Home / Articles / Nutrition / Biology Bash In Barrie

Biology Bash In Barrie
Notes from the Annual OEP Conference

By Dr. John M Berardi, Ph.D.
First published at www.t-mag.com, Feb 8 2002.

Printer friendly version

"Ah'm just an ol' fashioned exercise physiologist with a little biochemistry training, so what in God's creation is all of this?"

Those are the words that flashed (in my very best Vivian Leigh doing Scarlett O'Hara impersonation) across my initially overloaded and now numb cerebral cortex as I sat in frigid Barrie, Ontario listening to the following research presentation:

"The contractile mediated activation of Egr-1 occurs via an SRF dependent pathway in skeletal muscle cells."

You see, every year my lab mates, my PhD advisor, and I jump in a hopped up rental van (you know, the kind that have rear seat temperature control) and embark upon the three-hour, northbound journey from London, Ontario to Barrie, Ontario for the Annual OEP (Ontario Exercise Physiology) Conference.

While such conferences are always great occasions to learn about the latest research being done in the field, the unspoken reason for going to this meeting has shifted from gathering useful scientific findings to simply catching a glimpse of a different town and some new beautiful babies (as Vince Vaughn would call them).

The reason for this change in intention is the fact that the presentations given at these meetings have been shifting; subtly at first and then quite radically in the last few years, from integrated and applicable exercise physiology and nutrition research to the study of, what seems to me, molecular minutiae. So when I heard a talk entitled "Regulation of hsp72 gene expression is mediated by Protein Kinase A activation of HSF1 following physical exercise," only one thought remained in my head: "Frankly Scarlett, I don't give a damn."

While the focus of the actual talks at this meeting has become quite small in scope and incomprehensible to those without a book entitled "The Meaning of Not-So Self Evident Acronyms," there are always a few excellent and applicable presentations. In this article, I'll review the noteworthy presentations.

Noteworthy Presentation #1:

Fats, the Good, the Bad, and the Ugly

This year, nutriceutical researcher Dr. Bruce Holub from the Department of Human Biology and Nutritional Sciences at the University of Guelph gave an outstanding presentation on dietary fats with particular attention to the effects of fat on cardiovascular (CV) health. To be completely honest, I believe it to be one of the best presentations I've ever seen. Here are the key points:

#1 - Quit with the focus on blood cholesterol!

• While the current North American cardiovascular disease paradigm is centered on blood cholesterol management, cholesterol can't account for the declining CV health of the people. In fact, there is no difference in blood cholesterol levels between North Americans and the Japanese, but North Americans have a 626% higher CV disease mortality rate!
• While high levels of blood triglycerides as well as measures of platelet aggregation are better indicators of CV disease risk, cholesterol remains in the spotlight. For you X-Filers, some believe that this is the case for two reasons. First, as usual, the medical community is sluggish in accepting new research findings. Second, pharmaceutical companies have a stranglehold on the medical establishment, thereby imposing their interests in the success of cholesterol lowering drugs.
• Lowering cholesterol in your diet does not appreciably lower blood cholesterol or CV disease risk. In fact, decreasing dietary cholesterol by 35% only translates to a 2-3% drop in blood cholesterol.

#2 - Get rid of trans-fatty acids in the diet! They aren't just bad, they're eeevil!

• In a study published in the prestigious New England Journal of Medicine, the exercise and nutritional habits of 80,000 women were recorded for 14 years. The researchers found that the most important correlate of heart disease was the amount of trans-fatty acids in the diet.
• Higher amounts of trans-fatty acids in the diet lead to a lowering of "good cholesterol" (HDL) and an increase in bad cholesterol (LDL), total cholesterol, and lipoprotein (a).
• The typical North American consumes 10-15 g of trans-fatty acids per day. Ideally we should consume none (or at least less than a gram).
• The following diet provides 20 g of trans-fatty acids per day (scary, huh?):
  2 microwave waffles (4.5 g)
  1 small (1 serving) bag of chips (8 g)
  1 order of french fries (4.5 g)
  1 tablespoon margarine (3.5 g)
• Products that claim to be "Cholesterol Free" and "Low in Saturated Fat" often have the most trans-fatty acids. Unfortunately these are the products that most of the public thinks are "healthy."
• Breast-feeding women who eat a diet containing these relatively common amounts of trans-fatty acids are feeding their child milk that contains 35% of its fat as trans fatty acids. Yikes! Talk about child abuse!

#3 - Fish Oil (or EPA/DHA) is King!

• Omega 3 fatty acids (like fresh water fish oils) haven't gotten the medical attention they deserve because they don't lower blood cholesterol. However, they do lower blood triglycerides and platelet aggregation. Platelet aggregation is an indicator of how likely the platelets are to stick to the walls of your arteries, which causes plaque build-up, leading to eventual artery blockade (arteriosclerosis).
• Taking three grams of fish oil per day for only 30 days will decrease blood triglycerides by 35%.
• Taking nine grams of fish oil per day will decrease the severity of mental disorders such as mania and depression.
• Inuit (an Eskimo people) eat diets low in fruits and vegetables and also high in saturated fats and animal protein. Although this diet doesn't seem "heart healthy," these people have a very low risk of CV disease. Why? Well, the average Inuit eats 130 g of marine foods per day (1000 mg of fish oil) while the average North American eats only 13 g of marine foods per day (100 mg of fish oil).
• When fish oil is taken regularly after a myocardial infarction, there's a 40% reduction in subsequent death rate.
• Fish oil is rapidly burned in the mitochondrion (the cellular "power houses"); therefore it's not likely to be stored as body fat.
• Flavorless fish oil is now being added to foods like eggs (Omega Pro) and in the future you'll see flavorless fish oil added to many foods, including ice cream.

#4 - Recommendations and Review:

In order to keep your CV risk factors in check:

• Your carbohydrate sources should be foods like rolled oats, oat bran, beans, grapefruit, prunes, etc. as they are all high in fiber. A high fiber diet reduces CV disease risk.
• Eliminate as much of the trans-fatty acids (hydrogenated fats) from your diet as possible. Trans-fatty acids are the silent killers of our parents and will eventually do our children in as well! These fats are found in most processed and pre-packaged foods as well as foods that contain fat but claim that they're "Low in Saturated Fats and Cholesterol."
• Avoid fats high in Omega 6 fatty acids as they inflame the blood vessel walls and can lead to arteriosclerosis. Foods high in Omega 6's include vegetable oils (canola oil, etc.). Read your food labels to avoid these bad guys.
• Your dietary fat sources should be monounsaturated fats (olive oil) and Omega 3 fatty acids (flax seeds, flax seed oil, fresh water fish, fish oil, concentrated EPA/DHA).
• Even if you're too lazy to reevaluate your eating habits and eliminate all the evil fats, at least supplement your diet with a bunch of healthy fats like fish oil and Omega 3's.

Noteworthy Presentation #2:

Increased reliance on exogenous fatty acids in muscle recovering from intense stimulation

It's known that recovery from glycogen depleting exercise leads to:

• Glycogen resynthesis
• A decreased RER (respiratory exchange ratio). This ratio determines fat and carb use. The lower the RER, the more fat is being used as fuel.
• Increased EPOC (excess post exercise oxygen consumption). The EPOC represents the increased metabolism seen after exercise when compared to baseline.

While fat is preferentially burned after exercise, it isn't known where that fat comes from (endogenous intramuscular triglycerides OR exogenous blood triglycerides from adipose tissue).

In this study, after glycogen depleting exercise, rat skeletal muscle containing a mixture of fast twitch type II a and II b fibers (plantaris muscle) was excised, placed in a petri dish with a medium containing carbohydrates, insulin and fats. Carbohydrate metabolism and fat metabolism were measured 1.5 hours post exercise.

Researchers found the following:

• 30 minutes of stimulation decreased muscle glycogen from 122 mmol/g dry weight to 38.0 mmol/g dry weight.
• When carbohydrate was provided, muscle glycogen levels 1.5 hours after exercise were back up to about 61 mmol/g dry weight.
• During 1.5 hours of recovery, no glucose oxidation occurred in the muscle. This means all carbohydrates taken up in the muscle were stored to replenish the carbohydrate stores.
• There was a twofold increase in fat oxidation during recovery (40.2 nmol/g wet weight) when compared to resting fat oxidation (from 18.5 nmol/g wet weight). This fat was provided by exogenous sources, indicating that little intramuscular fat was used during recovery. Therefore, if applicable to in vivo (in the body) conditions, this means fat from adipose tissue is burned during recovery.
• There was no increase in fat storage during recovery. Therefore fat taken up into the muscle was not stored but burned.
• Insulin in the medium had no effect on fat oxidation; therefore post exercise fat burning was not impaired in the muscle by increased insulin.

Therefore, if these data are applicable to humans in vivo, they tell us that after exercise, the muscle stores all carbs provided to it; burns all fat provided to it (this fat coming from the blood and adipose tissue and not the muscle); and that high levels of blood insulin may not impair fat burning during the post exercise period.

Noteworthy Presentation #3

Expression of Hsp 70 in human skeletal muscle following single limb exercise

Heatshock proteins (Hsp) are an interesting family of "cellular chaperone" proteins that are responsible for protecting important cellular components from degradation during stress to the cell. Originally it was found that heating the cell induced the expression of these proteins (thus the name). However, a whole host of other stressors have been shown to increase heat-shock protein activity and expression.

In this study, researchers showed that exercise increases heat-shock protein activity in the muscle. Other factors increasing heat-shock protein expression in both skeletal and heart muscle include: estrogen, thyroid hormone, decreases in cellular temperature, and glycogen depletion.

Since heat-shock protein expression can protect against cardiac muscle damage as well as skeletal muscle atrophy arising from inactivity, a lot of research dollars are going to be spent in the hopes of finding novel ways to increase heat-shock proteins in the heart and skeletal muscles.

Noteworthy Presentation #4

The role of AMP-kinase as a regulator of leptin's stimulatory effects on fatty acid metabolism in rodent skeletal muscle

Both Leptin (a hormone released by fat cells) and AICAR (an experimental compound called 5-aminoimidazole-4-carboxamide) are known to increase fatty-acid oxidation (fat burning) while decreasing triglyceride esterification (fat storage).

This study was designed to examine whether these two agents operated on a similar signaling molecule, AMP-kinase. AMP-kinase is a cell signaling molecule that, when stimulated, causes an exercise-like increase in muscle insulin sensitivity leading to increased GLUT-4 (glucose transporter) expression and glucose uptake.

With the many interesting functions of AMP-kinase (increased muscle insulin sensitivity, increased muscle glucose uptake, increased fat burning, decreased fat storage), finding ways to manipulate this pathway may just be the holy grail of body-composition research.

Noteworthy Presentation #5:

No effect of glutamine in promotion of anabolism post-exercise

In this study, researchers examined the effects of two different post-exercise drinks. Drink one was a carbohydrate and amino acid drink. Drink two was the same drink with a big dose of added glutamine (0.3g/kg). Muscle glycogen resynthesis and protein metabolism was measured after 90 minutes of endurance exercise.

• During recovery, glycogen resynthesis was no different between the drinks.
• During recovery, protein synthesis was no different between the drinks.

The researchers concluded that no additional glutamine is necessary for improving protein synthesis or glycogen resynthesis in endurance athletes. However, other potential markers of recovery (immune function, markers of muscle damage) were not, however, measured.

Noteworthy Presentation #6:

VO2 kinetics and muscle EMG response pre and post fatiguing sprint bouts in highly trained cyclists

During high intensity endurance exercise, there's a lag time before the oxygen delivery and utilization systems of the body can catch up to the work rate. During this time an oxygen deficit is created and anaerobic energy sources are used, thus driving up blood lactate and potentially leading to early fatigue. If this lag time can be decreased, performance during high intensity endurance activity can be improved and fatigue delayed.

In this study, highly trained cyclists initially performed six minutes of cycling at 85% of peak VO2 (oxygen consumption). Then, after 10 minutes of rest, subjects performed three very intense 30-second cycle sprints separated by four minutes rest. After another four minutes rest, subjects again performed six minutes of cycling at 85% of peak VO2 (oxygen consumption).

The data from this experiment showed that after the three cycle sprints, the "lag time" in oxygen delivery and utilization was significantly reduced. This means that there would be less of an oxygen deficit and less lactic acid build up during the initial phases of endurance exercise.

While this information isn't new to most elite cyclists, all high-intensity athletes could take a lesson from these data. They provide one more reason for performing a high intensity warm-up immediately before an intense endurance exercise bout.

At this point, I'll conclude and spare you the pain of additional acronyms. Exercise physiology (once called physical education, or "gym") sure has come a long way, hasn't it?