Strategic Deconditioning

S

scientific muscle

New Member
This is specifically for Bryan Haycock, as the HST principles are his brain-child.
Deconditioning???

A lot if us continue to have doubts about how well deconditioning really works in the short-term. My thoughts are as follows: Does deconditioning really occur significantly enough to help combat RBE and aid continued hypertrophy in 9-14 days? It would seem to take significantly longer and of course then atrophy becomes a problem.
NWlifter once said he believes that deconditioning will only occur ast the same rate as neuro/muscular atrophy so its one step backwards to get one step forwards....in other words a waste of time.

I love HST, and I am very grateful to Bryan for presenting his research on the subject in a format all of us can understand. But I remain doubtful about this so-called 'Strategic Deconditioning' principle and its effects.

I would like to see Bryan post his thoughts and related research on the subject. Other relevant research papers anyone may have are welcome, but lets keep this thread about research and not just random opinions.

I don't have any relevant papers in my possession at this time, but I know Bryan, Dan and others do.
So please share and discuss!

Thanks.
smile.gif
 
To be fair, I will copy Bryan's post from the HST FAQ on the subject of deconditioning.
<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Though I wish I had more time to fully address your questions here, they will be more fully addressed in one of the HST books. In the mean time, we will try to use the most representative research of SD followed by retraining as we can find (with time constraints). The following study by Hortobágyi and colleagues (Hortobágyi, 2000) is one of the best I have found to date, with special reference to the adaptive changes to both deconditioning and retraining. Here is the full reference:

Hortobagyi T, Dempsey L, Fraser D, Zheng D, Hamilton G, Lambert J, Dohm L. Changes in muscle strength, muscle fibre size and myofibrillar gene expression after immobilization and retraining in humans. The Journal of Physiology 2000 April 1;524 Pt 1:293-304.

For those of you familiar with Medline the full text version is FREE.

But here are some important points brought to light by this and similar studies.

Deconditioning (including complete immobilization or even zero gravity)
1) In vivo studies suggest that a fall in the rate of protein synthesis rather than an increase in protein degradation is the predominant mechanism of atrophy at least during the first few weeks of immobilization in rats (Booth, F. W. &amp; Seider, M. J. (1979). Early changes in skeletal muscle protein synthesis after limb immobilization of rats. Journal of Applied Physiology 47, 974-977) as well as in humans (Gibson, J. N. A., Halliday, D., Morrison, W. L., Stoward, P. J., Hornsby, G. A., Watt, P. W., Murdoch, G. &amp; Rennie, M. J. (1987). Decrease in human quadriceps muscle protein turnover consequent upon leg immobilization. Clinical Science 72, 503-509)

2) In his pioneering work D. F. Goldspink (Goldspink, D. F. (1977). The influence of immobilization and stretch on protein turnover of rat skeletal muscle. The Journal of Physiology 264, 267-282) demonstrated that when the extensor digitorum longus of young rats was chronically stretched while immobilized, the muscle actually underwent hypertrophy. Although this chronic stretch may not be qualitatively equivalent to dynamic muscle lengthening, there is now cumulative evidence to suggest that strength gains (Dudley et al. 1991), muscle hypertrophy (Hather et al. 1991) and myosin heavy-chain (MyoHC) gene expression are specific to the type of mechanical loading (Booth &amp; Thomason, 1991), with greater adaptations occurring if the mechanical stimulus contains muscle lengthening or eccentric contractions compared with concentric contractions.

3) Even though strength loss correlated with muscle fibre atrophy (r = 0·75), the magnitude of strength loss (47 %) was almost 4-fold greater than the magnitude of fibre atrophy (11 %) [with 3 weeks of immobilization]

4) Greater type II than type I muscle fibre atrophy occurred after elbow immobilization in the triceps brachii (30 vs. 25 %, MacDougall et al. 1980), in the vastus lateralis after an 11 day space flight (36 vs. 16 %, Edgerton et al. 1995), lower leg suspension (12 vs. 6 %, Berg et al. 1993) and knee immobilization (19 vs. 15 %, Veldhuizen et al. 1993). In contrast, others reported that atrophy was greater in type I than type II fibres (46 vs. 37 %, Sargeant et al. 1977; 26 vs. 1 %, Häggmark et al. 1981). In the present work type I and type II fibres atrophied to about the same extent, 13 and 10 %.

Retraining
1) In the current work, resumption of spontaneous activity (i.e. just being up and around) for 2 weeks after the cast was removed resulted in about 90 % recovery of muscle strength and 95 % recovery of muscle fibre size. [That’s an 10% increase in muscle size in only two weeks WITH NO TRAINING!]

2) 3 weeks of immobilization significantly and uniformly reduced type I, IIa and IIx muscle fibre areas by 13, 10 and 10 %, respectively…Hypertrophy of type I, IIa and IIx fibres relative to baseline was 10, 16 and 16 % after eccentric and 11, 9 and 10 % after mixed training (all P &lt; 0·05) and these gains were significantly (P &lt; 0·05) greater than the hypertrophy after concentric training (4, 5 and 5 %). In addition, the type IIa and IIx fibres were significantly larger after eccentric than after mixed training

3) We observed a significantly faster rate of strength recovery when the exercise program contained eccentric contractions. Muscle strength recovery after 4 weeks was complete when subjects exercised with concentric contractions, whereas recovery to initial levels occurred about 2 weeks faster when pure eccentric contractions were used or added to concentric contractions…Not only was the rate of strength recovery faster with pure eccentric or mixed eccentric and concentric contractions but the strength gains and muscle fibre hypertrophy were also substantially greater compared with pure concentric contractions, confirming most (Komi &amp; Buskirk, 1972; Dudley et al. 1991; Hather et al. 1991; Hortobágyi et al. 1996a, b) but not all (Jones &amp; Rutherford, 1987; Smith &amp; Rutherford, 1995) prior reports. [We are not so interested in strength, but this info is demonstrative of the importance of eccentric training.]


Now this doesn’t speak much towards RBE, but it does demonstrate how muscle tissue responds differently after SD than it does during training. It’s a sliding scale of sensitivity and hypertrophy. When muscle is at its highest sensitivity, it grows most rapidly, and likewise, it grows more resistant to further growth at the same rate. I have other studies on RBE that I may be able to post later.

1. McHugh MP. Recent advances in the understanding of the repeated bout effect: the protective effect against muscle damage from a single bout of eccentric exercise. Scand J Med Sci Sports. 2003 Apr;13(2):88-97.

2: Thompson HS, Clarkson PM, Scordilis SP. The repeated bout effect and heat shock proteins: intramuscular HSP27 and HSP70 expression following two bouts of eccentric exercise in humans. Acta Physiol Scand. 2002 Jan;174(1):47-56.

3: Proske U, Morgan DL. Muscle damage from eccentric exercise: mechanism, mechanical signs, adaptation and clinical applications. J Physiol. 2001 Dec 1;537(Pt 2):333-45.

4: Stupka N, Tarnopolsky MA, Yardley NJ, Phillips SM. Cellular adaptation to repeated eccentric exercise-induced muscle damage. J Appl Physiol. 2001 Oct;91(4):1669-78.

5: McHugh MP, Connolly DA, Eston RG, Gleim GW. Exercise-induced muscle damage and potential mechanisms for the repeated bout effect. Sports Med. 1999 Mar;27(3):157-70.

6: Brown SJ, Child RB, Day SH, Donnelly AE. Exercise-induced skeletal muscle damage and adaptation following repeated bouts of eccentric muscle contractions. J Sports Sci. 1997 Apr;15(2):215-22.

7: Brown SJ, Child RB, Day SH, Donnelly AE. Indices of skeletal muscle damage and connective tissue breakdown following eccentric muscle contractions. Eur J Appl Physiol Occup Physiol. 1997;75(4):369-74.

8: Ebbeling CB, Clarkson PM. Exercise-induced muscle damage and adaptation. Sports Med. 1989 Apr;7(4):207-34.


- Bryan Haycock</div>
 
I don't want the thread to lose the focus you want, but I have 1 comment to make. There is, in my opinion, a sweet spot in terms of the deconditioning/atrophy curve where its not &quot;one step backwards to get one step forwards.&quot; It's probably highly variable between individuals as well. As far as my own case study, some of my best progress has come after layoffs. In my own experience, 9-14 has little if any effect for my genetics.
 
Well as far as actual papers you will be hard pressed to find any that have used ambulatory subjects.

Kadi did a study &quot;The effects of heavy resistance training and detraining on satellite cells in human skeletal muscles &quot; in which they trained then de-trained while looking at fiber size and sat cell activity.

tjp_387_f6.jpeg

Figure 6.  Fibre area
Mean cross-sectional area of muscle fibres before training (Pre), after 30 (T30) and 90 (T90) days of training and following 3 (D3), 10 (D10), 30 (D30), 60 (D60) and 90 (D90) days of detraining. * Significantly different from Pre; # significantly different from T90.

What makes this paper stand out is not only that they measured pre and post training and post training post de-training fiber size changes but they also noted some very interesting plastic changes in the sat cell population as well. More importantly these subjects were not bed ridden or suspended which puts a real world twist to the what can occur in a detraining state.
 
This one is interesting as well, even though it's on old farts like me, it still shows that some adaptations can take a while before returning to a pretrained state, in this case strength.

Strength training and detraining effects on muscular strength, anaerobic power, and mobility of inactive older men are intensity dependent.Fatouros IG, Kambas A, Katrabasas I, Nikolaidis K, Chatzinikolaou A, Leontsini D, Taxildaris K.
University of Thrace, Komotini, Greece. fatouros@otenet.gr

BACKGROUND: Although strength training (ST) enhances physical function in the elderly, little is known about the effect of training intensity on training and detraining adaptations in musculoskeletal fitness. OBJECTIVE: To determine the effect of exercise intensity on strength, anaerobic power, and mobility of older men subjected to a 24 week ST protocol followed by prolonged detraining. METHODS: Fifty two healthy but inactive older men (mean (SD) age 71.2 (4.1) years) were assigned to a control (n = 14), low intensity training (LIST; n = 18; 55% 1RM), or high intensity training (HIST; n = 20; 82% 1RM) group. They carried out a 24 week, whole body (10 exercises, two to three sets/exercise) ST programme followed by a 48 week detraining period. Upper and lower body strength, anaerobic power (Wingate testing), and mobility (timed up and go, walking, climbing stairs) were measured at baseline and immediately after training and during detraining. RESULTS: Although low intensity training improved (p&lt;0.05) strength (42-66%), anaerobic power (10%), and mobility (5-7%), high intensity training elicited greater (p&lt;0.05) gains (63-91% in strength, 17-25% in anaerobic power, 9-14% in mobility). All training induced gains in the LIST group had been abolished after four to eight months of detraining, whereas in the HIST group strength and mobility gains were maintained throughout detraining. However, anaerobic power had returned to baseline levels after four months of detraining in both groups. CONCLUSIONS: Higher intensity training protocols induce greater gains in strength, anaerobic power, and whole body physical function of older men. Moreover, higher intensity training may maintain the gains for more prolonged periods after training ceases.
 
Well I'm not Bryan but I did want to continue this discussion so here are a couple more studies.

The first is a recent one and although it does not deal with hypertrophy specifically it does again point to a much longer strength retention albeit these were seniors citizens and the same effect may not be true for the well trained younger populations.

J Strength Cond Res. 2007 Aug;21(3):813-8. Links
Detraining in the older adult: effects of prior training intensity on strength retention. Harris C, DeBeliso M, Adams KJ, Irmischer BS, Spitzer Gibson TA.
Center for Orthopaedic and Biomechanics Research, Department of Kinesiology, Boise State University, Boise, Idaho 83725, USA.

In this study, we assessed the influence of training intensity on strength retention and loss incurred during detraining in older adults. In a previous study, untrained seniors (age = 71.0 +/- 5.0; n = 61) were randomly divided into 3 exercise groups and 1 control group. Exercise groups trained 2 days per week for 18 weeks with equivalent volumes and acute program variables but intensities of 2 x 15 repetitions maximum (RM), 3 x 9RM, or 4 x 6RM. Thirty of the original training subjects (age 71.5 +/- 5.2 years) participated in a 20-week detraining period. A 1RM for 8 exercises was obtained pre- and posttraining and at 6 and 20 weeks of detraining. The total of 1RM for the 8 exercises served as the dependent variable. Analysis of variance procedures demonstrated significant increases in strength with training (44-51%; p &lt; 0.05), but no group effect. All training groups demonstrated significant strength decreases at both 6 and 20 weeks of detraining independent of prior training intensity (all group average 4.5% at 6 weeks and 13.5% at 20 weeks; p &lt; 0.04). However, total-body strength was significantly greater than pretraining values after the detraining period (all group average 82% at 6 weeks and 49% at 20 weeks; p &lt; 0.001). The results suggest that when older adults participate in progressive resistance exercise for 18 weeks, then stop resistance training (i.e., detrain), strength losses occur at both 6 and 20 weeks of detraining independent of prior resistance training intensity. However, despite the strength losses, significant levels of strength are retained even after 20 weeks of detraining. The results have important implications for resistance-trained older adults who could undergo planned or unplanned training interruptions of up to 5 months.

This next one is on resistance trained women and what is important to note is the hypertrophy response during the de-training period and then the retraining period. What isn't shown in the abstract is what the detraining period was, was it a complete non training period or was it a reduced training period?

J Appl Physiol. 1991 Feb;70(2):631-40. Links
Strength and skeletal muscle adaptations in heavy-resistance-trained women after detraining and retraining. Staron RS, Leonardi MJ, Karapondo DL, Malicky ES, Falkel JE, Hagerman FC, Hikida RS.
Department of Zoological and Biomedical Sciences, College of Osteopathic Medicine, Ohio University, Athens 45701.

Six women who had participated in a previous 20-wk strength training study for the lower limb detrained for 30-32 wk and subsequently retrained for 6 wk. Seven untrained women also participated in the 6-wk &quot;retraining&quot; phase. In addition, four women from each group volunteered to continue training an additional 7 wk. The initial 20-wk training program caused an increase in maximal dynamic strength, hypertrophy of all three major fiber types, and a decrease in the percentage of type IIb fibers. Detraining had relatively little effect on fiber cross-sectional area but resulted in an increased percentage of type IIb fibers with a concomitant decrease in IIa fibers. Maximal dynamic strength decreased but not to pretraining levels. Retraining for 6 wk resulted in significant increases in the cross-sectional areas of both fast fiber types (IIa and IIab + IIb) compared with detraining values and a decrease in the percentage of type IIb fibers. The 7-wk extension accentuated these trends such that cross-sectional areas continued to increase (nonsignificant) and no IIb fibers could be found. Similar results were found for the nonpreviously trained women. These data suggest that rapid muscular adaptations occur as a result of strength training in previously trained as well as non-previously trained women. Some adaptations (fiber area and maximal dynamic strength) may be retained for long periods during detraining and may contribute to a rapid return to &quot;competitive&quot; form.
 
Okay, I know I don't read studies as well as Dan, but is it just me or do these studies seem to support SD? It seems that a short break, while not resetting you totally back to untrained status, does seem to have a significant effect.

It looks like 10 days off actually resulted in an increase in the number of satellite cells, which then dropped a lot after 30 days. In the graph already posted in this thread the muscle fiber CSA was back to about the same as after 30 days of training, while not back to pretrained status, still wouldn't that make a difference when you return to training?
Again, I'm not an expert at reading this stuff, but it suggests to me that perhaps 10 days would be close to the optimal length for time off. Anything longer than that doesn't do much good. This is close to being in line with the suggested length for SD.

Is this what you guys got out of it or am I just way off?
 
I'm worse than Totentanz - completely dumb when it come to reading studies of the kind presented. Could someone summarize the ideal SD time, something like ... Less than XX days of SD is bad because blah-blah-blah-blah-blah, and more than XX days is bad because blah-blah-blah-blah-blah? Makes it much simpler to read.

This would be something I'd follow to the letter. In my almost two years of lifting, my shortest SD was 6 days, and my longest was 12 days.
 
Those are very interesting Dan, thank you.

They look at detraining but not potential deconditioning for the purpose of HST. Of course I don't suspect any study done on SD specifically for HST will be done any time soon!

But still, very good stuff Dan, especially the Kadi study.
 
The Kadi study was indeed interesting and I would love to see this repeated in trained subjects.

To answer Tot, the myonuclear domain increase significantly during the training yet with little to no new myonuclear numbers, therefore the classical explanation of sat cell nuclear donation did not readily occur in this case. What did occur is the domain size grew with concommittant increase in the sat cell pool number and hypertrophy.

Once training ceased the sat cell number remained increased yet the myonuclear domains gradually decreased and did not reach a significant decrease until 30 days. Yes at 10 days the number had decreased but not a significant amount.

Now you can look at this 2 ways, one way would be what you speculate. Detraining for 10 ten days is sufficient to cause the intital decreases seen and therefore this is a long enough period of time. The other way is to say that detraining for 10 days does very little to revert back to a pre-training state and in order to see a true reversion one would need to de-train for much longer time frames.

Importantly and what I think is worth mentioning is how the sat cell pool remains elevated for quite some time. This indicates that once proliferated they remain at the ready for future assaults, in some way you could classify this as another type of muscle memory phenomena.

Now whether or not de-training for a period of 10-14 days does truly revert the muscle cells decreased anabolic potential or not is yet to be studied. This is especiallly true in ambulatory subjects as most of the studies done have used either limb suspension or anti-gravity which total unloading may have a much more immediate and pronounced effect.

So with this study in mind one can absolutely say, yes there is a detraining effect in ambulatory subjects but the timeframe for this effect may be longer than those subjects who are experiencing a complete unloading period.
 
<div>
(scientific muscle @ Mar. 30 2008,17:16)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">They look at detraining but not potential deconditioning for the purpose of HST.  Of course I don't suspect any study done on SD specifically for HST will be done any time soon!

But still, very good stuff Dan, especially the Kadi study.</div>
Well actually the Kadi study is doing exactly that, looking at deconditioning as the plasticity of the nuclear domain is a training or de-training effect.
 
<div>
(Totentanz @ Mar. 30 2008,11:33)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">Okay, I know I don't read studies as well as Dan, but is it just me or do these studies seem to support SD? It seems that a short break, while not resetting you totally back to untrained status, does seem to have a significant effect.</div>
Well, the last study that Dan gave didn't seem to support SD, but the deconditioning period was very long (31 weeks). Doesn't sound very strategic to me!
 
Very, very interesting thread. Thanks to Sci for starting this and Dan for providing the studies. I will look into them in more detail as soon as I have the time.

Unfortunately, I don't have anything to add at this time, but the purpose of this post is double;

1. Bump. I would love to see Bryan replying.

2. Since it is hard to draw a definitive conclusion from the studies and an HST-specific deconditioning study seems a bit distant, maybe it would be interesting to start a new thread based on everyone's experiences on the subject. Of course it won't be scientific but most of the members of this forum have experimented with SD ourselves, so we might be able to collectively provide some positive feedback.

Thoughts, ideas?

Best regards,
Dimitris
 
Dan has already posted some of the most relevant research demonstrating the effects of Deconditioning (a.k.a. detraining) on muscle tissue. There are others but none that offer anything more than has been posted. There are no studies set up specifically to prove or disprove SD as I have outlined it for HST.

Perhaps what is lacking so far in this thread is an understanding of where I got the concept from. It didn’t come from reading research suggesting that detraining can be good for muscle growth. Instead, it came from frustration brought on by something called the Repeated Bout Effect (RBE). Anyone who has trained for more than 12-24 months knows that growth slows significantly over time.

I have been training for many years (~30 now). I have spent most of those years training at the mercy of the RBE. Understanding that RBE is a result of a specific stimulus, it was clear that only the opposite stimulus could do anything to reverse the growth-stagnating effects of the RBE.

Then, I came across a paper demonstrating the effect of detraining on fiber types. Basically training causes a shift in fiber types which persists (for a time) after training ceases. This shift facilitates hypertrophy. Many people experienced this inadvertently and called it “muscle memory” because of the heightened responsiveness of their muscle tissue to the loading stimulus when they resumed training.

So, I thought, once we can no longer increase the growth stimulus by adding weight, perhaps we can increase the sensitivity of the tissue to the load that we can apply? How? By temporarily creating an environment opposite that which caused the growth resistance in the first place…by detraining. But, because of the specific concern of hypertrophy (vs strength) I decided “deconditioning” was a more specific descriptor of what I was trying to accomplish.

My concern was about losing muscle while deconditioning. It had to be a period of time long enough to increase the growth responsiveness of the tissue, but not so long as to cause atrophy of actual contractile proteins. 10-14 days seemed to be enough. Personally, I feel those guys who have been lifting for many years could stand even longer deconditioning periods with no long term atrophy.

Over time, other benefits of deconditioning, and the periodic increase in rep ranges, began to manifest themselves. Specifically for those with joint pain. This was a welcome discovery. HST has always been a method for people who are life time lifters. After all, if you only intend on lifting for 6 months or a year, just push through to the end…don’t worry about deconditioning.

Ok, I don’t know if that helped this discussion or not, but that’s where the idea of SD came from. It is an attempt to overcome the stagnating effects of the RBE when other options aren’t possible. It’s geared towards lifters who intend on training for many years. It is a strategy that serves the most benefit to those who have already trained for several years. It is a way of increasing the sensitivity of muscle tissue to the loading stimulus once the RBE has become a significant barrier to further gains.
 
Thanks Bryan! I know you are a busy guy, but your input is greatly appreciated. Its good to know your thoughts on it, as I was wondering if any of your views had changed. It seems you are still quite confident in the HST principles as originally laid out. The more I learn, the more I see how thoroughly you thought out HST.

I can hardly wait until the HST book comes out, I am sure it will be an awesome read.
smile.gif
 
<div>
(Bryan Haycock @ Apr. 15 2008,1:08)</div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE">...
Over time, other benefits of deconditioning, and the periodic increase in rep ranges, began to manifest themselves. Specifically for those with joint pain. This was a welcome discovery. HST has always been a method for people who are life time lifters. After all, if you only intend on lifting for 6 months or a year, just push through to the end…don’t worry about deconditioning.
...</div>
Wouldn't this probably mean that it is best to use SD every 3 continuous HST cycles instead of 1?
 
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