So… I’m not a lanky bastard. I just have good SE?! YEhaaW! That’s such a validating life experience for me! I’m never running anything under 400m again! Oh wait… my shortest race is the quarter, danm.
Thanks for clearing that up.
This is very interesting. I have always been skeptical regarding how much hypertrophy is possible with someone who does a good amount of SE. I just havn’t been able to achieve it - one sub elite female (54s 400m) I train seems to have gone through this change despite doing a fair amount of cross section work. I was wondering this the other day… her muscles just look different to 2 years ago.
Has anyone done any examination of muscle fibres in trained and untrained race hourses? What accounts for this difference? Angle of pennation comes to mind while trying to imagine how a muscle can change its physical shape but I’m not an exercise physiologist so I could be thinking out of my arse 
Hakan others?
Just the facts.
Might be as you hope - or you might just be “dense” (Just kidding)
Charlie, I am glad you posted the above, it really confirms some things for me. I came to a very similar conclusion after Tellez explain to me the purpose of his “breakdown” (400,300,200) was to build strength and not for conditioning. I think it also explains why plyos were used over weights in his program.
Is this something to do with the myogenic tone?
Its probably to do with fast fibre adapting from fast twitch type II B to type II A, and for those talented individuals slow fibre converting to type II A also…
Strong neural activation=great endocrine response. More testostosterone=more fast fibers! But I guess that the jury is still out…
Concurrent Strength and Endurance Training: A Review.
Leveritt M.; Abernethy P.J.; Barry B.K.; Logan P.A. Sports Medicine 28, Number 6, 1 December 1999, pp. 413-427(15)
Abstract:
Concurrent strength and endurance training appears to inhibit strength development when compared with strength training alone. Our understanding of the nature of this inhibition and the mechanisms responsible for it is limited at present. This is due to the difficulties associated with comparing results of studies which differ markedly in a number of design factors, including the mode, frequency, duration and intensity of training, training history of participants, scheduling of training sessions and dependent variable selection. Despite these difficulties, both chronic and acute hypotheses have been proposed to explain the phenomenon of strength inhibition during concurrent training. The chronic hypothesis contends that skeletal muscle cannot adapt metabolically or morphologically to both strength and endurance training simultaneously. This is because many adaptations at the muscle level observed in response to strength training are different from those observed after endurance training. The observation that changes in muscle fibre type and size after concurrent training are different from those observed after strength training provide some support for the chronic hypothesis. The acute hypothesis contends that residual fatigue from the endurance component of concurrent training compromises the ability to develop tension during the strength element of concurrent training. It is proposed that repeated acute reductions in the quality of strength training sessions then lead to a reduction in strength development over time. Peripheral fatigue factors such as muscle damage and glycogen depletion have been implicated as possible fatigue mechanisms associated with the acute hypothesis. Further systematic research is necessary to quantify the inhibitory effects of concurrent training on strength development and to identify different training approaches that may overcome any negative effects of concurrent training.
Endurance training decreases serum testosterone levels in men.
Wheeler GD.; Singh M.; Pierce WD.: Epling WF.; Cumming DC.; J Clin Endocrinol Metab 1991 Feb;72(2):422-5
Abstract:
Cross-sectional studies have suggested that total and bioavailable testosterone levels are reduced in some male athletes. Such changes may be related to loss of body weight, increased serum cortisol, and/or alterations in LH pulsatile release. To determine how endurance training may affect androgen levels, we measured serum total testosterone, sex hormone-binding globulin, free androgen index, LH, FSH, PRL, cortisol, and weight in 15 previously sedentary males. We also examined pulsatile LH release in a subset of 5 subjects. Over 6 months of training, the men increased weekly running mileage to an average of 56 km/week. Total testosterone and free androgen index levels decreased significantly. PRL and cortisol also decreased, while single sample LH and FSH remained unchanged. There was a significant reduction in weight, which did not correlate with changes in serum testosterone levels. These data confirm previous findings of physiological reduction in serum testosterone.
All the best
Håkan Andersson
Sundsvall Sweden
I think there is a difference between Speed End and endurance as described in the study. I’d describe SE and STR as training elements competing for the same resources.
Judiciously applied, both will give the strong neural activation and favourable endocrine response postulated for STR work alone.
While there will be some difference in STR levels, I suspect much of it is due to this re-allocation of finite resources and it is my experience that STR levels may jump up dramatically upon the cessation/completion of the SE work to levels perhaps not attainable if SE had not been present at all.
During SE work, the same lengthening of the muscle, described earlier, changes the leverage for lifting slightly, also affecting lifting results during this period.
I definitely agree that there’s a difference between lactic anaerobic capacity/power (LAN) and endurance as described in the study, that is refering to aerobic capacity.
It’s my experience too that lactic anaerobic and Strength training can be difficult to combine, especially if you are trying to lift both qualities in the same period. And yes, these elements are competing for some similar sources, but there are also differences to be considered.
Lactic anaerobic training performed at maximal intensity most probably will stress the nervous system big time.
Lactic anaerobic work will increases hydrogen ion content and dramatically lowers ph, that most probably will release massive amounts of free radicals. With high free radical formation during exercise, resynthesis of muscle proteins could easily be disturbed.
Prolonged high intensity lactic exercise might also suppress the immune system, making adaptation to training less effective overall.
In my experience it’s much easier to combine Strength training with alactic anaerobic work and leave the lactic work until the end of macro cycle, when all the other qualities already has been developed.
With regards to racehorses. Thoroughbred racehorses are extremely fast twich, capable of producing extremely high levels of fatigue. Too much lactic anaerobic work for a horse has probably all the side effects that we experience training talented humans.
All the best
Håkan Andersson
First, I agree that strength is most easily advanced while doing alactic work. That’s why in a short-to-long approach, the most significant STR increases are in phase one (again, see the annual plan in the Vanc 2004 DVD)
The key concept with lactic anaerobic work is- judicious use. The East Germans always emphasized that there is no more important issue than the proper use and recovery from SE.
Interestingly though, sprinters often subjectively feel more CNS recovered when lactic levels are high because the work that causes it is not as hard on the nervous system- analogy, which is tougher: 2 x 300m or 10 x 60m with long recoveries?
A friend of mine -international level- has repeatedly observed good speed sessions after such workouts!
Also, this is one of the cases where lactate results can not help you much in monitoring the state of the athlete (e.g., a lactate measurement in the morning).
Not to mention there are more biochemistic principles at work than just lactic acid. Many enzymes, co-enzymes, buffers, neurotransmitters, endorphins, eicosanoids, peptides, hormones…etc. I think the most important thing we can say is that we know a little, but even our most knowledgable still don’t know a lot. I mean this in terms of all scientific backgrounds.
We have however made more of understanding at explaining why things happen. Unfortunately, it hasn’t really gained too much in terms of performance.
Pre-nuclear error:
10.3s on a cinder track with no blocks
Post-nuclear error
9.77 on a rubber track with precise timing
Not exactly the types of improvement we were hoping for when we thought we were so “advanced”…lol.
10.3s with inaccurate timing. Let’s say that with a rubber track and blocks they run 10.3 legal, over half a second improvement is huge–especially since two runs have the ability to be faster than 9.77 (BJ in Seoul and Mo in Edmonton) with a finish.
I second that, and with internet forums like the charlie francis website sharing information and allowing the exchange of ideas at a rate that is unpecedented. I think the moving average of top performances particularly in 100m will improve spike.
Soon a man will probably walk on the planet Mars, still we don’t know all the mechanisms that causes muscular fatigue. Very difficult areas though, were many things are to be explored.
Heard interesting speculations regarding blood ammonia (NH3) and CNS fatigue. It is well known that NH3 and lactate concentrations elevates during high intensive anaerobic exercises. At present, however, the lack of experience and lack of appropriate values still hinders the systematic use of NH3 measurements in the physiological monitoring of sports training.
NH3 is a small molecule that might penetrate true the blood brain barrier and interfere in different synopsis. The ph levels in the brain remain constant regardless of the intensity and duration of the exercise though.
I think that you will find a different stress on the CNS with lactic work than alactic but still, it might me more stressful than we think at present.
1060m might drain you brain from neurotransmitters but 2300m might be more toxic for the brain. Many people experience headaches after lactic work, why I don’t know but NH3 might have something to do with it?
Wild speculations here, far beyond my knowledge! Hope my old biology teacher doesn’t read this:-)
All the best
Håkan Andersson
Totally agree, where could I go to talk to some of the best trainers in the world anonymously?
Perhaps, or perhaps we will just get more confused because of all the conflicting oppinions?
The 10.3 was accurate timing. Eddie Tolan and Ralph Metcalfe both did 10.38 FAT at 1932 Olympic Games final. 3 years later Jesse Owens LJed 8.13m. 73 years later the WRs are 9.77 and 8.95.
Take in consideration the following factors of improvement:
- external factors : ground quality, shoes, outfits
- longer carriers (pre-War, the athletes retired much early than today, the average age for the all-time top 10 at 100m when achieving personal best was 23 years old, while today it is 27.)
- Professional sport (athletes are paid to run and have nothing else to think about)
- more attempts to break records (more countries involved in sports, higher number of meetings/competitions)
- advanced training methods (pre-War most of the athletes used to start training in Spring, later introduction of weight training…)
- human beeing is taller and heavier (stronger) today compared to 1932 (many factors for this mainly food)
- support of sport science/physiology/biomechanics/therapy?
Science has played a very poor role in this progression compared to the other 6 elements which are more than enough to explain a ridiculous 6% improvement between 1932 and 2005. That means that scientists (and coaches!) have little to do with the speed progression. Humility please!!!
One of advantage for older times is the lack of wind measurement. A dirt track and lousy footwear could, in theory, be compensated by a +5m/s tailwind. However, I agree with you pierrjean; though we know much more in scientific terms, very little has found a decisive practical implementation. Talented people will continue to dominate, unless, of course, genome-alteration is finding its way into sports.
There’s a monumental difference between ’applied medical science’ and ‘applied sport science’. Sport “science” is still 99% about translating and explaining sensible observations into the scientific discourse…