Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2022 Apr 12;14(8):1605.
doi: 10.3390/nu14081605.

Beyond the Calorie Paradigm: Taking into Account in Practice the Balance of Fat and Carbohydrate Oxidation during Exercise?

Jean-Frédéric Brun  1 , Justine Myzia  1 , Emmanuelle Varlet-Marie  2 , Eric Raynaud de Mauverger  1 , Jacques Mercier  1
Affiliations
Review

Beyond the Calorie Paradigm: Taking into Account in Practice the Balance of Fat and Carbohydrate Oxidation during Exercise?

Jean-Frédéric Brun et al. Nutrients. .

Abstract

Recent literature shows that exercise is not simply a way to generate a calorie deficit as an add-on to restrictive diets but exerts powerful additional biological effects via its impact on mitochondrial function, the release of chemical messengers induced by muscular activity, and its ability to reverse epigenetic alterations. This review aims to summarize the current literature dealing with the hypothesis that some of these effects of exercise unexplained by an energy deficit are related to the balance of substrates used as fuel by the exercising muscle. This balance of substrates can be measured with reliable techniques, which provide information about metabolic disturbances associated with sedentarity and obesity, as well as adaptations of fuel metabolism in trained individuals. The exercise intensity that elicits maximal oxidation of lipids, termed LIPOXmax, FATOXmax, or FATmax, provides a marker of the mitochondrial ability to oxidize fatty acids and predicts how much fat will be oxidized over 45-60 min of low- to moderate-intensity training performed at the corresponding intensity. LIPOXmax is a reproducible parameter that can be modified by many physiological and lifestyle influences (exercise, diet, gender, age, hormones such as catecholamines, and the growth hormone-Insulin-like growth factor I axis). Individuals told to select an exercise intensity to maintain for 45 min or more spontaneously select a level close to this intensity. There is increasing evidence that training targeted at this level is efficient for reducing fat mass, sparing muscle mass, increasing the ability to oxidize lipids during exercise, lowering blood pressure and low-grade inflammation, improving insulin secretion and insulin sensitivity, reducing blood glucose and HbA1c in type 2 diabetes, and decreasing the circulating cholesterol level. Training protocols based on this concept are easy to implement and accept in very sedentary patients and have shown an unexpected efficacy over the long term. They also represent a useful add-on to bariatric surgery in order to maintain and improve its weight-lowering effect. Additional studies are required to confirm and more precisely analyze the determinants of LIPOXmax and the long-term effects of training at this level on body composition, metabolism, and health.

Keywords: FATmax; LIPOXmax; calorimetry; carbohydrate oxidation; fat; fat metabolism; indirect calorimetry; lipid oxidation; maximal fat oxidation (MFO); myometabokines; peak fat oxidation; sleeve gastrectomy; substrate oxidation; training.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The classical picture of Brooks and Mercier’s “Crossover concept” redrawn from our personal database of more than 5000 exercise calorimetries (see text). This hypothesis assumes that there is a major shift in the balance of substrates used for oxidation during exercise grossly around 50% of the maximal aerobic capacity, when carbohydrates represent more than 70% of the sources of energy for the exercising body. Oxidative use of fat culminates below this level, and close to it or slightly above it, blood lactate increases and the ventilatory threshold occurs. Note that the ordinates for % of fat oxidation and % of CHO oxidation are not symmetric, in order to better visualize the crossover. In a series of more than 5000 exercise calorimetries, we find that the crossover point is, on average, at 55.1% of VO2max but exhibits a wide variability among individuals.
Figure 2
Figure 2
An example of exercise calorimetry performed on a 75-year-old male subject explored for training prescription in grade-2 obesity (weight 99.3 kg, body mass index: 36 kg/m², percentage of fat: 27.7%, VO2max ACSM: 19.7 mL/min/kg). Four 6-min steps were performed: 20, 40, 70, and 100 watts. The crossover point is found at 68 Watts (i.e., 56% of maximal aerobic power) and the LIPOXmax is found at 51 Watts (i.e., 42% of maximal aerobic power). The MFO is 297 mg/min, i.e., 8.2 mg/min/kg of muscle mass. CHO represents 100% of the oxidized substrates above 100 watts, i.e., 82% of maximal aerobic power. It can be seen that over the range of intensities applied during the test, CHO oxidation can be approximately modeled as a straight line (carbohydrate cost of the watt) whose slope is, in this individual, 0.24 mg/min/kg/watt.
Figure 3
Figure 3
Schematic representation of the events explaining the “bell-shaped curve” of lipid oxidation when exercise intensity increases (see text). Lipolysis is not the limiting step and is still active far above the “crossover point”, but lipid oxidation is inhibited by the metabolites generated by the increase in the rate of CHO oxidation, which becomes the dominant fuel. At this intensity level, blood lactate increases because of the high rate of carbohydrate processing. Therefore, the LIPOXmax (intensity where lipid oxidation reaches its top) occurs below the “crossover point”, the rise in blood lactate, and the ventilatory threshold. The drawing of lipid oxidation is obtained from our database including 5258 calorimetries, and the point of maximal lipid oxidation occurred at 47 ± 1% of VO2max. At the level of LIPOXmax, individuals oxidized 209.5 ± 1.37 mg/min of lipids. This level is widely variable among individuals. Lactate data are from [59] and intramuscular lipolysis from [60]. HSL: Hormone-sensitive lipase activity.
Figure 4
Figure 4
The lipid oxidation zone or “LIPOX zone” corresponds to a level of light to moderate exercise (usually 30–50% of VO2max, quoted from “very light” to “moderate” on scales of perceived exertion, and corresponding in practice to 50–70% of the maximal heart rate (HRmax). Equivalences between % of VO2max and % heart rate reserve (HRR) and % VO2 reserve are calculated according to [154,155].
Figure 5
Figure 5
Schematic representation of physiological situations that modify the asymmetrical dome-shaped curve of lipid oxidation.
Figure 6
Figure 6
An attempt to summarize hormonal influences that shift the balance of substrates towards more carbohydrate vs. more fat oxidation. As indicated in the text, this issue remains poorly investigated.
Figure 7
Figure 7
Follow-up of a cohort of 12 obese patients regularly followed over 96 months (results partially presented in [33] and further updated in January 2022). This is the continuation of previously presented shorter follow-up studies [17,18,231,256]. Results show that the weight-lowering effect of LIPOXmax training persists over more than 8 years.
Figure 8
Figure 8
An example of exercise calorimetry in a patient exhibiting a markedly ‘biphasic’ profile of substrate oxidation during exercise. Opposite effects on eating behavior of the two zones of the balance of substrates may, in part, explain why exercise targeted toward fat oxidation induces weight loss [30,344]), while short bouts of exercise targeted toward higher intensities in the zone of predominant oxidation of CHO may induce overeating and paradoxical weight gain [345].
Figure 9
Figure 9
An example of the biphasic profile of substrate oxidation in a 48-year-old woman who suddenly gained weight after discontinuing sport practice. Current weight is 96 kg (percentage of body fat 37.6%). The LIPOXmax occurs at 64 watts (i.e., 42% VO2max), and MFO at this level is 282 mg/min. However, the optimal level of fat/carbohydrate oxidation ratio (OLORFOX) [352] occurs at a lower power intensity at 23 watts, so the target heart rate can be proposed as 82 b/min, rather than 92 bpm, if one wants to spare carbohydrates.
Figure 10
Figure 10
Summary picture. Maximal oxidation during exercise is determined by genetic background and gender, as well as hormones (catecholamines, GH, estradiol), exercise habits, and nutrition. It is a rather stable and reproducible parameter, unless subjects change their lifestyle, and is impaired in various pathologic conditions (obesity, diabetes, sleep apnea, bariatric surgery). This level or others closely related can be used for targeting exercise training. There is now good evidence that in the middle term (2–6 months), this variety of exercise training improves mitochondrial function, VO2max, lipid oxidation during exercise, parameters of glucose disposal, LDL cholesterol, and low-grade inflammation. Fat mass decreases and fat-free mass are maintained. In diabetics, the decrease in HbA1c elicited by this variety of training is of the same magnitude as that of other protocols (−0.6%). In fact, the effects on VO2max, blood pressure, and circulating levels of lipids at 2–6 months are less pronounced than those of higher-intensity protocols and interval training. A moderating effect on sedentarity-associated overeating is also reported by several studies and occurs over the first week. Long-term effects are only reported by a limited number of nonrandomized studies but they appear to be prolonged (up to 7 years), inducing a gradual improvement in body composition (loss of central and limb fat mass, maintenance of muscle mass) and blood pressure. Whether such prolonged training can have other beneficial effects is not yet known. More studies are needed to better describe and understand all these processes.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Perez-Martin A., Mercier J. Stress tests and exercise training program for diabetics-Initial metabolic evaluation. Ann. Endocrinol. 2001;62:291–293.
    1. Dériaz O., Dumont M., Bergeron N., Després J.P., Brochu M., Prud’homme D. Skeletal muscle low attenuation area and maximal fat oxidation rate during submaximal exercise in male obese individuals. Int. J. Obes. Relat. Metab. Disord. 2001;25:1579–1584. doi: 10.1038/sj.ijo.0801809. - DOI - PubMed
    1. Achten J., Gleeson M., Jeukendrup A.E. Determination of the exercise intensity that elicits maximal fat oxidation. Med. Sci. Sports Exerc. 2002;34:92–97. doi: 10.1097/00005768-200201000-00015. - DOI - PubMed
    1. Romijn J.A., Coyle E.F., Sidossis L.S., Gastaldelli A., Horowitz J.F., Endert E. Regulation of endogenous fat and carbohydrate metabolism in relation to exercise intensity and duration. Am. J. Physiol. 1993;265:E380–E391. doi: 10.1152/ajpendo.1993.265.3.E380. - DOI - PubMed
    1. Bergman B.C., Brooks G.A. Respiratory gas-exchange ratios during graded exercise in fed and fasted trained and untrained men. J. Appl. Physiol. 1999;86:479–487. doi: 10.1152/jappl.1999.86.2.479. - DOI - PubMed