Research Review: IBE Conference Review
What I did on my summer vacation: Found out all about muscles as molecular and metabolic machines.
This week’s review is going to be a little different, because instead of reviewing an article I’m going to highlight a conference.
In the beginning of June I went to the Olympics of exercise conferences: The International Biochemistry of Exercise (IBEC) conference.
Instead of every four years this conference happens every three years, but just like the Olympics, people from around the world attend. In fact, each continent was represented, except for Antarctica. Maybe next time. (I’m sure there’s a “March of the Penguins” joke in there somewhere.)
The speakers and attendees are mostly exercise physiologists/biochemists and even some molecular biologists. More importantly, most of the speakers and attendees are exercise enthusiasts. They included a lot of marathon runners, a few Ironman participants, hockey players, rugby players and even a few resistance exercisers. Generally, this would be described as a trained group.
Just like every good high school prom, this conference has a theme. Thankfully for those of us who hated the Under the Sea concept with poorly painted glow-in-the-dark jellyfish, this year’s conference theme was Muscles as Molecular and Metabolic Machines. Thus most of the talks were about how muscle (skeletal rather than heart muscle) works at a molecular level and how muscle uses fat, sugar and proteins.
Muscles as molecular and metabolic machines
Many studies were done on cells or animals. (By the way, any research on live critters, whether people or animals, is regulated by an ethics board, with the goal of keeping stress and discomfort to a minimum.)
But why not do all experiments on people? Many molecular techniques are difficult, if not impossible, to do on people. Scientists look for other things that can represent how people would respond.
For example, most of the genetic work can’t be done on people, because manipulating the genes of people is an ethical no-no and it would take a very long time to get results. Compare human pregnancy (9 months) to pregnancy for a mouse (3 weeks).
While non-people work is necessary, converting knowledge from cells (in an incubator) and animals is not always possible. And even though most of the presentations were on non-people studies, I’m going to focus on the people stuff, since I’m a person and so are you. All literate mice can start their own blog.
Mitochondrial DNA shifting in older adults following resistance exercise training
Dr. Mark Tarnopolsky from McMaster University (Hamilton, ON) talked about how age related muscle loss (sarcopenia) leads to muscle weakness, functional impairments, loss of independence and increased falls.
One component of muscle, the mitochondria (sub-cellular machine that provides energy), becomes dysfunctional during sarcopenia. As we age, mitochondria have a buildup of genetic mutation (specifically DNA deletions) that probably causes the dysfunction.
The good news is that six months of resistance exercise decreases genetic abnormalities in mitochondria! How? Right now, the best guess is that exercise decreases mitochondrial genetic abnormalities because new muscle cells (satellite cells) with normal mitochondria are being added to the muscle.
Influence of aging & long-term unloading on the structure & function of human skeletal muscle
Dr. Todd Trappe from Ball State (Muncie, IN) talked about how muscle unloading in young people leads to muscle loss (atrophy).
In this case, muscle unloading means bed rest — people lay in bed 24 hours a day. In Trappe’s research, unloading causes a rapid decrease in muscle volume (size) in the first 2-4 weeks, but then levels off. Interestingly, most of the muscle volume lost is from the lower body (40% loss).
Even though there is a decrease in the amount of muscle with bed rest, there is no decrease in quality of the muscle. Quality means that the muscle can generate the same amount of power for a given size (watt/litre).
Women lose more muscle mass than men overall and at a faster rate than men, possibly due to sex differences in hormones. This extra loss of muscle (atrophy) in women appears to be from more loss of type IIa muscle fibres than men.
Again, resistance exercise seems to save the day. Resistance exercise at relatively high intensity (and low volume) is effective at preventing loss of muscle mass. Only few minutes of activity/muscle group every 3 days helped prevent muscle loss in people lying in bed 24 hours/day. In addition, aerobic exercise may be beneficial to target type I fibers.
Dr Trappe also examined the effects of nutrition in preventing muscle loss. He found that nutrition alone (leucine-enriched high-protein diet) didn’t help with muscle loss — it actually made it worse. But exercise + nutrition + bed rest gave the best results — 26% better than exercise + nutrition without bed rest.
So you want to increase gains? Quit your jobs and don’t do anything but exercise, eat and sleep!
Why bother with bed rest? Because from the ages of 25 to 75 years old there is 20-30% loss in muscle mass — comparable to complete bed rest for 30-60 days. Thus bed rest is used to look at muscle loss that may be related to age related muscle loss.
NASA and other space agencies are very interested in muscle loss, as when people go into space their muscles do little to no work because of the lack of gravity. Bed rest is used as a cheaper way of looking at preventing atrophy in space.
For those of us not going into space, I’ll focus on the effect of aging on muscle loss. As Dr. Tarnopolsky also pointed out, as we age we lose muscle. Partially this is because you lose around 30-50% of your muscle fibres. But you lose more muscle function (strength) than can be attributed to loss of muscle fibres alone.
So something else is going on. We don’t know what this is, but it might be neural. In other words, the nervous system may also play a role.
Anabolic resistance – effects of aging, sexual dimorphism and immobilization on human muscle protein turnover
Dr Michael Rennie from the University of Nottingham discussed muscle protein turnover – basically the difference between how much muscle protein you make (muscle protein synthesis) and how much muscle protein you break down. The main portion of his talk looked at factors that change muscle protein turnover.
Nutrition is the first factor. Availability of amino acids is a major driver of protein synthesis – particularly essential amino acids (these include branched chain amino acids).
This may come as a surprise to many, but there is no sex difference in fed muscle protein metabolism between young men and women. However, older women have lower levels of protein synthesis compared to older men.
Also, older people have less of an increase in protein synthesis than young people with amino acids. Insulin normally decreases the amount of protein breakdown in the young. But with older people this insulin response is much less.
So as we age you get less protein synthesis when eating amino acids and more protein breakdown with the same amount of insulin. It’s a double whammy.
A cool aside: As if there weren’t enough reasons to take fish oil, Dr. Rennie shared a recent but unpublished study from his lab that showed that fish oil for 8 weeks (4 g per day) in the presence of amino acids increased muscle synthesis. So if you haven’t been convinced to take regular fish oil for fat loss, cardiac health or joint health then maybe the chance of bigger muscles will finally convince you.
Impact of resistance exercise on human skeletal muscle: Protein and exercise dose effect
Dr. Stewart Phillips from McMaster University has spent most of his research career looking at protein balance in muscle and how nutrition and exercise change that dynamic.
In his talk he presented some really cool results and some controversial ones.
He covered a lot of material, so I’m going to give them to you in point form:
- Trained people have a smaller window of protein synthesis post-work out than untrained people. In trained people there is a sharp peak followed by a dramatic drop, while untrained hit the same peak but it stays high longer. This may be because untrained protein synthesis don’t seem to be specific. The untrained muscle makes protein for everything: mitochondria, sarcoplasmic reticulum and myofibrillar protein (actin and myosin) compared to target protein synthesis (myofibrillar) in trained.
- Consuming 20 g of whey protein immediately before or after resistance exercise increases protein synthesis. Okay you probably knew that taking in whey right before or after exercise increased your muscle hypertrophy, but now you know why – you’re making more protein (but still breaking down the same amount).
- More protein (>20g) didn’t further increase protein synthesis – up to 40 g of protein from whey didn’t increase protein synthesis, but it did increase protein oxidation in young and in old (70 years old).
- Comparing 4 sets of 90% RM to failure to 30% RM to failure resistance exercise found no difference in muscle protein synthesis. In other words, the intensity (as % of max) didn’t seem to matter as much as muscular failure.
- Comparing exercise with low hormonal response (single preacher arm curls) with high hormonal response (leg press and single preacher arm curls) found no difference in muscle protein synthesis between groups – there was an increase in testosterone and cortisol in the high hormonal response.
Molecular responses to strength and endurance training: Are they incompatible?
Dr John Hawley from the RMIT University in Budoora Australia looked at whether strength and endurance training negatively impacted each other. The short answer – yes. But you knew that, didn’t you?
To look at this question more closely, Dr Hawley combined resistance and endurance exercise in consecutive bouts (one right after the other) in people who had experience in both types of training.
Resistance training was 8 sets of 5 reps of 80% RM leg extensions. Endurance training was 30 minutes of 70% VO2 peak. Either they did the resistance training first or the endurance training first.
Looking at molecular markers (specific proteins – mTOR and AMPK), Dr. Hawley concluded that “undertaking divergent exercise modes one after the other clearly influences the molecular profile typically associated with exercise in either mode alone.”
After this talk a lively discussion began on how all this research was done on people who were fasted (they hadn’t eating in awhile) and that if they had eaten or had some whey protein the results would be different.
Dr Hawley did mention that they work with elite swimmers and have separated their endurance and resistance training into a morning and night, which has lead to gains in muscle mass. Whether this was because of nutrition (they could eat more closer to each training bout) or because of the separation of the two type of training was up for debate.
Molecular responses to high-intensity interval exercise
Dr. Martin Gibala from McMaster University talked about HIIT – but a really short intense version of HIIT.
This involved 30 seconds of all-out cycling, followed by a 4 minute break. After the break, subjects would do the 30 all-out seconds again. There were 4 “rounds” in total.
After less than 15 minutes of total exercise (6 exercise sessions over 2 weeks) Dr Gibala found increases in mitochondrial enzymes and improved aerobic performance. Molecularly, changes in specific proteins (PGC-1a mRNA and p-AMPK, p-38) responsible for aerobic improvements happened with this really short HIIT. Also, Dr. Gibala mentioned that this type of HIIT does positively impact cardiovascular measures.
Also, worth mentioning is that while this type of training is very short and is effective it also is very hard. So 30 seconds on “kinda hard” is not good enough. You need 30 seconds of all-out, gut-busting effort.
While I didn’t go through all the talks, I’ve tried to give you highlights of the talks that I think you would have most liked to have seen. These were the most directly applicable to you – though there was some cool animal work that I didn’t go into.
For those interested in reading more about the talks, Applied Physiology, Nutrition and Metabolism vol 34 (3) for June 2009 has reviews written by many of the speakers at the IBEC conference.
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