T Nation

Coffee before fasted-state cardio?

Please bear with me, as I’m a bit of a newbie to the nutrition scene.

Okay, we know:

  1. Caffeine causes a rise in insulin levels.

  2. Fat metabolism during exercise is inhibited in the presence of high insulin levels.

Based on 1 and 2, wouldn’t it follow that coffee before fasted-state AM cardio is a bad idea?

Don: What makes you think that caffeine causes an insulin response when no other nutrients are ingested simultaneously? It seems to hold true that when eating carbohydrate at the same time as ingesting caffeine will cause transient insulin insensitivity and glucose intolerance.

However, I do not believe that such will be the case when caffeine (i.e. coffee) is ingested in the fasted state, nor with a protein and fat meal. On the contrary, coffee or caffeine ingestion at this time (i.e. before fasted-state cardio or with a protein and fat meal) might actually prove beneficial.

This should increase plasma free-fatty acids, and with stable insulin levels, this should bode well since the body will be primed to mobilize those fatty acids right to the muscles’ mitochondria for oxidation.

Green tea is a much better choice in my book.

Both of your statements are incorrect.

Joel

Okay Joel, I’ll bite. What’s the correct response?

Fa Q Joel, I was stating an opinion!
Green Tea is thermogenic with very little caffine and besides it has a ton of anti oxidants.

Joel, disregarding statement number one, could you expand on statement number two being incorrect?

It’s pretty much a physiological principle that insulin will inhibit hormone sensitive lipase, both in the muscle and in adipose tissue, which will lead to inhibition of fat breakdown.

In addition, elevated insulin levels will lead to or are indicative of elevated glucose oxidation. This latter point is associated with elevated malonyl-CoA levels, which are thought to inhibit fat oxidation by inhibition of Carnitine Palmitate Transferase, which shuttles FFA into the muscle mitochondria.

Thanks, Joel.

Joel! That is what a five year old would say, explain your answer. We expect more from someone of your standing. Why are they wrong? Who is wrong? I think timbo just about hit the nail on the head.
Caffeine doesn’t raise insulin, it may prove to make the subject less glucose tolerent meaning glucose levels would remain higher after ingesting carbs, so insulin cant do its “job”.
as for high insulin level reducing the ability to burn body fat that seems pretty well accepted to me.

I have covered this as has Berardi on the forum before, thus the reason why I did not elaborate; the information is already out there. I posted at least 4 research studies that showed no difference in substrate utilization during or after exercise when a carbohydrate, insulin releasing meal was consumed prior to exercise. Berardi even posted a study which showed a greater EPOC when subjects consumed milk and glucose. Insulin does not seem to make a difference w/ exercise. This is true at “rest,” but the physiological responses to exercise can’t be overridden by a little insulin.

What about a recent French study that found that trainees consuming a straight whey protein drink before training gained more muscle and less fat than those that consumed a whey/carb combo? I haven’t seen the study myself but a number of whey protein manufacturers are citing it all over the place. Is there anything to it?

Don: Did you read my first post? Therein lies an answer to question numero uno.

J-Rule: Thanks for the reply, my friend. Are those studies posted here on the forum, or could you be so kind as to direct a blind young T-Man to such?

Here is a quote from Berardi:

“Besides, the effects of exercise on fuel mobilization are more powerful than a small insulin increase.”

Here are 4 studies that I posted:

  1. Int J Sports Med 1999 Aug;20(6):384-9

Cardiovascular and metabolic responses during 30 minutes of treadmill exercise shortly after consuming a small, high-carbohydrate meal.

Diboll DC, Boone WT, Lindsey LR.

Procedure: Subjects either fasted or consumed a small, high-carb meal prior to 30 mins of treadmill running.

Results: No difference in substrate utilization during exercise.

  1. Appl Physiol 1991 Dec;71(6):2088-93

Effect of feeding and fasting on excess postexercise oxygen consumption.

Bahr R, Sejersted OM.

Procedure: Subjects fasted or consumed a small meal prior to strenous exercise.

Results: No difference in EPOC (substrate utilization post exercise) between groups.

  1. : J Appl Physiol 1999 Feb;86(2):479-87

Respiratory gas-exchange ratios during graded exercise in fed and fasted trained and untrained men.

Bergman BC, Brooks GA.

Procedure: Subjects exercised after an overnight fast or 3 hours after breakfast.

Results: There was a difference at extremely low intensities, but not at intensities that any T-man would work out at.

  1. : Med Sci Sports Exerc 1999 Mar;31(3):464-71

The effect of a preexercise meal on time to fatigue during prolonged cycling exercise.

Schabort EJ, Bosch AN, Weltan SM, Noakes TD.

Procedure: Subjects exercised in a fasted state or 3 hours after consuming 100g of carbs.

Results: It took longer for the CHO group to fatigue, and again, no difference in substrate utilization.

Here is another quote from Berardi:

“If you check out my Biology Bash In Barrie article I covered a study (I know, it’s in VITRO data) that showed that exercised muscle incubated in a carb and fat medium preferentially stores carbs and burns fat (even in the presence of insulin).”

Here is a study posted by Berardi:

“The effects of various intensities and durations of exercise with and without glucose in milk ingestion on postexercise oxygen consumption. Lee YS, Ha MS, Lee YJ. This study shows that during high intensity exercise with supplement nutrient intake (glucose+milk) actually INCREASES EPOC without changing RER. This means increase total calorie expenditure at the same relative proportion of fat oxidized (i.e. more total fat burned with the drink provision) (The RER was measured 2 hours post exercise).”

Joel

J-Rule: Thanks a lot, brutha. I’m going to delve into those. I’m not at all arguning against the post-exercise period and fat metabolism then, no, sir. I’m feelin’ you on that front.

The reason I questioned the assessment of substrate utilization during exercise in the post-absorptive state (i.e. after eating CHO) was because this is what I have been “schooled” to believe, with convincing data and physiology to support such, by my professors.

Now, if I can uncover some information to the contrary and build a solid base for an argument, this would be great.

Thanks again, J-Rule. I didn’t mean to “question” you, and I hope it didn’t come across as such. It seems the more I learn, the less I know:-)

Im not convinced. sure there are four studies showing this, that and whatever. i cant be bother looking them up right now, or getting the actual study to check methodogy and the actual results (conclusion are different to results and can be equally flawed) to check whether there WAS significant difference (statisticaly significant doesnt always mean not signifiacnt). im going with the real world result on this one, tghe lab is not always right, and there are some crappy studies out there.
I cant say if these studies are or not because i have no the time to look for them and check them out. if anyone has the full studies of any of these PM them my way.
Cheers
whetu

There is a difference between being critical and simply not accepting the research. Do a search on pubmed and there you will find the studies and abstracts that I mentioned, but interestingly enough, nothing will come up that shows consuming a meal before cardio effects substrate utilization during or after exercise. I already conducted the search because I too believed that this couldn’t be the case, but all I found was study after study telling me that I was wrong. Now, I’ve come to grips w/ the research.

J-Rule: I’ve been doing a bit of research myself–not to much:-) And, like you were originally, I’m still of the camp that insulin is going to inhibit lipolysis. Here is some literature worth a look:

Montain, SJ, MK Hppoer, AR Coggan, EF Coyle (1991). Exercise metabolism at different time intervals after a meal. J Appl Physiol 702(2): 882-888.

Jensen, MD, et al (1989). Insulin regulation of lipolysis in nondiabetic an IDDM subjects. Diabetes 38:1595-1601.

Horrowitz, JF et al (1997). Lipolytic suppression following carbohydrate ingestion limits fat oxidation during exercise. Am J Physiol 273 (Endocrinol Metab 36): E768-E775.

I think I can come up with a few more, as these are just from a couple of articles from my readings packet for Advanced Ex Phys II.

Timbo:

The first study has individuals consuming ~1g C/lb of body weight as their pre cardio meal. I don’t know that anyone is consuming a couple hundred carbs pre workout. And even w/ these large consumption, the difference between groups wasn’t all that much.

The second study has nothing to do w/ exercise and cant be compared to substrate utilization during exercise. Also, you’re dealing w/ diabetics in this study, not healthy individuals. Anytime you are going to make a statement about insulin for the general population, it’s probably best if the subjects in the study aren’t insulin f-ed up.

I looked for the third study but couldn’t find it.

Lastly, I think people are getting caught up in an issue that doesn’t really matter: substrate utlization during exercise. We are talking about gram difference in fat utilization at best; that isn’t going to make a difference. If you want to get some real benefit from cardio activity, then you need to have a great EPOC, and this only happens w/ higher intensity exercise. High intensity interval training has been shown to elevate metabolism for up to 48 hours post exercise; this is really when you start to get the fat loss benefits of cardio. Now imagine if we decided not to eat for 48 hours because our bodies are still in “fat burning” mode…you see what I’m saying?

Bottom line; do your HIIT and stop worrying about the little details like substrate utlization during exercise; it’s so small that it doesn’t even matter. And besides, there is a lot of data to support that it remains unaffected anyway when a normal meal is consumed pre workout.

Point well-taken, J-Rule.

I am also of the camp that believes not that the substrate utilization during exercise is most important. I am also a proponent of high-intensity intermittent aerobics, so I echo your feelings there as well.

However, what I am primarily concerned with is that, actually, during all times of the day–besides when at rest–we are basically just at different degrees of exercise. So, if lipolysis is inhibited at something like 25% VO2max, when the greatest percentage of energy is derived from fat, then you’d really not want to interfere with this.

J-Rule, believe me, I see exactly what you’re saying. Keep pounding away, and you’ll get through to me:-)

Timbo wrote: However, what I am primarily concerned with is that, actually, during all times of the day–besides when at rest–we are basically just at different degrees of exercise. So, if lipolysis is inhibited at something like 25% VO2max, when the greatest percentage of energy is derived from fat, then you’d really not want to interfere with this.

Okay, so how would you not interfere w/ this? Don’t eat all day? Do that and say bye bye to your leptin levels which will cause your body to be reluctant to use fat for energy. Also say bye bye to muscle protein, because gluconeogenesis will surely occur.

You can’t just say, oh, I’m going to be walking in the mall at 5 oclock, so let’s make sure I have a P + F meal at 3. You’ll put yourself through hell worrying about little stuff like that when it will make a 1% difference at best.

J-Rule, that was kinda funny, bro:-) Actually, reading over the “Lose Muscle-Gain Fat” thread, it seems plausible that optimal meal timing and composition is very beneficial for body composition athletes.

Now, is that something we didn’t already know and practice or what? Man, I can’t believe I just typed that directed at you, J. Don’t take offense to that. It just seems that your comment about eating a P/F meal during times of lower activity levels seemed condescending, when in fact, it’s rather applicable and makes sense.

Anyway, I picked up this abstract today. Just some more thought to add to the conversation.

[quote]J Clin Invest 2002 Dec;110(11):1687-93

Malonyl coenzyme A and the regulation of functional carnitine palmitoyltransferase-1 activity and fat oxidation in human skeletal muscle.

Rasmussen BB, Holmback UC, Volpi E, Morio-Liondore B, Paddon-Jones D, Wolfe RR.

Department of Surgery, University of Texas Medical Branch, Galveston, Texas, USA. blakeras@usc.edu

Physiological hyperglycemia with hyperinsulinemia reduces fat oxidation in skeletal muscle. The mechanism responsible for this decrease in fat oxidation in human muscle is not known and may contribute to the development of insulin resistance. We hypothesized that the transfer of long-chain fatty acids (LCFAs) into the mitochondria via carnitine palmitoyltransferase-1 (CPT-1) is inhibited by increased malonyl coenzyme A (malonyl-CoA) (a known potent inhibitor of CPT-1) in human muscle during hyperglycemia with hyperinsulinemia. We studied six healthy subjects after an overnight fast and during an induced 5-hour period of hyperglycemia with hyperinsulinemia. Muscle fatty acid oxidation was calculated using stable isotope methodology combined with blood sampling from the femoral artery and vein of one leg. Muscle functional CPT-1 activity was assessed by concurrently infusing an LCFA tracer and a CPT-independent medium-chain fatty acid tracer. Muscle biopsies were obtained from the vastus lateralis after the periods of fasting and hyperglycemia with hyperinsulinemia. Hyperglycemia with hyperinsulinemia decreased LCFA oxidation, but had no effect on LCFA uptake or medium-chain fatty acid oxidation across the leg. Malonyl-CoA concentration significantly increased from 0.13 +/- 0.01 to 0.35 +/- 0.07 nmol/g during hyperglycemia with hyperinsulinemia. We conclude that hyperglycemia with hyperinsulinemia increases malonyl-CoA, inhibits functional CPT-1 activity, and shunts LCFA away from oxidation and toward storage in human muscle.[/quote]