Trying to understand DOMS and HST

[LucidLight]

First of all Let me start by saying that until I found this website I fell squarely into the HIT camp. As I read more and learn the actual science behind muscle building I started to rethink things. However I need to get some stuff clearified before I can adapt my way of thinking.

1. What exactly is DOMS (delayed onset muscle soreness)? What is happening chemically before and during DOMS? Is the muscle actually healling from an intense or unaccustomed work out or is something else happening?

2. It has been proven that negatives promote better strength gains (not sure about size gains) and that negatives or eccentic contractions will promote the occurrence of DOMS and the level of soreness you are obtain. So, wouldn't DOMS be a good indicator for progressing to something your muscle is not used to doing? Why not keep trying to do more intense exercise every workout?

3. What is the chemical reason that going to failure taxes your CNS more than not going to failure. Negatives are in a sence "failure". The weight is so heavy that you fail to move the weight concentricly and are only able to slow its decent.

4. Is DOMS and indicator that you have taxed your CNS? If it is, shouldn't you wait longer before your CNS is recovered before working out again?

5. I believe that one workout of going to failure will promote more muscle\strength growth than just one workout of using HST principles. Is this so? Isn't just the fact that HST allows you to train 2 to 3 times more that makes it better, not the intensity of the individual work out?

6. Does DOMS have any direct negative effects other than the soreness limiting your ability to have an effective workout.
Does it chemically hinder the growth of new muscle tissue?

I think once I understand these question I will be much more willing to jump on the HST bandwagon. Even if I am not, this site has been most excellent in understanding the basics of muscle growth.

 

[imported_dkm1987]

Quote[/b] (LucidLight @ April 11 2005,1:24)]1. What exactly is DOMS (delayed onset muscle soreness)? What is happening chemically before and during DOMS? Is the muscle actually healling from an intense or unaccustomed work out or is something else happening?

2. It has been proven that negatives promote better strength gains (not sure about size gains) and that negatives or eccentic contractions will promote the occurrence of DOMS and the level of soreness you are obtain. So, wouldn't DOMS be a good indicator for progressing to something your muscle is not used to doing? Why not keep trying to do more intense exercise every workout?

1. Coudreuse JM, Dupont P, Nicol C. summed it up well in a review last year

Quote[/b] ]Acidosis, muscle spasm and microlesions in both connective and muscle tissues may explain the symptoms. However, inflammation appears to be the most common explanation. Interestingly, there is strong evidence that the progression of the exercise-induced muscle injury proceeds no further in the absence of inflammation. Even though unpleasant, DOMS should not be considered as an indicator of muscle damage but, rather, a sign of the regenerative process

2.Although DOMS can be a sign, growth can occur even with out DOMS and therefore using the DOMS factor to identify if growth is happening wouldn't be the best indicator.

Quote[/b] ]Delayed-onset muscle soreness does not reflect the magnitude of eccentric exercise-induced muscle damage.

Nosaka K, Newton M, Sacco P.

Exercise and Sports Science, Graduate School of Integrated Science, Yokohama City University, Yokohama, Japan.

This study investigated the relationship between delayed-onset muscle soreness and other indicators of muscle damage following eccentric exercise. Male students (n = 110) performed 12 (12ECC), 24 (24ECC), or 60 maximal eccentric actions of the elbow flexors (60ECC). Maximal isometric force, relaxed and flexed elbow joint angles, upper arm circumference, and plasma creatine kinase activity were assessed immediately before and after, and for 4 days after exercise..... Because of generally poor correlations between DOMS and other indicators, we conclude that use of DOMS is a poor reflector of eccentric exercise-induced muscle damage and inflammation, and changes in indirect markers of muscle damage and inflammation are not necessarily accompanied with DOMS.

I'll let others touch on the rest

 

[vicious]

DOMS is the holy grail, the 42, and That Which Has No Name of bodybuilding. Just ask Vince.

Lucid, if you have a lot of time (oh, a weekend or so), do a search for member littledoc. There's a pretty scary thread that covers a crap load of philosophical and physiological theory about why intensity, HST, and why we don't go all-out with every workout. It's rambling, yet interesting. And you'll get to meet Vince.

cheers,
Jules

 

[imported_dkm1987]

Quote[/b] (vicious @ April 12 2005,8:20)]Just ask Vince.  

Lucid, if you have a lot of time (oh, a weekend or so), do a search for member littledoc.  

How about we don't

Here is that thread and a couple more. As our man Vicious said please make sure you have time to read this it will take a while

littledoc's thread

Vince Thread 1

The Biggie, 37 pages

There are more if you wish to take the time out of your life. Please note the recurring theme that eminates from Vince.

 

[vicious]

Quote[/b] ]the Biggie, 37 pages

 

 

 

 

 

 Mother of God . . .

Lucid: in a sense, the given HST program is both a practical application and on-hand teaching tool of current theories on physiology pertaining to muscle hypertrophy. You may, in the end, try something very different (say, DC training), but you'll never see training the same way again.

In regards to your DOMS inquiry, the HST program holds to the belief that the best long-term gains are derived from moderate, but frequent and consistent stimulation of growth executed over a long period of time. The underlying assumption, of course, is that each session stimulates some growth, which will not always be true with HIT and many other programs.

cheers,
Jules

 

[imported_dkm1987]

Quote[/b] (vicious @ April 12 2005,9:06)]

Quote[/b] ]the Biggie, 37 pages

 

 

 

 

 

 Mother of God . . .

I wish you had been coming around then, it would have been quadruple interesting with your input

 

[vicious]

You'd mean it would have been quadruple as long.  Here, Bryan, we wrote your book for ya!  

Vince is cool in my book.  If you argue science, he'll say he doesn't believe in the science.  If you argue anecdotal evidence, he'll cite Flex magazine as his anecdotal evidence.  And if you still argue with him, he'll repost.  This man should run as a Republican!  

Hmm, caught this in the 37-page thread . . .

Quote[/b] ]"Chris Cormier's trainer had him on a HST routine [with great success] - possibly currently also...

Holy crap. You guys understand that if Cormier eventually becomes the Man who overthrew Coleman . . .

cheers,
Jules

 

[LucidLight]

Thanks guys. It is going to take a while to get thought all that info. What I would like to know is why would one set to failure of like 12 reps tax the CNS more, than 2 sets of 10 reps.

 

[imported_dkm1987]

Quote[/b] (LucidLight @ April 14 2005,3:27)]What I would like to know is why would one set to failure of like 12 reps tax the CNS more, than 2 sets of 10 reps.

Working to failure invokes different balances within the muscles infrastructure, Phosphorus levels, Ca++ Levels, magnesium, glycogen and a whole list. Over time chronic peripheral fatique can accrue into acute Central Fatique, this can lead to overtraining symtoms. Once overtrained the body then MUST recoup/recover. We simply avoid this in order to work out more frequently. Therefore 2 sets of ten reps is less fatiqueing to the peripheral tissue than working to all out failure, if your two sets of 10 are not fatiqueing in nature.

There is a whole thread here called "Training to failure, indespensible for growth or not" from last year give it a once over.

 

[Bryan Haycock]

Quote[/b] (LucidLight @ April 14 2005,2:27)]Thanks guys. It is going to take a while to get thought all that info. What I would like to know is why would one set to failure of like 12 reps tax the CNS more, than 2 sets of 10 reps.

neural output goes up as fatigue goes up, even if the force produced declines at the same time.

I participated in an interesting study when I was in grad school. It was an EMG set up where we looked at the effects of fatigue on EMG output.

We hooked up the biceps and then compared different scenarios. One was a steadily increasing load while holding the biceps/arms at 90 degrees. It created a nice slope. Then we compared a fixed load but let the biceps fatigue under that load. At first the EMG was pretty steady, no real increase. But then all of a sudden when you hit that "wall" where fatigue begins it sloped up just like the increasing load condition.

Not to mention other artifacts like synchronization etc.

So, the point is, as long as the weight is heavy enough, there is no need to strain the nervous system if you don't have to. Either way the muscle will get the same stimulus based on how much weight and how many times you lift it. One way will just increase fatigue and delay recovery.

Strength training is a different issue of course.

 

[NWlifter]

DOMS


The sensation of tenderness appears to be triggered by the loss of cellular calcium homeostasis (Clarkson, Cyrnes, McCarmick, Turcotte, & White, 1986; Friden & Lieber, 1997' Jackson, Jones, & Edwards, 1984) due to the activity-induced disruption of sarcomeres. A high intracellular calcium concentration activates proteolytic and lipolytic systems that initiate the degradation of cellular structures (Armstrong, 1990). Because this inflamatory process has a time course smilar to that of the heightened tenderness (Lieber, Schimtz, et al., 1994) and thre is an appropriate activation of the immune system (Malm, Lenkel, & Sjodin, 1999), the sensation of soreness is usually attributed to the inflammatory response.

 

[yshemesh]

"how about we don't"
lmao

i could get DOMS from lots of pushups
that doesn't mean they provided a better stimulus for growth than my 5rm bench. so now that that crap is outta the way --

i want to put another issue on the table, that has something to do with this intensity/failure. the new wave on the board of clustering and stopping the set when you start slowing down, anything to avoid fatigue. i tried it for a few weeks.

first, i'd think it's much less helpful for added strength benefits, correct ? ( yeah i know it's HST, but still )
when i stopped trying to avoid fatigue so much, i realized i could lift much more than i was. once, in the middle of a set, i was thinking, let's see where i can take this. the weight started to slow down at 5, but i kept pushing and i got 10 !!
and yeah i was still able to keep up with frequency.

i'm NOT saying clustering doesn't work. just that it promotes wussiness !!!!!!!!!! if not done correctly.

 

[imported_dkm1987]

Quote[/b] (yshemesh @ April 15 2005,4:22)]i'd think it's much less helpful for added strength benefits, correct ? ( yeah i know it's HST, but still )
when i stopped trying to avoid fatigue so much, i realized i could lift much more than i was. once, in the middle of a set, i was thinking, let's see where i can take this. the weight started to slow down at 5, but i kept pushing and i got 10 !!
and yeah i was still able to keep up with frequency.

As Bryan pointed to above, strength is different, and pushing yourself to failure when STRENGTH training does have benefits.

There is also the issue of strength endurance, IE going to 10 reps vs. 5.

But honestly is you were working with your 5RM, and you acheived 10 reps then it wasn't your true 5RM.

Lastly, Bryan has pointed out many times that if someone can work to failure and has the recouperative power needed to maintain frequency, then do it. Unfortunately most do not and burn out or injury happens, hampering frequency.

 

[yshemesh]

the point was, when i clustered i wasn't even looking to challenge my RM's. like you pinted out.

 

[NWlifter]

Hey DKM, on the fatigue, failure stuff....

I just received Komi's "Strength and Power in Sport", it's quite enlightening so far. He mentions a couple things in chapter two of the book. Just getting started and already getting some good info.!

He's speaking of the growth of FT and the slow conversion process of fiber types and sub-types

1) FT will not hypertrophy without high frequency stimulation. This doesn't mean 'to failure' but it does mean it 'appears' the rate coding at least has to get up there a bit. Which means not stopping a set 'too soon'

2) Regular (daily, even 5% of a day) stimulation of a fiber will cause it to produce type I or slow MHC molecules. He talks how this is not a problem if the load is lower, so that only ST fibers are receiving this daily stimulation, he says if higher loads are used then FT fibers are recruited and will start producing a slower MHC.

So far, GREAT book!

Ron

 

[imported_dkm1987]

Quote[/b] (NWlifter @ April 15 2005,10:03)]1) FT will not hypertrophy without high frequency stimulation. This doesn't mean 'to failure' but it does mean it 'appears' the rate coding at least has to get up there a bit. Which means not stopping a set 'too soon'
2) Regular (daily, even 5% of a day)  stimulation of a fiber will cause it to produce type I or slow MHC molecules. He talks how this is not a problem if the load is lower, so that only ST fibers are receiving this daily stimulation, he says if higher loads are used then FT fibers are recruited and will start producing a slower MHC.
So far, GREAT book!
Ron

1. What is defined as too soon, how would one know? Without an EMG on hand to look at this one can only assume, enough TUT without necessarily going to failure. So we get back to what's enough TUT, looking at Aagard, Enoka and others there is a specific adaptation neurally to training and this "Conditoining Effect" affects both tissue specific response and neural response, so it goes back to Bryan's statement of it varies based on conditioning.

2. 5% of a 24 hour day is 1.2 hours, so I can definately see this as a correlation to ST, but are you trying to say that above 85% of RM work will still increase type 1 isoform. If so I would have to agree because you are still working type 1 motor units along with type II. But to say that when consistenly working above 85%RM intensities that more type II isoforms will shift towards a ST MHC then I wold have to say that goes against the studies I have seen.

Or am I misreading what you are saying?

 

[NWlifter]

Quote[/b] ]1. What is defined as too soon, how would one know? Without an EMG on hand to look at this one can only assume, enough TUT without necessarily going to failure. So we get back to what's enough TUT, looking at Aagard, Enoka and others there is a specific adaptation neurally to training and this "Conditoining Effect" affects both tissue specific response and neural response, so it goes back to Bryan's statement of it varies based on conditioning.

True, it's hard to know when 'too soon' is. I found a study comparing frequencies of stimulation, at low frequencies hypertrophy was indeed not evident. The problem might be related to that a fiber at low frequencies is not experiencing fused tetanus, this means there is no direct solid tension on the fiber.
(neurally: One thing to remember, once trained, we can maximally activate our muscles, most the 'neural' stuff that happens after that is related to coordination and sub-conscious cheating to ease the load. )

Quote[/b] ]2. 5% of a 24 hour day is 1.2 hours, so I can definately see this as a correlation to ST, but are you trying to say that above 85% of RM work will still increase type 1 isoform. If so I would have to agree because you are still working type 1 motor units along with type II. But to say that when consistenly working above 85%RM intensities that more type II isoforms will shift towards a ST MHC then I wold have to say that goes against the studies I have seen.

Yes and no...
Every study I have seen involving weightlifting, shows conversion of IIb(x) to IIa MHC. Long isometrics or too frequent of stimulation appears to simulate a need for postural muscle. This is the conjecture on why even IIa fibers will start producing type I isoforms with too frequent of stimulation.
Ron

 

[NWlifter]

Here is an excerpt from Goldspink
http://bst.portlandpress.co.uk/bst/030/0285/bst0300285.htm

At one stage it was thought that the frequency (he means frequency as in HZ) of stimulation was the important factor in determining fibre type transition. However, it was shown that higher stimulation frequencies were just as effective in producing the fast-to-slow switch [ 7]. Using plaster-cast limb immobilization, stretch alone was found to induce fast fibres to lay down slow-type sarcomeres [ 8], and under these conditions virtually no electromyograph signal can be detected [ 9]. Therefore it is unlikely that stimulation frequency is the primary determinant of muscle phenotype. Instead, it appears to be the particular physical activity that this induces that is important, rather than the electrical stimulation itself. In our experiments, more complete reprogramming of the muscle was obtained when stretch was combined with high-frequency stimulation. This indicates that the signal for the fast-to-slow change is mechanical strain. This makes physiological sense, as it can be argued that the muscle cells, by responding to isometric overload, are adapting to an increased postural role.


http://ajpregu.physiology.org/cgi/content/full/276/2/R414

The purpose of this study was to determine the effect of endurance-oriented exercise on myosin heavy chain (MHC) isoform regulation in human skeletal muscle. Exercise consisted of 1 h of cycle ergometer work per day at 75% maximal oxygen consumption for seven consecutive days. Muscle was obtained before the first bout of exercise, 3 h after the first bout of exercise, and before and 3 h after the final exercise bout on day 7 (n = 9 subjects). No changes in MHC mRNA (I, IIa, IIx) were evident after the first exercise period. There was, however, a significant (P < 0.05) decline (30%) in MHC IIx mRNA 3 h after the final training bout. An interesting finding was that a higher pretraining level of MHC IIx mRNA was associated with a greater decline in the transcript before (r = 0.68, P < 0.05) and 3 h after (r = 0.82, P < 0.05) the final exercise bout. These findings suggest that MHC IIx mRNA is downregulated during the early phase of endurance-oriented exercise training in human skeletal muscle but only after repeated contractile activity. Pretraining MHC IIx mRNA content may influence the magnitude of this response.

 

[imported_dkm1987]

Ron, just for you  

Be sure to work your way though the references

<a href="http://jap.physiology.org/cgi/content/full/90/1/345" target="_blank">Plasticity in Skeletal, Cardiac, and Smooth Muscle
Invited Review: Effects of different activity and inactivity paradigms on myosin heavy chain gene expression in striated muscle</a>

 

[NWlifter]

Hey that was good stuff! Thanks! So regular OR intermitant use of muscles shifts isoforms to the IIa type. OR IIb to IIx. And it seems that's good as elite weightlifters have high proportions of IIa fibers. That clears a lot of this up

I liked this abstract from the references...

Quote[/b] ]Resistance training frequency: strength and myosin heavy chain responses to two and three bouts per week.

Carroll TJ, Abernethy PJ, Logan PA, Barber M, McEniery MT.

Department of Human Movement Studies, The University of Queensland, Brisbane, Australia.

Seventeen subjects performed resistance training of the leg extensor and flexor muscle groups two (2/wk) or three (3/wk) times per week. Changes in the relative myosin heavy chain (MHC) isoform contents (I, IIa and IIx) of the vastus lateralis and isometric, isokinetic and squat-lift one-repetition maximum (1 RM) strength were compared between conditions after both a common training period (6 weeks) and number of training sessions (18). After 6 weeks and 18 sessions (9 weeks for the 2/wk group), increments in 1RM strength for the 3/wk and 2/wk groups were similar [effect size (ES) differences approximately 0.3, 3/wk &gt; 2/wk], whereas the 2/wk group presented greater isokinetic (ES differences = 0.3-1.2) and isometric (ES differences approximately 0.7) strength increases than the 3/wk condition. A significant (P &lt; 0.05) increase in MHC IIa percentage was evident for the 2/wk group after 18 sessions. Both training groups exhibited a trend towards a reduction in the relative MHC IIx and an increase in MHC IIa contents (ES range = 0.5-1.24). However, correlations between changes in the strength and MHC profiles were weak (r2: 0.0-0.5). Thus, isometric and isokinetic strength responses to variations in training frequency differed from 1RM strength responses, and changes in strength were not strongly related to alterations in relative MHC content

This was cool too....

Quote[/b] ] the dose-response study revealed that as few as 10 contractions (40 s) per training session were capable of elevating the expression of the fast type IIX MHC mRNA isoform by approximately 250%. These collective findings demonstrate that high-resistance training is a powerful modulator of MHC protein isoforms and that pretranslational mechanisms are very sensitive to even small amounts of high-resistance training.

This is great right here, it doesn't talk about CSA gains, but it does point to the idea that high rate coding ISN'T required to stimulate the protein machinery!

Quote[/b] ] mechanical loading, not stimulation frequency per se, plays a key role in determining the plasticity of myosin heavy chain (MHC) protein isoform expression in muscle undergoing resistance training.

This is really comforting and assures that most the transitions are within the type II isoforms

Quote[/b] ]Neither I MHC composition nor type I fiber percentage changed with training.