White Paper: MAF Exercise Heart Rate – How it can help improve health and sports performance

White Paper - HR

This paper defines the MAF HR, discusses its importance, and relates it to other standard physiological parameters.

Dr. Philip Maffetone

I. Introduction

Heart-rate monitoring is essential to exercise prescription by health practitioners, coaches, athletes and others. It helps individuals track their relative exercise intensity in real time. The MAF Method1 uses heart-rate monitoring to help individuals exercise at an intensity that allows them to maintain and improve health while also creating lasting fitness gains.

Besides being easily measurable by chest-strap, wrist, and other types of monitors, the heart rate corresponds to various physiological markers of metabolic activity, including substrate utilization (the use of different metabolic fuels to power activity).2,3,4

Substrate utilization, typically measured through gas-exchange parameters such as respiratory exchange ratio (RER), is an excellent indicator of relative activity levels. At the highest level of exercise intensity, the greatest amount of fuel is provided by glucose and its derivatives (stored glycogen, lactate, and blood glucose), which we refer to in shorthand as “sugar.” In the lower ends of activity, a larger percentage of energy is provided by free fatty acids and triglycerides — which we shorten in this paper to “fats.” However, aerobically fit athletes still burn fat at a high intensity of activity (see Table 1).

MAF WP Table 1

At 155 HR this athlete can run 5:25 per mile pace. Note the continued use of fat for energy even at a relatively high-intensity HR of 169.

Defining ‘MAF HR’

The MAF Method looks at critical changes in substrate utilization to define “low-intensity exercise” in opposition to “high-intensity exercise”:

Low-intensity exercise is associated with high fat-burning (called Fatmax), and high-intensity exercise is associated with reduced fat-burning and high sugar-burning. Some authors also use Fatmax as a threshold measure for exercise prescription, often referring to it as aerobic threshold (AerT).3,4,5

Because of the correspondence of heart rate to markers of substrate utilization and other metabolic activity, the MAF Method identifies the Maximum Aerobic Function Heart Rate (MAF HR) as the heart rate which corresponds with AerT and Fatmax. As we shall see, AerT, Fatmax, and consequently the MAF HR, indicate where the body is most advantageously positioned to:

  • Reap health benefits from exercise.
  • Develop the aerobic system to increase work rate (running speed, cycling power, etc.) and performance.
  • Improve the physiological systems necessary to recover from exercise of
    all intensities.

Estimation of Exercise Intensity

Exercise prescribed according to relative intensity is a mainstay in exercise science literature. It is intended to produce exercise stress that is approximately equivalent between individuals with different absolute exercise capacities.6 The traditional and common approach has often been to prescribe exercise intensity as a percentage of maximum oxygen consumption (VO2max) or maximum heart rate (HRmax).

Exercise intensity prescribed at a percentage of these parameters does not necessarily place individuals at an equivalent intensity above resting levels. Some individuals will fall above or below metabolic thresholds of substrate utilization at the same percentage of VO2max or HRmax.

Furthermore, the most widely used estimation methods of exercise intensity by many exercisers observe subjective parameters (such as the “talk-test”) or statistical observations about a population that have no allowances for individualization (such as heart-rate zones, the 220 Formula and others). In addition, most individuals do not accurately obtain VO2max, HRmax, RER or other physiological parameters with which to calculate a training intensity. As such, the MAF Method proposes separating exercise intensity in terms of substrate utilization:

  • Aerobic: a lower-intensity activity with high fat-burning (and sugar-sparing) potential.
  • Anaerobic: a higher-intensity, lower fat-burning and higher sugar-burning activity.

Exercising at a Lower Intensity

The overwhelming majority of exercise should occur at a low intensity to keep the body healthy, build the aerobic system and improve fat-burning.7 Modern humans are physiologically better adapted to exercise intensities similar to ones their hominid ancestors evolved with rather than those supported by modern societies. These would have included daily bouts of prolonged, low-intensity, aerobic-based activities, which are primarily fueled by the body’s long-term energy source: fats.8 Lower-intensity exercise has been described as “regenerative”3 since it activates and develops the organs, systems, and processes that together exhibit a series of interrelated functions.
These include:

  • Endurance exercise capabilities.9,10
  • Protection from metabolic syndrome.11,12,13
  • Recovery from high-intensity activity.14,15
  • Resilience to oxidative stress (aging).16

All these abilities stem from the body’s ability to reliably and continuously draw from an abundant fuel source (fats) and a near-limitless supply of reactant (oxygen).

A high level of fat-burning bolsters the metabolism and creates positive health outcomes due to its epigenetic effects on gene expression.17

The diverse mechanisms implicated in these abilities include the respiratory and cardiovascular systems (lungs, heart and blood vessels), but most importantly the slow-twitch aerobic (Type I) muscle fibers which, in addition to oxidizing fats,18 assist anaerobic (Type II) muscle fibers in their function during high-intensity efforts.14

High-intensity activity is associated with using a more powerful fuel (sugar) which is nevertheless much more limited than fats. Using sugar for energy allows the body to increase its energy production and work rate far beyond what the rate of oxygen uptake allows. When the rate of sugar usage exceeds the supply of oxygen, this sugar is burned anaerobically, or outside the presence of oxygen.

Anaerobic function creates higher levels of physical and biochemical stress,16 decreases immune function19, 20 and muscle repair,21 increases inflammation,22 increases the risk of muscle injury (most common in fast-twitch fibers),23 and impairs fat-burning.24 These conditions are also associated with poor (or a lack of) recovery, and are common components of and contributors to the overtraining syndrome.25

Greater fat oxidation is therefore a hallmark of low-intensity training and aerobic activity. It corresponds to a lower RER, and occurs at a lower percentage of maximum oxygen consumption (VO2max) than sugar-burning (typically around 75 percent, although health, fitness, age and other factors can raise or lower this number).3 As activity levels (and therefore RER and oxygen consumption) rise, so does sugar-burning.

Because anaerobic activity impairs fat-burning, we can extrapolate that Fatmax occurs just before the onset of anaerobic activity and the production of its main by-product, lactate.3 The onset of increasing lactate is also indicative of the start of glycogen depletion.26 As noted above, this point is referred to as the aerobic threshold (AerT) and Fatmax, which coincides with the MAF HR.

Calculating the MAF HR: The 180 Formula

The AerT is located at an exercise intensity that is often described as a percentage of VO2max. This is sometimes referenced as 75 percent but it varies with and is largely determined by endurance training and subsequent fitness, health status and age.3,27 For example, AerT occurs at a lower percentage for those who are untrained, ill, or elderly. Values may be slightly higher for very well trained elite athletes (such as an AerT of 80%+ of VO2max), and lower for untrained individuals (AerT as low as 55% of VO2max). The AerT occurs at a higher percentage for adolescents, and at a lower percentage for those over age 60.28

After a few years of determining the MAF HR in individuals via an array of clinical assessments, including age, a comprehensive physical evaluation, gait analysis, health and fitness history, with confirmation using measures of gas exchange,29 it became clear that a heart rate equivalent to 180-age could constitute the beginnings of a potential formula for determining a person’s MAF HR (see Table 2). The 180 Formula indicates that certain modifications must be made depending on a person’s health and fitness status. These idiosyncrasies influence where the AerT and Fatmax, and therefore the MAF HR, will occur.

Table 2

The 180 Formula for determining MAF HR

Subtract your age from 180, then modify from one of the categories below:

  1. If you have or are recovering from a major illness (heart disease, any operation or hospital stay, etc.) or are on any regular medication, subtract an additional 10.
  2. If you are injured, have regressed in training or competition, get more than two colds or bouts of flu or other infection per year, have seasonal allergies or asthma, or if you have been inconsistent or are just getting back into training, subtract an additional 5.
  3. If you have been training consistently (at least four times weekly) for up to two years without any of the problems just mentioned, keep the number (180-age) as maximum.
  4. If you have been training for more than two years without any of the problems listed above, and have made progress in athletic competition without injury, add 5.

Exemptions:
The 180 Formula may need to be further individualized for athletes over the age of 65. For some, up to 10 beats may have to be added for those in category (d) in the 180 Formula, and depending on individual levels of fitness and health. This does not mean 10 should automatically be added, but that an honest self-assessment is important.

For athletes 16 years of age and under, the formula is not applicable; rather, a heart rate of 165 may be best.

Prescribing Aerobic Exercise

Speed or power at the MAF HR is an important physiological predictor of endurance performance. Studies show that submax thresholds are the best predictors of endurance performance in runners, cyclists, race walkers and other athletes, as well as in the performance of untrained people.30,31

The MAF Test was developed in order to track the improvement of the aerobic system across time (see Table 3). For a runner, this test may consist of a 3- to 5-mile run on an oval, 400-meter track, while recording the time per mile (or kilometer). The MAF Test should be preceded by a 15-minute warm-up and performed under consistent conditions (same shoes, weather, time of day, etc.) Other activities can also be used for the MAF Test, including cycling and rowing by measuring power, swimming by measuring laps, etc.

MAF WP Table 3

Increasing speed at the same submax HR translates to improvement in aerobic function and fat-burning, and can predict faster race performances.32 It has also been long known that aerobic contribution to energy during maximal exercise such as competition is significant, and increases with the duration of the event.30 See Table 4.

MAF WP Table 4

The 180 Formula is not a replacement for properly executed laboratory tests that determine the AerT, Fatmax and other metrics, although it usually corresponds with them. Given that the 180 Formula is applicable to a majority of the population, it can help individuals monitor workouts, improve fitness and build health. This makes it very useful to those who do not have access to regular laboratory testing.

References

  1. Maffetone P. White Paper. An Introduction to MAF: Maximum Aerobic Function. Independent; 2016.
  2. Montgomery P, Green D, Etxebarria N, et al. Validation of Heart Rate Monitor-Based Predictions of Oxygen Uptake and Energy Expenditure. J Strength Cond Res. 2009;23(5):1489-1495.
  3. Meyer T, Lucía A, Earnest C, Kindermann W. A Conceptual Framework for Performance Diagnosis and Training Prescription from Submaximal Gas Exchange Parameters: Theory and Application. Int J Sports Med. 2005;26:S38-S48.
  4. Kindermann W, Simon G, Keul J. The significance of the aerobic-anaerobic transition for the determination of work load intensities during endurance training. Eur J Appl Physiol. 1979;42(1):25-34.
  5. Londeree BR. Effect of training on lactate/ventilatory thresholds: a meta-analysis. Med Sci Sports Exerc. 1997;29(6):837-843.
  6. Mann T, Lambert RP, Lambert MI. Methods of prescribing relative exercise intensity: physiological and practical considerations. Sports Med. 2013;43(7):613-25.
  7. Maffetone P. Complementary Sports Medicine. Champaign, IL: Hum Kinet; 1999.
  8. Boullosa D, Abreu L, Varela-Sanz A, Mujika I. Do Olympic Athletes Train as in the Paleolithic Era? Sports Med. 2013;43(10):909-917.
  9. Hickson RC, Rennie MJ, Conlee R, et al. Effects of increased plasma fatty acids on glycogen utilization and endurance. J Appl Physiol. 1977; 43: 829-833.
  10. Holloszy JO, Coyle EF. Adaptations of skeletal muscle to endurance exercise and their metabolic consequences. J Appl Physiol. 1984; 56: 831-838.
  11. Ellis AC, Hyatt TC, Hunter GR, Gower BA. Respiratory quotient predicts fat mass gain in premenopausal women. Obesity. 2010; 18(12): 2255-2259.
  12. Mattson M, Allison D, Fontana L, et al. Meal frequency and timing in health and disease. Proc Natl Acad Sci. 2014; 111(47): 16647-16653.
  13. Schutz Y. Abnormalities of fuel utilization as predisposing to the development of obesity in humans. Obesity Res. 1995; 3(2): 173s-178s.
  14. Haseler LJ, Hogan MC, Richardson RS. Skeletal muscle phosphocreatine recovery in exercise-trained humans is dependent on O2 availability. J Appl Physiol. 1999; 86:2013-8.
  15. Astrand PO and Rodahl K. Textbook of Work Physiology. New York, McGraw-Hill 1977.
  16. Powers SK, Jackson MJ. Exercise-Induced Oxidative Stress: Cellular Mechanisms and Impact on Muscle Force Production. 2008. Physiol Rev. 2008;88(4): 1243-1276.
  17. Volek J, Noakes T, Phinney SD. Rethinking fat as a fuel for endurance exercise, Eur J Sport Sci. 2015; 15:1, 13-20.
  18. McArdle W, Katch F, Katch V. Exercise Physiology. 3rd ed. Philadelphia, PA: Lea & Febiger; 1991.
  19. Putman CT, Jones NL, Hultman E, et al. Effects of short-term submaximal training in humans on muscle metabolism in exercise. Am J Physiol. 1998;275:E132–E139.
  20. Walsh N, Gleeson M, Shepard R et al. Position statement part one: immune function and exercise. Immunol Rev. 2011;17:6-63.
  21. Szivak T, Hooper D, Dunn-Lewis C et al. Adrenal Cortical Responses to High-Intensity, Short Rest, Resistance Exercise in Men and Women. J Strength Cond Res. 2013;27(3):748-760.
  22. van de Vyver M, Engelbrecht L, Smith C, Myburgh K. Neutrophil and monocyte responses to downhill running: Intracellular contents of MPO, IL-6, IL-10, pstat3, and SOCS3. Scand J Med Sci Sports. 2015.
  23. Blankenbaker DG, De Smet AA. MR imaging of muscle injuries. Appl Radiol. 2004:14–6.
  24. Boyd A, Giamber S, Mager M, Lebovitz H. Lactate inhibition of lipolysis in exercising man. Metabolism. 1974;23(6):531-542.
  25. Kreher JB and Schwartz JB. Overtraining Syndrome. A Practical Guide. Sports Health. 2012 Mar; 4(2): 128–138.
  26. Billat V, Sirvent P, Py G, Koralsztein J, Mercier J. The Concept of Maximal Lactate Steady State. Sports Med. 2003;33(6):407-426.
  27. Emerenziani GP, Gallotta MC, Meucci M et al. Effects of Aerobic Exercise Based upon Heart Rate at Aerobic Threshold in Obese Elderly Subjects with Type 2 Diabetes. Int J Endocrinol. 2015 May 18;2015.
  28. Bassett DR, Howley ET. Limiting factors for maximum oxygen uptake and determinants of endurance performance. Med Sci Sports Exerc. 2000 Jan 1;32(1):70-84.
  29. Høeg T, Maffetone P. The Development and Initial Assessment of a Novel Heart Rate Training Formula. Poster presented at the Medicine & Science in Ultra-Endurance Sports 2nd Annual Conference; May 2015; Olympic Valley, CA, USA.
  30. Achten J, Gleeson M, Jeukendrup AE. Determination of the exercise intensity that elicits maximal fat oxidation. Med Sci Sports Exerc. 2002; 34: 92-97.
  31. Dantas JL, Doria C. Detection of the Lactate Threshold in Runners: What is the Ideal Speed to Start an Incremental Test? J Hum Kinet. 2015 Mar 1;45(1):217-24.
  32. Yoshida T, Chida M, Ichioka M, Suda Y. Blood lactate parameters related to aerobic capacity and endurance performance. Eur J Appl Physiol Occup Physiol. 1987;56:7–11.

Special thanks to Ivan Rivera for assistance in writing and editing, Hal Walter for editorial and Simon Greenland for formatting.

Join the discussion 11 Comments

  • Art Bourque says:

    Dr. Maffetone:

    Great piece; I circulated it to family and friends.

    I am so fortunate to have “discovered” you over a decade ago. Every day I observe examples of athletes overtraining or eating/drinking refined carbs and sugar. Last night I watched the excellent documentary “All of Nothing” about the Arizona Cardinals’ 2015 season. On of the stories was about the discovery that great defensive back Patrick Peterson has Type 2 diabetes. Yet, Gatorade bottles are everywhere during various team meetings. The disconnect is amazing.

    Please keep spreading the word, Dr. Maffetone. Your work is saving lives and making the quality of life better.

    Art Bourque

  • laura tancredi says:

    Hello, can you help me with race strategy in general and for the upcoming Chicago Marathon. i hope this question is applicable to anyone across the board. While i understand MAF philosophy and nutrition and have implemented all Phil’s recommendations over the last 5 weeks i am still unclear about what happens on race day? Assuming one’s MAF is not in line (slower then) race day goals what do you do? Are we always supposed to race in an anaerobic higher then MAF state? My MAF is 137. my fastest marathon is a 3:38. My goal in 4 weeks for chicago is a 3:35 (and i’m running NYC just 4 weeks after). When i started this program in early August i was running at MAF bet a 10- 11 min/mile (taking into account alot of summer travel and altitude changes). During my 20 mile run yesterday i essentially ran between a 9-10 min/mile with some early miles in the 8:45 range and the later miles in the 10:15 range. But when it comes to race day in Chicago do i need to run according to MAF or if i want to try to reach my goal i will need to run an 8:15 pace well outside my MAF? Is that the goal anyway? if you are training say a fast 10K or half marathoner and they start with an 8:30 MAF and a year later get to a 6:30 MAF but normally race at a 5:45? is this expected? IS one even after years of MAF ever able to get their MAF to the race pace? or is that not part of the formula and i can run in an anaerobic state? and if so know i will be doing more sugar burning wondering how i compensate with fueling that day and what are your best marathon race day food recommendations that i can stash in my pockets? nut butters, avocado, honey etc? thank you!

    • Laura:

      Check out this research article on marathon race pace. Essentially, we believe that marathoners race best (with exceptions, of course) when their pace is about 15 seconds faster than the first mile of their MAF test. The problem is that if you run any faster than that—that 8:15 pace you want to run in Chicago—your glycogen stores will become depleted too fast and your body won’t be able to keep up that speed. Your best bet is to stay close enough to your 1st mile MAF (within 15 seconds) that your glycogen stores don’t become depleted. The reason the marathon race pace is always faster than MAF is because you want to be using your muscle glycogen stores enough for them to become completely depleted by the end of the race but not before.

      In other words, if your 1st mile MAF pace is say, a 9 min mile pace, it would be very very difficult (not to mention extremely stressful and unhealthy) to be able to keep a 8:15 marathon pace. But most likely, if you do try, you’ll find that you’ll hit the wall at around mile 18 and have to reduce your speed the rest of the way—and possibly run a 8:45 or 9 minute average anyway. So one of the reasons marathon strategy is to run just above your MAF pace (but not too high) is because you don’t have much of a choice in the matter: too slow and you could run at that same speed for 5 or 10 more miles. Too fast and you’ll slow down well before the finish line.

      So you are running in a mildly anaerobic state. However, when the body is running mostly aerobically (as in the case of the marathon), all the systems that prolong its ability to stay active become active. Conversely, as soon as the body becomes too anaerobic, all the endurance systems—which include but are not limited to aerobic muscle fibers—switch their functions: They stop being the body’s main drivers and instead work more to support the functioning of the anaerobic (short-term) system in order to protect the body. So, suppose that you’re running a marathon at your lactate threshold (quite anaerobic). Even if you could replace every single sugar molecule you are burning, you wouldn’t be able to run a marathon at that intensity. And that’s not because you aren’t fueled—you are—but because the engine that uses the kind of fuel you are ingesting is built for a much shorter timescale than that of a marathon.

      What ingesting sugar does during a marathon is not primarily to feed your muscles (although it does do a bit of that), but to feed your brain. If your blood sugar levels remain steady and your brain remains well-fueled, it won’t have to compete with your muscles for fuel: the muscles are using mostly fats, and the brain is using sugar. In fact, athletes “hit the wall” when blood sugar drops low enough that the brain starts competing with the muscles for sugar. When this happens the brain goes to extreme measures to stop athletic activity. These extreme measures produce the feeling of incredible fatigue we get when we hit the wall.

      To fuel your brain, anything that you can digest well is a good idea. It’s just fine to eat honey or energy goos or gel shots as long as you start consuming them about 40 minutes after the onset of athletic activity.

      I hope I’ve answered your questions!

  • panos says:

    Hello

    During my daily commute with my bike, i am trying to stay at or below my maf hr.
    I have noticed that when i go 1 or 2 beats above my maf hr, my breathing changes a little bit and i need to take a deeper breath.
    Why is that happening ? Do i cross so kind of limit/threshold ?

    Thank you
    Panos

    • Panos:

      You are most likely exceeding your first ventilatory threshold (VT1), which occurs just a few BPM above your aerobic threshold (a.k.a. MAF HR). So, that you have to breathe more heavily a couple of beats per minute above your MAF HR tells me that the 180-Formula is giving you a very accurate reading of your physiological aerobic threshold. If you want to read more on this topic, check out reference 3 on the white paper. It’s a worthwhile read in its entirety, but in particular there’s a graphic towards the end that shows where VT1 occurs relative to the aerobic threshold. (I think they call VT1 something like AerT/GE, or “AerobicThreshold/GasExchange”).

  • Captain Fancy says:

    Hi & thank you for the great work. I have The Big Book of Endurance Training & listened to all the podcasts! I have a question on the scientific calculation of the MAF heart rate in a sports lab… at what point does one decide the ideal HR if you have a table like the one above (table 1) showing the % of fat v sugar burned at various heart rates? Assuming that you can get tested what should you be asking for and how do you decide upon the ideal HR? Thank you, Jon.

    • Look for your FAT MAX (maximum rate of fat-burning), also known as your aerobic threshold or “First lactate threshold” (LT1). That’s your MAF HR. The percentage of fats vs. carbs burned only somewhat correlate to that.

  • peter says:

    Hi,

    Just going to start MAf-training as base building for next 3 months, after 1,5 years of 80/20 training with more moderate distance training. My question is if its appropriate to incorporate som short strides(20 sec) after my MAF runs, just to keep some sort of reminder for the legs regarding coordination/speed as well as neuro gains. And what about strength training with focus on core and legs/calfs? Can you do it together with MAF without loosing development?

    My last question is regarding 180 formula, shall you still use this formula if you know that I.E standard maxpuls formula is a bit low for me. Im 35 years old, with maxpuls this year at 192 bpm.

    Thanks,
    Peter

  • Hi, 46 Male, well trained over last 7 years in Triathlon with 70.3 & full last 2 years. adopting the MAF method & HFLC although I do seem to have a low range regarding heart rate. my Max is 159 during an 18:40 5k, my sole 1/2 marathon 1:29:40 145bpm, top 5% Age Group in Ironman Races incl 70.3 Worlds. have been running & riding at 134bpm for 3 weeks, runs feel easy (8-8:10/mile for 13 miles) biking 7-7.5 rpe 210watts 2-3hrs.
    have just been for a Metabolic rate test which gave me an Aerobic Threshold of just 116bpm! 56.2% cals from fats dropping to just 35.8% at 131bpm.
    have just done a run @116bpm and 9:43/mile!
    can you confirm that 116 is in fact the rate at which I should be training regardless of how easy it feels and how far away from 180-age it is?

    would really appreciate your help.
    thanks
    Simon

  • patch adam says:

    Hi,
    My question is regarding the effect of temperatures on MAF ie in summers should the MAF be modified , increased by x number as even on a field test the LTHR in summers is higher than in winters

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