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Four Years of Frigidity
Notes from the 2003 OEP Conference

By Dr. John M Berardi, Ph.D.
First published at www.t-mag.com, Feb 21 2003.

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"What the heck is a 'snow squall' anyway?" I asked myself as I packed my suitcase and prepared to embark on a 3-day science extravaganza. My lab mates and I were getting ready to trek a few hundred miles north to Barrie, Ontario for the 2003 OEP (Ontario Exercise Physiology) Conference.

The weather reports warned of "snow squalls," but I thought it was just a fancy term for snowstorms and snowstorms are nothing to worry about. Heck, I've got 4-wheel drive.

A few hours later, while barrelling toward Barrie, I learned what a snow squall looks and feels like. The formal definition is a brief, but intense fall of snow that greatly reduces visibility and which is often accompanied by very strong winds. Nowhere in the definition was the fact that snow squalls also may cause roughly a doubling of the time it takes to get to your destination. Neither was it mentioned that snow squalls can cause cars to burst into flame, which can further slow you down.

Since this trip marked my fourth year to OEP — and my fourth year arriving late at OEP due to weather/traffic conditions — I'll have to remember the snow-squall theory of travel for next year.

Once nestled into the hotel — warm, safe, secure, and committed to not leaving the hotel, lest I become an unwilling participant in Snow Squall Fury 2003 — it was time to experience Science Squall 2003. A Science Squall is defined as a brief but intense research experience in which 20 presentations, 15 minutes in length, are presented, back to back, over a five-hour span of time. A Science Squall, when attended by some of the top researchers in the country, is also accompanied by reduced objectivity and very strong opinions.

For your reading pleasure, here are a few of the noteworthy presentations.

Abstract Title — Effects of Creatine on GLUT4 Translocation, Glucose Uptake, and Glucose Metabolism in L6 Rat Skeletal Muscle Cells (Ceddia et al).

Okay, so you're stuck on the title. Let me give you a quick glossary of the terms and then I'll tell you what the researchers found. For starters, GLUT4 translocation is the process by which the GLUT4 receptor, a glucose transporter that's stored deep inside of the cell, migrates to the cell membrane to facilitate glucose uptake. GLUT4 translocation occurs in response to insulin signaling and also occurs massively after exercise — thus the post-exercise "window of opportunity." L6 rat skeletal muscle is a cell type in which insulin stimulation of glucose uptake occurs predominantly via GLUT4 translocation. Therefore, if the GLUT4 mechanism is thought to be affected, the L6 cells are the ones you want to study.

Recently, several research studies have suggested that creatine supplementation can actually increase the GLUT4 receptor content in muscle as well as increase muscle glycogen concentration. This would be an interesting mechanism of action for creatine since it would lead to increased insulin sensitivity and increased storage of carbohydrate in the muscle — thus improving nutrient partitioning.

In this study, researchers at York University investigated the hypothesis that creatine might regulate glucose metabolism by increasing insulin sensitivity in skeletal muscle. They incubated L6 muscle cells with or without creatine for 48 hours. Then, insulin and glucose were added to the medium. They then measured the amount of glucose oxidized, the amount of glucose stored as glycogen, and the amount of GLUT4 translocation.

After insulin stimulation, GLUT4 translocation was increased. In addition, the incorporation of glucose into glycogen and the oxidation of glucose both were increased. However, this effect was not impacted by the presence of creatine. Interestingly, creatine alone (before insulin stimulation) increased cellular metabolism, leading to greater glucose oxidation. However, creatine did not seem to increase insulin sensitivity.

This in vitro study ("in a dish"), along with a few other similar studies, has demonstrated that acute (short duration) glucose uptake is not impacted by creatine supplementation. However, other investigations have shown increases in muscle glycogen and GLUT4 content in vivo ("in a human").

This simply indicates that creatine may affect glucose metabolism, thereby increasing baseline glucose oxidation and chronic muscle glycogen storage in humans over a longer time frame than an acute study can measure.

Abstract Title — The Effect of Short Sprint Intervals on Muscle Metabolism and Performance During Intense Aerobic Cycling (Hughes et al).

Traditionally, aerobic training has consisted of long-duration aerobic exercise performed at/below critical power or the lactate threshold. These sessions have been known to be quite long and when performed daily, can lead to the accumulation of huge training volumes.

Recently, many investigators have demonstrated that intense sprint or interval training might lead to more rapid improvements in performance, maximal oxygen consumption, and important thresholds like the lactate threshold and critical power. These results have been demonstrated in both elite and untrained men and women.

In this study, the investigators examined whether a mere three high-intensity training bouts per week for two weeks could lead to increased aerobic performance, maximal oxygen consumption, and anaerobic power.

Subjects performed intense Wingate sprint cycling (cycling as fast as they can for 30 seconds at a resistance of 10% x body mass) on M, W, and F of two consecutive weeks. On the first Monday, subjects performed 4 sprints with 4 minutes rest between sprints. On days 2, 3, 4, and 5, subjects performed 5, 6, 7, and 8 sprints with 4 minutes rest between sprints. Finally, on day 6 they repeated the protocol from day 1.

As a result of a mere 17 minutes of actual exercise (and 150 minutes of "workout time" — including rest periods), subjects increased their max anaerobic power by 12%. While maximal oxygen consumption was unchanged, the most interesting finding of the study was that cycle time to exhaustion (at 80% of max) was increased by 101%. In other words, before the 6 cycling bouts, the subjects cycled for about 25 minutes before they were exhausted. After the 6 cycling bouts, subjects lasted a whopping 51 minutes.

Metabolically speaking, muscle glycogen was 25% higher at rest and glycogen utilization was lower during the ride to exhaustion.

This study, along with a number of recent investigations, hopefully illustrates the need for very high-intensity work in endurance athletes. By using both distance work and high-intensity work, a time-efficient training regime can be created that will allow for both adequate recovery as well as impressive adaptation.

Abstract Title — Ingestion of Caffeinated Coffee Impairs Blood Glucose Homeostasis in Response to Either High or Low Glycemic Index Cereals in Non-Obese Males (Kacker et al).

Uh, oh — this topic again! The last time I discussed the negative effects of caffeine on glucose tolerance and insulin sensitivity, I got hate mail from just about everyone. It appears that no one wants to give up their caffeine, not even the scientists at OEP. That's right, several caffeine-oholic researchers in the audience got all twisted up over this one and created a bit of a stir. One even mentioned that caffeine, to him, was like an essential food group, and therefore it couldn't be all that bad. Regardless, here's the data.

In this study, a group of young, healthy, non-obese males consumed coffee (5mg/kg of caffeine) and then, 60 minutes later, consumed 75g of carbohydrate as either a high-GI meal (Crispix and skim milk) or a low-GI meal (all bran and skim milk).

While caffeine didn't have an effect on blood glucose or insulin after an overnight fast, caffeine consumption resulted in:

• 29% increase in insulin after high-GI meal (vs. decaf.)
• 44% increase in insulin after low-GI meal (vs. decaf.)
• 146% increase in blood glucose after high-GI meal (vs. decaf.)
• 220% increase in blood glucose after low-GI meal (vs. decaf.)

Again, whether we like it or not, it's becoming clear that caffeine does negatively impact glucose disposal, insulin response, and the glycemic index. The subjects in this study were regular caffeine users but did go through a 48h withdrawal before the test day, so I asked the researchers involved in this study whether this effect would be as pronounced without the withdrawal period. While they weren't sure, they did tell me that they are collecting those data as you read this and they should be published in the near future.

The big question I keep getting is whether or not the negative effects of caffeine will impact body composition. Since caffeine does increase metabolic rate and fat mobilization, the negative effects on glucose and insulin function may be neutralized with respect to body comp. However, since glucose and insulin homeostasis are linked to health, it's important to realize that even if coffee doesn't make you fatter, it may impair your ability to deal with carbohydrates.

Glycemic Index of Different Breakfast Cereals is Not Due to Glucose Entry into Blood But by Glucose Removal by Tissue (Schenk et al.)

As many of you know, the glycemic index is calculated by the total amount of glucose that appears in the blood after a test meal divided by the amount of glucose that appears in the blood after a reference meal (white bread or glucose). However, the factors contributing to the blood glucose rise and fall often aren't discussed, presenting an incomplete picture of the glycemic index.

After eating a meal, blood glucose will rise in proportion to the rate of appearance (Ra) of glucose in the blood (how fast the meal was digested and absorbed). However, the rate of appearance isn't the only determinant of glycemia. During the time that glucose is appearing, the amount of glucose we can measure in the blood is also determined by the amount of glucose that's concomitantly taken up by the tissues, or the rate of disappearance (Rd). Therefore, the glycemic index/blood glucose = Ra - Rd.
Usually, when a food is high GI, we assume that it's rapidly digested and absorbed, leading to a high glucose response. In addition, we assume that insulin will rise in proportion to this measured glucose rise, leading to antilipolytic effects and lipogenesis. Likewise, when a food is low GI, we assume that it is slowly digested and absorbed, leading to a low glucose response. Again, leading to a small insulin response and minimal impact on fat storage or fat loss.

As you can see, the assumption is that Ra, or the rate of entry of the carb into the blood, determines GI. In other words, a high GI meal has a high Ra while a low GI meal has a low Ra. This study points out that the assumption commonly made is far too simplistic.

In this investigation, two different breakfast cereals were studied. The first cereal was a high-GI cereal (corn flakes; GI = 151) while the second cereal was a low-GI cereal (all bran; GI = 54.5). After consuming 50g of each available carbohydrate, blood glucose and insulin concentrations were measured for two hours.

Of course, the total glucose measured in the blood reflected the large difference in GI. The corn flakes promoted a much larger blood glucose rise than the all bran.

Interestingly, though, when labeled glucose was used to trace the glucose Ra and Rd, the glucose Ra into the plasma wasn't different between cereals, meaning that both cereals were digested and absorbed at the same rate.

How, then, might the glycemic index have been different? Well, the Rd from the blood was much faster in the all bran group, meaning that the reason that the glucose concentrations in the blood were lower with all bran was not that it was slower to digest and absorb.

How could this be? Well, enter our friend insulin. Since insulin concentrations were 75% higher immediately after the low GI, all-bran meal, it stands to reason that the blood glucose cleared out much more quickly in this group. Therefore the reason the high GI corn flakes group had a larger rise in blood glucose is because they got a smaller insulin response and a slower clearance of the blood than the low-GI group.

So why the big insulin response with bran? Well, it could be the fact that the bran meal contained 15g of protein while the corn flakes meal contained only 1g of protein. Since protein promotes a large insulin response when combined with carbohydrate, the all bran cereal may have a low GI for the same reasons milk has a low GI — the protein content. In both types of low-GI meal, the low blood glucose response is probably due to the large insulin response and the subsequent rapid uptake into the tissues (Rd).

While this study adds a whole lot of confusion with respect to selecting appropriate carbohydrate choices (since it now looks like all bran might be worse than even corn flakes in terms of the insulin response), I believe that it does indicate that the insulin index might turn out to be a better determinant of carbohydrate quality than the glycemic index.
Now, we just need to convince some researchers to get us a comprehensive list of the insulin index of foods instead of the glycemic index. In the interim, don't freak out and draw all sorts of weird conclusions. Remember, the best determinant of whether a food is "good" or "bad" for your physique progress is how you look when it's regularly eaten.

Hyperoxic Training Improves Cardiorespiratory Response and Performance to Heavy Exercise (Perry et al).

Breathing air that contains a higher percent-oxygen concentration can lead to an increased aerobic work capacity. This study investigated whether increased oxygen provision (60% oxygen) during training would lead to increased training intensity and a subsequent increase in maximal oxygen consumption and exercise performance.

Subjects trained on a bicycle ergometer 3 days per week. During each training session they exercised at 80-85% of max HR, performing intervals of 4 minutes on and 2 minutes off for 60 minutes. During training the HR range was maintained by increasing workload. In the hyperoxic group, a 12% higher load was required to maintain the same % of max HR.

At the end of the 6 weeks of training, subjects required an average load increase of 16% to maintain 80-85% of HR max. However, as indicated, the hyperoxic group needed to use 12% more load throughout in order to maintain the appropriate HR range.

At the end of the 6 weeks of training, both groups of subjects were tested under normoxic conditions. While there seemed to be no differences in max oxygen consumption, the hyperoxic group showed a 100% improvement in time to exhaustion at 90% of max while the normoxic group showed only a 50% improvement in time to exhaustion at 90% of max.

These data indicate that training under hyperoxic conditions can increase the amount of work an athlete can perform during each training session. After several training sessions, this increased workload translates into increased performance under normoxic conditions.

And there you have it — my fourth OEP conference, my fourth year of frigidity. Remind me to convince someone else to drive next year!