficient as possible If your objective is to avoid using extra energy, a simpler strategy is to skip all the pedaling, and stay home and "remain seated" while just watching TV. Is it possible that my apparent increase in tolerance of lactic acid while on a bike between last year and this year is from increased mitochondria in my upper body from skiing? Not my first guess. I'd guess that the most critical factor in operating successfully at higher levels of lactic acid production is _transport_ : moving the excess lactic acid quickly out of the muscle fibers that are producing it. Which points to the importance of building capillary density. (Which contradicts the focus on mitochondria in recent announcements this biochemist -- but does explain why altitude training and EPO are so effective for endurance performance, by increasing the transport capacity of capillaries). Of course it couldn't hurt to have more mitochondria available elsewhere in the body -- I'm just not sure if there's a shortage of them, or if you can mobilize them to "burn" lactic acid when there's nothing additional useful for them to do with it. But then maybe that's the point of some of those "wasted" motions which the second-tier regional "experts" are forever pointing out as flaws in the technique of the world champions -- to mobilize otherwise irrelevant mitochondria to "clear" excess lactic acid. I haven't heard whether elite endurance athletes develop increased capability in the _liver_ to recycle lactic acid (back into glucose). It's rather inefficient from an energy utilization perspective -- but so what, that's what energy drinks are for. For bicycle time-trials I have been using my measured LT of 163 HR to pace myself. However, in group start races I often have my HR way above that and even feel good for extended periods at 173 I'd guess that relying too much on heart rate as a measure of what's happening in your muscle fibers and peripheral transport gradients is going to yield all kinds of spurious "phenomena" that need to be explained. There's some web page where Stephen Seiler lists at least five different ways that heart rate shows spurious observations that have no basis in the what's happening with effective muscular propulsion. Ken |
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Reading this as far as I can comprehend, rings a bell with me.
In mountainbiking, there's this thing called singlespeeding. I'm honoured to be 2003 and 2005 Dutch Champ with that. On some types of courses. With short climbs and long flats, singlespeeds are stunningly fast. And as the rider, you get the impression you're just doing what's required to keep going, or not to be dropped. With just one gear ratio, climbs are hard (low rpm, lots of anaerobic strangth required), flats are hard (spinning out, not able to get power down). Climbs you attack to get them over with, and hopefully not be forced to walk. Flats, you spins till it hurts, and coast (recover) till you slow back down to the comfort zone, and spin back up. After a SS race I'm much much much more tired than with gears (forced to give my all, all the time), but specific parts of courses it's just a really FAST way to get cross country. This whole new look at lactic acid might offer answers WHY singlespeeds are fast. Singlespeeders even win races overall, and it's not even rare anymore. When I first had a lactate test, I was just getting into serious cycling training. I was a rookie. I had a lactate peak of 3.3 or so, around 165-170bpm. LT was 182-185 back then, and I recorded 1.1 in that zone. So near LT heartrate, my body actually cleaned up the built up lactate somehow. When I trained by myself, the 165-170 zone was NOT fun. Hurt like hell. It was an undertrained zone for me, so I worked on it with 10-15min intervals. If I'd push on to higher heartrates, it would be like a relief "ah, that's better!". Before I got to train seriously, I did weekly sunday rides over marked courses, 40-60km most of the time. Flat out. Mostly flat. strong competition, so I really had to dig deep. In those days I could get that famous rush of being in pain, but loving it, going a notch faster still. I lost that feeling since. And I lost the speeds I could generate. But now I can climb steeps hills, back then I had to use the smallest gear to get up a fly-over, while my weight never changed much. But especially, for fun I often trained on 5km time trails. A 620m course with 2 corners that forced me to lift off just a bit. I kept attacking my own best times, and got good at it. Immense pain, obviously. My trainer figured that way of training made me so fast, and so clean of lactate at the LT heartrate. |
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snip!
If you train lactate training then you also adapt to this via enzymes and musclefiber composition etc with all the pro and cons that follows. One bad thing is the limited storage of carbohydrates. What are these pros and cons? And what do you mean by lactate training? Joseph |
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good resort for christmas/new year | Dino | North American Ski Resorts | 0 | July 13th 03 06:32 AM |