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Paul Kayley
05-27-2007, 05:04 AM
Muscle glycogen depletion in the recruited muscle fibers used during a specific endurance activity is a powerful trigger for endurance adaptations. The latest recommendation on the endurance grape vine relates to muscle glycogen - "Train low and race high!"

This makes a lot of sense to me. Although getting the balance right is critical to avoiding over-training and stalled adaptation.

Mike ODonnell
05-27-2007, 08:04 AM
Makes sense as you carb load before a race....so you are not going to train in hyperglycemic state....always good to train harder and then make the race easier...train single speed, run with resistance/up hill, etc....

Greg Everett
05-27-2007, 10:49 AM
paul - how depleted are we talking here?

Paul Kayley
05-28-2007, 02:46 PM
Hey Greg, thats a very good question. IMO&E, total depletion at the end of a training session would be counter productive, as it would be a taking the stimulus a couple of steps too far, resulting in cell damage and the need for prolonged recovery.

The volume and intensity of the training used would of course depend upon the fiber range being targeted. It is quite easy, with experience, to feel the point where you start to near the 'bottom of the tank' in terms of muscle glycogen(MG). This is the point in a training session where I start to back off. Going home feeling tired but not completely wiped out. The term 'train low, race high' isn't suggesting training in a depleted state, it is discouraging continuously and repeatedly carboloading the cells.... this just gives the athlete more work to do in order to stimulate change. Its training with a constant tail wind!

It might be worthwhile mentioning that the MG stored in a single muscle cell is locked in that cell, exclusively for that cell's use. It cannot be accessed for use by other muscle cells or to bolster ebbing blood glucose levels. This also means that the stimulus of MG depletion is also cell specific.

I've probably missed loads out, so ask away if I have... thats a rushed answer as I'm rushing about!

Greg Everett
05-28-2007, 03:32 PM
Interesting... Looking forward to reading more on this.

Derek Simonds
05-29-2007, 02:59 PM
I have been thinking about your post for most of the day. If you are an endurance athlete that eats a mostly paleo / low carb diet are you already on the low side pre-exercise?

I did a 2 hour ride with my sister on Saturday that turned into a little more of a hammer than originally planned as we rode out with a 20 knot tailwind. Oops! I definitely was at the "bottom of the tank" when we got back. I ate my normal meat, salad and small amount of carb meals for the remainder of the day. Sunday morning we did a 45 minute high intensity ride with a 20 minute tempo transition run. It ended up being a pretty tough brick. Afterwards I couldn't eat right away but when I could I was ravenous.

What made me think about this is how I was eating in the past when constantly training for triathlons. It was definitely more carb focused. Today I train 3 days a week endurance and I don't feel like I need the extra carbs except Sunday when I was so hungry I could have ate the paper plate my food was served on.

This also played into a question that I was going to ask Paul. On my heart rate monitor during the Saturday ride it showed that I burned 1734 Kcal's. Is the only factor in determining calories burned average heart rate over time? I am sure there is some algorithm that the watch uses to calculate the calories burned, but does muscle glycogen depletion come into play for calories burned?

Meaning if I worked out for 1 hour and felt near the bottom of the tank at an average heart rate of 140 and the monitor showed 900 Kcal's versus working out for 1 hour at an average heart rate of 140 but not feeling depleted did the first example actually burn more calories?

I hope this made some sort of sense, as is appears I am rambling again.

Paul Kayley
06-01-2007, 08:51 AM
Hi Derek,

I had to read this a fews times, but I think I know what you are asking...

Meaning if I worked out for 1 hour and felt near the bottom of the tank at an average heart rate of 140 and the monitor showed 900 Kcal's versus working out for 1 hour at an average heart rate of 140 but not feeling depleted did the first example actually burn more calories?

Both burn the same calorific total, the latter will burn less fat calories. The relative contribution of fats to total energy output is inversely proportional to exercise intensity, and a low to moderate exercise intensities its also proportional to muscle glycogen depletion.

When talking about 'the tank' I am refering to muscle glycogen stores, not liver glycogen. Exercising with low liver glycogen, unless you are ketone adapted or fueling on the go, will lead to an early knock and curtail workout capacity. I suspect that following your second workout, because you delayed eating, your liver glycogen stores will have been low following the workout, and then continued to deplete into the used muscles. When the liver empties too much, IME, a ravenous hunger ensues which seems to dominate all powers of self control... its linked with other hormonal triggers like ghrelin etc.

The key - train low, but dont entertain extremes. I will post more later on this...as usual I'm pushed for time...

Derek Simonds
06-01-2007, 09:43 AM
Thanks that is actually what I thought. Not all the stuff about the liver but the burning fat part :D.

I can't wait to read more.

Paul Kayley
06-02-2007, 03:48 PM
This study relates to what I've been rambling on about....

J Appl Physiol. 2005 Jan;98(1):93-9. Epub 2004 Sep 10. Related Articles, Links

Skeletal muscle adaptation: training twice every second day vs. training once daily.

Hansen AK, Fischer CP, Plomgaard P, Andersen JL, Saltin B, Pedersen BK.

Dept. of Infectious Diseases M7641, and The Copenhagen Muscle Research Centre, Rigshospitalet, Blegdamsvej 9, DK-2100 Copenhagen, Denmark.

Low muscle glycogen content has been demonstrated to enhance transcription of a number of genes involved in training adaptation. These results made us speculate that training at a low muscle glycogen content would enhance training adaptation. We therefore performed a study in which seven healthy untrained men performed knee extensor exercise with one leg trained in a low-glycogen (Low) protocol and the other leg trained at a high-glycogen (High) protocol. Both legs were trained equally regarding workload and training amount. On day 1, both legs (Low and High) were trained for 1 h followed by 2 h of rest at a fasting state, after which one leg (Low) was trained for an additional 1 h. On day 2, only one leg (High) trained for 1 h. Days 1 and 2 were repeated for 10 wk. As an effect of training, the increase in maximal workload was identical for the two legs. However, time until exhaustion at 90% was markedly more increased in the Low leg compared with the High leg. Resting muscle glycogen and the activity of the mitochondrial enzyme 3-hydroxyacyl-CoA dehydrogenase increased with training, but only significantly so in Low, whereas citrate synthase activity increased in both Low and High. There was a more pronounced increase in citrate synthase activity when Low was compared with High. In conclusion, the present study suggests that training twice every second day may be superior to daily training.

I also believe that the following study helps to demonstrate that endurance athletes' dont need to be quite so obsessive about rushing to refill muscle glycogen with high starch diets... the body's ability to conserve and efficiently partition glucose is under-estimated, especially in response to glycogen sapping exercise.

J Physiol. 2003 May 1;548(Pt 3):919-27. Epub 2003 Mar 21. Links
Skeletal muscle fat and carbohydrate metabolism during recovery from glycogen-depleting exercise in humans.

* Kimber NE,
* Heigenhauser GJ,
* Spriet LL,
* Dyck DJ.

Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph, Ontario N1G 2W1, Canada.

The primary aim of the present study was to determine whether intramuscular triacylglycerol (IMTG) utilization contributed significantly to the increase in lipid oxidation during recovery from exercise, as determined from the muscle biopsy technique. In addition, we also examined the regulation of pyruvate dehydrogenase (PDHa) and changes in muscle acetyl units during an 18 h recovery period after glycogen-depleting exercise. Eight endurance-trained males completed an exhaustive bout of exercise (approximately 90 min) on a cycle ergometer followed by ingestion of carbohydrate (CHO)-rich meals (64-70 % of energy from carbohydrate) at 1, 4 and 7 h of recovery. Duplicate muscle biopsies were obtained at exhaustion, and 3, 6 and 18 h of recovery. Despite the large intake of CHO during recovery (491 +/- 28 g or 6.8 +/- 0.3 g kg-1), respiratory exchange ratio values of 0.77 to 0.84 indicated a greater reliance on lipid as an oxidative fuel. However, there was no net IMTG utilization during recovery. IMTG content at exhaustion was 23.5 +/- 3.5 mmol (kg dry wt)-1, and remained constant at 24.6 +/- 2.6, 25.7 +/- 2.8 and 28.4 +/- 3.0 mmol (kg dry wt)-1 after 3, 6 and 18 h of recovery. Muscle glycogen increased significantly from 37 +/- 11 mmol (kg dry wt)-1 at exhaustion, to 165 +/- 13, 250 +/- 18, and 424 +/- 22 mmol (kg dry wt)-1 at 3, 6 and 18 h of recovery, respectively. PDHa was reduced at 6 and 18 h when compared to exhaustion, but did not change during the recovery period. Acetyl-CoA, acetylcarnitine and pyruvate contents declined significantly after 3 h of recovery compared to exhaustion, and thereafter remained unchanged. We conclude that IMTG has a negligible role in contributing to the enhanced fat oxidation during recovery from exhaustive exercise. Despite the elevation of glucose and insulin following high-CHO meals during recovery, CHO oxidation and PDH activation were decreased, supporting the hypothesis that glycogen resynthesis is of high metabolic priority. Plasma fatty acids, very low density lipoprotein triacylglycerols, as well as intramuscular acetylcarnitine stores are likely to be important fuel sources for aerobic energy, particularly during the first few hours of recovery.

This serves to demonstrate just how precious glucose stores are to the athlete's body. Fat burning even in the presence of insulin until depleted MG is restored! However, there is another side to this. It has been demonstrated that following carbo-loading, to supra-normal MG levels, that CHO is burned at an increased rate until CHO levels level out. It appears that the body likes a nice balance, not too much, nor too little. Personally, I find that my muscles dont operate so well when CHO-loaded, they feel all jammed up and sore. Following a few days rest I'll get this feeling if I've over-filled my legs... it then takes a couple of hours of training before my legs feel loose and able to fire effectively with all cyclinders!

Derek Simonds
06-02-2007, 06:25 PM
Thanks for posting the info Paul. I like what I am reading. I also really like the 2 a days with 1 day recovery. On the F, S and S I can train that way so it looks like I will adapt my schedule and work 2 on Friday and 2 on Sunday with some active recovery on Saturday.

Garrett Smith
06-03-2007, 06:47 AM
The body is smarter and more efficient than most give it credit for???

You don't say... ;-)

When I was a carb-crazy lacto-ovo vegetarian triathlete, all I got for it was:
Fried immune system
Lost about 15# of muscle
Hypoglycemia
Holier-than-thou attitude (about diet and exercise)

I'm so glad I'm away from that now. I still bike and run (x/c now it's only hard and fast), and may enter some sprint tri's for fun in the future (so much for fun that I'll do them on my commuter fixie). I love training on low carbs, low food intake in general.

How long will this idea take to penetrate the endurance masses? At least it's out there for the smart ones to find/figure out...

Paul Kayley
06-03-2007, 07:46 AM
When I was a carb-crazy lacto-ovo vegetarian triathlete, all I got for it was:
Fried immune system
Lost about 15# of muscle
Hypoglycemia
Holier-than-thou attitude (about diet and exercise)...

Yes... but going to those extremes has rewarded you with the wisdom you possess today grass hopper!

How long will this idea take to penetrate the endurance masses? At least it's out there for the smart ones to find/figure out...

Lets hope that the normal sea guls stay with their flocks... allowing the few Jonathan Livingstons among us to push our way forward, relying not upon talent or brute force, but upon the appliance of intelligence and a willingness to explore! Its a much more meaningful journey too!

Paul Kayley
06-04-2007, 10:06 AM
Thanks for posting the info Paul. I like what I am reading. I also really like the 2 a days with 1 day recovery. On the F, S and S I can train that way so it looks like I will adapt my schedule and work 2 on Friday and 2 on Sunday with some active recovery on Saturday.

The 2 a day theory does definately work, its been around for decades. One just has to read into how the best training results are elicited by the top swimming and running coaches through the years, the empirical evidence is there. What interests me is the question why? Yes, its reported to have a stronger long term impact upon gene transcription, but why? Could this be related to modern nutrition... are mutiple daily training sessions necessary because of the rapid glycogen replenishment techniques so often used by athletes, and would fewer sessions be called for to affect the same adaptive responses if a more 'normal' diet were followed?

I personally dont like having to train 2-3 x per day in the same sport, it just gets too boring. However, I believe that the same effects may be achieved by training just once per day whilst backing off (not totally laying off) the starches, and relying more upon hepatically controlled sugar levels and slowly replenished muscle glycogen levels. The signals should be the same - muscle glycogen levels are being regularly stressed, the rate of replenishment is barely matching the rate of depletion per cycle, therefore adaptions to conserve levels are initiated... that is - increased glycogen storage capacity per cell, increased mitochondrial reticulum density, increased membrane glucose transport capacity, improved capillarisation, and increased aerobic capacity to improve ATP yield per glucose molecule, etc, etc... blah, blah, blah..

Dave Van Skike
06-04-2007, 10:52 AM
every one of your posts makes my head hurt. that is all.

Paul Kayley
06-04-2007, 12:17 PM
every one of your posts makes my head hurt. that is all.

Every time I post, its because my head hurts!

Dave Van Skike
06-04-2007, 01:39 PM
Every time I post, its because my head hurts!

It's ok Dude, let it go... we're here for you.

Robb Wolf
06-04-2007, 02:13 PM
every one of your posts makes my head hurt. that is all.

LOL! There's some support! HA!

Robb Wolf
06-04-2007, 02:14 PM
Paul-
I DO think you are onto something here. I think intermittent fasting can bring about some of these changes as well.

Derek Simonds
06-04-2007, 06:47 PM
Paul do you think that for the 2 a days to be effective they have to be the same sport? I know that Gordo Has had great results from his epic camps. He has also crushed some people that weren't ready but mostly they have had great results. I have had luck with 2 a days but in different sports.

Thinking about what we are trying to accomplish though it would make sense that you would have to work the same muscles that had already been depleted. I wonder if an AM run and a PM bike would be as effective as an AM longer tempo run with a PM fartlek / interval run? I will have to try and see how I feel after each.

My head hurts also but this is why I am on this forum the opportunity for intellectual growth is staggering. I am staggered just in case anyone wondered.

Paul Kayley
06-05-2007, 01:29 AM
Derek, I am glad you know about Gordo. He is an amazing example of what can be achieved in the endurance world with the application of what appears to be limitless enthusiasm. I'm not in touch with how Gordo trains today, although its probably very similar to previously if he's still pushing his 'Epic Camps'. He is a clear proponent of very high weekly volumes per sport, which works obviously. However, I suspect this is the long way around... for IM training reverse periodisation would likelycreate the same results if done correctly. Gordo is the first to admit that he only possesses modest talent as far as VO2max is concerned, but he has trained an ability to churn out work at a high relative % of his max for long periods, by maximising his muscular endurance capacities. If you read into his diet, which he also has nailed, you will see that he is very careful with his carb intakes, especially starches. He appears to get most of his carbs from fruits, veg, dairy, and fueling on the go using sports products.

I couldnt train as much as Gordo does, its too much sacrifice. Yes its highly admirable, but there is more to life than spending 8+ hours per day flip-turning, pedalling, and trail bashing. To me LSD training is like reading a long book from the beginning every day trying for longer each day to get further into the book in an attempt to near the end, when more can be achieved with the intelligent use of a book mark and a few fresh pages per day!

Paul do you think that for the 2 a days to be effective they have to be the same sport?
For example, there is cross over (maybe 50%) from running to biking, &VV. But training at muscular level is highly cell specific, only the recruited cells will be affected.

I wonder if an AM run and a PM bike would be as effective as an AM longer tempo run with a PM fartlek / interval run? I will have to try and see how I feel after each.
A 2 a day bike day, followed by a 2 a day run day, would work. Or a double short brick day... 90min brick am, 60 min brick pm ... would take some enthusiasm though! Alternatively, as I'm suggesting, train once per day in each sport, as many times per week as possible, at a high aerobic output, whilst monitoring your carb intake. (If training at this intensity for 6 S-B-R per week the body would be struggling to meet glycogen replenishment rates with a high starch diet anyway...thats why well executed tri training works so damn well!)

Derek Simonds
06-05-2007, 12:23 PM
Gordo has a page on his website which I consider Mandatory Reading for anyone considering making a change to their diet. I have used it with many people in the last 3 years. Just in case anyone hasn't read it here it is.

http://www.coachgordo.com/gtips/nutrition_body_composition/nutrition_101.html

The only problem I personally will have with your S B R in one day idea is that I will not be able to easily split it up in to 3 different time slots. I don't have access to a shower at work so a run during lunch is out. I will have to try and find the closest pool, I could see an early AM bike, a lunch swim with an evening run.

If I could make that happen 1 day a week I could do a long ride on Sat AM with a follow up ride Sat PM and a bike - run brick Sun AM (90) and PM (60). I will still need to pick up another swim but it should work out pretty well.

I am getting ready for vacation which means no lifting for 10 days, just swimming and easy running. I am pretty stoked. I will be laying out my training schedule while I am away and plan on starting 2 weeks from now. Thanks for lots of great ideas in this thread.

Paul Kayley
06-05-2007, 01:18 PM
Paul-
I DO think you are onto something here. I think intermittent fasting can bring about some of these changes as well.

I'd be interested to hear your thoughts on this Robb. I have used IF in the past when I was experimenting with a Warrior style diet. I enjoy the challenge of IFing. I got the feeling whilst doing it that it helped with improved tissue repair.

Robb Wolf
06-05-2007, 02:27 PM
So long as the caloric intake is solid I think it really enhances recovery. I think the adaptations are VERY endurance/metcon specific as well.

Many people have noticed an improvement in max strength...people like Kurtis Bowler who have really pushed that max strength element. That is honestly surprising to me as the adaptations seem to favor a fiber type conversion and tendency towards endurance adaptations. It could be that one will not create a TOP level Olifter, PL'er or sprinter on intermittent fasting, the well fed state is very favorable to the type 2b fiber type expression, but for the endurance athlete or strength-endurance athlete it may be very beneficial.

Paul Kayley
06-05-2007, 04:15 PM
Another study of interest

***
Am J Physiol Endocrinol Metab. 2005 Dec;289(6):E1023-9. Epub 2005 Jul 19. Related Articles, Links

Glucose ingestion during exercise blunts exercise-induced gene expression of skeletal muscle fat oxidative genes.

Civitarese AE, Hesselink MK, Russell AP, Ravussin E, Schrauwen P.

Dept. of Human Physiology, Pennington Biomedical Research Center, 6400 Perkins Road, Baton Rouge, LA 70808, USA.

Ingestion of carbohydrate during exercise may blunt the stimulation of fat oxidative pathways by raising plasma insulin and glucose concentrations and lowering plasma free fatty acid (FFA) levels, thereby causing a marked shift in substrate oxidation. We investigated the effects of a single 2-h bout of moderate-intensity exercise on the expression of key genes involved in fat and carbohydrate metabolism with or without glucose ingestion in seven healthy untrained men (22.7 +/- 0.6 yr; body mass index: 23.8 +/- 1.0 kg/m(2); maximal O(2) consumption: 3.85 +/- 0.21 l/min). Plasma FFA concentration increased during exercise (P < 0.01) in the fasted state but remained unchanged after glucose ingestion, whereas fat oxidation (indirect calorimetry) was higher in the fasted state vs. glucose feeding (P < 0.05). Except for a significant decrease in the expression of pyruvate dehydrogenase kinase-4 (P < 0.05), glucose ingestion during exercise produced minimal effects on the expression of genes involved in carbohydrate utilization. However, glucose ingestion resulted in a decrease in the expression of genes involved in fatty acid transport and oxidation (CD36, carnitine palmitoyltransferase-1, uncoupling protein 3, and 5'-AMP-activated protein kinase-alpha(2); P < 0.05). In conclusion, glucose ingestion during exercise decreases the expression of genes involved in lipid metabolism rather than increasing genes involved in carbohydrate metabolism.

Paul Kayley
06-05-2007, 04:16 PM
And another...

Med Sci Sports Exerc. 2006 Nov;38(11):1945-9. Links
Role of AMP-activated protein kinase in the molecular adaptation to endurance exercise.

* Winder WW,
* Taylor EB,
* Thomson DM.

Department of Physiology and Developmental Biology, Brigham Young University, Provo, UT 84602, USA. William_winder@byu.edu

What are the molecular signals induced by muscle contraction that result in an increase in GLUT4, hexokinase 2, mitochondrial oxidative enzymes, and other adaptations to endurance exercise training? Could repetitive activation of AMP-activated protein kinase (AMPK) be responsible in part? There is substantial evidence for a role of AMPK in inducing adaptations to endurance training: 1) AMPK is activated in response to muscle contraction; 2) chronic chemical activation of AMPK results in increases in GLUT4, hexokinase 2, UCP-3, and citric acid cycle enzymes; 3) muscle contraction and chemical activation of AMPK both result in increases in PGC-1alpha, a transcriptional coactivator involved in stimulation of mitochondrial biogenesis; and 4) increases in muscle PGC-1 alpha, delta-aminolevulinic acid synthetase, and mitochondrial DNA induced by chronic creatine phosphate depletion in wild-type mice are not observed in dominant-negative AMPK mice. These observations lend credence to the hypothesis that AMPK activation induced by muscle contraction is responsible in part for adaptations to endurance exercise training.

Paul Kayley
06-21-2007, 01:32 AM
It looks like Dr Seiler and I share some common beliefs.....

From Dr Seiler (taken from the Sport Science List) regarding nutrition. Food for thought:

As a non-nutritionist I have tried to follow along in the excellent discussion catalyzed by Dr. Bill Meisner's original posting. The crux of the discussion from my exercise physiologist's perspective has been "do athletes need micronutrient SUPPLEMENTATION to optimize performance?" I am going to throw the discussion a wicked curveball now by asking essentially the OPPOSITE (and perhaps heretical?)
question: "Do athletes need nutritonal DEPLETION to optimize adaptive signalling and, thereby, performance?"

Let me explain with reference to some key examples. I will begin with the macronutrient carbohydrate and the issue of glycogen depletion.
Over the last 30 years I think it is fair to say that prevention of intramuscular glycogen depletion during exercise and competition (and rapid repletion after) has been a major focus of human performance research and a major cash cow for the sports nutrition industry.
During this same period, the sheer volume of training performed by endurance athletes has risen substantially, if not dramtically. The goal of training is to signal adaptive processes that enhance performance (and not just to accumulate hours in training diaries).
So the question I pose is this: "Are certain aspects of nutritional depletion during, or subsequent to, exercise stress actually important modulators of the adaptive signalling process?"

In this case of glycogen depletion, I believe the answer may well be "YES." Read for example this abstract (this paper came out electronically a year ago):
__________________________________________
Hansen AK, Fischer CP, Plomgaard P, Andersen JL, Saltin B, Pedersen BK. J Appl Physiol. 2005 Jan;98(1):93-9. Skeletal muscle adaptation:
training twice every second day vs. training once daily.


Low muscle glycogen content has been demonstrated to enhance transcription of a number of genes involved in training adaptation.
These results made us speculate that training at a low muscle glycogen content would enhance training adaptation. We therefore performed a study in which seven healthy untrained men performed knee extensor exercise with one leg trained in a low-glycogen (Low) protocol and the other leg trained at a high-glycogen (High) protocol. Both legs were trained equally regarding workload and training amount. On day 1, both legs (Low and High) were trained for 1 h followed by 2 h of rest at a fasting state, after which one leg (Low) was trained for an additional 1 h. On day 2, only one leg (High) trained for 1 h. Days 1 and 2 were repeated for 10 wk. As an effect of training, the increase in maximal workload was identical for the two legs.

However, time until exhaustion at 90% was markedly more increased in the Low leg compared with the High leg. Resting muscle glycogen and the activity of the mitochondrial enzyme 3-hydroxyacyl-CoA dehydrogenase increased with training, but only significantly so in Low, whereas citrate synthase activity increased in both Low and High. There was a more pronounced increase in citrate synthase activity when Low was compared with High. In conclusion, the present study suggests that training twice every second day may be superior to daily training.
__________________________________

So, we glycogen load, push carbohydrate, and preach to our athletes the importance of a high carbohydrate diet. And yet, part of the adaptation process seems to actually DEPEND on periods of marked cellular depletion of glycogen. Perhaps one reason we need so much training volume these days is that it takes longer to reach a level of cellular depletion that is necessary to signal further adaptation in already adapted muscle?

What about free radicals (reactive oxygen species, ROS)? ROS production is an obligatory side-effect of aerobic metabolism. Oxygen is volatile and poisonous. Clearly, excessive ROS production is toxic to aerobic organisms because evolution has equipped them with an impressive array of ROS quenching compounds and enzymes that occupy both the aqueous (ascorbic acid and glutathione, for example) and lipid regions (a-tocopherol or Vit E, for example) of cells. This defence system has captured the attention of biomedical science for the last 20 years.

HOWEVER, it did not take very long after the "ROS as intracellular enemy" wave of research kicked in that serendipitous observations were made suggesting that these ROS were not all bad. I actually had one of these myself 15 years ago. I was using isolated heart perfusions to study some aspects of heart recovery after a "heart attack". I wanted to artificially induce free radical damage by infusing H2O2, hydrogen peroxide, into the perfusate of thse rat hearts. To my surprise, a low dose of H2O2 actually increased myocardial contractility! Higher doses did do damage, but what I observed was nowhere in the literature, and I figured people would think I was nuts if I tried to say that free radicals enhanced contractile function, so I moved on. Now we know that ROS play a role in numerous intracellular signalling processes, including adaptive signalling. Read for example, this abstract:
-----------------------------------------------------------

Gomez-Cabrera MC, Borras C, Pallardo FV, Sastre J, Ji LL, Vina J.
Decreasing xanthine oxidase-mediated oxidative stress prevents useful cellular adaptations to exercise in rats. J Physiol. 2005 Aug 15;567 (Pt 1):113-20. Epub 2005 Jun 2.

Reactive oxygen or nitrogen species (RONS) are produced during exercise due, at least in part, to the activation of xanthine oxidase. When exercise is exhaustive they cause tissue damage; however, they may also act as signals inducing specific cellular adaptations to exercise. We have tested this hypothesis by studying the effects of allopurinol-induced inhibition of RONS production on cell signalling pathways in rats submitted to exhaustive exercise.
Exercise caused an activation of mitogen-activated protein kinases
(MAPKs: p38, ERK 1 and ERK 2), which in turn activated nuclear factor kappaB (NF-kappaB) in rat gastrocnemius muscle. This up-regulated the expression of important enzymes associated with cell defence (superoxide dismutase) and adaptation to exercise (eNOS and iNOS).
All these changes were abolished when RONS production was prevented by allopurinol. Thus we report, for the first time, evidence that decreasing RONS formation prevents activation of important signalling pathways, predominantly the MAPK-NF-kappaB pathway; consequently the practice of taking antioxidants before exercise may have to be re- evaluated.
----------------------------------------------------------------

This brings me to the passage posted by Annie Wetter that prompted me to play devil's advocate here in the first place:


------------------------------------------------------
One last point and then I will let you go. A recent study (Christensen
Br J Nutr 88:711-717;2002) assessed the dietary intake of 12
adolescent male Kenyan runners. These boys were of Kalenjin
ethnicity, the group from which most of the Kenyan distance running
talent emerges. Although micronutrient intake was not determined,
their average daily intake of 3100 kcals was composed of foods only
locally available. Most (90%) of their calories were provided by
plant foods, with 81% of their energy coming from two foods, maize
and beans. How such a limited, unfortified diet allows for youth in
this area to develop world-class potential is a very interesting
research question.
------------------------------------------------------------

I don't want to stretch this notion to far, but is it possible that we
should look at this seeming mismatch between diet and performance
among these great runners as another indicator that we may be actually "over nourishing" our athletes during certain phases of the training process?

If we never allow glycogen levels to bottom out in training, do we
dampen the adaptive signals of training? If we flood the system with antioxidants prior to exercise, do we dampen intracellular signalling
in important ways?

One thing I think we can agree on is that the environmental pressures that formed intracellular signalling mechanisms over many thousands of years were NOT characterized by nutritional EXCESS and easily accessed carbo-loading bars, antioxidant cocktails and the like.

Just a little food for thought.

Dr Seiler

Garrett Smith
06-21-2007, 05:30 AM
Awesome info, Paul. Thank you.

Derek Simonds
06-21-2007, 12:59 PM
I wanted to artificially induce free radical damage by infusing H2O2, hydrogen peroxide, into the perfusate of thse rat hearts. To my surprise, a low dose of H2O2 actually increased myocardial contractility! Higher doses did do damage, but what I observed was nowhere in the literature, and I figured people would think I was nuts if I tried to say that free radicals enhanced contractile function, so I moved on.

OOOH I know (hand raised)!!!! "Hormesis"

Paul some fascinating information. I have a contratrian thought I will post later just as a thought because I believe the direction we are heading is correct.