|Training in general||cyclomoteur|
Dec 5, 2001 7:24 PM
|Have you guys went with killing intervals in this winter or still sticking to a basic training ?
Let's say basic training is HR<75-80%
Dec 6, 2001 6:26 AM
|I've started my second base cycle (I start racing in the 2nd week of March w/ training races in February) and therefore have included Tempo work for this 4 week block. I'm still simply building my aerobic engine, strength, and leg speed. During the next 4wk training block Tempo work continues and also introduces cruise intervals which are AT training (but still essentially aerobic). Other people who have their first peak planned later in the season are probably just starting structured base training. My first peak cycle is planned for April, hence the early start.
Doing AT/over AT work will make you stronger if you start doing them now, but being strong in January is pretty useless. It's a long season (I race from March to October). Doing this type of work on a substandard aerobic foundation actually limits your top end gains. It's like building the roof of a house first, then trying to pour the foundation.
The longer/deeper your base period, the higher your peak later in the season. More importantly, working at lower intensity level trains your body to use fat as an energy source. When your body becomes adept at doing this you'll have more glycogen in the tank late in races (because you're burning primarily fat) when you need to go anaerobic or put in big efforts (break aways, bridging gaps etc.).
People that ride hard year round tend to plateau and not get significantly stronger because they haven't build solid/deep/well-rounded fitness.
Check out either Joe Friel's book or Ed Burke's Serious Cycling - they should be very helpful to you.
Of course, if hammering year round is what you want to do, have at it. Keep in mind though, that pros are piling on easy miles right now. Every coach, physiologist, and other elite endurance athletes WITHOUT EXCEPTION practice periodization in their training plans.
If I recall correctly you're fairly young (17 I think?). Now is a good time for you to build good training habits to build a solid future as a racer/cyclist. Keep an open mind and try to learn as much as you can. Good Luck.
|Bobo, You've Done Your Homework. Good job. (nm)||Jon|
Dec 6, 2001 7:02 AM
|Bobo, You've Done Your Homework. Good job. (nm)||Zipper|
Dec 6, 2001 7:37 AM
|I concur. You know there are guys out there right now hammering away. Your friends are doing it, my friends are doing it. Be disciplined and stay the course. The guys I know that were interval training this time of the year last year were good in the early season races, but couldn't finish the season and missed out on some great races.|
|Moderately long response||jstonebarger|
Dec 6, 2001 10:11 AM
|"working at lower intensity level trains your body to use fat as an energy source"
This is true, but moderate to high intensity work trains your body faster and raises your VO2max to boot.
"pros are piling on easy miles right now"
I'm not a pro. Is the original poster? If he rides 20,000 miles this year some of them had better be easy, I suppose. Otherwise, I think his time could be better spent.
"Every coach, physiologist, and other elite endurance athletes WITHOUT EXCEPTION practice periodization in their training plans"
This may be true, but your implication is not. Granted, anyone who lives in a northern climate will change their training while there's snow on the ground: periodization. We all need easy days and days off to recover: periodization. Most of us only race six months a year: periodization. This doesn't mean we need to log thousands of easy miles to build a base.
The best arguement Burke makes in "Serious Cycling" for easy miles: Your but will thank you later on!
|Moderately long response||Kyle|
Dec 6, 2001 2:43 PM
|"This is true, but moderate to high intensity work trains your body faster and raises your VO2max to boot."
This is a question of volume vs. intensity--you can't effectively substitute one for the other. In a world with no such thing as overtraining and fatigue, we would do daily high volume/high intensity workouts. In the real world, we have to back off on intensity to increase volume (though a 3-4 hr ride in the 'aerobic zone' isn't all that easy IMHO.) Small off season declines in VO2 can be easily made up in the pre/early season with intervals.
"This may be true, but your implication is not. Granted, anyone who lives in a northern climate will change their training while there's snow on the ground: periodization. We all need easy days and days off to recover: periodization. Most of us only race six months a year: periodization. This doesn't mean we need to log thousands of easy miles to build a base."
The human body cannot be in top shape at all times, and it's adaptation to stress tends to level out after a time. Periodization makes a great deal of sense for creating successively higher peaks over numerous seasons--not just because weather and race schedules dictate it. If periodization was just a convienience, it seems that pro riders would simply do the same workout week in and week out, spending half the year in Europe and half in Australia.
The best arguement Burke makes in "Serious Cycling" for easy miles: Your but will thank you later on!
I don't understand this statement. Because of the long periods on the bike and the fact that less weight is being distributed to your feet, this kind of training is harder on your tail than anything.
|Moderately long response||jstonebarger|
Dec 7, 2001 7:21 AM
|High volume/low intensity training is not an effective way to train: it makes injury much more likely and trains us to go slow (specificity).
Periodization comes in many shapes and sizes, and in itself makes no arguement for low intensity work.
Burn out is a real threat to any athlete. Taking a break, whether its a day off a week or a month off each fall, provides needed rest for both body and mind. Then, when we start training again, jumping too hard too fast makes injury likely (especially with high-volume training). If this all results in a familiar yearly pattern (convenient for most due to weather) let's take it for what it is and not glorify the simplistic analogy of a "base" for future training.
I don't understand Burke's point either. (Obviously he thinks we'll adapt to saddle pressure with time.) My point is that there aren't a lot of solid arguments for low-intensity "base" training.
|Can you quantify moderate to high intensity?||Pack Meat|
Dec 7, 2001 9:31 AM
|Try not confuse base training with easy, it's just a different kind of difficult. The best explaination that I've heard for base training at less than high intensity relates to the development of capillaries deep into the muscles. The theory is, and yes I believe it is just a theory but it makes sense, that working at levels around 75 to 80% of max HR encourages growth of the fine capillaries in the muscles. These small blood vessels are easily damaged by high intensity work so to accomplish growth is this system you can't go to hard. Increased cap. density increases VO2 max with greater delivery of O2 to the muscles which explains why proponents of base training state that a solid base increases the duration and level of peaks in the season.
BAse training is a good time to wor on other things such as pedaling technique that will make you faster as well. Base training is not simply riding slowly.
Good question from the original poster. Knowledge is power.
Share the Road.
|Can you quantify moderate to high intensity?||jstonebarger|
Dec 7, 2001 10:22 AM
|Granted, the off season is a great time to work on skills neglected during the season (I know I rarely get in a ride longer than 60 miles before racing ends). But capillarie growth, and the resulting rise in VO2max, is greatest after highly intense work, not base miles.
There are some advantages to logging big miles--weight control and more efficient fat metabalism--and any rider will have to moderate their work intensity so as to keep the pace for 2-3 hours or more. But those base miles won't raise VO2max. Quite the opposite: endurance training tends to detrain speed and power.
|Some confusion here (longish)...||Kyle|
Dec 7, 2001 1:16 PM
|Capillary growth (in number, not size) does not relate in any meaningul way to VO2max. VO2 is essentially an adaptation of the heart (ie increased blood volume, ventricular hypertrophy and perhaps better diastolic filling due to the resulting slower HR.) This is a fairly quick adaptation that seems to respond best to 2min+ efforts between 90-95% of maxHR. These are usually done in intervals to increase total volume and not because intervals have any real magic (ignoring for a moment the possibiliy of improved aterial/veinous stretching.)
Lactate Threshold results from the skeletal muscles adapting to endurance work--primarily by increasing the number of capillaries feeding the muscle fibers O2, and increasing the number and size of mitochondria which allow for improved fat metabolism. These adaptation will allow for a higher percentage of maximum power output to be maintained with less lactate resulting.
The size of your endurance engine can be expressed as:
VO2max X LT (as a % of VO2max)
An example of a very fast biker would be 80 x .9=72. An example of a very mediocre rider (me) might be 58*.83=48. Unfortunately, a big difference...
So now the question we've been debating--what's the best way to improve muscular endurance (and therefore LT.) IMHO, there are different answers for different people. It seems that someone with an 80/20 fast to slow twitch fiber makeup would have different training needs than a person with the opposite makeup.
Overall, though, hard efforts can have the effect of frying fast twitch muscle fibers and creating a great deal of blood lactate, thus making us feel 'burnt' after a relatively short workout that actually has barely even stressed our slow twitch muscles (which are difficult to fatigue.) Therefore, there might be some benefit to going longer at a more moderate pace. Fast twitch fibers might hardly be stressed at this level (they are recruited last) but slow twitch will get a serious workout (maybe.)
There is also the possibility of switching type IIb fibers to more fatigue resistant IIa fibers--something that would probably take long easy efforts (perhaps because as you burn out slow twitch fibers, fast twitch fibers must adapt to endurance work.) Studies have shown that elite endurance athletes have almost no IIb fibers (though there may be a chicken and the egg problem with that argument.) This is perhaps the 'detraining of speed and power' you were talking about--and the reason most sprinters climb poorly.
So what effort level? Certainly not VO2 intervals all the time--there's no reason to maintain a peak VO2 in the offseason, and this kind of training is very stressful.
So the question is: Aerobic zone for 3hrs, or Tempo for an hour?
Hard to say--lots of factors at work including genetics, suseptability to overtraining, etc. The answer is probably a mix of both but I guess you just have to figure out what works for you.
|ummm, right.... yea, what he said||Pack Meat|
Dec 7, 2001 2:30 PM
|I think that gave me a better understanding than what I had before. What's your backgound, md of some sort or phd?
Share the Road.
|Anal retentive training geek. w/no education (nm)||Kyle|
Dec 8, 2001 7:40 AM
|Peripheral Adaptations Also Affect VO2 max||Jon|
Dec 8, 2001 6:49 PM
Not to detract from your central point, but central limiters are not the only factors governing VO2max.
You not only have to have a well developed pump and transport system to achieve high aerobic
capacity, but the ability of the cells to oxidize glucose. So mitochondrial size and density as well
as aerobic enzyme production are equally important. Some workouts are theorized to specifically
develop these faculties: moderate aerobic endurance workouts, tempo work, as well as high
intensity long sprint intervals. The latter workouts in one study produced dramatic results in 40K time
trial performance, due the researchers thought to their stimulative effects on aerobic enzyme production.
|I'd argue that it depends...||Kyle|
Dec 8, 2001 9:21 PM
|You're right in the instance of a person who is really out of shape but has a naturally high VO2 (and thus simply wouldn't have the skeletal muscle in place to draw all that O2), or a sport in which O2 consumption isn't super high (best example: wheelchair athletes.)
The other side of the spectrum would be a fit XC skier, who brings in so many muscle groups that demand will always exceed supply.
Interestingly, road biking is kind of on the fence between these two. I'm open to the suggestion that a very efficient, very genetically gifted, road cyclist who is not in top condition could not reach VO2 max while seated.
Haven't read the study you cited--the suggestion that oxidative enzyme production is independent of mitochondrial size/density sounds interesting though. Good papers are hard to find in this area--samples are always really small, time periods are always short, and it seems like they always use non-athletes who would benefit from any kind of training...
|I'd argue that it depends...||Jon|
Dec 9, 2001 10:52 AM
|We may have a small misunderstanding going on here. I was referring specifically to the trainability |
of VO2 max, whatever one's genetic ceiling, not the ability of a person to achieve VO2 max during
a workout. And obviously, measured VO2 max is going to increase as one's ability to utilize oxygen in
the production of ATP is increased, hence the importance of peripheral conditioning achieved during
base and build periods. There have been a few studies done in which vVO2 max as well as time
to exhaustion increased in the absence of measured increases in cardiac output. The first, cited
by Owen Anderson, was a rat experiment at Berkeley was back in the eighties. The rats, as a result
of interval training, dramatically increased their running speeds and time at VO2 max without an apparent
change in central capacity. It later dawned on the researchers that the training had dramatically
increased enzyme production, thus allowing the rats to utilize unused central aerobic potential.
Veronique Billat has taken this idea further in her workout designs having runners do repeats
at vVO2 max. Anderson argues that these workouts improve VO2 max, lactate threshold, running
economy, and vVO2 max, sort of a quadruple whammy. The upshot is that these physiological
measurements are a result of a complex of physiological processes and abilities and cannot be
so neatly compartmentalized as we sometimes think. This is a somewhat academic point and should
not detract from the original points made in this thread by yourself and some others.
|Way too boring for anyone but Jon to read...||Kyle|
Dec 9, 2001 4:36 PM
|I know we're getting bogged down in minutiae here, but I find your point interesting.
It makes perfect sense to me that interval training would increase running speeds and time at VO2 max by increasing oxidative capacity in the skeletal muscles of rats (and perhaps running economy--I don't know, I used to live in Baltimore and even the fat rats seemed pretty quick.)
But is the skeletal muscles' aerobic efficiency a contributor to VO2max? The fact that the best XC skiers test slightly higher than the best bikers suggests that there may be is some small component of VO2 that is affected by exercise efficiency and is therefore muscle related (though body position might be a contributor here too.)
Think of the test: You ride 'til you drop while a mask measures the amount of O2 you consume. The test ends when your O2 consumption stops compensating for increased workload. But why does it stop responding? Because your muscles have reached their oxidative capacity and therefore don't need further O2 delivered? Because your cardio system has reached it's capacity for delivering oxygenated blood? Or, as you say, is it a little of both?
Another interesting question is why skeletal muscle adaptations are long term, whereas significant improvements in VO2 are hard to come by after only a few months of hard training. Also, wouldn't it be true that in a highly efficient sport (back to skiing, here) that the oxidative efficiency of the muscles would be pretty much irrelevant, due to the enormous O2 demands of nearly every muscle working simultaniously at capacity?
Having said all that, I'm a big enough man to that my statement was overly cut and dried. You're almost certainly right that muscular adaptations play some role in VO2. In my defense, though, I think we're talking about a very small role in untrained people and an almost immeasurably small role in well trained athletes...
|Way too boring for anyone but Jon to read...||Jon|
Dec 9, 2001 6:37 PM
|Before we drive everyone with a shred of sanity off the board, this will be my last contribution to this |
discussion! I would guess that the role of peripheral adaptation in trained people would be very
small, whereas it might be more significant in the untrained. I got into this discussion with my
course instructor in ex. phys. He thought that there is a peripheral contribution, simply from a
deductive viewpoint. The guy that coaches in a club I belong to is a doctoral candidate in
exercise physiology, and when we resume our Spring group torture sessions with him I'm
going to pop the question and see what he says.
|My last post on this, too. I swear...||Kyle|
Dec 10, 2001 9:20 AM
|Something we haven't considered in our respective arguments is what comes between the heart and the muscles--blood.
It seems that raising hematocrit levels would increase VO2max without increased cardiac output. It's unlikely that this was the reason for improvements in the rat study you cited (due to the effects of athletic induced anemia) but it is still a concept that has interesting implications to the 02 delivery vs 02 consumption debate.
Anyway, no real point here, other than it's something you might want to bring up when you talk to your friends.
Dec 10, 2001 9:28 AM
|Do you have any references for high level endurance athletes having very little or no IIb (IIx) fibers? I've kind of been looking for this info, I would expect given the adaptive nature of fast-twitch fibers that this could or would be the case.|
Dec 10, 2001 12:12 PM
|I've never actually read a study that set out to prove this, I've only seen mentions of the phenomenon in papers focusing on another subject.
The problem here is cause/effect. Do elite athletes lose their IIB fibers because of training, or are elite athletes born with no IIB fibers, and therefore become elite? As far as I know, there is no indesputable evidence either way--though that doesn't necessarily mean its not out there--I may have just missed it.
I think the popular theory now is that IIa&b fibers are convertable with training. I'm sure there are people out there who still disagree with this, though.
|Debunking the theory...||Wayne|
Dec 7, 2001 10:53 AM
|I believe Eddy B. (the cycling coach) put forth this theory that you had to go easy with lots of miles to stimulate capillary formation and that lactic acid would destroy them if you went too hard. On another newsgroup, Dr. Coogan, an exercise physiologist, said this was total bunk, and that acually the high pressures on capillary walls associated with hard efforts has been shown to be a stimulus for increased capillary formation. (I hope I have that right and didn't misrepresent anyone!)
I can think of several reasons for a base phase of high volume (or at least moderate volume)/relatively low intensity work:
1) Mentally it is not very demanding to ride easy (although it may be boring), if you figure there is only so much water in the well, you need to reserve that water for the season when your going to need alot of drive and motivation for hard training and racing.
2) Much of the stimulus for adaptation to endurance training is probably provided by just the easy riding (sure it's not going to put you in tip-top shape but it will stimulate your body to adapt without wearing you out mentally or physically.)
3) The adaptations to the hard efforts are just the icing on the cake and necessary for peak fitness but come at the price of mental fatigue and possible injury.
4) It's good for fat burning, the longer you go (within a workout) at a relatively low intensity, the greater % of your ATP is being provided by oxidation of fats rather than glucose. I'm not sure if this means you will burn more fat at higher intensities but at least you're getting rid of your fat stores rather than your glycogen.
|injury and fat||jstonebarger|
Dec 7, 2001 11:20 AM
|You're much more likely to injure yourself with high mileage than with high intensity. Much more likely. (Discounting crashes and problems from bad fit, almost all of cyclists injuries are "overuse injuries.")
While it's true that you burn a higher percentage of fat during low-intensity work, you burn fewer calories overall so you lose less weight. Also, why would your body ever learn to store more glycogen & burn fat better if you never deplete your glycogen stores to begin with?
|injury and fat||allervite|
Dec 7, 2001 4:36 PM
|Overuse is a relative term. Both volume and intensity can injure you no doubt, but all of my "Overuse injuries" came from intense efforts i.e. a hill or long sprint. A five mile hill is a long hill, but no serious cyclist would consider that a long ride! You would have to ride a long ways with a heart rate of 160 bpm to get an overuse injury. I once rode from sun-up to sun-down and suffered no overuse injuries. I have suffered "Overuse injuries" on hard short rides of about 20-30 miles more times than I would have liked. I have never hurt myself on a casual century.
You burn a higher percentage of fat compared to glycogen at lower intensities. That is fact no matter who you are. That is why at lower intensities you teach your body to use fat as a fuel.
At high intensities you are burning no fat. That is until you bonk. At this point your glycogen levels are so low that your brain tells your body "No more intensity". Now your body will switch to fat and you will be physically unable to maintain any intense effort.
If you take an untrained sedentary person and put him on a high volume low intensity plan, he will become fit slower than if you put him on a low volume high intensity plan. However, if you put him on a high intensity low volume plan he will not get as fit as he would if you put him on a low intensity high volume plan and then switched him to a high intensity low volume plan.
|injury and fat||Wayne|
Dec 8, 2001 7:34 AM
|You're taking a too literal definition of overuse. It's really a term used to distinguish a class of injuries such as tendinitis, bursitis etc. from more acute traumatic type injuries. In my experience, overuse injuries are almost always associated with high forces/intensities more so than volume (not that this isn't a factor) and even more so are associated with a relatively dramatic increases in intensity (volume) over what your body is adapted to. This is also one of the arugments for a base period of low intensity work: that it allows your muscular system to adapt to the cycling motion without the really high stresses of high-intensity work. I've treated plenty of weightlifters with tendinitis who maybe do 50 or so reps of an exercise a week and still have the problem, which doesn't even begin to compare to the 10's if not 100 of thousands of reps a cyclist experiences every week.
I totally agree with you about the total calories burnt, but at high intensities (even moderate intensities like a tempo or hard aerobice pace) most of your calories are coming from glycogen and or intra muscular fats (as opposed to free-fatty acids from adipose tissue) at threshold you're almost exclusively burning glucose/glycogen. Also at low intensities, say < 65% VO2 max, the longer you go the greater the percentage of fat you burn for energy and the greater the percentage of fat that is Free fatty acids rather than Intramuscular fat becomes. I would think this is what your looking to get rid of and the off-season/base period seems the time to do this. It just seems like to me there are some good arguements for including a high or mod volume of low intensity work early in the season, there is plenty of time to allow for adaptations to the high intensity glycogen depleting stuff as the season approaches and doing it early carries too much of a risk of burn-out by the time the season gets in full swing.
|re: Training in general||Dream plus|
Dec 7, 2001 5:08 AM
|It all depends on whether you want to adopt a training program that specifies this type of periodization or not. If you choose to, then you have to trust and believe that it's right or it won't work.
In my experience there are plenty of guys who hammer year round who are faster than I am. Some of these guys don't really do structured training at all - just fast group rides several times a week. For me, I know I would not hold up to well doing this but for them it seems to be OK.
Some people enjoy the planning and structure that comes from a periodized training program. I think that's part of it. The other part for me is just when I'm sick of what I'm doing, I get to introduce something new. I also feel that I can train effectively with a plan, mostly on my own and on my own schedule, and recovery is part of it. Do what you think will work for you. If your young enough, you can experiment a little. If you are talented and fast enough you can get away with a lot of mistakes. If you're serious, get a coach.
Good luck. Mike
|My 2 Cents...||Wayne|
Dec 7, 2001 6:10 AM
|Dream says, "In my experience there are plenty of guys who hammer year round who are faster than I am." This is just not good reasoning, you don't know if they are faster than you because of their training or inspite of it or if their training method is irrelevant to them being faster than you. I would argue your talent (genetics, development, etc.) is in all probability the largest determinant of your ultimate success in cycling (or any sport for that matter).
The question is, how do you maximize whatever talent you have through training, diet, etc.?
I'm only aware of 2 major endurance training ideas that account for the increase in human performance (think of running world records since these control for technology advances and environmental conditions so much better than cycling) over the last half century. They are interval training and periodization, I believe the introduction of these training methods both saw more dramatic drops in world record running times then were previously typical. Interestingly I believe there had been a fairly linear small steady drop in world record running times (since the mid '70s when periodization became widespread?) until the introduction of EPO (late '80's/ early 90's) and since then there has been a non-linear relatively dramatic drop in times. Interestingly many of them set by Kenyans who typically live in Germany or Italy and are trained by doctors.
So, in my opinion
1) if your not using periodization and interval training you're probably selling yourself short.
2) That being said, and assuming everyone is out riding their bikes and training hard without overdoing it, incorporating proper training methods can probably make the difference between being a cat. 4 and cat. 3, or your local cat. 2 bad-ass, and maybe a national level cat. 1, but it ain't going to turn a good cat. 3 into Lance Armstrong.
|My 2 Cents...||Jon|
Dec 7, 2001 10:37 AM
|Let me add a couple more comments. First, there is no hard and fast scientific evidence to back |
up periodization. However, when Tudor Bompa refined the Russians' methods and introduced them to the
Romanian athletes, world records started to fall. Second, the rule of specificity indicates that the body
adapts to specific stressors, then plateaus. When these plateaus occur, the training stimulus or
stressor needs to be changed. Periodization facilitates this process. Third, there does seem to
occur over time--and it's different for different athletes--a certain neurohormonal fatigue from intense
interval training and racing. These central systems need to rest and rejuvenate from time to time. And
fourth, there is the element of psychological burnout and fatigue from sustained, intense training and
racing. Enough said. Do as you please and observe the effects!
|Rest vs. low-intensity||jstonebarger|
Dec 7, 2001 11:27 AM
|Is there some reason that rest would be less likely to overcome fatique than low-intensity mileage would?
I have no problem with periodization. What I don't understand is why it is now thought of as synonomous with high volume/low intensity training.
|Rest vs. low-intensity||Wayne|
Dec 8, 2001 7:07 AM
|I don't know that periodization is necessarily thought of as synomonous with high volume/low intensity training but I think "base work" usually is. Maybe only in the sense that a yearly periodization program usually has some component of high volume/low intensity work.
Rest probably is better to overcome fatigue than low-intensity mileage but what stimulus does it provide for endurance adaptation?
If your looking at your whole year, not riding for the month of January will not only not provide any stimulus but you will detrain. Whereas if you just went out and rode consistently easy for that month you would detrain less, probably still provide some stimulus for muscular adaptations (increase mitochondria, aerobic enzymes, capillarization, etc.), burn more fat than sitting on your ass, and not really stress the mind or body all that much leaving you in a much better position to start working in intensity in March or whenever.
If you mean during a given training week is rest better than an easy spin, I don't know if anyone has ever looked at that. Probably depends on your level fitness, experience, how much training you've been doing etc.
|* new questions : rest - muscular fibers - capillar vessels and VO2||cyclomoteur|
Dec 7, 2001 3:46 PM
|3 part :
1-Does crazy intervals (15/15 (15sec sprint - 15sec relax) until you can't turn the crank) need more rest then normal base training (75-80%HR)?
2-Could somebody explains me simply what are the types of fibres and whats their job ? (link or book would be appreciated)!
3-Are you guys sure that more small capillar vessels are built when doing base training then killing intervals, and does it REALLY improves VO2?
|* new questions : rest - muscular fibers - capillar vessels and||peloton|
Dec 8, 2001 1:49 PM
|1) Yes- When you do intervals, you break down more of the body and that requires more rest. This means both sleep sort of rest, and more rest in between your next set of intensity. Remember that rest IS training. You don't recover to get stronger without it.
2) You have different types of muscle fibers in your body to accomplish different things. They can be broken down simply by what is referred to as 'twitch' times. A twitch is how fast the muscle fiber contracts and how forcefully. You have probably heard people refer to slow twitch or fast twitch muscle fiber. Slow twitch muscle fiber has greater oxidative capacity. There is more mitochondria, and aerobic enzymes, but they don't develop as much force as fast twitch fibers. They are frequently referred to as type I muscle fibers. They have the ability to contract more slowly, but more steadily over time. Then you have the fast twitch muscle fibers, of which there are two kinds, type IIa and IIb (IIb is also called IIx if you were doing comparison based on myosin heavy chains. More myosin is faster).Fast twitch muscle fibers give you the ability to move very quickly, but not for as long. Fast twitch muscle fibers like these can produce great force, and have more anerobic capacity, enzymes, and things like creatine phosphate. IIa is your classic fast twitch muscle fiber. Pure speed, and highly glycotic. Type IIb is also fast twitch, but more oxidative. Type IIb can be trained to have greater oxidative capacities and therefore greater endurance. IIa will not adapt to endurance training like this.
3) Base training is going to build up your capillary and microvascular systems. You have roughly 500-900 capillaries per square millimeter in your body. There are a lot of factors on this too. Genetics, cross-sectional muscle size, and training will all affect it. Capillary to fiber ratio has been shown to be improved over a 12 week endurance training program by from 5-20%. This is untrained people though, so athletes will have less of a difference. Building up your capillarity will have an effect on your aerobic ablilities, but it is only one piece of a large puzzle.
Dec 9, 2001 7:36 AM
|Good questions man.||Pack Meat|
Dec 10, 2001 8:44 AM
|I learned a lot.|
|Fibre type confusion!||Wayne|
Dec 10, 2001 10:03 AM
|I'll take this oppurtunity to do a little self-promotion. We recently did a review article for the journal Physical Therapy (v. 81, pps. 1810-1816, 2001) on muscle fibre types. You can get to this online through the apta.org website if you care to. Basically alot of confusion arises over fiber types because there are several different ways to type a fiber and to make it a little more confusing a couple of methods don't always agree with one another. So fibers that are the same type under one method can be different using another method. Further adding to the confusion, what used to be called type IIb (the faster of the 2 fast twitch fiber-types) is now properly called IIx, we have the genes for IIb fibers but do not express them (only small mammals do). True (small mammal) IIb fibers are even faster than IIx fibers, this has some interesting implications for human athletic performance (and cheating) if someone figures out how to turn-on our type IIb genes.
Adding even more to the confusion, peloton, has it backwards; IIa fibers are the slower of the fast-twitch fibers and tend to be more oxidative/less fatiguable and IIb (really IIx) are the faster usually heavily glycolytic/fatiguable fibers, this most accurately applies to untrained individuals. All fibers are heavily trainable including the type IIx, and can greatly increase their oxidative capacity, furthermore as volume of activity increases type IIx fibers tend to covert to type IIa. It's possible, although somewhat controversial if any type II fibers convert to type I (slow-twitch) fibers with typical training type activities. Lastly, it's not "more myosin" that is faster, but actually the myosin protein itself that largely determines the contractile speed of the fiber. The myosin protein molecule (Type I, IIa, or IIx each coded for by a separate gene) is what actually hydrolyzes an ATP molecule each time it ratchets along the actin molecule, the faster it can do this the faster the muscle fiber contracts. If you have more myosin (and the companion actin molecules) a fiber will produce more force, since force is directly proportional to cross sectional area, but it won't be any faster than the smaller fibers of the same type.
That was more than anybody cared to know, right?
|Fibre type confusion!||Jon|
Dec 10, 2001 10:51 AM
|Geeks of the world unite! This (to me at least) is super interesting. What is it in Type II myosin |
that determines speed of ATP hydrolysis? I would assume you're talking about hydrolysis at
the ATP binding site? Also, I thought that the conversion rate of Type IIX to Type IIA was not really
very significant. That the "trainability" of these fibres was really pretty marginal and occurred
slowly over a fairly long training period. Without "crashing the board" could you give us (me!) a
little primer on the latest in this area? Thanks.
|Fibre type confusion!||Wayne|
Dec 10, 2001 11:17 AM
|I'm not sure what about the myosin molecule itself determines the ATP hydrolysis rate and therefore the contractile speed of the fiber. Maybe something to do with the ease at which an ATP molecule can "find" it's way and bind to the site?
I'm not sure about how readily convertable IIx fibers are to IIa (that's why I asked above if the poster could provide a reference for his statement that almost all II fibers being type IIa in endurance trained athletes), but I'm sure about all fibers being highly trainable and capable of increasing their oxidative capacity including IIx fibers. I know it's been shown that IIa fibers will convert to IIx fibers in astronauts exposed to micro-gravity, and muscle below the level of injury in persons with spinal cord injuries will convert to almost all IIx fibers within a couple of years of injury (this even includes type I fibers). Basically, the less you use a muscle the faster it becomes and the more you use it the slower it becomes. That's why I wouldn't be terribly surprised if professional cyclist had almost no Type IIx fibers in their quads. It's also been shown in animals subjected to chronic electrical stimulation (so a contraction every second for a couple of weeks) that the muscle will become almost all type I. It also becomes very weak, so don't rush out and buy one of those abtronic stimulators and start stimulating your legs! As far as I know, no one has demonstrated that with typical endurance training Type II fibers will convert to Type I fibers.
|Where could I find some good info on...||Kyle|
Dec 10, 2001 3:47 PM
|the trainability of different fiber types?
Specifically, I've never seen any really compelling research on how the different fibers react to volume vs. intensity. For instance, if I do a single squat with maximum weight, would this stress (and therefore cause adaptation) in my type I fibers? Or is it impossible to stress a type 1 fiber with a single effort, no matter how intense? Conversely, if I train at an aerobic intensity, will type II fibers be affected?
|Very good question !||cyclomoteur|
Dec 10, 2001 5:02 PM
(I really have no idea of the awnser though ...)
|Not sure that it's out there||Wayne|
Dec 11, 2001 7:41 AM
|With weight-training all fibers, including Type I, hypertrophy, there is some evidence that with endurance training there is selective hypertrophy of Type I fibers but I think this is far from conclusive. If you are performing a true maximum effort all of your motor units will be activated and in fact at submaximal efforts your slow Type I units should be activated first. Here's why: Some basic neuroscience is necessary, your central nervous system (CNS) controls the force from a muscle in two ways:
1: By recruiting more motor units (a motor unit is the alpha motor neuron in the spinal cord and all of the muscle fibers that it innervates, ranging from maybe as few as only 2 or 3 fibers in muscles that require very fine control such as your hand or eye muscles upwards of several 100 fibers per some large motor units in postural muscles like your quads etc. but there will be range of motor unit sizes in each muscle only the limit of the ranges will vary)
2: The motor units that are recruited can be activated at differing frequencies from a few Hertz upwards of 70+ Hz per second. At low frequencies the motor unit will not be generating its maximal force, but at a given frequency it will produce its max force (the frequencies required to achieve this varies depending on the contractile speed of the muscle, a faster motor unit requires a higher frequency for the muscle fibers to summate and produce their max force).
All the fibers ennervated by a given motor neuron are typically of the same type, this probably highlights the important influence of the descending drive from the CNS on the expression of the genes within the fibers that determine the fiber type.
The Henneman Size Principle:
If you ramp up force from a muscle, first the small motor units will be recruited and gradually larger ones until they are all being recruited and driven at maximal frequencies. Small motor units tend to be Type I whereas larger ones tend to be type II.
This makes perfect sense since you produce low forces all the time you want the motor units to be fatigue resistant (think something like typing) and you want them to be small so you have fine motor control (again typing). That is, by bringing in or dropping out motor units the force only varies slightly. It all gets a bit more complicated if your trying to move very fast, but with very fast movements you can't produce much force so they're not really appropriate for weight-training anyway.
So the short answer to your first question is, if you're doing a true one-rep max all of your motor units should be recruited and presumably receiving a stimulus for hypertrophy. I would say at sub-maximal efforts (say a 10 rep effort to failure) again your Type I's are probably being recruited every rep whereas, maybe some of the Type II fibers wouldn't be brought in until your really fatigued on the last couple of reps (or maybe they're all being recruited and the last couple of reps get harder because some of the fatiguable Type II fibers are giving out?).
In response to your second question if you were just doing an easy ride I would imagine there would be some Type II fibers (esp. IIx) that may not get recruited, but the longer (and harder) you go the more likely it would be that some of your type I and esp. type IIa fibers would become glycogen depleted and essentially crapped out, forcing your CNS to start bringing in some less "ideal" fibers to achieve the desired force. Of course this all assuming a steady force output, if your were doing hill sprints or LT threshold intervals, etc. you're probably going to recruit all of your fibers at some point. One suggestion I've seen for hitting the less recruited fibers is to go out and do a 1.5 - 2 hour steady aerobic ride to glycogen deplete some of the fibers you normally use and then do intervals including some longish tempo stuff to "force" your CNS to recruit some of the motor units you might not normally be using and thereby hopefully supply some stimulus to them to adapt to endurance exercise.
|Not sure that it's out there||Jon|
Dec 11, 2001 8:39 AM
|Jim Martin, an ex. phys. and cycling coach, likes back to back long rides, ridden at high cadence, |
because Type 1 fibres become depleted and Type II are therefore recruited--and possibly
converted? over a period of time.
Dec 11, 2001 8:57 AM
|Before getting too old for the sport, I was very interested in (okay, obsessed with) rock climbing.
Years ago, it became clear to many high-level climbers that a very effective way to train was to do power one day, then what we called power/endurance the next day. Then one or two days off.
Power training in climbing is probably more extreme than any other sport--often involving one-off efforts that are just below injury level. An example (practiced by a guy in Salt Lake) is to drop from a ledge and catch a 2x4 screwed to an overhanging wall 3ft below. This either promotes excellent recruitment patterns, or retires you. Another training method would be doing climbs with every move near your limit, generally burning off at about 5 moves.
What's interesting about this (to a sick few) is that the next day, training at a moderate level (say, doing laps for ten minutes on an overhanging wall until failure) did not seem to be greatly affected by the prior day's workout. Additionally, this training schedule seemed more effective than the classic day on/day off--even with the same intensity and volume in any given week.
So all this got me to thinking--is it possible that endurance adapted fibers can only be stressed by volume? By this I mean that at high levels of intensity, IIa/x fibers might fry and cause failure before the (as you pointed out--fully recruited) Type I fibers are even warmed up.
If this is the case, it has significant training implications:
1: After an intensity day (sprint work/weight room) a high volume aerobic day can be done without worrying about overtraining the skeletal muscle. This debunks the current theory you should follow a hard interval day with a recovery day, or a day off.
2: Aerobic level training may (in some ways) be more effective than LT efforts, due to the fact that it take high volume to cause Type I failure and thus force Type II fibers to adapt to aerobic efforts. Another benefit here is that this level of effort (even at significantly higher volumes) is less systemically stressful. So you could theorize that even if Tempo training is twice as effective as aerobic training at improving LT, you would show better long term improvement by training aerobically for double the volume (as a practical matter, the pattern the pros have fallen into based on results.)
In any event--great thread...
|You guys are amazing.....||Len J|
Dec 11, 2001 10:22 AM
|and I think I only understood about half of what you are saying. Thanks, I think I'll print this thread out & get some old biochemestry texztbooks out & try to translate it. My gut says there is an awful lot of value in understanding this thread.
|A lot of us will do the same||cyclomoteur|
Dec 11, 2001 11:09 AM
|Where could I find some good info on...||allervite|
Dec 11, 2001 9:18 AM
|Yes and yes, but not a very big yes to your first question. Burke covers this in his books. You can train slow twitch to act like fast twitch and vice versa, but fast twitch will always be more powerful than slow, and slow will always have more endurance than fast.|
|Where could I find some good info on...||Jon|
Dec 11, 2001 10:36 AM
|With respect to overall aerobic adaptation I'd agree with the high volume hypothesis. This is |
why the pros do such enormous volumes. Having achieved optimal aerobic adaptation through
volume, however, I'd think that threshold work is necessary to optimally raise LT due to lactate
Another interesting point, some research has shown high intensity sprint intervals to be as effective
in raising aerobic power and endurance as the more traditional, longer LT intervals. The hypothesis
is that the recovery periods allowed for rapid clearance of lactic acid, while the short, but intense
sprinting stimulated aerobic enzyme production. This effect was most pronounced in 30 sec.
sprints with four minute recoveries.
On the applied side, I personally have found one day of sprint intervals, followed by a long ride or
even a tempo seems to work really well, better than back to back tempos. However, following the
day two of the block I need some recovery. I do believe that all this mix and match stuff does
have a lot to do with patterns of fibre type recruitment.
|Where could I find some good info on...||peloton|
Dec 11, 2001 10:57 AM
|I read an interesting study on medline recently about the differences in sprint training by gender as well. In 30 bike sprints, female athletes use 50% less glycogen, and produce less lactate than their male counterparts. They did produce slightly less power overall when compared by lean body mass ratio to the men though by 8%. It made me think of how we train our male and female athletes. Too frequently the same, when there are obvious biomechanical and metabolic differences to take into consideration. There are so many factors to take into consideration when setting up a training program that it is mind boggling.|
|Where could I find some good info on...||Jon|
Dec 11, 2001 11:21 AM
|Is this due to a higher ratio of Type I muscle fibre in women compared to men? Or a difference |
in enzyme production? Or what? Interesting.
|Here it is||peloton|
Dec 11, 2001 12:22 PM
|Jon- This came from the Journal of Applied Physiology's website. There are a lot of graphs to go with this there that you might want to check out too.
The link is- http://jap.physiology.org/cgi/content/full/87/4/1326?ijkey=nASP4DqOrpaXY
Metabolic response in type I and type II muscle fibers during a 30-s cycle sprint in men and women
Mona Esbjörnsson-Liljedahl1, Carl Johan Sundberg2, Barbara Norman1, and Eva Jansson1
1 Division of Clinical Physiology, Department of Medical Laboratory Sciences and Technology, Karolinska Institutet, Huddinge University Hospital, S-141 86 Huddinge; and 2 Department of Physiology and Pharmacology, Karolinska Institutet, S-114 86 Stockholm, Sweden
The acute metabolic response to sprint exercise was studied in 20 male and 19 female students. We hypothesized that the reduction of muscle glycogen content during sprint exercise would be smaller in women than in men and that a possible gender difference in glycogen reduction would be higher in type II than in type I fibers. The exercise-induced increase in blood lactate concentration was 22% smaller in women than in men. A considerable reduction of ATP (50%), phosphocreatine (83%), and glycogen (35%) was found in type II muscle fibers, and it did not differ between the genders. A smaller reduction of ATP (17%) and phosphocreatine (78%) was found in type I fibers, and it did not differ between the genders. However, the exercise-induced reduction in glycogen content in type I fibers was 50% smaller in women than in men. The hypothesis was indeed partly confirmed: the exercise-induced glycogen reduction was attenuated in women compared with men, but the gender difference was in type I rather than in type II fibers. Fiber-type-specific and gender-related differences in the metabolic response to sprint exercise might have implications for the design of training programs for men and women.
anaerobic metabolism; vastus lateralis; Wingate test
SPRINT EXERCISE leads to a major reduction in muscle ATP and phosphocreatine (PCr) content as well as a considerable reduction in glycogen content and a subsequent accumulation of lactate in both muscle and blood. These metabolic alterations seem to be fiber type specific. For instance, during sprint exercise the type II fibers lose much more ATP and glycogen (6, 15, 29) than do type I fibers. There are no studies, to our knowledge, in which gender-related differences in the fiber-type-specific metabolic response to sprint exercise have been addressed. It has been demonstrated, at the systemic level, that women have lower concentrations of blood lactate and plasma catecholamines than do men after sprint exercise (13, 26). In addition, glycolytic enzyme activities are lower in muscle from women than from men (10, 14, 31). Thus gender-related differences in metabolic response to sprint exercise, locally in the exercising muscle, are to be expected. We hypothesized that the reduction of muscle glycogen content during sprint exercise would be smaller in women than in men and that a potential gender difference in glycogen reduction would be greater in type II than in type I fibers. The latter hypothesis is based on the observation that the glycogen reduction is greater in type II than in type I fibers (15) and on the concept that women, to a lesser degree than men, may recruit/activate their muscle fibers (e.g., Ref. 4), especially type II fibers, during sprint exercise inasmuch as these fibers have a higher activation threshold than do type I fibers (18). To elucidate whether there are gender-related differences in the acute metabolic response to sprint exercise, the exercise-induced reduction of glycogen and high-energy phosphates was analyzed in type I and type II fibers in both men and women.
Subjects. Twenty men and nineteen women (students at a college for sports and recreation instructors) volunteered for the study. None of the subjects was at an elite or competitive athletic level. They did participate in leisure-time sports (e.g., various ball games and jogging for the men and mainly calisthenics, aerobics, and jogging for the women). During class hours, all subjects took part in the same theoretical and practical classes (physical exercises). A questionnaire was used to estimate the physical activity level during leisure time. The subjects answered nine different questions, from which an activity index (minimum value 5.5 and maximum value 20.5) was calculated (22). As estimated by this questionnaire, the physical activity level did not differ between the genders (Table 1). Anthropometric data for the subjects are given in Table 1. Fat-free mass was estimated from skinfold measurements (triceps, biceps, and subscapula; Ref.
All experiments were performed in the morning after an overnight fast. The subjects were asked not to perform any heavy exercise during the 24-h period preceding the experiment. Fourteen of nineteen female subjects were on oral contraceptives (11 subjects on 3-phase and 3 subjects on 1-phase pills). All subjects had regular menstrual cycles. To reduce the interindividual variation in hormone levels of the female subjects, all experiments were performed between day 12 and the last day of the menstrual cycle. The subjects were fully informed about the procedures and potential risks of the experiment and gave their consent to participate. The study was approved by the Ethics Committee of the Karolinska Institutet.
Experimental protocol. After familiarization, conducted at least 24 h before the experiment, a 30-s cycle sprint was performed (Wingate test; Ref. 1) on a mechanically braked cycle ergometer (Cardionics, Bredäng, Sweden). The subjects were instructed to pedal as fast as possible with an individual braking load set at 0.075 kp/kg body wt. A sensor-microprocessor assembly counted flywheel revolutions. The flywheel progression per pedal revolution was 6 m. Average power for 5-s periods was automatically printed. Peak power (i.e., the highest 5-s power) and mean power (the average power during the 30-s duration) were calculated. In addition, peak and mean power were adjusted for body mass and fat-free mass. This was done in a multiple-regression model, where peak or mean power was chosen as the dependent variable. Gender, together with body mass or fat-free mass, was chosen as independent variables (see also Statistics).
An indwelling catheter was inserted into an antecubital vein ~20 min before exercise. Two milliliters of blood were sampled ~2 min before exercise and subsequently at 3, 6, and 9 min after exercise (with the subjects in the supine position). Skeletal muscle biopsies were obtained from the vastus lateralis with the needle-biopsy technique (3) before and within 10 s of the cessation of exercise. Both biopsies were obtained from the same leg and skin incision, frozen in isopentane precooled with liquid nitrogen within a further 5 s, and stored at 70°C until later analysis.
Histochemical and morphological analyses. The biopsy taken before exercise was mounted in an embedding medium and analyzed histochemically for fiber types (I, IIA, IIB, and IIC) with a myofibrillar ATPase stain. Cross-sectional fiber area was measured morphologically by planimetry from an NADH-dehydrogenase stain. The relative number of the different fiber types (%type I, %type IIA, %type IIB, and %type IIC) and the relative area of the different fiber types (fiber type area) were calculated. In addition, mean type I, type IIA, and type IIB fiber areas; weighted mean fiber area of all fiber types combined; and weighted mean fiber area of the two type II fiber populations (IIA and IIB) were calculated. For more information about the histochemical and morphological analyses, see Jansson and Hedberg (22).
Single-muscle-fiber preparation procedures and analyses. After histochemical analysis of the preexercise biopsy, the rest of this biopsy and the one taken after exercise were freeze-dried, and ~100 single-fiber fragments were dissected from each biopsy. These were classified histochemically as fiber type I or II (12) and thereafter divided into separate pools of type I and type II. The mean weight of the pools was 40 µg (range 15-75 µg).
The fiber pools used for analysis of lactate, ATP, ADP, IMP, inosine, hypoxanthine, and PCr were extracted in 20-55 µl (depending on the weight of the pool) 0.4 M perchloric acid containing 0.06 M phenol red at 0°C. The pH of the extracts was brought to 8.2 by adding 1 M KOH. An HPLC technique, which has been described by Sellevold et al. (30), was used to determine the amounts of the metabolites in the fibers. The injection volume was 10 µl, and isocratic ion-pair reversed-phase assay (250 ¥ 4.6-mm, 5-µm Nucleosil 120-C18 column) was used. The mobile phase used for separation consisted of 215 mM potassium dihydrogen phosphate (pH 5.6), containing 2.4 mM tetrabutylammonium hydrogen sulfate and 3.5% acetonitrile. ATP, ADP, IMP, inosine, and hypoxanthine were detected at 254 nm (model 440, Waters) and PCr at 206 nm (model 481, Waters) with two detectors connected in series.
The fiber pools used for glycogen analysis were digested by adding 20 µl of 1 M KOH, and then glycogen was extracted by vigorously mixing and warming the samples for 15 min at 50°C. The extracts were neutralized by addition of 0.25 M HCl. Amyloglycosidase was added to break down glycogen to glycosyl units (17), which were then measured by a fluorometric enzymatic method (24).
Blood analyses. Blood lactate was analyzed in neutralized perchloric acid extracts of whole blood by a fluorometric enzymatic method (24).
Methodological error. Methodological error (imprecision) for glycogen, ATP, ADP, IMP, and PCr was determined by analyzing extracts from two corresponding pools and was found to be between 5 and 8%.
Statistics. Unless otherwise stated, values in the text are means ± SD. The gender difference in exercise-induced blood lactate accumulation was tested by Student's t-test for groups. The exercise-induced accumulation of blood lactate was defined as the change between the preexercise and the peak value. The peak value was defined as the highest of the 3-, 6-, or 9-min postexercise value. For the single-muscle-fiber variables (ATP, ADP, IMP, PCr, glycogen, and lactate), an ANOVA was applied to compare the exercise-induced responses between genders and in different fiber types. Gender and muscle fiber type (I or II) were chosen as independent variables and exercise-induced changes in various muscle metabolites as dependent variables. If a significant (P < 0.05) interaction effect was found between gender and fiber type, a contrast analysis was applied to identify the interaction (7). Student's t-test was applied for paired observations or groups. The P values (all analyses) were accepted as statistically significant at P < 0.05.
Multiple-regression analyses were applied to analyze the influence of gender, body mass, and fat-free body mass (independent variables) on peak or mean power outputs (dependent variables). Multiple-regression analyses were also used to analyze the influence of gender, glycogen content before exercise, and exercise-induced increase in IMP or decrease in ATP content (independent variables) on the exercise-induced decrease in glycogen content and exercise-induced increase in muscle lactate content or muscle lactate content after exercise (dependent variables).
(Table 1). Absolute values of peak and mean power output were 27 and 30% lower, respectively, in women than in men. When peak and mean power output were adjusted for body mass, the women still presented lower peak (15% lower; P < 0.001) and mean power outputs (18% lower; P < 0.001) than did the men. When the power output was adjusted for fat-free body mass, there was a gender difference only for the mean power (8% lower in women than in men; P = 0.03).
Fiber types and size (Table 1). There were no gender differences in the relative numbers of different fiber types. The relative area of type II fibers was smaller in women than in men. The cross-sectional area of type I fibers, on the other hand, was not statistically different between the genders. The cross-sectional area of type IIA and type IIB fibers and the weighted mean fiber area was 33, 31, and 20% smaller, respectively, in women than in men.
Blood lactate. The exercise-induced increase (peak value preexercise value) in blood lactate concentration was 22% smaller in women than in men (Fig. 1).
Metabolites in muscle: fiber-type comparisons (Table 2). Before exercise, there were no differences in ATP, ADP, IMP, or lactate content in the two fiber types. Glycogen content was ~1.2 times higher (P < 0.0001) and PCr was 1.1 times higher (P = 0.02) in type II than in type I fibers.
Sprint exercise induced a different metabolic response in type I than in type II fibers for most of the assessed metabolites. The reduction in ATP was ~3 times greater (P = 0.0001) in type II than in type I fibers, and the reduction in PCr content was 1.1 times greater (P = 0.003). The ADP content increased by 12% in type I, whereas there was no change in type II fibers. The accumulation of lactate was 1.4 times greater in type II than in type I fibers, and the accumulation of IMP was 2.5 times greater in type II (P = 0.0001). The glycogen reduction was approximately twofold greater in type II than in type I fibers in the women. In men, however, no difference in glycogen reduction was found between the two fiber types.
There were no detectable amounts of inosine or hypoxanthine in either type I or type II fibers before or after sprint exercise (detection limit was 0.05 mmol/kg dry muscle).
Exercise-induced changes in ATP, ADP, IMP, and PCr content did not differ between men and women either in type I or type II fibers. Similarly, exercise-induced changes in glycogen and lactate in type II fibers did not differ between the genders. In type I fibers, however, the exercise-induced glycogen reduction was found to be 42% smaller in women than in men (gender; P < 0.02). The lactate content in type I fibers was 20% lower in women than men (gender; P = 0.01) after exercise. Furthermore, exercise-induced increase in lactate content in type I fibers tended to be smaller in women than men (gender; P < 0.09). After adjustment for the interindividual variation in the exercise-induced IMP accumulation in type I fibers (see DISCUSSION for further explanation), the gender differences in exercise-induced glycogen reduction and lactate content after exercise in type I fibers were further augmented (P < 0.01 and P < 0.0001, respectively). The gender difference in the exercise-induced increase in lactate content in type I fibers was significant at the level of P = 0.006 after adjustment for the interindividual variation in the type I exercise-induced IMP accumulation. In type II fibers the adjustment for exercise-induced accumulation of IMP did not reveal any gender-related difference in metabolic response in type II fibers.
Correlations. Exercise-induced glycogen reduction correlated with glycogen content before exercise both in type I fibers (men, P = 0.003; women, P = 0.02) and in type II fibers (men, P = 0.02; and women, P = 0.004). However, in type I, but not in type II, fibers the regression lines were significantly different between men and women: at a given preexercise value of glycogen, the reduction in glycogen content was smaller in the women (P = 0.02).
Our hypothesis that the reduction in glycogen content in the type II fiber pool would be attenuated in women compared with men during sprint exercise was not confirmed: sprint exercise reduced the glycogen content in type II fibers similarly in both men and women by ~140 mmol/kg dry muscle. Similarly, the exercise-induced lactate accumulation and the lactate content after exercise did not differ between the genders in type II fibers (~120 mmol/kg dry muscle). An extensive reduction of the ATP content in type II fibers to approximately one-half of the preexercise value occurred in both genders. The lack of a gender difference in exercise-induced metabolic changes in type II fibers indicates that an attenuated recruitment/activation of type II fibers in women compared with men during sprint exercise is not likely.
The finding that the exercise-induced reduction in glycogen content in type I fibers was smaller in women than in men was unexpected. The smaller glycogen reduction in type I fibers in women was supported by the lower lactate content in the same fibers after exercise. A lower muscle lactate content in women than men after a 30-s cycle sprint has earlier been shown in biopsies that were not dissected into single fibers (20). Bell and Jacobs (2) also found a gender difference in glycogen degradation in women, as estimated from a histochemical glycogen staining, during repeated bouts of maximal isokinetic knee extensions. However, they found lower degradation in women in both fiber types. The discrepancy between the results of the present study and those of Bell and Jacobs may be related to the different exercise protocols or to the different techniques used for quantification of glycogen.
It is thought that the rate of glycogenolysis increases as a response to an increased ADP content and/or a decreased ATP content. An increased IMP content most likely reflects such a disturbed energy balance (e.g., Ref. 21). Therefore, the rate of glycogenolysis ought to relate to the increase in IMP content. In fact, a strong correlation was found between IMP and lactate accumulation during exercise in the present study (Figs. 3 and 4). However, for type I fibers, the regression lines describing the relationship between lactate and IMP accumulation were significantly different for the male and female subjects (different y-axis intercept). This means that, for a given increase in IMP, the women demonstrated a lower exercise-induced lactate content than did the men. This could be due to a limiting phosphorylase activity in women by either lower maximal velocity (Vmax) or higher Michaelis constant (Km) for the enzyme or lower concentrations of alternative stimulators, such as cAMP as discussed below. In type II fibers, however, no gender differences were found either before or after adjustment for exercise-induced accumulation of IMP.
The gender difference in the average rate of glycogenolysis over the 30-s exercise in type I fibers occurred despite a lack of gender difference in net ATP or PCr reduction or IMP accumulation in these fibers. This would indicate that type I fibers were activated/recruited to a similar degree in the two genders. The similar metabolic activation of the high-threshold type II fibers in both men and women, together with the principle of orderly recruitment of motor units (18), makes it unlikely that there would be a gender difference in the recruitment/activation of the low threshold type I fibers. Therefore, we do not think that the smaller glycogen reduction in type I fibers in the women was due to a lower recruitment/activation of these fibers.
One possible explanation, however, for the lower rate of glycogenolysis in type I fibers in the women is the lower activity (lower Vmax or higher Km) of enzymes limiting the anaerobic ATP-regenerating pathway in women. Women are known to have lower Vmax activities of lactate dehydrogenase, phosphofructokinase, and glycogen phosphorylase (see Ref. 10). However, we have found that the greatest gender difference in lactate dehydrogenase activity is found in type II fibers (M. Esbjörnsson-Liljedahl, C. Sylvén, and E. Jansson, unpublished observations). Therefore, the lack of gender difference in the rate of glycogenolysis in type II fibers may argue against gender differences in glycolytic enzymes as the main explanatio
|Here it is||Jon|
Dec 11, 2001 4:21 PM
If I read this correctly, the researchers don't have an explanation for the effects they observed, right?
Their initial hypothesis that glycolytic inhibiting enzymes may have been responsible did not bear out.
|Here it is||peloton|
Dec 12, 2001 7:13 AM
|I gathered the same, Jon. What I found interesting wasn't so much that their hypothesis didn't pan out, but the effects that they did observe. Just the fact that there are differences in the lactate and gylcogen usage and production in males and females shows that there may be different ways to train each more effectively. All too often I think we train women the same way we train men, even though there are differences. There have to be some ways to take advantage of these metabolic and biomechanical differences to develop more specific training by gender.
In a lot of ways I find this field interesting because there is so much we don't know. They couldn't find out why there were differences in this study, and there are so many other things we are unsure of as well. I think we'll see some huge advances in training continue over the next few years.
Dec 12, 2001 8:46 AM
|Tongue-in-cheek: for sure Jeannie Longo is not gonna beat Cipollini in a sprint!! But for |
the rest of it, what are the training implications? This data bears out the general drift in
gender-specific research that indicates that women might have an innate endurance
advantage, most strongly borne out for swimmers. So how does a coach compensate
for less overall power and a higher glycolytic threshold for women? Train to compensate
for weaknesses or train to strengths? I think sometimes the research just tells us what
our hardwired limiters are.
Dec 12, 2001 10:42 AM
|I don't think Cipo has to worry in a sprint against Longo, but she did beat him in a time trial last year at some small UCI stage race!
I agree that sometimes research shows us what our innate limits might be, but that can give us an idea of what we need to concentrate on in training. Let's say a great sprinter needs to work on endurance so as to be able to get to the end with the peloton to be able to put that sprint to work (Nothstein?). Work to the weakness. I think that better knowledge of physiology between genders or even ages can give us a better idea of how to effectively train an individual. Another example might be how we know that we lose power (type IIa fibers) as we age. Our endurance does become better though. To maintain power on the bike though, we know we need to train for it to maximize the ability we do have. I think that there are factors like this between different genders and age groups that could be better understood to create more effective training programs to minimize our weakness and get better overall performance. Sometimes I just think a lot of the training programs that I see are too one dimensional, and don't even show consideration for individual differences. People want to quantify everything in the most simple way.
|True enough. (nm)||Jon|
Dec 12, 2001 11:48 AM
Dec 12, 2001 11:54 AM
|I think it was Leontjien Zijlaard-van Moorsel who beat Cipo by 2 seconds! Which is |
why I brought up the comparison in context of the discussion. So your preliminary
thoughts as a coach would be to train to weaknesses? e.g. more sprint training for
Dec 12, 2001 3:18 PM
|You are right. It was Zijlaard-van Moorsel, not Longo.
My thoughts are usually that you are only as good as your weakest link. I guess it is somewhat situational though. Not going to try to turn a downhiller into a slalom skier or visa-versa. Climber to sprinter in cycling terms I guess. When it is a skill that is required though for the proper situation, my feeling is attack it and make it strong if that is where you are lacking. IE- a good downhiller might be faster on the flats with more flexiblility to be more supple and low in their tuck if the flexibility was lacking and weak. Maybe their turning is good though, and we need to focus on the flexibility and gliding to really get faster. I guess I view physiology the same way. Go for what is weak, and make it strong to bring up the whole to a new level.
|Where could I find some good info on...||Wayne|
Dec 11, 2001 12:40 PM
|I believe Chris Boardman used the 30 sec. max effort intervals in his training for his hour record attempt. For cross season, I've also been doing a sprint workout on Tuesdays, but then threshold (or even max effort) intervals on Wednesdays. I've been surprised how little a sprint workout takes out of me, it really seems to be the longer intervals that are very demanding and require the most recovery time.|
|Fibre type confusion!||peloton|
Dec 11, 2001 10:51 AM
|Thanks- I did mix the two fibers types up there.
Maybe I did over-simplfy myosin and it's role by stating that more myosin was faster. What you said is true about the type of myosin and it's myosin heavy chain isoforms determining the contractile speed force capacity of the protein filament. As a muscle fiber hypertrophies, the contractile speed of the muscle fiber does not get any faster. It does produce more force though. There is more actin/myosin as a result of the hypertrophy. Because the muscle fiber can now exert more force the effect on it's leverage changes. Let's say it was third class extension of the biceps brachii. Just flexion, no supination of the forearm. More force applied at the fulcrum ( the elbow joint here), would result in greater speed at the distal end (the hand). There may not have been a change in speed at the level of the muscle fiber, but there has been a change in the capacity to do biomechancial work. That is the same reason why someone with more type II fiber can move faster. More force acting on leverage creating more speed. What I said before was too simple to show what I meant. I do believe that there is some merit to the idea of more force being able to create more speed, although it is more complex than just saying more myosin is a reason for that.
Wayne, I tried quickly to find your article this morning, but wasn't able to. Could you steer me the right way in finding it? Is it on Medline? I would love to check it out. Thanks
|Fibre type confusion!||Wayne|
Dec 12, 2001 5:32 AM
Dec 12, 2001 7:25 AM
|I do have a question though. Do you know of anywhere I could look to learn more about the genetic and chemical differences between the 7 human muscle fiber types, (from slowest to fastest): types I, IC, IIC, IIAC, IIA, IIAB, and IIB. Generally the information that I find only includes types I, IIa, and IIx for humans. Anything you might know of would be appreciated. Thanks|
|Not specifically, but....||Wayne|
Dec 12, 2001 10:37 AM
|I think I can answer the question. The 7 fiber types are based on myosin ATPase staining characteristics of single fibers. The mysosin heavy chain (MHC) is the ATPase and that is what primarily determines the contractile speed of a muscle fiber. In human skeletal muscle there are three MHC Type I, IIa, and IIx. If muscle fibers were all pure, that is, didn't contain any mixes of MHC there would only be three types of myosin ATPase fibers, I, IIA, and IIB. But there are mixed fibers, so when you stain them a mixed MHC I and IIa will stain somewhere in between pure I and IIA, so you end up with IC (more MHC type I than Type IIa) or IIC (about equal Type IIa and Type I MHC)and IIAC (more type IIa than Type MHC). A myosin ATPase type IIAB would contain both MHC IIa and IIx. Because these divisions are arbitrary and qualitative(afterall they split mixed Type I and IIa fibers into 3 types, IC and IIC and IIAC but mixed type IIx and IIa fibers into only 1 type, IIAB) and you're inferring the underlying protein difference in the fibers from the way the fiber stains in response to chemicals, I think most researchers prefer looking directly at the myosin content of the fibers.
Thus your type I, IIa and IIx. There are fibers that co-express the type I and IIa genes or IIa and IIx. These techniques are qualitative so you can take a mixed fiber and say it contains 30% Type I MHC and 70% Type IIa MHC (If you used myosin ATPase staining for this fiber it would be a Type IIAC). This of course doesn't lend itself to nice neat mixed fiber categories beyond saying it's a mixed fiber. Anyway, mixed fibers make up a relatively small percentage of the total fibers anyway (so most muscle fibers are pure). And with exercise (both strength and endurance training) there is a reduction in the percentage of mixed fibers.