Tag Archives: carbohydrate

Implementing low carbohydrate availability training- Part 2

by Kedric Kwan CISSN. There is definitely a discrepancy between mitochondrial adaptation and performance. After reading the literature, there are a few factors that needs to be accounted for during the implementation to optimise both the mitochondrial adaptation and performance outcome. The first factor is to ensure that the second bout of exercise is commenced with low muscle glycogen levels.

Not doing so might not facilitate the desired adaptation which can translate to performance. This could be seen in an acute study done by Cochran and colleagues (2010) who had 10 active males participated in a trial where they were split into two groups, both groups performed 5 x 4 minutes bout of cycling at 90-95% heart rate reserve followed by a 3 hour recovery where both groups consumed the drinks provided. One group ingested a high carbohydrate drink (HI-HI) and the other ingested a placebo drink (HI-LOW). After the 3 hour recovery, the same exercise protocol was repeated. The HI-LOW group showed greater increased of p38 MAPK compared to the HI-HI group. However the increase of PGC-1α and cytochrome c oxidase (COX IV) mRNA which plays a role in the synthesis of ATP increased with no difference between groups. This is due to the fact that both groups started the second bout of exercise with similar muscle glycogen content.

In addition, to further emphasize the importance of muscle glycogen content, two different studies measured the activity level of AMPK. Using a cycling model one study showed that AMPK levels were not different in both groups despite one group consuming CHO during exercise (Lee Young et al., 2006). This was in contrast to the result by Akestrom et al (2006) which showed a higher increase in the group that consumed a placebo drink. This could be caused by the different exercise mode used in the experiments due to a cycling model used by Lee Young and colleagues whereas Akestrom and colleagues used a single knee extensor model. The nature of the single knee extensor model is highly concentrated and possibly targeted the carbohydrate glucose supplementation which spared muscle glycogen which explains the difference in findings between the two studies. Another interesting study found that carbohydrate ingestion during endurance exercise resulted in similar increases in CS levels with the placebo group. An incremental maximal cycling test also showed similar improvements in both groups (Nybo et al., 2009). This was also only conducted after an overnight fast with no glycogen depletion prior which further indicates the role of glycogen on these adaptations.

The last study that really cements the role of muscle glycogen is done by Lane and colleagues (2015) This study was done to examine the effects of sleeping with low carbohydrate availability on acute training responses and this showed greater upregulation of signalling proteins involved in fat oxidation but fail to show an increase of upregulation of markers of mitochondrial biogenesis. The participants recruited in this study were highly trained and it is well documented that trained individuals have a higher capacity to store glycogen compared to untrained. Despite muscle glycogen content was reduced by 50% but because of the high level of starting muscle glycogen, participants started the second exercise bout with reduced muscle glycogen but the levels were not low enough to illicit changes in mitochondrial adaptation that was hypothesized to occur. This shows that the actual content of muscle glycogen seems to play a larger role than the relative amount of muscle glycogen. What is the sweet spot for muscle glycogen content to illicit a response is still unclear and hopefully future research will shed some light on it.

The more trained you are, the greater cellular disruption you would need to cause an adaptation, hence there seems to be an inverse relationship between training status and muscle glycogen level. The more well trained you are, lower muscle glycogen levels might be needed to create additional adaptation. If you’re relatively untrained, performing exercise after a long bout of fasting might be able to cause some form of improvement.

Another factor that to take into account during implementation is the intensity or stimulus from the training bout. As mentioned above, p38 MAPK is one of the regulators of the master regulator of mitochondrial biogenesis, PGC-1 α. Research have shown that p38 MAPK is sensitive to the stress that is being imposed during training and it is also regulated by the reactive oxygen species (ROS) induced during exercise. In fact, oxidative stress seems to be higher after a short bout of high intensity exercise compared to a submaximal steady state exercise (Olcina et al., 2008) further showing the role of intensity in regulating this protein. The hypothesis that higher exercise intensity would cause higher oxidative stress leading to higher levels of p38MAPK seems valid. Hence, a constant intensity might not be able to illicit significant adaptation for the trained athlete.

The other upstream protein, AMPK seems to response to exercise stimulus and intensity as well. Nielsen and workers (2002) showed that at the end of a 20 minute exercise bout at 80% VO_2max AMPK levels were reduce.d This is possibly due to the fact that AMPK response to a change to the initial bout of intensity and reduces thereafter. Another study showed that AMPK activation was lowered after 3 weeks of moderate intensity at the same workload. This could be caused by the initial adaptation to the initial stimulus and that intensity wasn’t sufficient to further induce additional adaptation in later stages (McConell et al., 2005).

Most training bouts used in the studies used fixed bout of exercise, an example from one study used a high intensity training model consisting of 8 x 5 minutes of all-out effort alternating with 1 minute of recovery for 3 weeks (Hulston et al., 2010). It is possible that because the exercise bouts did not increase, a “tolerance” was built up to it. Hence a reduced stimulus of exercise intensity took place further into the training intervention. Moreover, how much time of the 5 minute all-out effort was actually maximal effort because I doubt that anyone could sustain an all-out effort for 5 minutes. Shorter bouts of all-out efforts such as the one used in Sprint Interval Training (SIT) might be able to elicit a stronger stimulus. In fact, Granata et al (2015) showed that SIT actually increased PGC-1 α and p53 much higher than regular high intensity training or sub-lactate threshold training even though total work done was lower in the SIT group. However, this study was not done in a limited carbohydrate availability state but the importance of intensity should be noted from this study. Given that the activation of these two upstream regulators responses to the exercise stimulus and intensity, it make sense that some form of progressive overload is needed to induce some form of additional improvement that could translate into performance.

In a discussion with Professor John Hawley (you should know who he is, if you don’t, you haven’t been reading up enough) he said that currently measurement tools might not be sensitive enough to show a statistical significance on performance when training with a reduced carbohydrate availability, so if tools aren’t sensitive enough, the only possible way I could think of is to create additional performance large enough to be detected. While the verdict on performance isn’t actually out yet, future studies that is conducted with much better methods might actually create more performance changes using a “train low” method strategically.

For the general lay person wanting to implement some form of reduced carbohydrate availability training, you could probably start by doing some form of fasted exercise or simply performing two bouts of exercise with no carbohydrate in between sessions. While the exact amount of muscle glycogen depletion would not be accurate, I believe most readers here aren’t elite endurance athlete hence there might still be small additional benefits to us.

A very interesting study I would like to conduct which would benefit meathead powerlifters like myself would be to actually examine if performing resistance training with reduced glycogen availability could improve endurance performance compared to actually performing resistance training in a carbohydrate fed state. If this hypothesis works, simply restricting carbohydrate consumption prior to lighter lifting sessions might actually improve our aerobic capacity without the need of too much additional cardio.

And yes, despite being a powerlifter, I still see the importance of the aerobic system so if it’s possible to kill two birds with one stone solely through lifting, I would be highly interested to do a study as such.

Take home message: As far as the evidence would suggest, training with low glycogen/carbohydrate availability and periodizing it to a well thought of training schedule can bring about additional benefits. No study have shown a decrement in performance which would be a relief to most wanting to experiment with it.

This field of research is relatively new and there would definitely be more studies coming out in the near future. I hope I’ve given some insight on the mechanism behind how low glycogen/carbohydrate availability training works and the physiology and biochemistry lessons didn’t bore you out of your minds!

Fun Reading for My Fellow Geeks

Akerstrom, T., Birk, J., Klein, D., Erikstrup, C., Plomgaard, P., Pedersen, B. and Wojtaszewski, J. (2006). Oral glucose ingestion attenuates exercise-induced activation of 5’-AMP-activated protein kinase in human skeletal muscle. Biochemical and Biophysical Research Communications, 342(3), pp.949-955.

Cochran, A., Little, J., Tarnopolsky, M. and Gibala, M. (2010). Carbohydrate feeding during recovery alters the skeletal muscle metabolic response to repeated sessions of high-intensity interval exercise in humans. Journal of Applied Physiology, 108(3), pp.628-636.

Granata, C., Oliveira, R., Little, J., Renner, K. and Bishop, D. (2015). Training intensity modulates changes in PGC-1α and p53 protein content and mitochondrial respiration, but not markers of mitochondrial content in human skeletal muscle. The FASEB Journal, 30(2), pp.959-970.

Hulston, C., Venables, M., Mann, C., Martin, C., Philip, A., Baar, K. and Jeukendrup, A. (2010). Training with Low Muscle Glycogen Enhances Fat Metabolism in Well-Trained Cyclists. Medicine & Science in Sports & Exercise, 42(11), pp.2046-2055.

Lane, S., Camera, D., Lassiter, D., Areta, J., Bird, S., Yeo, W., Jeacocke, N., Krook, A., Zierath, J., Burke, L. and Hawley, J. (2015). Effects of sleeping with reduced carbohydrate availability on acute training responses. Journal of Applied Physiology, 119(6), pp.643-655.

Lee-Young, R. (2006). Carbohydrate ingestion does not alter skeletal muscle AMPK signaling during exercise in humans. AJP: Endocrinology and Metabolism, 291(3), pp.E566-E573.

McConell, G., Lee-Young, R., Chen, Z., Stepto, N., Huynh, N., Stephens, T., Canny, B. and Kemp, B. (2005). Short-term exercise training in humans reduces AMPK signalling during prolonged exercise independent of muscle glycogen. The Journal of Physiology, 568(2), pp.665-676.

Nielsen, J., Mustard, K., Graham, D., Yu, H., MacDonald, C., Pilegaard, H., Goodyear, L., Hardie, D., Richter, E. and Wojtaszewski, J. (2002). 5â€²-AMP-activated protein kinase activity and subunit expression in exercise-trained human skeletal muscle. Journal of Applied Physiology, 94(2), pp.631-641.

Nybo, L., Pedersen, K., Christensen, B., Aagaard, P., Brandt, N. and Kiens, B. (2009). Impact of carbohydrate supplementation during endurance training on glycogen storage and performance. Acta Physiologica, 197(2), pp.117-127.

Olcina, G., Munoz, D., TimÃ³n, R., Maynar, M., Robles, M., Caballero, M. and Maynar, J. (2008). Oxidative Stress And Antioxidant Response In Trained Men After Different Exercise Intensities. Medicine & Science in Sports & Exercise, 40(Supplement), pp.S384-S385.

The Case for Carbs – Part 1

by Kedric Kwan CISSN. The world of carbohydrates can be one plague with controversy. It seems like people tend to polarize the intake of carbohydrates from either completely low to no carbohydrate or having a high carb diet all day, every day. It’s either cotton candy or some gross sugar-free substitute. And somewhere in that morass of social media confusion, lies the truth.

When the role of carbohydrate is concerned, it is mainly involved in keeping muscle glycogen and blood glucose elevated to facilitate exercise performance.

Classic studies have shown the role skeletal muscle glycogen content plays in sustaining exercise or sporting performance. My favourite one in particular is this study done in soccer players. The finding of the summary is in the table below:

	High Glycogen	Low Glycogen
Muscle glycogen at start of game:	100%	50%
Muscle glycogen at half time:	40%	7%
Muscle glycogen at full time:	10%	0%
Distance covered first half	6,100m	5,600m
Distance covered second half	5,9000m	4,1000m
Total distance covered	12,000m	9,7000m
Percentage walking	27%	50%
Percentage sprinting	24%	15%

This study basically showed that the football players with higher glycogen covered a staggering 1,300m more and sprinted more and walked less compared to the ones who had low muscle glycogen (Saltin 1973).

I don’t like white rice said no Asian ever.

You should be convinced now that carbohydrates do play a huge role in both exercise and sporting performance. However, just because something is good doesn’t mean that constantly consuming a ton if it will bring additional benefits.

In the endurance world, performance is definitely affected by carbohydrates and recent studies have indeed demonstrated that (Leckey et al., 2015, Torrens et al., 2016). However, in 8 longitudinal studies evaluating the relationship between a high carbohydrate diet (HCHO) and moderate carbohydrate diet (MCHO), 5 studies showed no difference in performance improvement of HCHO compared to MCHO when it came to the actual performance test (Burke et al., 2004).

This leaves us with the question, is constantly having high carbohydrate availability the best way to maximize endurance performance? Or could strategically periodizing phases of training with low carbohydrate availability enhance performance to a greater extent?

Mitochondrial physiology

In order to fully understand the content of this article we need to understand a little physiology of endurance performance. Besides the role the heart plays, the two ways someone can increase their endurance performance is by increasing the number of mitochondria also known as mitochondria volume density or by improving mitochondrial function. This article will focus mainly on the increasing of mitochondrial volume density also known as mitochondrial biogenesis, instead of its function.

Mitochondria is the site where energy in the form of ATP is produced so the more mitochondria we have, the more ATP we can produce which theoretically leads to an improvement of performance. Since the improvement of performance could be thought of the accumulated response from an acute exercise bout, constant training would result in an improvement of endurance performance through increased mitochondrial volume.

Something that governs the increase of mitochondria is the transcription factor called Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α). This has been labelled as the “master regulator” of mitochondrial biogenesis and training in a state of reduced carbohydrate availability seems to augment this by upregulation upstream regulators and protein kinases that are involved in the signalling pathway for mitochondrial biogenesis.

One of the major protein kinases that up regulates PGC-1α is the protein kinase called AMP- activated protein kinase (AMPK). This protein responses mainly to energy availability and the ratio of AMP to ATP, a higher level of AMP concentration simply signals that energy availability is low and AMPK will be upregulated (Alexander and Walker, 2011). Another protein kinases is the p38 mitogen-activated protein kinase (p38 MAPK) which is a protein that is sensitive to stress that takes place during exercise mainly in the form of cellular perturbation and oxidative stress. This two proteins act downstream on PGC-1α, increasing it’s activity hence up regulating mitochondrial biogenesis.

Besides PGC-1α, another protein called p53 has also been implicated in the role of mitochondrial biogenesis. Similar to how PGC-1α is upregulated by AMPK and p38 MAPK, p53 is also one of the downstream targets of those proteins.

Training with low carbohydrate availability – the evidence.

One of the most common ways to reduce carbohydrate availability is to train twice a day without ingesting any form of carbohydrate after the first exercise bout. What happens when exercise is commenced with low carbohydrate availability is that the cellular perturbation is increased and energy availability would be greatly reduced hence AMPK and p38 MAPK activity would increase and act on it’s downstream targets. This was first seen in a study done by Hansen and workers (2005) in which they recruited a group of seven untrained males and have them perform single leg knee extensions at 75% maximal power out (P_max). One leg trained twice a day, every other day (LOW) while the other once a day, every day (HIGH). This training protocol lasted 10 weeks. Only water was ingested while training the LOW leg to ensure that the second bout of training was commenced with lower glycogen stores while the HIGH leg that was trained once every other day trained with regular glycogen levels. After 10 weeks the LOW leg showed higher a increase of Citrate Synthase (CS) which is a marker of increased mitochondrial volume and HAD which shows greater oxidative capacity, compared to the HIGH. The LOW leg also performed better in a time to exhaustion test (TTE) compared to the HIGH.

This study was definitely a huge pain to go through and in most countries, it wouldn’t even get approved by ethics. Hence ecological validity isn’t particularly high but this was simply a “proof of principle” study that eventual lead to more studies being done. Another thing to take note of is that this study was done with untrained population and the effects on trained population might be different

To create a study that had greater real world application, a similarly study was done using a cycling model on 12 endurance trained cyclist or triathletes. Using a similar design in a cycling model, one group trained twice a day with both steady state (SS) and high intensity interval training (HIIT) done on the same day (LOW) every other day while the other group once a day, every day (HIGH) alternating between SS and HIIT for 3 weeks. Participants cycled for an initial 100 minute of SS cycling followed by 8 x 5 minutes of HIIT at 75-80% P_max(Yeo et al., 2008).

The LOW group was given only water while the high group had no nutritional restriction. In the first two weeks, the LOW group had reduced power output compared to the HIGH but that stabilized in the third week. After 3 weeks, biopsies showed a higher increase in CS and β-HAD in the LOW in agreement to the results reported by Hansen et al. The LOW group also had higher lipid oxidation compared to the HIGH. A 60 minute time trial was also performed to measure performance improvement but there was no difference between groups. Unlike the study done by Hansen et al which showed an improvement in both mitochondrial adaptation and performance (TTE) Yeo et al couldn’t display an additional performance benefit despite enhance mitochondrial adaptation in the LOW group.

Hulston and colleagues (2010) performed what was almost a replication of the study conducted by Yeo et al with small changes in different training parameters and what they showed was consistent with the previous findings, as markers of mitochondrial adaptation (CS and β-HAD) and lipid oxidation increased while a drop in power output was seen in the low group and both groups showed similar improvement in a time trial test.

Despite the lack of performance improvement, most acute studies done would be in agreement with the chronic studies showing additional improvement in markers of mitochondrial adaptation (some acute studies did not show improvements but will be touched on below). Using a cycling model, Psilander and colleagues (2013) recruited 10 subjects to investigate the acute response to training with reduced glycogen availability on highly trained athletes. They performed exercise either in a high glycogen session or low glycogen session with at least a week in between sessions. On the first day, a protocol to deplete glycogen was done for both high and low sessions. The high session then consumed two high carbohydrates meal and returned for the exercise test 14 hours later, whereas the low session was commenced 14 hours later after consuming two low carbohydrate meal. The exercise test consist of 6 intervals of 10 minutes with 4 minutes of active rest in between intervals. The first interval started at 72.5% Vo₂ max and subsequent intervals were reduced by 2.5% making the last interval 60% of Vo₂ max. A muscle biopsy obtained 3 hours post test showed a greater increase in PGC-1α expression with also an increase of the mitochondrial enzyme pyruvate dehydrogenase lipoamine kinase isoenzyme 4 (PDK-4).

In a different study, increases of PDK- 4 and Carnitine palmitoyltransferase I (CPT-1), another mitochondrial enzyme was higher in the group that performed exercise in a lower glycogen state (Bartlett et al., 2013). 8 participants performed a glycogen depletion protocol in the evening lasting 68 minutes. Participants returned the next morning to perform High Intensity Training (HIT) running for 6 x 3 minutes at 90% Vo₂ max. Participants exercised either in a high (HIGH) carbohydrate state or low (LOW) carbohydrate state. In the HIGH state, participants were fed carbohydrate before, during and after HIT while in the LOW state, no carbohydrate was fed before, during and after HIT. Participants switched groups (HIGH to LOW or LOW to HIGH) and repeated the protocol with a minimum of 7 days rest between protocols. Phosphorylation of p53 was also higher in LOW compared to HIGH but the increase of PGC-1α was similar between both groups.

So far every exercise protocol here has been done using an endurance exercise model, for all the meat heads out there, don’t lose hope as there is one study that used resistance training to investigate similar hypothesis.

Low carbohydrate availability and resistance exercise.

In this study, Camera and workers (2015) recruited participants to perform resistance exercise to investigate the acute response on mitochondrial adaptation. A group of 8 healthy fit males were recruited and they performed a glycogen depletion protocol on one leg. Participants then consumed a low carbohydrate dinner and returned the next morning to perform resistance exercise after an overnight fast to ensure one leg would perform the exercise in a low glycogen state. Participants then performed 8x 5 minutes at 80% of their 1RM with 3 minutes rest in

Check out Pauline’s glycogen filled skeletal muscles.

between legs. The leg that performed resistance exercise in a low glycogen state had greater phosphorylation of p53 compared to the normal leg and PGC-1α also had a higher increase in the low glycogen leg.

As far as the acute and chronic changes in mitochondrial adaptation is concerned, it’s safe to say that training in a low glycogen/carbohydrate state definitely enhances this response. When it comes to performance, it’s not so clear cut.

Two other studies showed increases in both mitochondrial adaptations but when it came to the actual performance test, improvements were similar across both groups with no additional performance outcome (Morton et al., 2009, Van Proeyen et al., 2011).

Low carbohydrate availability and greater performance improvement.

However there are two studies that have been published recently that shows an improvement in performance. The first was done by Cochran and workers (2015) which showed that high intensity interval training (HIIT) performed twice a day with the second bout in a glycogen reduced state showed an improvement in a 250kj time trial compared the control group. This training protocol lasted 2 weeks. Another study was published early this year that showed that by simply altering the timing of intake of carbohydrate resulted in both a reduction in body fat and improved performance in a stimulated triathlon test (Marquetz et al., 2016).

In brief, both groups performed two bouts of exercise. The first bout of exercise took place in the evening and consisted of 8 x 5 minutes of maximum aerobic power followed by 60 minutes of cycling at 65% maximum aerobic power. The sleep low group restricted carbohydrate from their meals after the first bout of exercise up till the second bout of exercise whereas the control group maintained carbohydrate availability with throughout the recovery period up till the second exercise bout and a carbohydrate drink was consumed during the second bout of exercise. After the second bout of exercise, the sleep low group then consumed large amount of carbohydrates to match the amount consumed by the control group. Both groups were given a protein drink before bed and total energy intake was matched between groups.

Improvements in triathlon simulated trial, decreased in heart rate and rate of perceived exertion took place only in the sleep low group whereas the control group showed no noticeable difference. This study is significant because it’s the first and only study that showed an improvement in performance in a group of highly trained athletes whereas the previous studies (Hansen et al and Cochran et al) was done in untrained individuals.

This is almost all the evidence there is on training with low carbohydrate availability and I hope that it has given some insight on the mechanism on how it works.

I’ve purposefully left out some evidence from the literature because I plan to include that in the next part where we will touch on the implementation of low carbohydrate availability training and how to optimise it to get a performance outcome. Part 2 coming soon!

References

Alexander, A. and Walker, C. (2011). The role of LKB1 and AMPK in cellular responses to stress and damage. FEBS Letters, 585(7), pp.952-957.

Bartlett, J., Louhelainen, J., Iqbal, Z., Cochran, A., Gibala, M., Gregson, W., Close, G., Drust, B. and Morton, J. (2013). Reduced carbohydrate availability enhances exercise-induced p53 signaling in human skeletal muscle: implications for mitochondrial biogenesis. AJP: Regulatory, Integrative and Comparative Physiology, 304(6), pp.R450-R458.

Burke, L., Kiens, B. and Ivy, J. (2004). Carbohydrates and fat for training and recovery. Journal of Sports Sciences, 22(1), pp.15-30.

Camera, D., Hawley, J. and Coffey, V. (2015). Resistance exercise with low glycogen increases p53 phosphorylation and PGC-1α mRNA in skeletal muscle. European Journal of Applied Physiology, 115(6), pp.1185-1194.

Cochran, A., Myslik, F., MacInnis, M., Percival, M., Bishop, D., Tarnopolsky, M. and Gibala, M. (2015). Manipulating Carbohydrate Availability Between Twice-Daily Sessions of High-Intensity Interval Training Over 2 Weeks Improves Time-Trial Performance. IJSNEM, 25(5), pp.463-470.

Hansen, A., Fischer, C., Plomgaard, P., Andersen, J., Saltin, B. and Pedersen, B. (2005). Skeletal muscle adaptation: training twice every second day versus training once daily. Scand J Med Sci Sports, 15(1), pp.65-66.

Leckey, J., Burke, L., Morton, J. and Hawley, J. (2015). Altering fatty acid availability does not impair prolonged, continuous running to fatigue: evidence for carbohydrate dependence. Journal of Applied Physiology, 120(2), pp.107-113.

Marquet, L., Brisswalter, J., Louis, J., Tiollier, E., Burke, L., Hawley, J. and Hausswirth, C. (2016). Enhanced Endurance Performance by Periodization of CHO Intake. Medicine & Science in Sports & Exercise, p.1.

Morton, J., Croft, L., Bartlett, J., MacLaren, D., Reilly, T., Evans, L., McArdle, A. and Drust, B. (2009). Reduced carbohydrate availability does not modulate training-induced heat shock protein adaptations but does upregulate oxidative enzyme activity in human skeletal muscle. Journal of Applied Physiology, 106(5), pp.1513-1521

Psilander, N., Frank, P., Flockhart, M. and Sahlin, K. (2012). Exercise with low glycogen increases PGC-1α gene expression in human skeletal muscle. European Journal of Applied Physiology, 113(4), pp.951-963.

Saltin, B. (1973). Metabolic fundamentals in exercise. Medicine & Science in Sports & Exercise, 5(3), pp.137-146.

Torrens, S., Areta, J., Parr, E. and Hawley, J. (2016). Carbohydrate dependence during prolonged simulated cycling time trials. European Journal of Applied Physiology.

Van Proeyen, K., Szlufcik, K., Nielens, H., Ramaekers, M. and Hespel, P. (2010). Beneficial metabolic adaptations due to endurance exercise training in the fasted state. Journal of Applied Physiology, 110(1), pp.236-245.

Yeo, W., Paton, C., Garnham, A., Burke, L., Carey, A. and Hawley, J. (2008). Skeletal muscle adaptation and performance responses to once a day versus twice every second day endurance training regimens. Journal of Applied Physiology, 105(5), pp.1462-1470.

About the Author: Kedric Kwan CISSN

Kedric is a performance nutritionist (CISNN) certified through the International society of sports nutrition (ISSN) and is currently pursuing his MSc. His researc
h is currently focusing on
carbohydrate and it’s effect on sports performance with a particular interest in the molecular signalling pathways. He has worked with professional football players, powerlifters and endurance athletes but his current clientele consist of strength/power athletes and the general weekend warrior. His aim is to able to translate the ABC soup of complex science into something palatable for the general population. He is also a competitive powerlifter and when he is not spending time nerding over science or lifting heavy weights, he enjoys indulging in ice cream and reading about superheroes. If you enjoy any of the aforementioned things, feel free to drop him a holla!

Rice Rice Baby

by Jose Antonio PhD FISSN. I really like white rice. You know the sticky kind that you can pick up with your fingers and throw down the gullet. I mean 1.4 billion Chinese couldn’t all be wong. I’ve heard a million times how brown rice, which tastes like tree bark mixed with bread crust dipped in dog food, is soooo much better than the white variety. Growing up eating rice the way most families consume potatoes and bread, I rarely go a day without consuming some white stuff. So is the white stuff so bad? Is it like eating fried Twinkies or Oreos? Well grasshopper, empty your cup of tea and follow me down the path of truth and enlightenment. LOL. Actually, just read the rest of this silly article and let’s hope you’re entertained as well as edified.

One study stated that “higher consumption of white rice is associated with a significantly increased risk of type 2 diabetes, especially in Asian (Chinese and Japanese) populations.”¹ Yikes, that’s me! Does being a ‘Pacific Islander’ count? Also, “consumption of brown rice in place of white can help reduce 24-h glucose and fasting insulin responses among overweight Asian Indians.”² Shitfire I’m glad I’m not an overweight Asian Indian. Either way, that study was an acute one. And then we have this extensive case-control study which looked at the association between white rice-based food consumption and the risk of ischemic stroke in a southern Chinese population. Information on diet and lifestyle was obtained from 374 incident ischemic stroke patients and 464 hospital-based controls. They found that the average weekly intake of rice foods appeared to be significantly higher in cases than in controls. Increased consumption of cooked rice, congee, and rice noodle were associated with a higher risk for ischemic stroke after controlling for confounding factors. So is this evidence of a link between habitual rice food consumption and the risk of ischemic stroke in Chinese adults?³ Maybe.

Now keep in mind what exactly a case control study is. It is a design used in epidemiological research. Basically what scientists do is compare subjects who have a certain condition (e.g. high blood pressure) with those who do not (e.g. are normal blood pressure) and then identify the factors that may lead to that condition. Folks aren’t given a treatment per se. The categories are statistical ones, not biological ones. This study design is far inferior to the gold standard of science, the randomized controlled trial in which subjects are randomized to a ‘treatment’ or ‘placebo/control’ group. Thus, there is an actual intervention to see if a ‘treatment’ has an effect and minimizes bias.

So indeed it is true that epidemiologic studies have suggested that higher consumption of white rice (WR) is associated with increased risk for type 2 diabetes mellitus. And short term data shows that the glucose and insulin response is lower with brown vs white rice. What if you actually substitute white rice with brown rice, should we not then see a benefit? Especially if done over a period of several months?

Let’s see what this particular study showed. A total of 202 middle-aged adults with diabetes or a high risk for diabetes were randomly assigned to a white rice (WR) or brown rice (BR) group and consumed the rice ad libitum (free access to rice) for 4 months. Metabolic risk markers were measured. So what happened? Did the WR group get ill? Did the BR group become healthier than a triathlete? They basically found no between-group differences for any markers. However, blood LDL cholesterol concentration decreased more in the WR group compared to the BR group; this effect was observed only among participants with diabetes. On the other hand, diabetics had a greater reduction in diastolic blood pressure in the BR group compared to the WR group. So what’s the net-net? Nothing! There’s in essence no difference.⁴

Most non-Asians consume rice about as frequently as a homeless man in Miami takes long bubble baths. I mean have you ever seen a Chinese guy ask for brown rice? When an Asian orders brown rice instead of white, it would be like the Dallas Cowboy Cheerleaders cheering for the Washington Redskins. Ain’t gonna happen. So for my brothas and sistas who are of the ‘Asian’ denomination (hey, that rhymes), go ahead and eat plenty of white rice. But, and this is a big but, not the J-Lo big butt, but the but with just one ‘t.’ Exercise like you’re being chased by an angry Doberman Pinscher! If you exercise hard enough, long enough and frequently enough, I seriously doubt that eating brown or white rice will make a helluva difference.

So next time you’re at PF Changs, go for the white stuff:-)

References for the Science Nerds

[1] Hu EA, Pan A, Malik V, Sun Q: White rice consumption and risk of type 2 diabetes: meta-analysis and systematic review. Bmj 2012, 344:e1454.

[2] Mohan V, Spiegelman D, Sudha V, Gayathri R, Hong B, Praseena K, Anjana RM, Wedick NM, Arumugam K, Malik V, Ramachandran S, Bai MR, Henry JK, Hu FB, Willett W, Krishnaswamy K: Effect of Brown Rice, White Rice, and Brown Rice with Legumes on Blood Glucose and Insulin Responses in Overweight Asian Indians: A Randomized Controlled Trial. Diabetes technology & therapeutics 2014.

[3] Liang W, Lee AH, Binns CW: White rice-based food consumption and ischemic stroke risk: a case-control study in southern China. Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association 2010, 19:480-4.

[4] Zhang G, Pan A, Zong G, Yu Z, Wu H, Chen X, Tang L, Feng Y, Zhou H, Li H, Hong B, Malik VS, Willett WC, Spiegelman D, Hu FB, Lin X: Substituting white rice with brown rice for 16 weeks does not substantially affect metabolic risk factors in middle-aged Chinese men and women with diabetes or a high risk for diabetes. The Journal of nutrition 2011, 141:1685-90.

Bio – Jose Antonio PhD – Science guy, paddler, avid MMA fan, www.theissn.org

Glycogen: more than just an energy source?

By Mark Hearris. It is well documented that glycogen is the predominant fuel source oxidised during moderate-intensity exercise and that during exercise endogenous muscle glycogen is dramatically reduced, limiting exercise capacity (Bergstrom et al, 1967; Hermansen, Hultman & Saltin, 1967; Ahlborg et al, 1967; Hargreaves et al, 1984). It is well regarded that the onset of fatigue is associated with severe depletion of one’s muscle glycogen stores leading to hypoglycaemia and, as a result, limiting exercise capacity. In light of this, attention should be focused on nutritional interventions that aim to maximise endogenous glycogen stores (liver and muscle) before training sessions or competitive events. This strategy should allow training to be commenced with optimal glycogen stores that can be maintained throughout the exercise bout. The proposed mechanisms that explain exogenous carbohydrate supplementation include a muscle glycogen “sparing” effect (Tsintzas & Williams, 1995) and the maintenance of high blood glucose oxidation rates (Coyle et al, 1986).

However is glycogen more than just a simple energy source? In recent years, the role of glycogen has evolved into that of a regulator of cell signalling (Hawley et al, 2006). In light of this, it is suggested that carbohydrate availability is a potent modulator of the subsequent adaptations to exercise. Furthermore, there is accumulating data that provide evidence to suggest commencing exercise with reduced carbohydrate availability enhances the transcriptional rate of several genes associated with training adaptations. Recent research has suggested that commencing training with “low” muscle glycogen leads to enhanced training adaptations when compared with “normal” glycogen levels. (Hansen et al, 2005; Yeo et al, 2008; Hulston et al, 2010) including increases in resting muscle glycogen, citrate synthase activity and the rate of whole body fat oxidation. In spite of this, however, it is important to critically assess; what are the “costs” of training with “low” glycogen levels and how can these be minimized?

It is suggested that training intensity may suffer as a result of “training low” as well as increases in ones perception of effort (RPE). However, could simply rinsing the mouth with a carbohydrate (CHO) solution be the answer to this problem? Initial research by Carter and colleagues (2004) suggested rinsing the mouth with a CHO solution improved cycle time trial performance compared with a taste-matched placebo. Similar results have been shown in a handful of studies in both cycling and running protocols with seemingly no increases in effort (Whitham & McKinney, 2007; Pottier et al, 2010; Rollo et al, 2010). The proposed ergogenic effect of this intervention lies within activated regions of the brain that are responsible for reward and motor control (Chambers, Bridge & Jones, 2009) and not due to a metabolic effect. As a result, a CHO would not interfere with the cell signalling processes associated with “training low” and therefore allow optimal training adaptations.

BIO: Mark is currently a final year undergraduate student studying Sport & Exercise at Liverpool John Moores University. In regards to providing Sport Science support, Mark has previously worked at Blackburn Rovers & Liverpool FC where he was responsible for monitoring training session loads and other physiological variables of players. During the coming season, Mark will also be responsible for providing nutritional support to Blackburn Rovers sport science department. Marks particular research interests lie in the field of skeletal muscle metabolism and the role of nutrition in modulating adaptations to training.

References

1. Ahlborg, B. J., Bergstrom, J., Ekelund, G., & Hultman, E. (1967). Muscle glycogen and electrolytes during prolonged physical exercise. Acta Physiologica Scandinavica, 70, 129 – 142.

2. Bergstrom, J., Hermansen, L., Hultman, E., & Saltin, B. (1967). Diet, muscle glycogen and physical performance. Acta Physiologica Scandinavica, 71, 140 – 150.

3. Burke, L. M. (2010). Fueling strategies to optimize performance: training high or training low? Scandinavian Journal of Medicine & Science in Sports, 20, 48 – 58.

4. Carter, J. M., Jeukendrup, A. E., & Jones, D. A. (2004). The effect of carbohydrate mouth rinse on 1-h cycle time trial performance. Medicine and Science in Sports and Exercise, 36, 2107 – 2111.

5. Chambers, E. S., Bridge, M. W., & Jones, D. A. (2009). Carbohydrate sensing in the human mouth: effects of exercise performance and brain activity. Journal of Physiology, 587.8, 1779 – 1794.

6. Hansen, A. K., Fischer, C. P., Plomgaard, P., Anderson, J. L., Saltin, B., & Pedersen, B. K. (2005). Skeletal muscle adaptation: training twice every second day vs. training once daily. Journal of Applied Physiology, 98, 93 – 99.

7. Hargreaves, M., Costill, D. L., Coggan, A., Fink, W. J., & Nishibata, I. (1984). Effect of carbohydrate feedings on muscle glycogen utilization and exercise performance. Medicine and Science in Sports and Exercise, 16, 219 – 222.

8. Hawley, J. A., Tipton, K. D., & Millard-Stafford, M, L. (2006). Promoting training adaptations through nutritional interventions. Journal of Sport Sciences, 24, 709 – 721

9. Hermansen, L., Hultman, E., & Saltin, B. (1967). Muscle glycogen during prolonged and severe exercise. Acta Physiologica Scandinavica, 71, 129 – 139.

10. Hulston, C. J., Venables, M. C., Mann, C. H., Martin, C., Philp, A., Baar, K., & Jeukendrup, A. E. (2010). Training with low muscle glycogen enhances fat metabolism in well-trained cyclists. Medicine and Science in Sports and Exercise, 42, 2046 – 2055.

11. Pottier, A., Bouckaert, J., Gillis, W., Roels, T., & Derave, W. (2010). Mouth rinse but not ingestion of a carbohydrate solution improved 1-h cycle time trial performance. Medicine & Science in Sports & Exercise, 42, 798 – 804.

12. Rollo, I., Cole, M., Miller, R., & Williams, C. (2010). Influence of mouth rinsing a carbohydrate solution of 1-h running performance. Medicine & Science in Sports & Exercise, 42, 798 – 804.

13. Tsintzas, K., & Williams, C. (1998). Human muscle glycogen metabolism during exercise: Effect of carbohydrate supplementation, Sports Medicine, 25, 7 – 23.

14. Whitham, M., & McKinney, J. (2007). Effect of a carbohydrate mouthwash on running time-trial performance. Journal of Sports Sciences, 25, 1385 – 1392.

15. Yeo, W. K., Paton, C. D., Garnham, A. P., Burke, L. M., Carey, A. L., & Hawley, J. A. (2008). Skeletal muscle adaptation and performance responses to once a day versus twice every second day endurance training regiments. Journal of Applied Physiology, 105, 1462 – 1470.

‘Multiple Transporter’ Carbohydrates

By Scott Robinson.

Supplementation of carbohydrate (CHO) sources (e.g. glucose or glucose polymers), has been widely observed to increase exercise capacity, most notably during prolonged exercise at moderate to high intensities (1). These effects are largely attributed to a prevention of hypoglycaemia and the maintenance of high rates of CHO oxidation towards the latter phases of exercise when endogenous stores are either low or depleted (2). On this basis, it appears somewhat intuitive for athletes to seek methods of maximising their rate of CHO oxidation in the hope that a greater contribution from exogenous sources will increase exercise capacity through the ‘sparing’ of endogenous sources.

Background: Whereas it was once thought that 1 g.min-1 was the absolute maximum rate of CHO oxidation, more recent advances demonstrate convincingly that this rate is, in fact, much higher (in excess of 1.5 g.min-1; 3). To understand maximum CHO oxidation rates, it is important to understand what limits this. In an eloquent series of studies from Asker Jeukendrup’s lab in Birmingham, it was found that limitations to CHO oxidation were in the absorptive process most likely because of a saturation of carbohydrate transporters (for review see 4). They demonstrated that glucose oxidation rate is limited by a sodium-dependent glucose transporter (SGLT1), which, once saturated, the additional feeding of this carbohydrate will not result in greater intestinal absorption and increased oxidation rate (5). HOWEVER, other sugars are limited by different transport mechanisms (GLUT5 in the case of fructose). Thus, it was proposed that the use of different transporters might increase total carbohydrate absorption (see Figure 1).

Figure 1. The oxidation rate of glucose plus fructose in a combined drink is higher than the oxidation rate of similar amounts of either glucose or fructose alone (4)

Research study 1: Wallis et al. (2005; 6) tested this hypothesis by investigating the oxidation of combined ingestion of maltodextrins and fructose during cycling exercise. In this study, eight trained cyclists performed three exercise trials, with each comprising of 150 min cycling at 55% maximum power output. During each trial, subjects received a solution providing either 1.8 g.min-1 of maltodextrin (MD), 1.2 g/min-1 of maltodextrin + 0.6 g/min-1 of fructose (MD+F), or plain water. Results revealed that peak exogenous carbohydrate oxidation (last 30 min of exercise) was ~40% higher with combined MD+F ingestion compared with MD only ingestion. The authors concluded that ingestion of large amounts of maltodextrin and fructose during cycling exercise enables exogenous carbohydrate oxidation rates to reach peak values of ~1.5 g.min-1, which is much higher than oxidation rates from ingesting maltodextrin alone.

Performance Implications: Since these studies, it has been demonstrated that the ingestion multiple carbohydrate transporters i.e. glucose+fructose, exerts favourable influences on subjects’ ratings of perceived exertion (7) and endurance capacity (time to fatigue; 8). What is more, increased CHO oxidation with multiple transporter carbohydrates is well-regarded to be accompanied by increased fluid delivery and improved oxidation efficiency, thus reducing the likelihood of gastrointestinal distress (9).

Research study 2: Currell and Jeukendrup (2005; 8) investigated the effect of ingesting a glucose+fructose drink compared with a glucose-only drink (both delivering CHO at a rate of 1.8 g∙min^-1) and a water placebo on endurance performance. Eight male trained cyclists performed120 min of cycling exercise at 55% Wmax followed by a time trial of approximately 1h duration. Results revealed a staggering 8% quicker time to completion during the time trial in the GF condition when compared with the G condition (times, 4022 s compared with 3641 s for FG and G, respectively). Total CHO oxidation did not differ significantly between GF (2.54 +/- 0.25 g∙min^-1)and G (2.50 g∙min^-1), indicating that there was a sparing of endogenous CHO stores in the GF trial, because GF has been shown to have a greater exogenous CHO oxidation than G.

Take home message: In sharp contrast to the original guidelines, the new recommendations are dictated by the type and duration of exercise. Multiple transportable carbohydrates, ingested at high rates (1.8-2.4 g∙min^-1), are likely to improve exercise performance during ultra-endurance events of duration 3 h or more by reducing rating of perceived exertion and increasing time to fatigue. Such feeding strategies are not necessary for shorter duration events seeing that saturation of gut glucose transporters would be unlikely, especially if access to additional CHO is limited (e.g. team sports where fluid breaks are limited to unscheduled breaks in play and half-time).

BIO: Scott is a First Class Honours Sports Science graduate from the Research Institute of Sports and Exercise Sciences, at Liverpool John Moores University. He acquires a range of experience in both playing and coaching sport having represented Stoke City Football Club at Youth level and coached football at the International Youth Games. Scott has been an Assistant Sports Scientist at Blackburn Rovers Football Club and Everton Football Club for the 2010/2011 and 2011/2012 seasons, respectively. He has also partaken in Sports Science related research for FIFA, where he travelled across Europe as part of a multi-national team of sports scientists and athletes. Scott is currently completing his Masters of Science in Sports Physiology, where his research focuses on creating the optimal sports drink for soccer performance, after which he is due to begin a PhD within the Exercise Metabolism Research Group at the University of Birmingham, in September. Contact info: scottr38@hotmail.co.uk and Twitter is @scottrobinson8

References

Coyle EF, Coggan AR, Hemmert MK & Ivy JL. Muscle glycogen utilisation during prolonged strenuous exercise when fed carbohydrate. J Appl Physiol. 1986; 61: 165-172.
Bosch AN, Dennis SC & Noakes TD. Influence of carbohydrate ingestion on fuel substrate turnover and oxidation during prolonged exercise. J Appl Physiol. 1994; 76: 2364-2372.
Jentjens RL, et al. Oxidation of combined ingestion of glucose and fructose during exercise. J. Appl. Physiol. 2004; 96: 1277-1284.
Jeukendrup, AE, Gleeson, M. Sport Nutrition, Leeds, UK, Human Kinetics. 2010.
Jentjens RL, et al. Oxidation of exogenous glucose, sucrose and maltose during prolonged cycling exercise. J. Appl. Physiol. 2004; 96: 1285-1291.
Wallis GA, et al. Oxidation of combined ingestion of maltodextrins and fructose during exercise. Med Sci Spo & Exer. 2005; 37: 426-432.
Jeukendrup AE, et al.Exogenous carbohydrate oxidation during ultraendurance exercise. J. Appl. Physiol. 2006; 100: 1134-1141.
Currell K, Jeukendrup AE. Superior endurance performance with ingestion of multiple transportable carbohydrates. Med Sci Sports Exerc. 2008; 40: 275-281.
Jeukendrup AE. Carbohydrate feeding during exercise. Eur J Sport Sci; 8: 77-86.