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Started By Analyzer (CDA, id, U.S.A.)

Started on: 2/11/2006 1:37:49 PM, viewed 2168 times
Energetic info. for Jeff

I′ll post articles, followed by posts, studies ect. Give me a few to get them all up before replying 🙂

This Topic has 63 Replies: Displaying out of 63 Replies:

Analyzer (CDA, id, U.S.A.) on 2/11/2006 1:37:59 PM


revised edition

Ron Sowers


There are several paths that lead to upregulated protein synthesis in resistance training. It would be naive to focus completely on any one, or to neglect the aspects of any one of the various signaling factors. Many times, a means is thought of as the actual stimulation. Or more simply, a method of applying a stimulation is deemed as an actual path of stimulation. An important marker for the hypertrophic stimulus, lies in the energetic cost of the set, usually in reference to the time span per amount of energy consumed. This is the energetic theory.


The energetic theory is one in which the energetic cost of the contractions, or sum of contractions, is used as a measurement tool for the upregulation of protein synthesis.(14) Many debate this, usually from a lack of understanding. An opposing point might be, that running or aerobics burn ample energy but are not a good stimulus for hypertrophy. This is true, but is wrongly applied to this theory. The energetic cost is more related to the time factor.(5,9,14,21) ie ATP turnover per time period. A muscle fiber uses ATP to break the contraction bonds, and burns it in proportion to the rate at which the sarcomeres are crossbridging.(5) This rate is determined by the neurological input frequency. (rate coding) Exercise which is of low intensity, calls for slower contractions of the motor unit pools. Thus, total energy for the exercise session might be high, but the rate at which ATP is turned over, is low.

The science of the energetic theory is based upon the action of mTOR (mammalian target of rapamycin). mTOR is a regulator of protein synthesis in a muscle cell, simply, it monitors and adjusts protein metabolism (synthesis/degradation) in response to energy requirements. mTOR is very sensitive to amino acids and insulin. How the process appears to work, is AMP-activated protein kinase (AMPK) blunts mTOR during contraction. By mTOR slowing protein synthesis, more ATP is available for use during the contractions. When contractions cease, mTOR rebounds to a higher level, increasing protein synthesis to a greater than resting levels. The presences of amino acids at this time also seem to be required. It′s possible that a high ATP turnover, such as found during heavy or high intensity contractions, blunts mTOR to a maximum or close to maximum level, causing the highest level of rebound afterwards. The rebound level may or may not be proportion, or somehow related to the rate of ATP turnover and/or the time it is blunted. (5,14)


The reason aerobics or endurance activities do not cause this effect, is due to the lower levels of tension. High rates of ATP turnover require high frequency contractions (rate coding).(9) The way in which the CNS manipulates activity is by the level of required effort. First order is to increase recruitment levels, once recruitment becomes full, then, and only then, will firing frequencies be increased. Depending in the muscle or muscle group in question, full recruitment will occur anywhere from approximately 40% (for smaller muscles such as those of the hand) to possibly 95% (upper thigh musculature) of maximum momentary MVC. Other muscles of the torso usually fall somewhere inbetween, such as biceps at approx. 70-80% of momentary maximum MVC. (16,17,18,22)

Note: The reason "momentary" maximum MVC is stressed, is to emphasize that the resistance does not have to be that particular percentage of fresh maximum force (percent of 1RM), but that anytime that level of effort is required, recruitment follows these patterns. For example, if your biceps reach full recruitment at 80% of 1RM, and your 1RM is 100lbs, a single rep with 80 pounds will induce full recruitment, as will the last several reps of a set with your 10RM, where fatigue has limited your strength. Anytime your CNS is putting out a "greater than the minimum" level of effort for full recruitment, rate coding is employed afterwards for further force requirements.


A first thought is usually, "Why not just train to failure?". As far as energetics are concerned, yes, going to failure, and even beyond would cause a high sustained ATP turnover. However, if prudence is not used, there may be a price to pay. Both short term, and long term. For short term, failure training and sustained high frequency type contractions may cause failure in the EC (excitation contraction) systems. Failure may lie in the local propagation of the neural signals.(23) And, it may cause a lengthy recovery period.(24) What this means, is your muscles may be long recovered and ready to go before your local neural system is up to performing those types of contractions with any meaningful intensity again. For long term, over-doing ′ultra high effort training, may also induce a mental toll. This may cause an overtraining of the CNS and systemic factors. Symptoms such as those found with depression may become evident. Loss of appetite, loss of desire, etc. This is not to say one should avoid training hard, or avoid pushing themselves. Caution and intelligent planning/monitoring of recovery factors is recommended.(11,12,24)


How do we know that energetics are even a viable marker? First, studies using occlusion have found rapid increases in size and strength, with very low resistance.(6,7) The fatigue induced from the lack of blood flow, causes the muscles to reach full recruitment and high levels of rate coding with very low whole muscle tension. Damage, or micro-trauma is low to non-existant but marked hypertrophy is still evident. Further, what was once thought to be damage, is now seen to be more of the remodeling process.(13) The smeared Z lines found in exercised muscle cells, are much more evident several days after exercise. If damage from the contractions were causing this, they would be seen immediately. Since their prominence is greater days afterwards, it shows the process of recovery has caused this rather than the acute effects of exercise. Why is this important? This effect (smeared Z lines) is sometimes, but not always, in accordance with DOMS. One of the best explanations of DOMS, describes the effects stemming from high intra-cellular calcium concentrations initiating the process, and the time course of the immune system following the time course of the soreness.(15) High peak tension, eccentrics, and many other aspects of training, including high frequency contractions, can increase intra-cellular calcium concentrations through various means.(3) We′ve all experienced increased levels of DOMS with higher levels of intensity and/or the volume of exercise. Obviously, both of these applications (intensity and volume) are increasing the stimulation of the remodeling process.

Also, a measurement variable, termed TTI (Tension Time Integral), where the average true tension is computated, (4,5) is directly proportional to the energetic cost of a contraction. Even tension signaling factors, such as P70 (70-kDa ribosomal S6 kinase, an important marker for hypertrophy) (9,10) can be tracked by calculating the TTI of the contractions. One can then extrapolate, that ATP turnover (the energetic cost/time) is proportional to the stimulation induced by resistance based contractions. (5,6,7,8,21)

Means To an End

What your seeking, is protein upregulation. Your means is through an application of external resistance that will induce full recruitment and higher levels of rate coding. These factors have been shown to induce a hypertrophic effect. Whether synthesis levels increase beyond degradation levels depends mostly on genetics, recovery factors and proper nutrient timing.


1) Human Skeletal Muscle Hypertrophy Jose Antonio, Ph.D.

2) Carey-Smith R, Rutherford OM: The role of metabolites in strength training. Eur J Appl Physiology

3) Calcineurin Is Required for Skeletal Muscle Hypertrophy* Shannon E. Dunn, Jennifer L. Burns, and Robin N. Michel 1999

4) Influence of tension time on muscle fiber sarcolemmal injury in rat diaphragm

Ercheng Zhu, Alain S. Comtois, Liwei Fang, Norman R. Comtois, and Alejandro E. Grassino

5) Tension-time index, fatigue, and energetics in isolated rat diaphragm: a new experimental model Paul F. Klawitter1 and Thomas L. Clanton2 2003

6) Skeletal muscle size and circulating IGF-1 are increased

after two weeks of twice daily “KAATSU” resistance

training T. Abe, T. Yasuda, T. Midorikawa, Y. Sato, C. F. Kearns, K. Inoue, K. Koizumi, N. Ishii 2005

7) Effects of resistance exercise combined with moderate vascular occlusion on muscular function in humans. Takarada Y, Takazawa H, Sato Y, Takebayashi S, Tanaka Y, Ishii N.

8) CONTROL OF THE SIZE OF THE HUMAN MUSCLE MASS Michael J. Rennie,1,4 Henning Wackerhage,1 Espen E. Spangenburg,3 and Frank W. Booth 2 2004

9) Intracellular signaling specificity in skeletal muscle in response to different modes of exercise Gustavo A. Nader and Karyn A. Esser 2001

10) Phosphorylation of p70S6k correlates with increased skeletal muscle mass following resistance exercise Keith Baar1,2 and Karyn Esser2 1999

11) Resistance exercise overtraining and overreaching. Neuroendocrine responses.

12) Spinal and Supraspinal Factors in Human Muscle Fatigue

S. C. Gandevia Prince of Wales Medical Research Institute, Prince of Wales Hospital and University of New South Wales, Sydney, Australia

13) Evidence for myofibril remodeling as opposed to myofibril damage in human muscles with DOMS: an ultrastructural and immunoelectron microscopic study. Yu JG, Carlsson L, Thornell LE.

14) Regulation of mTOR by amino acids and resistance exercise in skeletal muscle. Deldicque L, Theisen D, Francaux M.

15) Enoka; Neuromechanics of Human Movement 3rd edition (Clarkson, Cyrnes, McCarmick, Turcotte, & White, 1986; Friden & Lieber, 1997′ Jackson, Jones, & Edwards, 1984; Armstrong, 1990; Lieber, Schimtz, et al., 1994; Malm, Lenkel, & Sjodin, 1999)

16) Enoka; Neuromechanics of Human Movement 3rd edition (Deluca, LeFever, McCue & Xenakis, 1982a; Kukulka & Clamann, 1981; Van Cutsem et al,. 1997)

17) Intermuscle differences in activation. Behm DG, Whittle J, Button D, Power K.

18) Influence of exercise and training on motor unit activation. Sale DG.

19) Effects of low-intensity resistance exercise with short interset rest period on muscular function in middle-aged women. Takarada Y, Ishii N.

20) Fatigue contributes to the strength training stimulus. Rooney KJ, Herbert RD, Balnave RJ.

21) Mechanism of work-induced hypertrophy of skeletal muscle. Goldberg AL, Etlinger JD, Goldspink DF, Jablecki C.

22) Motor unit activity during long-lasting intermittent muscle contractions in humans. Christova P, Kossev A.

23) Behavior of motor units in human biceps brachii during a submaximal fatiguing contraction. Garland SJ, Enoka RM, Serrano LP, Robinson GA.

24) Neuromuscular disturbance outlasts other symptoms of exercise-induced muscle damage.Deschenes MR, Brewer RE, Bush JA, McCoy RW, Volek JS, Kraemer WJ.

Analyzer (CDA, id, U.S.A.) on 2/11/2006 1:39:42 PM

Size and Strength

Ron Sowers

(this is a ′sister′ article to "What inroad are you traveling?"


This can be a confusing subject to analyze. I was confused, repeatedly, for years with this one. It really appeared to me (as with many others) that a person′s gain′s in size and strength, (the ratios) can vary depending on training. The answer is yes and no. The qualifications? It depends on what you consider the size of and how you gain your strength.

What science says

The strength of a muscle is very proportionate to it′s CSA (cross sectional area). This fact both enlightens and confuses. On the one hand, we know that size and strength are tied with close constraints. On the other, were perplexed when we gain strength and see no concurrent size increase. What we miss, is this. Science is looking at the increase in fibril CSA. These are the actual contractile elements within the muscle. If the number of these are increased, there will be more crossbridges per area and the muscle′s strength will increase proportionally.

Exercise performance

Another area we fail to recognize is the comparison of getting better at an exercise vs. actual muscular strength increase. The latter will produce size increases, the former may, or may not. If your bench press poundage increases from an increase in the number of fibrils ( in the involved musculature), then your strength increase will reflect a size increase. However, if your bench press has increased due to slight alterations in ROM, increased neural coordination, or finding a better ′groove′, you may not see much, or any increase in size.

Where the house of cards collapses with training programs

First on the list is impatience. "I trained like X for 3 months, I added 50 lbs to my bench and gained no size!". If this happened, then yes, your training didn′t allow for muscle growth. But why? Ask yourself these questions and be honest as one of these must be the answer.

1) Did you let your form drift, so that even though you added weight each week, in reality you were keeping the stress the same?

2) Did you ′know′ the exercise well enough that the neural learning curve was finished?

3) Did you change exercises during that time, or hand spacing, grip, etc. so that you never could completely finish the ′learning′ of the exercise?

4) Did you just ′hoist′ the weight, or did you use the exercise to ′work′ the muscles?

Other programs producing ′more size per strength′

When science checks the CSA of a muscle, they use sophisticated methods. They know that using a tape is highly inaccurate. MRI, ultrasound, as well as other methods are used to actually ′see′ inside. Intramuscular glycogen, fat, water retention, etc. can all change the external size of a muscle. You may have used a high volume program and noticed quick size gains. But if you didn′t gain strength proportionately, (while keeping form, ROM, etc. all consistant) you cannot be sure your size came from an increase in fibril numbers. In fact, if you didn′t increase strength rapidly in accordance with the size, you most definately did not gain your size from fibril hypertrophy.

Back to the nitty-gritty

If you (insert name here) add a certain amount of fibrils, you (insert name again) will gain a certain amount of strength. It does not matter one iota how you added those fibrils, neither your exercise volume or intensity will alter your personal ′strength to size′ ratio. The only thing that can cause a change in the appearance of your strength to size ratio (besides beginner′s neural learning) is a change in the performance of the exercise.

What can one do?

Make darn sure you train in such a way that when you record a strength increase, it′s really a strength increase. If you have to, time your reps, have your training partner (if you have one) holler at you for altering your form or ROM (range of motion). Make sure, you stimulate the muscle to grow, and that growth shows up as a strength increase. Do not try to use strength increases as a means to force growth. If you grow, you will need to add weight to the bar to keep within your desired rep range.

Analyzer (CDA, id, U.S.A.) on 2/11/2006 1:41:41 PM


After years of research and putting as many pieces of the puzzle into place as I could, mTOR seemed to be the one common signal factor amoungst all progressive scenarios. Methods, even if less efficient, that however did still induce hypertrophy, along with heavy weights, occlusion, etc, etc., all could be traced back to this factor.

It explains why we have to train ′hard′ (intense), why heavy works, why volume works (but is less efficient), why occlusion training works, cumulative fatigue train, yada yada.

All the things that happen during high levels of rate coding go right along with all the key elements we look for in stimulation.

* High intracellular calcium (calcineuron, latent damage/remodeling)

* High ATP turnover (mTOR signaling for increased protein synthesis)

* Tetanic contractions (maximum per fiber force, maximum strain)

* ect.

Analyzer (CDA, id, U.S.A.) on 2/11/2006 1:42:06 PM

Study abstract

Regulation of mTOR by amino acids and resistance exercise in skeletal muscle.

Deldicque L, Theisen D, Francaux M.

Institut d′Education Physique et de Readaptation, Universite catholique de Louvain, Place Pierre de Coubertin 1, Louvain-la-Neuve, Belgium, [email protected]

Resistance exercise disturbs skeletal muscle homeostasis leading to activation of catabolic and anabolic processes within the muscle cell. A current challenge of exercise biology is to describe the molecular mechanisms of regulation by which contractile activity stimulates net protein breakdown during exercise and net protein synthesis during recovery. Muscle growth is optimized by combining exercise and appropriate nutritional strategies, such as amino acid (AA) and carbohydrate ingestion. The effects are integrated at the level of one central regulatory protein, mTOR (mammalian target of rapamycin). mTOR is a complex protein integrating signals of the energetic status of the cell and environmental stimuli to control protein synthesis, protein breakdown and therefore cell growth. mTOR is known to be activated by insulin, and the mechanisms involved are well documented. The ways by which exercise and AA lead to mTOR activation remain partially unclear. Exercise and AA use different signalling pathways upstream of mTOR. Exercise seems to recruit partially the same pathway as insulin, whereas AA could act more directly on mTOR. During resistance exercise, the activity of mTOR could be acutely blunted by AMP-activated protein kinase (AMPK), thus inhibiting protein synthesis and enhancing AA availability for energy metabolism. During recovery, the inhibition of mTOR by AMPK is suppressed, and its activation is maximized by the presence of AA. There appears to be a requirement for a minimal concentration of plasma insulin to stimulate muscle protein synthesis in response to resistance exercise and AA ingestion.

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