Performance nutrition. Part 2 of 6:
How do your muscles use fuel to produce energy during exercise?
Thomas Solomon, PhD.
What you’ll learn:
Increases in exercise intensity alter the mix of fuels your muscles use: faster running pushes the muscles to rely more on stored carbs (glycogen) and circulating blood glucose.
But, the muscles always “burn” glucose, even at low intensity, so the body is never “off the hook” for supplying it.
Because the muscles keep using glucose, the long-duration exercise will eventually drain the body’s available glucose stores — basically, the “pint-glass of glucose” runs low over time.
But, don’t stop there! Scroll down to fully educate yourself on the details, nuances, and nerdy bits.
In part 1 of this series, you learnt how your organ systems fit together, how much fuel you have available in your body, and how metabolism can be measured. You are now ready to understand why the size of your bodily fuel stores, aka your “bucket load of fatty acids and pint-glass of glucose”, are so relevant to performance.
So, let’s dig in…
If your body stores lots of fat but little carbohydrate, it is useful to know how these fuels are “burned” during exercise because this will help you understand how to optimise your performance. As you embark on your journey into the world of substrate oxidation, there is an obvious question to ask yourself...
How does your body use its stored fuels during exercise?
At rest, your body “drip-feeds” energy from its fuel stores to keep all your basic functions plodding along. The amount of energy you “burn” at rest is your resting metabolic rate (your RMR). When you get up and start moving, the rate at which energy is used increases above your resting metabolic rate and this increase is relative to the rate of work (or intensity) of your movement. For example, when you stand up there, is a small increase in your energy expenditure above resting levels; when you walk slowly (~3 kph), there is about a 2-fold increase in energy expenditure; a 10-fold increase if you run at 10 kph; and about a 20-fold increase if you run at 10 kph up a 10% incline. You can conceptualise this as follows:
The increase in your rate of energy expenditure (kcals per minute) is proportional to the increase in your work rate (intensity).
And
The total amount of energy used (kcals) is proportional to your total duration of work (minutes).
During physical work (exercise), the kcals (or kiloJoules) predominantly come from fatty acids and glucose. Your muscles “burn” fatty acids taken up from those circulating in the blood and those broken down from fat droplets stored in your muscle cells (aka intramyocellular triglycerides, IMTG). Your muscles also “burn” glucose taken up from the blood and glucose broken down from glycogen stored within muscles. Within your muscle cells, chemical energy (ATP) is generated from fatty acids and glucose by oxygen-requiring (aka aerobic) oxidative processes in the mitochondria plus a little bit coming from glucose via non-oxygen-requiring (aka anaerobic) non-oxidative processes outside the mitochondria. Compared to regular folks, endurance athletes have adapted to store large amounts of IMTG and glycogen in their muscles and they have adapted to store the majority of their IMTG and glycogen right where they are needed; next to the mitochondria. Plus, endurance athletes have more mitochondria and higher activities of their metabolic enzymes, allowing athletes to produce more energy, more efficiently than regular folks.
Pretty darn cool.
Feel free to use and share this figure, but please give credit to Thomas PJ Solomon PhD @veohtu
But it gets a little more complicated than that because as your rate of work increases, different types of fuel are preferentially used to produce the energy you need. It is like fatty acids and glucose start competing to be the ones that are “burned” — “I want to jump in the fire!” … “No. I want to jump in the fire!” … Weirdos.
How do we know this?
The first observations that the body “burns” different proportions of fat and carbohydrate to produce energy during exercise, was made in 1920 by August Krogh and Johannes Lindhard. Subsequent work added to our knowledge but, in the 1990s, a series of highly-detailed mechanistic studies from the labs of Bob Wolf (Romijn et al. 1993) and Anton Wagenmakers (van Loon et al. 1999 and van Loon et al. 2001) used stable isotopes of glucose and palmitate (a fatty acid), combined with indirect calorimetry, and tissue biopsies, to measure whole-body and tissue-specific glucose and fatty acid “flux” (aka, the rate of transport from the blood into tissues and vice versa) and “oxidation” (aka the rate of burning) during low-, moderate-, and high-intensity exercise in trained cyclists and untrained folks.
These studies firstly showed that the high level of adipose tissue lipolysis (aka fat breakdown in fat tissue) does not further increase with increasing exercise intensity (from low, 25% VO2max, to high, 85% VO2max) but intramuscular lipolysis (aka fat, or IMTG, breakdown in muscle) does. However, adipose tissue release of fatty acids into blood decreases with increasing exercise intensity, causing reduced availability of fatty acids in the blood at higher exercise intensities. This might imply that the decrease in fat “burning” with increasing exercise intensity is possibly due to the lower amounts of fatty acids available in the blood. That aside, the decrease in fatty acid availability with increasing exercise intensity is compensated for by an increase in glucose availability, as shown by increasing glucose appearance into the blood (from the liver) with increasing exercise intensity, and a corresponding increase in glucose “burning”.
Say whaaat?
To summarise that rant:
Your body always makes fuel available to the working muscle to support the increasing energy requirement as exercise intensity increases.
and
There is an intensity-dependent change in the relative contribution of different types of fuel (from fatty acids to glucose) as exercise intensity increases.
Next, it was found that during prolonged exercise (2-hours), blood glucose is used to produce energy at low (25% VO2max, aka a walk), moderate (65% VO2max, aka an easy run), and high (85% VO2max, aka a marathon-paced run) intensities. Over a 2-hour moderate-intensity bout, for example, blood glucose use and blood fatty acid use progressively increase while muscle glycogen and muscle fat (IMTG) use decrease (because the muscles’ available glycogen and IMTG stores become depleted).
The important take-home from that is:
Your muscles always use blood glucose even during low-intensity exercise, putting pressure on the liver to release enough glucose to prevent hypoglycemia (low blood sugar).
Image copyright © Thomas Solomon. All rights reserved.
Feel free to use and share this figure, but please give credit to Thomas PJ Solomon PhD @veohtu
Next, if an endurance-trained athlete and an untrained person complete a prolonged (2-hour) workout at the same absolute workload as (e.g. both riding at 150 watts or running at 12 kph), total energy burned (kcals per hour) is about the same but the trained folks “burn” way more fat and way less glucose. In fact, the lower glucose oxidation rate in a trained athlete is explained by a lesser reliance on muscle glycogen use and (liver-derived) blood glucose use.
This means that:
Endurance training causes “fat adaptation” to help spare your precious glycogen stores during exercise… But, you probably already knew that.
Finally, this series of studies showed that as a trained athlete makes the transition from moderate to high-intensity exercise (roughly the equivalent as transitioning from your easy run pace to your marathon pace), fatty acid oxidation rates (fat “burning”) decrease while glucose oxidation (glucose “burning” of glucose taken up from the blood and glucose broken down from muscle glycogen) increase. These observations contribute to those which led to George Brooks’ “crossover concept”, the point at which you switch from predominantly fat to predominantly carbohydrate use during increasing intensity exercise (read more about that in a previous post at veohtu.com/fatoxidationrates). Furthermore, these studies found that the decrease in fat “burning” is explained by a decrease in the use of fatty acids freely circulating in the blood, and fatty acids broken down from triglycerides circulating in the blood, and fatty acids broken down from triglycerides stored in muscle (IMTG). Plus, with increasing intensity, the activity of the enzyme (called CPT1) that shuttles fatty acids into the muscles’ mitochondria so they can be “burned” was also found to be decreased. In other words, fatty acid delivery to the mitochondria (the part of the muscle cell that “burns” fat to produce energy) is decreased as exercise intensity increases.
Image copyright © Thomas Solomon. All rights reserved.
Feel free to use and share this figure, but please give credit to Thomas PJ Solomon PhD @veohtu
What can you put in your performance nutrition toolbox?
So, coming back to that question: How does your body use its stored fuels — its bucket load of fatty acids and pint-glass of glucose — during exercise? … The important nuggets of my rant to embed in your cerebellum are that:
Increasing your intensity during exercise — moving faster — will increase your muscles’ reliance on glucose to produce energy.
And
Because your muscles always “burn” glucose, even during low exercise intensity, long-duration exercise will eventually deplete available glucose stored in your body.
This knowledge might prompt an obvious question: How long will your bodily fuel stores allow you to go? Well, tune in for the next part of this series to find out.
Until then, keep training smart…
Thanks for joining me for another “session”. I’m passionate about equality in access to free education. Please help keep the content alive by buying me a beer and leaving me a 5-star review. Also, follow @veohtu on X, Facebook, and Instagram. To receive updates on my new articles, nerd alerts, and training tools, subscribe to my newsletter at veothu.com/subscribe.
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Who is Thomas Solomon?
My knowledge has been honed following 20+ years of running, cycling, hiking, cross-country skiing, lifting, and climbing, 15+ years of academic research at world-leading universities and hospitals, and 10+ years advising and coaching in athletic performance and lifestyle change.
I have a BSc in Biochemistry, a PhD in Exercise Science, and over 90 peer-reviewed publications in medical journals.
I'm also an ACSM-certified Exercise Physiologist (ACSM-EP), an ACSM-certified Personal Trainer (ACSM-CPT), a VDOT-certified Distance Running Coach, and a UKVRN Registered Nutritionist (RNutr).
Since 2002, I’ve conducted biomedical research in exercise and nutrition and have taught and led university courses in exercise physiology, nutrition, biochemistry, and molecular medicine.
And, with my personal experience of competing on the track (800m to 10,000m), the road (5 k to marathon), on the trails, and in the mountains, by foot, bicycle, cross-country ski, and during obstacle course races (OCR), I deeply understand what it's like to train and compete — I've been there, done it, and gotten sweat, mud, and tears on my t-shirt.
Disclaimer: I occasionally mention brands and products, but it is important to know that I don't sell recovery products, supplements, or ad space, and I'm not affiliated with / sponsored by / an ambassador for / receiving advertisement royalties from any brands. I have conducted biomedical research for which I’ve received research money from publicly-funded national research councils and medical charities, and also from private companies, including Novo Nordisk Foundation, AstraZeneca, Amylin, the A.P. Møller Foundation, and the Augustinus Foundation. I’ve also consulted for Boost Treadmills and Gu Energy on R&D grant applications, and I provide research and scientific writing services for Examine.com. Some of my articles contain links to information provided by Examine.com but I do not receive any royalties or bonuses from those links. Importantly, none of the companies described above have had any control over the research design, data analysis, or publication outcomes of my work. I research and write my content using state-of-the-art, consensus, peer reviewed, and published scientific evidence combined with my empirical evidence observed in practice and feedback from athletes. My advice is, and always will be, based on my own views and opinions shaped by the scientific evidence available. The information I provide is not medical advice. Before making any changes to your habits of daily living based on any information I provide, always ensure it is safe for you to do so and consult your doctor if you are unsure.
