An individual’s ability to metabolize fat has significant ramifications for maximal exercise performance. There is a relationship between exercise intensity, fat oxidation, and carbohydrate oxidation. For example, as exercise intensity increases, fat oxidation decreases while carbohydrate oxidation increases. This can be understood through metabolic gas analysis, where VO2 and VCO2 are measured. By measuring the ratio between the volume of carbon dioxide produced to the volume of oxygen consumed per unit of time, you can calculate a respiratory exchange ratio (RER), which allows you to estimate the type of fuel used for oxidation.
Since both fats and carbohydrates differ in the amount of oxygen used and carbon dioxide produced during oxidative phosphorylation, you can divide VCO2 by VO2 to calculate RER. Typically, RER values will fall between 0.7 and 1.0, with values closer to 0.7 indicating that more fat is oxidized and values closer to 1.0, indicating that more carbohydrate is oxidized. In most cases, RER will increase as exercise intensity increases, and given this relationship, we can define the exercise intensity at which maximal fat oxidation occurs as the ‘Fatmax’.
As you can see in the image above, when fat oxidation is expressed as a function of exercise intensity, a parabolic curve is formed. All things being equal, the higher an individual's fitness level (defined by an increased VO2max), the greater their Fatmax will be. Mechanistically this makes good sense since the same adaptations that lead to an increase in VO2max like enhanced skeletal muscle blood flow and oxygen extraction will also lead to an increased ability to oxidize fat. VO2max can be defined as the maximum integrated capacity of the pulmonary, cardiovascular, and muscular systems to uptake, transport, and utilize oxygen, respectively. Given this fact, it stands to reason that any improvements in VO2max will come with a concomitant increase in either oxygen delivery or utilization. Increases in oxygen delivery can come through various mechanisms, including increases skeletal muscle capillarization and increased maximal cardiac output. In addition to enhanced blood flow to the working skeletal muscles, these training adaptations will also augment the substrate-exchange surface for fatty acids to enter into myocytes, leading to a greater fat oxidation capacity and a ‘glycogen sparing effect. Because of the relationship between exercise intensity, oxygen availability, and fat oxidation it’s been suggested that NIRS (near-infrared spectroscopy) may be used to identify an individual's Fatmax non-invasively.
The question of whether or not NIRS can be used to determine Fatmax was recently investigated by Zurbuchen and colleagues in their paper titled, Fat Oxidation Kinetics Is Related to Muscle Deoxygenation Kinetics During Exercise. Interestingly, the investigators found a relationship. Between muscle deoxygenation kinetics and fat oxidation, their specific findings indicated that shallower deoxy-hemoglobin kinetics with a right-shifted deoxy-hemoglobin breakpoint was associated with higher fat oxidation, and Fatmax shifted to higher absolute exercise intensities. The following image from the paper mentioned above is of particular interest:
Note that the deoxy-hemoglobin breakpoint and Fatmax for this individual both occur at the same percentage of VO2peak in this individual. Interestingly, the same relationship appears to hold true for both trained cyclists and untrained individuals, as seen in the image below:
Knowing this, we can use relatively simple NIRS breakpoint tests to determine what paces an individual's Fatmax occurs at on a range of modalities. For example, if you're working with a rower, you might put them on a concept 2 erg and have them row for 4:00 at 150 watts, then each subsequent 4:00 block, you increase the power output by a fixed amount (say, 50 watts) until failure.
What's interesting about ramp tests of this sort is that while power output increases linearly, physiologic metrics like blood lactate, oxygen consumption, muscle oxygenation, and fat oxidation do not. When calculating breakpoints with NIRS data, we’ll want to use the deoxy-hemoglobin measurements increase of muscle oxygen saturation (SmO2) or oxygenated hemoglobin (O2Hb) since they are less affected by blood volume under the NIRS probe. Even though the Moxy monitor does not provide a deoxyhemoglobin measurement directly, we can back-calculate it from the THb and SmO2 data with the following formula: Deoxy hemoglobin = ((100 - %SmO2)/100))*THb.
You can see Deoxy hemoglobin from a rower's vastus lateralis muscle plotted against their power output on an incremental step test in the picture above. Note the nearly linear increase in deoxyhemoglobin 400 watts, at which points a break occurs. This 'break point' demarcates the crossing of an intensity threshold and an increased reliance on glycolytic energy sources. You'll also notice that deoxyhemoglobin plateaus towards the end of the test. This indicates that the athlete has 'maxed out' their oxygen extraction capabilities, and given that they were no longer able to increase their oxygen supply, then failed shortly after, thus ended the test and causing deoxyhemoglobin to drop down rapidly after the test ends.