Join Date: May 2007
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
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.
Happiness is success.
Contentment is wealth.