We asked our friend and colleague, Ian Craig to write a blog post for us about exercise and fat metabolism. He proposes some interesting new research about the importance of personalisation.
We all have a large resource of fat - even us skinnies have enough to run continuously for a few days. So, in order to maximise our fat utilisation and metabolic efficiency, it makes a lot of sense to understand the dynamics of fat metabolism during exercise. For example, should we be accumulating high volumes at low exercise intensities as with the theory of Long Slow Distance (LSD), or should we jump on the current exercise bandwagon of high-intensity interval training (HIIT)?
This is an apparently simple question about human metabolism and from what we read in popular magazines and exercise books, you would think that we already had all the answers. However, the big problem with these, often extreme, approaches is that they all still follow the one-size-fits-all principle; albeit, a slightly different one from a few years ago. Additionally, in my experience, this physiological question of metabolic specificity is extremely complicated and it is one that I don’t presume to answer.… not today anyway.
Long Slow Distance (LSD)
As illustrated in the sample heart rate zones chart (Figure 1), for many years the fat burning zone has been the nemesis of the gym industry - during my time as an exercise specialist, I met many disappointed people who had just spent six months exercising at slow poke pace, only to have ended up with just as many grams of fat sitting on their hips as when they had started. To put the fat burning zone intensity into context, I would rate the 50 to 65% of maximum heart rate in the chart as ‘very easy to ‘easy’.
To check the scientific integrity behind the ‘fat burning zone', I plunked those exact words into Pubmed and without any search restrictions, I found….. one paper: Carey et al (1) noted that there was considerable overlap between the ‘aerobic’ and ‘fat-burning’ zones, such that training for fat oxidation and training for aerobic fitness are not mutually exclusive. Additionally, they suggested that the great variability in physiological response to exercise that occurred between individuals, should preclude the prediction of the fat burning zone, indicating a need for measurement in the laboratory.
Looking at the studies that appear to support a LSD training style, I’ll share two with you:
- - 16 recreationally active individuals cycled for 120mins at 60 per cent VO2peak. By muscle biopsy, it was shown that FAT/CD36 (a fatty acid translocating protein) contents increased 75 per cent by the end of the bout (2).
- - During 120mins of cycling at 60 per cent VO2peak, CHO oxidation slowly decreased and fat oxidation increased, corresponding with a mild drop in the respiratory exchange ratio (RER). Following exercise, the content of FAT/CD36 on the mitochondrial membrane increased by 59 per cent (3).
These studies are good support that to increase fat oxidation during exercise, it helps to go long. However, if we look at the actual intensity chosen by the investigators (60 per cent VO2peak), it is actually quite a bit higher than the typical fat burning zone intensity and would be described as ‘steady state’ rather than ‘easy’.
Figure 1 - a sample heart rate zones chart typically found in a gym
High Intensity Interval Training (HIIT)
We’re now in the era of military fitness training regimes in the park and CrossFit killer ‘workouts of the day’. According to a Men’s fitness article (4): “If your goal is to burn fat, intervals better be part of your program…. The magic of high intensity interval training lies in its ability to keep you burning fat even after you leave the gym…. Trainers refer to this phenomena as excess post-exercise oxygen consumption or EPOC.” Basically; the more intense and voluminous the workout, the longer your body will sit in a state of heightened metabolism, meaning increased basal fat metabolism.
Interestingly, it is above 60 to 70 per cent VO2max that the EPOC values really become highly significant, which as you will see in a moment, is the range of intensities that correspond with the theoretical maximum flux rate of fat metabolism.
Here are two research studies supporting the HIIT method:
- - It was a research study by Tremblay and colleagues in the 1990’s (5) that really brought HIIT training to the front of people’s minds: eight men and nine women undertook a 20-week endurance-training (ET) programme and five men and five women undertook a 15-week high-intensity intermittent-training (HIIT) programme. The mean estimated total energy cost of the ET programme was 120.4 MJ, whereas the corresponding value for the HIIT programme was 57.9 MJ. Despite its lower energy cost, the HIIT programme induced a more pronounced reduction in subcutaneous adiposity compared with the ET programme, plus muscle 3-hydroxyacyl coenzyme A dehydrogenase (HADH) enzyme activity, a marker of the activity of beta-oxidation, was significantly greater after the HIIT programme.
- - Just like the LSD trials above, it has also been shown that six weeks of high-intensity interval training increased mitochondrial FAT/CD36 by 51% (6).
LSD vs. HIIT - head to head trials
Just as I was careful not to promise you conclusive support for one type of exercise training or another, the limited research that has directly compared both scenarios, bears out this need for inconclusiveness. Here are two well constructed studies that compared continuous moderate exercise with high intensity interval training:
- - Nine sedentary subjects cycled for 90 min with two protocols: continuous exercise at 67 per cent VO2max (CE) and interval exercise comprising of 12 secs at 120 per cent, alternating with 18 secs at 20 per cent of VO2max (IE). The duration of exercise and work performed with CE and IE was identical. The researchers demonstrated that the mRNA content for major regulators of mitochondrial biogenesis and lipid metabolism increased after CE and IE exercise, with no significant differences between the exercise scenarios (7).
- - Thirty-four recreational endurance runners were randomly assigned either to a Weekend-Group (WE) or an After-Work-Group (AW) for 12 weeks (8). WE completed 2 hrs 30 min of continuous endurance running per week, composing of two sessions on the weekend. AW performed four 30 min sessions of high intensity training plus a 30 min endurance run weekly, always after work. Both training methods resulted in improvements in body composition and weight. AW improved relative peak oxygen uptake by 18.6% compared to 7.1% in WE. The velocity at lactate threshold improved by 20.5% in AW and 12.9% in WE. The time to finish the half-marathon was not significantly different between the groups. The authors concluded that both exercise scenarios had similar outcomes in terms of body composition improvements and recreational exercise outcomes, but that physiological performance measurements were favoured by high intensity training.
The physiology of fat
So far, despite many years of research, I’ve been able to tell you a fat load of inconclusiveness. However, what you have hopefully learned from this exercise is not to trust popular claims when it comes to something as complicated as the human body.
To expand our inquiry, let’s look at some basic physiology. Figure 2, constructed by Prof Roger Harris (9) is one of my favourite illustrations - it demonstrates the basic fact that the rate and the volume of ATP (energy) production is dictated by your fuel source and whether you are exercising aerobically or anaerobically. You can see, rightly so, that fat metabolism is the most dominant fuel during low-intensity/high-volume exercise and that carb metabolism becomes the most dominant fuel during increasing more intense exercise. But, we cannot separate fat and carb metabolism: even during low intensity exercise, carbs are the preferred source of fuel and will therefore be burned alongside fat, and during all but the most intense exercise, fat provides background ‘slow-burn’ energy.
Figure 2 - illustration of macronutrient contributions during exercise
To return to my original question, it would be interesting to know where the fat metabolism peaks and therefore what kind of exercise is needed to make the most of this invaluable fuel source. Birmingham University scientist, Asker Jeukendrup, performed a series of experiments in the early 2000’s with colleagues:
- - Eighteen moderately trained cyclists performed a graded exercise test to exhaustion and found that *Fatmax was equivalent to 64 +/- 4 per cent VO2max (10). The contribution of fat oxidation to energy expenditure became negligible above 89 +/- 3 per cent VO2max.
- - Achten & Jeukendrup (11) suggested from exercising data that accumulation of plasma lactate was strongly correlated to the reduction seen in fat oxidation with increasing exercise intensities. The first rise of lactate concentration occurred at the intensity that elicited maximal fat oxidation rates. At last, somebody who made a lot of sense - it linked with the notion that the reduction in long-chain fatty acid transport into the mitochondria could be a consequence of the accumulation of hydrogen ions during high-intensity exercise.
These experiments clearly show that the notion of low-intensity exercise being maximally stimulatory to fat metabolism, is false. We actually need to be working quite hard, near lactate threshold intensities, to challenge and develop our fat metabolising abilities. It’s not to say that LSD training doesn’t have its importance - it is required for a long-distance athlete to become more metabolically efficient when exercising and to learn to endure the biomechanical challenges of long distances.
HIIT can stimulate fat metabolism during exercise up to a point, but the athlete will experience diminishing returns as the intensity increases. Sure, there is the EPOC element, but there is the question of whether you simply wish to increase your metabolism overall, or to become better at metabolising fat during exercise.
Genetics of fat metabolism
If it was as easy as exercising at 64 per cent VO2max, or an equivalent percentage of maximum heart rate, to maximally stimulate fat metabolism, we could all use set equations. But, it’s not that simple. There is the small question of genetics.
Respiratory Exchange Ratio (RER) is a measurement used to represent the ratio of CO2 produced by a person compared to O2consumed. The RER for carb metabolism on its own is 1.0 and for fat, it is 0.7. In a laboratory, we can therefore determine the relative utilisation of these fuels by checking RER levels at rest or during sub-maximal exercise. The very interesting part is that testing reveals very low RERs in some people, meaning a higher reliance on fats, and high RERs in others, meaning a higher reliance on carbs. For example:
- - Goedecke et al (12) found a large inter-individual variability in resting RER (0.72–0.93), that persisted during exercise of increasing intensities.
- - Venables et al (13) demonstrated that RER ranged from 0.82 to 0.95 at rest and that maximum fat oxidation (MFO) rate ranged from 25 to 77 per cent VO2max. 34 per cent of this variance in MFO was accounted for by FFM, physical activity, VO2max, gender and fat mass.
These massive variances in fat metabolising abilities match up well with my clinical observations. Some people can rise early on a Sunday morning, have a quick cup of coffee and head out on their bike for five hours, only sipping water on the way. Others rely on a good carbohydrate breakfast and then guzzle sports drinks and energy bars throughout the ride, followed closely by breakfast No 2. You can see from the Venables study (13) that some of this variance in fat metabolism can be influenced by fitness and body composition, things that we can somewhat control. Additionally, a high-fat diet has been shown to increase rates of fat metabolism during exercise, but these manipulations are not sufficient to account for such large individual differences.
In genetic science, we have a large amount of information with regards to differences in fat metabolism and weight management. Most of this research has unfortunately not been translated into the sports sector, although there are some signs of this question being addressed:
- - Kruppel-like factor 15 (KLF15) deficient mice cannot appropriately shift toward lipid utilisation during endurance exercise and therefore rely on excessive consumption of carbohydrate fuels (14).
- - In obese women who underwent a VO2max test, those who had the Beta-2 Adrenergic Receptor (ADRB2) Glu27 polymorphism had a significantly higher respiratory exchange ratio (RER) than the Gln27 (wild type) group, suggesting a lower post-exercise fat oxidation (15).
Concluding remarks and future research
These two genetic research observations may be highly significant in terms of how we utilise fats and carbs during exercise. Some individuals may metabolise fats extremely poorly and we could assume that they would have high RER (towards carb metabolism) and low MFO rates during exercise. This information could be hugely valuable in an exercise setting and would also raise further interesting questions:
- - Is a poor fat oxidizer at a disadvantage for long distance endurance events?
- - Would they experience a lower training effect from LSD exercise and more from high-intensity training, that is more carb-dependent?
- - Would the opposite apply for a good fat metaboliser, or do we also need to study carb metabolism to answer that question?
- - Would a high-fat, low-carb diet be detrimental to a poor fat metaboliser’s energy and training outcomes?
We could develop quite a list of potential research enquiries that assessed people as individuals. Suffice to say; the relationship between exercise and diet choice, genetics and fat metabolism is not an simple one. But, we could still make a start: with a new piece of metabolic equipment available to myself, Zac van Heerden (FSN May-Jun 2015) and colleagues, we’re starting to evaluate resting and submaximal RER levels in cyclists and triathletes. Additionally, I’m in discussion with DNAlysis Biotechnology to add a short SNP panel on exercising fat metabolism, into their DNA Sport test. Cross-correlating metabolic and genetic information, as well as well formulated client questions, should hopefully start to expand our understanding of this subject.
*Fatmax - the intensity at which maximum fat oxidation occurs
You can order Ian's book online here:
- Carey D (2009). Quantifying differences in the “fat-burning” zone and the aerobic zone: implications for training. J Strength Cond Res. 23(7):2090-2095.
- Bradley N et al (2012). Acute endurance exercise increases plasma membrane fatty acid transport proteins in rat and human skeletal muscle. Am J Physiol Endocrinol Metab. 302:E183–E189.
- Holloway G et al (2006). Mitochondrial long chain fatty acid oxidation, fatty acid translocase/CD36 content and carnitine palmitoyl- transferase I activity in human skeletal muscle during aerobic exercise. J Physiol. 571:201–210.
- Duvall J. Eight amazing fat-burning intervals. Men’s Fitness. http://www.mensfitness.com/training/cardio/8-amazing-fat-burning-intervals
- Tremblay A et al (1994). Impact of exercise intensity on body fatness and skeletal muscle metabolism. Metabolism. 43(7):814-818.
- Talanian J et al (2010). Exercise training increases sarcolemmal and mitochondrial fatty acid transport proteins in human skeletal muscle. Am J Physiol Endocrinol Metab. 299:E180–E188.
- Wang L et al (2009). Similar expression of oxidative genes after interval and continuous exercise. Med Sci Sports Exerc. 41(12):2136-2144.
- Hottenrot K et al (2012). Effects of high intensity training and continuous endurance training on aerobic capacity and body composition in recreationally active runners. Journal of Sports Science and Medicine. 11:483-488.
- Harris R (2007). Metabolism. Powerpoint Presentation - University of Chichester. Presented at the Centre for Nutrition Education Competitive Athlete module.
- Achten J et al (2002). Determination of the exercise intensity that elicits maximal fat oxidation. Med Sci Sports Exerc. 34(1):92-97.
- Achten & Jeukendrup (2004). Relation between plasma lactate concentration and fat oxidation rates over a wide range of exercise intensities. Int J Sports Med. 25(1):32-37.
- Goedecke J et al (2000). Determinants of the variability in respiratory exchange ratio at rest and during exercise in trained athletes. Am J Physiol Endocrinol Metab. 279:E1325–E1334.
- Venables M et al (2005). Determinants of fat oxidation during exercise in healthy men and women: a cross-sectional study. J Appl Physiol. 98(1):160-167.
- Haldar S et al (2012). Kruppel-like factor 15 regulates skeletal muscle lipid flux and exercise adaptation. Proc Natl Acad Sci U S A. 109(17):6739-6744.
- Macho-Azcárate T et al (2002). A maximal effort trial in obese women carrying the beta2-adrenoceptor Gln27Glu polymorphism. J Physiol Biochem. 58(2):103-108.