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Old 05-07-2008, 12:43 PM   #21
Brandon Oto
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Re: Leg Power - Increased performance

Put more simply, you can't lift fast what you can't lift at all...

Interesting last remark, though. Are you saying maximum power is achieved with EITHER 30% (or in this ballpark -- I hear 40% as well) max weight, or 30% max speed (which would mean 70% weight)? I know folks like Westside like their DE work somewhere around 70% 1RM or so (60? 80?), which would jibe with this.

By the way, could one of you go through and define the specific muscle fiber terminology? I think most of us are stuck on basic fast- or slow-twitch.
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Old 05-07-2008, 01:11 PM   #22
Justin Lascek
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Re: Leg Power - Increased performance

Quote:
Originally Posted by Brandon Oto View Post
Put more simply, you can't lift fast what you can't lift at all...

Interesting last remark, though. Are you saying maximum power is achieved with EITHER 30% (or in this ballpark -- I hear 40% as well) max weight, or 30% max speed (which would mean 70% weight)? I know folks like Westside like their DE work somewhere around 70% 1RM or so (60? 80?), which would jibe with this.
Keep in mind the following:

Power = work / time Work = force x distance

So: Power = (force x distance) / time
Force being strength, d/t being speed

So that means that power is the product of both strength and speed. Given that speed diminishes with an increased load, the most power would be achieved if you produce one-third of the maximum force at one-third the maximum velocity (to answer the question).

Of course you can do power (i.e. Olympic lifts and such) movements at higher loads, but speed will be reduced in such a case. Research shows that a load of 30 to 50% is ideal for developing power.

Edit: This doesn't mean you couldn't increase the load higher than the 30 to 50% range in a training program to ultimately increase power. However, if in a single bout of lifting you wanted to maximize your power, and you knew what your maximum force and speed of the movement were, then you would use one-third of that max force and one-third of that max speed.

For the sake of splitting my post up, I'll define the muscle fiber terminology in the next post.

Last edited by Justin Lascek : 05-07-2008 at 01:37 PM. Reason: Additional information
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Old 05-07-2008, 01:35 PM   #23
Justin Lascek
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Re: Leg Power - Increased performance

Quote:
Originally Posted by Brandon Oto View Post
By the way, could one of you go through and define the specific muscle fiber terminology? I think most of us are stuck on basic fast- or slow-twitch.
All righty...

Type I fibers are the "slow-twitch fibers". They have a high level of aerobic endurance. These fibers are efficient at producing ATP (the energy that the muscle fibers use for muscle contraction) from the oxidation of carbohydrate and fat.

So you can probably discern that these are the fibers involved with muscular endurance.

Type II fibers are the "fast-twitch fibers". They have relatively poor aerobic endurance in comparison to the Type I fibers. They perform anaerobically, or without oxygen. So, the ATP is formed through anaerobic pathways (a la the ATP-PCr (phosphocreatine) system). The Type II fibers are broken up into Type IIa and IIb (or IIx depending on the text/researcher), and even more depending on how technical you want it. There are slight differences, but you can look at them both as the "fast-twitch fibers" for simplicity since they pretty much do the same thing, which is produce short durations of strength and speed.

So, concerning muscle fibers:

A muscle fiber is made up of hundreds to thousands of myofibrils. The sub-unit of a myofibril is a sarcomere, which is the basic contractile unit of muscle. Myofibrils are made of sarcomeres that are joined end to end.

Here's a pic (safe):
http://www.mhhe.com/biosci/esp/2001_...s/anm5s5_1.jpg
The whole structure is the muscle fiber. Those sections within it are myofibrils. Then the myofibrils consist of the longitudinal links of sarcomeres.

Anyway, within the sarcomeres are the myosin and actin. To put it easily and briefly, these contract the sarcomere, which contracts the myofibril, which contracts the muscle fiber. Here is a video of that contraction at the smallest level (safe):
http://www.sci.sdsu.edu/movies/actin_myosin_gif.html

There's kind of a lot going on in it, but you can see the myosin binding to the actin and ratcheting the head to pull the actin filament down, thus creating a contraction.

So, in that post where I referenced hypertrophy, the research shows that it's most likely due to the increase in these components of the muscle fiber to increase the size of that fiber.

Did that help at all?
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Old 05-07-2008, 02:27 PM   #24
Brandon Oto
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Re: Leg Power - Increased performance

Thanks -- this is great stuff. For sure it's going to get linked to in the future. What's your background btw, Justin?

Now, how eager are you to talk about what happens to the muscle fibers when we do various sorts of resistance training? (high/low rep, heavy/light weight, fast/slow, etc.).
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Old 05-07-2008, 06:18 PM   #25
Steven Low
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Re: Leg Power - Increased performance

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Originally Posted by Justin Lascek View Post
Regardless of whether or not the ratio can change, all I'm saying is that what I thought Jake was asking was about the ratio of fibers. It was simply the semantics of the question, not the content.

But, since we're talking about it:

"Some recent evidence, however, suggests that endurance training, strength training, and muscular inactivity may cause a shift in the myosin isoforms. Consequently, training may induce a small change, perhaps less than 10% in the percentage of type I and type II fibers. Further, both endurance and resistance training have been shown to reduce the percentage of type IIx fibers while increasing the fraction of type IIa fibers.

IIx and IIa types are fairly adaptable to training because they have oxidative and glycolytic capabilities. I wouldn't actually call that a shift in fiber type.

But sure I'll run with this.. there is SOME evidence of hyperplasia except we don't really know what causes it yet, so it's not really worth arguing about. All of the "lower" animals like birds seem to have hyperplasia fairly well ironically.. kind of interesting that it's been eliminate or at least inhibited in humans.


Studies of older men and women have shown that aging may alter the distribution of type I and type II fibers. As we grow older, muscles tend to lose type II motor units, which increases the percentage of type I fibers" (40, Wilmore 2008).

Interesting. Did they speculate as to why?

"Sprinters and jumpers usually have great concentrations of fast-twitch fibers. These fiber types are also found in high concentrations in muscles on which these athletes rely, such as the gastrocnemius. On the other hand, distance runners usually have greater concentrations of slow-twitch fibers" (68, Hamill 2003).

It's not a coincidence that a marathoner's muscles are lean while the sprinter's are thicker. Type I fibers are smaller than the Type II fibers since they don't produce as much force as the Type II fibers (and they also have a difference in motor unit recruitment).

I wouldn't say this is indicative of anything at all. The people who will do well in sprinting will be born with higher amounts of fast twitch while the opposite is true for marathoning. Doesn't mean there is hyperplasia or anything.

As for differences in recruitment.. one would hope so given the differences between power and endurance training...


Now, concerning hypertrophy, there are postulated mechanisms for fiber hypertrophy and fiber hyperplasia.

Fiber hypertrophy "could be explained by more myofibrils, more actin and myosin filaments, more sarcoplasm, more connective tissue, or any combinations of these" (207, Wilmore 2008)

Textbook myofibrillar and sarcoplasmic hypertrophy.

Fiber hyperplasia, on the other hand, has involvement with satellite cells.
"It has more recently been established that satellite cells, which are the myogenic stem cells involved in skeletal muscle regeneration, are likely involved in the generation of new muscle fibers" (209, Wilmore 2008).

Here is something else that is interesting:
"Muscle injury can lead to a cascade of responses, in which satellite cells become activated and proliferate, migrate to the damaged region, and fuse to existing myofibers or combine and fuse to produce new myofibers" (209, Wilmore 2008).

I don't know how these researchers define "muscle injury", but in some cases normal exercising can be considered an "injury" to the muscle. If that's the case, then CrossFitting (and other forms of activity in this 'community') could qualify because it is intensive exercise. If "muscle injury" includes the realms of normal to intense exercise, then it may acceptable to assume some satellite cell involvement for repair, but generally this seems to be for a more serious muscular injury.

Satellite cell donation also occurs with myofibrillar hypertrophy to increase cross sectional area.. hence increase in size of the cell. Well, that's why the muscle cells tend to be multinucleated anyway with larger muscles having more nuclei donated.

With rhabdomyolysis there needs to be regeneration of muscle fibers (because many are destroyed) and the process to regain strength is very slow often taking months for recovery (ask some CFers who have had rhabdo about that, heh). So there definitely is some mechanism of hypertrophy for skeletal muscle regeneration although I am pretty sure it does NOT occur under normal circumstances.

If anything, I would **speculate** with humans that hyperplasia is regulated to (1) high output of anabolic hormones like testosterone/GH and (2) extreme stress response probably mediated by possibly cytokines/interleukins exerting some effect on satellite cells.


There are instances where researchers differ on physiological concepts of the human body (Delayed Onset Muscle Soreness is an example), so all research must be taken into account to prevent a biased view. Interesting stuff.

DOMS is still being debated. Especially since it present inflammation-like response without actually any inflammation. I am going to look into this more in the future.
-------------------------

Quote:
Thanks -- this is great stuff. For sure it's going to get linked to in the future. What's your background btw, Justin?

Now, how eager are you to talk about what happens to the muscle fibers when we do various sorts of resistance training? (high/low rep, heavy/light weight, fast/slow, etc.).
Simplifying what Justin said to a few lines:

Type I - slow twitch - low force production, high endurance capabilities as they contain many mitochondria for oxidative phosphorylation

Type IIa - fast twitch - moderate-high force production, reliance on glycolytic and oxidative phosphorylation for energy

Type IIb - fast twitch - high force production, total reliance on phosphocreatine and glycolysis for energy, fatigue quickly

Muscle -> fascicles -> muscle fibers -> myofibrils -> sarcomere

Sarcomere are the units that actually contract. When myofibrillar hypertrophy occurs (normal hypertrophy from 'strength' training generally speaking) there is an increase in the amount of myofibrils (made up of actin & myosin) which increases the cross sectional area of the muscle.

Here's a bit of stuff from the new and improved v1.1 of "how to construct a workout routine".. haven't elaborated much more on it but... wfs
http://www.powerathletesmag.com/wfor...php?f=1&t=1037

Quote:
The central nervous system (CNS) is composed of the brain and spinal cord and is primarily responsible for handling sensory input, information processing and decision making and the primary thing in training which is obviously motor output. Once the brain makes a decision, it stimulates the primary motor cortex in the brain to send action potentials down to motor neurons which innervate specific muscles.

Along these lines, the motor neurons innervate specific muscle fibers. Each motor neuron has approximately three to thousands or so muscle fibers it innervates. The less fibers that a motor unit has, the more precise and fine movements you can get. Therefore, the dexterity of your hands comes from many motor units with fewer numbers of muscle fibers in each unit as opposed to the quadriceps which have few motor units with many more muscle fibers because its movements are on a larger scale. A motor unit innervates RANDOM fibers without each muscle (so they can be on different fascicles).

These motor units are grouped according from high to low depending on the force production needed. If the force production needed is low, the first motor units recruited are “low threshold” which are primarily composed of slow twitch (type I oxidative) fibers. This is primarily because slow twitch fibers have very strong endurance qualities and can sustain contractions because of the energy produced by oxidative phosphorylation for hours. Secondly, we have our “medium threshold” motor units which are composed mainly of fast twitch (type IIa oxidative-glycolytic) fibers which contract with a higher force (and speed) than the slow twitch fibers. These derive energy from glycogen and then through oxidative phosphorylation as the energy need exceeds the muscle's glycogen stores. Lastly, we have fast twitch (type IIb glycolytic) fibers which contract the fastest out of all of the fibers. These fibers use energy from glycogen only and therefore tire very quickly as their glycogen stores run out.
So with low weight and high reps mostly low threshold fibers are activated which is basically your nice type I slow twitch fibers because they are built for endurance. Marathoners obviously have this.

With high weight low reps at about 85-90% 1 RM or >3RM you have FULL recruitment of all muscle fibers due to the nature of the heavy weight being a high threshold load. Well, not *all* muscle fibers in your muscles but the amount you can actually activate due to CNS inhibiting actual full contraction of all muscle fibers you have literally. Thus, strongmen and powerlifters tend to have heavier hypertrophy of type II fibers namely because their force production is greater and they bear a greater brunt of the force. So heavy lifting is a bit biased towards type II fiber hypertrophy.

With POWER work (lifting fast), the tendency is for high threshold motor units to be recruited. This is why Oly lifters and sprinters have the tendency to have their type IIb fibers hypertrophied the most and poor endurance capabilities.

Slow lifting depending on the intensity of the repetition will probably preferentially recruit slow twitch because the high force production is not needed unless it's like a max effort lift where the weight moves slow anyway. So.. depends on what kind of repetition it is.

Uhm, if you want any extra explanations beyond this... sure.
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Last edited by Steven Low : 05-07-2008 at 06:23 PM.
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Old 05-07-2008, 08:36 PM   #26
Justin Lascek
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Re: Leg Power - Increased performance

I wanted to clarify that the first quote wasn't indicating anything about hyperplasia. There's all kind of quasi-boring studies done on animals, and even very few studies on humans, but I am with you on the fact that it's unattainable in humans.

And the satellite cell involvement in rhabdomyolysis would make sense since, according to where I've seen the research at, there is satellite involvement in "muscle injury", of which rhabdo is the most severe kind (if I'm ever urinating myoglobin, I'm not gonna be happy).

You mentioned how the satellite cells increase the cross-sectional area of the muscle fibers. While this may be possible or believed by some folks, the researchers and exercise physiologists that I've been around for the past couple years attribute hypertrophy (AKA increase in cross-sectional area) to the increases in (to simplify my reference) the contents of the muscle fiber.

What I mean by that is you attribute one thing, I another. Since there is a discrepancy in research, I don't think one or the other can solely be the cause for hypertrophy. For the time being, you and I cannot ignore the other's point until research clarifies the mechanism.

Also the fact that DOMS is still debated was my point exactly. Some of the causes of mechanisms that go on in our bodies when we exercise aren't completely solidified, and I was using DOMS as one of those examples of something that has differing opinions.

Good stuff, but I'll get to the rest tomorrow.
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Old 05-07-2008, 09:50 PM   #27
Steven Low
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Re: Leg Power - Increased performance

For myofib it's definitely mainly increase in actin-myosin chains.. although satellite cell donation is involved too b/c of muscle repair (well, hypertrophy is caused more or less by mechanical stress so it fits). Peh, it's really both that increase CSA but really only myofib does stuff for strength.

Per wiki (if you trust that source... )
http://en.wikipedia.org/wiki/Satellite_cell

Quote:
When muscle cells undergo injury, quiescent satellite cells are released from beneath the basal lamina. While normally in a post-mitotic state, they become activated and re-enter the cell cycle. Proliferating myoblasts then undergo myogenic differentiation, becoming post-mitotic, and form new myotubes and fuse with existing muscle fibres. This leads to repair of the injured site.

The presence of fibroblasts during muscle repair can lead to the formation of scar tissue that can lead to impaired muscle function.
Yeah, hyperplasia is a bit shady though. In the grand scheme of humans it doesn't matter too much since well it doesn't involve training and humans don't get much of it anyway.

I wonder.. if sarcoplasmic hypertrophy is involvement of increased sarcoplasm due to or related to satellite cell donation (because of the sarcoplasmic donation of satellite cells...). Would be interesting to see if there's any studies on bodybuilders having a greater proportion of multinucleated muscle cells than say a regular human or other sports that don't damage muscle fibers as much.
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Old 06-08-2008, 09:54 AM   #28
Justin Lascek
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Re: Leg Power - Increased performance

Hey folks. I don't know if anyone is still interested in this thread, but I said I would reply (even though it's more than a month later). Apologies on that -- over that time I've had to graduate, start an internship, continue working as a personal trainer, and start working as a strength coach (as well as getting my CF in!).

Quote:
Me:
It's not a coincidence that a marathoner's muscles are lean while the sprinter's are thicker. Type I fibers are smaller than the Type II fibers since they don't produce as much force as the Type II fibers (and they also have a difference in motor unit recruitment).

Steven's reply:
I wouldn't say this is indicative of anything at all. The people who will do well in sprinting will be born with higher amounts of fast twitch while the opposite is true for marathoning. Doesn't mean there is hyperplasia or anything.
Just for clarification, I wasn't insinuating hyperplasia was going on. People certainly excel in the areas that they have a genetic pre-disposition for, but if I went from power lifting for five years to running/marathoning for the next five (or more) years, there would definitely be a change in my body. I attribute that to the ratio of slow twitch to fast twitch fibers changing as an adaptation to training, not hyperplasia. Just wanted to clear up my position!
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Quote:
Steven:
If anything, I would **speculate** with humans that hyperplasia is regulated to (1) high output of anabolic hormones like testosterone/GH and (2) extreme stress response probably mediated by possibly cytokines/interleukins exerting some effect on satellite cells.
Agreed. I still view satellite cell involvement as something that occurs with heavily damaged muscle (rhabdo) and not regular, typical hypertrophy. That's coming mostly from what I've been taught from my professors whose job it is to know the research through and through. A small component is from my understanding of the research, but my understanding is in no way holistic of all research on the matter (like my professor's understanding).
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Quote:
Steven:
DOMS is still being debated. Especially since it present inflammation-like response without actually any inflammation. I am going to look into this more in the future.
I am too. About a year ago I had to do a bit of research. I typed out a list of "fun facts" pertaining to DOMS, but it was longer than I thought it would be, and it doesn't exactly fit with the scope of this thread. I'll post it in a new thread and hopefully it can open up a discussion (particularly your thoughts Steven) and help the awareness/knowledge of DOMS.

I also will continue to finish responding to the rest of this thread, but will go ahead and post this so it isn't an unnecessarily lengthy post!
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Old 06-08-2008, 10:03 AM   #29
Justin Lascek
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Re: Leg Power - Increased performance

Quote:
Originally Posted by Steven Low View Post
For myofib it's definitely mainly increase in actin-myosin chains.. although satellite cell donation is involved too b/c of muscle repair (well, hypertrophy is caused more or less by mechanical stress so it fits). Peh, it's really both that increase CSA but really only myofib does stuff for strength.

Per wiki (if you trust that source... )
http://en.wikipedia.org/wiki/Satellite_cell



Yeah, hyperplasia is a bit shady though. In the grand scheme of humans it doesn't matter too much since well it doesn't involve training and humans don't get much of it anyway.

I wonder.. if sarcoplasmic hypertrophy is involvement of increased sarcoplasm due to or related to satellite cell donation (because of the sarcoplasmic donation of satellite cells...). Would be interesting to see if there's any studies on bodybuilders having a greater proportion of multinucleated muscle cells than say a regular human or other sports that don't damage muscle fibers as much.
Ha, I like Wiki except when research/empirical evidence is split on certain topics.

Would you say bodybuilders are damaging their muscle fibers more than, say, a CrossFitter? Or an olympic lifter? A power lifter? I'm biased in my distaste for bodybuilders because of their their lack of functional compound movements that have a neuroendocrine hit (among plenty of other reasons that are irrelevant to the discussion). Most of them squat, deadlift, and press, but not much other than that. But I see your point when you say "a regular human", since they don't have a regular body chemistry because of the supplementation they go through.
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Old 06-08-2008, 10:51 AM   #30
Skylar Cook
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Re: Leg Power - Increased performance

Quote:
Originally Posted by Justin Lascek View Post
Just for clarification, I wasn't insinuating hyperplasia was going on. People certainly excel in the areas that they have a genetic pre-disposition for, but if I went from power lifting for five years to running/marathoning for the next five (or more) years, there would definitely be a change in my body. I attribute that to the ratio of slow twitch to fast twitch fibers changing as an adaptation to training, not hyperplasia. Just wanted to clear up my position!
I agree there'd be a change in your body, but I'm not so sure that a change in the ratio of fibers would take place. As I understand it, your Type II fibers would atrophy after stopping the lifting, but wouldn't decrease in number. They'd just get smaller. Correct me if I'm wrong, but I'm under the impression that it's impossible to change the RATIO of fibers (measured by number of each type) without hyperplasia. Now if you mean ratio by mass/size, that's different.
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