Wednesday, September 9, 2015

Fractional Utilization, Low Carbohydrate Diets and Running Performance

Fractional utilization refers to the fraction of VO2max that an athlete sustains during an event. It varies between events and between athletes. An athlete can sustain a greater percentage of VO2max for a shorter duration (5000m vs. 10,000m). Fractional utilization is sometimes referred to as lactate threshold. While the concepts are related, they are not the same.

Consider an athlete with a VO2max of 70 ml/kg/min: If we find that he can average 90% of VO2max over the course of a 5000m run, he averages 63.0 ml/kg/min for the race. If he averages 86% of VO2max during a 10,000m run, he averages 60.2 ml/kg/min.

Athletes may train for years, increasing fractional utilization. By increasing fractional utilization, an athlete will be able to complete a distance at a greater percentage of VO2max. For example, if that same athlete increases his fractional utilization during the 5000m to 93%, he can now average 65.1 ml/kg/min. That 2.1 ml/kg/min increase in utilization means more O2 is consumed. Assuming running economy does not change, more ATP is generated from aerobic metabolism for muscle contraction and the athlete completes the 5000m faster.

But what happens if economy decreases?

Economy has traditionally been measured by recording O2 uptake at certain running velocities. If an athlete consumes less O2, that means he's become more economical. We can also compare economy between athletes. The athlete that consumes the least amount of O2 for any given running velocity is the most economical at that pace. Economy gives us an indication of how much substrate, or which substrate, is being used for locomotion. One issue with a low carbohydrate diets is that more O2 is required to completely oxidize fatty acids than is needed for glucose. This means, economy suffers. And when economy suffers, pace declines for any given percentage of VO2max.

To my knowledge, low carbohydrate diets have no beneficial effects on VO2max or fractional utilization. And if VO2max and fractional utilization are unchanged (while economy is decreased) performance suffers; no matter the distance. The athlete may still only be able to complete the 5000m at 90% of VO2max, but more O2 is being used for substrate oxidation (decrease economy), and the ATP yield per unit of O2 consumed is decreased.

Dr. Ronald J. Maughan does a great job summarizing this issue with low carbohydrate diets here, beginning just after 23:00 and going to 34:00.

"The challenge is not to spare carbohydrate by promoting fat use. The challenge is rather to increase carbohydrate storage; and to increase carbohydrate utilization."

Thursday, August 13, 2015

So you want to "burn fat?"

Potential for Improving Endurance Performance through Substrate Conservation

We know skeletal muscle needs ATP to contract and there are different pathways from which ATP can be synthesized. During endurance exercise, inevitably, some combination of glucose/glycogen and fatty acids will be used for substrate. Utilizing fatty acids for ATP synthesis could be beneficial for endurance athletes because humans have a virtually unlimited supply fatty acids, whereas stored carbohydrate is relatively limited - demonstrated below:

135,000 Cal from stored fat is roughly enough energy for a 65 kg person to run 2000 km (R. Margaria et al, 1963).
A decreased reliance on carbohydrate and a subsequent increased reliance on fatty acids during exercise should help to "spare" muscle glycogen. Accepting the well documented theory that low muscle glycogen causes fatigue, one can see how glycogen sparing can potentially extend performance or allow for an acceleration late in a race.

"Glycogen sparing" is widely recognized as a potential ergogenic strategy, but the best training techniques to maximize fatty acid oxidation are still hotly debated.

Conventional Training for "Fat Burning"

Some time ago, people noticed; at certain intensities individuals rely more on the different metabolic pathways and substrates to synthesize ATP. Low intensity exercise can be sustained through oxidation of fatty acids, while high intensity exercise relies more on the oxidation of carbohydrate from blood glucose and/or glycogen. This principle became the foundation upon which weight loss programs and training regimes were built. The birth of the "Fat Burning Zone" was inevitable.

The exact intensity range of the "Zone" is still being debated - research indicates that it varies from individual to individual (Achten et al., 2002, Carey, 2009). The general consensus is that it occurs at a relatively low intensity, near 60-65% of VO2max. Somewhere down the line, coaches, physiologists or athletes took this data and assumed since maximal fat oxidation rate (MFO) occurs at low intensities, it is best to train at low intensities for long durations to increase one's ability to oxidize fatty acids. Example: Maffentone

One Problem: The Paucity of Data

Unfortunately, for the long-slow-distance enthusiast, these notion that training in the "zone" improves his fat oxidation rate more so than training at a higher intensity is not supported by the literature. When it comes to fat oxidation, it doesn't seem to matter whether an athlete trains at or above the intensity that corresponds to MFO (Alkahtani et al., 2013). In 2004, Achten and Jeukendrup wrote:
To the best of our knowledge no studies have investigated
which training is most effective in inducing changes in fat metabolism.
The effects of intensity and duration of training programs on
fat oxidation should be investigated to predict such changes.

The Physiological Model:

If we work our way through the physiological model, it becomes more apparent how one could potentially improve his maximal fat oxidation rate - increasing his aerobic capacity (VO2max). Suppose a marathon runner trains hard and improves his VO2max. For simplicity's sake let's assume his running economy (RE) and fractional utilization at marathon pace remain the same after training.

Increasing VO2max alone will not change the percentage of VO2max or the percentage of lactate threshold/pH threshold the marathon can be run at - so it will not change substrate utilization (indicated by respiratory exchange ratio). Increasing VO2max will translate to a faster pace at any given percentage of max, again - assuming RE doe snot change. Increased running speeds require more ATP, and O2 consumption. Where does the additional ATP come from? It comes from increased oxidation of substrate (carbohydrate and fatty acid).

Further, if an athlete increases VO2max and then can run the same pace at a lower percentage of VO2max, he is likely to rely less on carbohydrate and more on fatty acid metabolism.

Yes, increased VO2max ↔ increased fatty acid oxidation → increased performance.

What about "Aerobic Base?"

For too long, aerobic metabolism has been misunderstood - looked at as a separate entity from anaerobic metabolism. But, it's more complicated than that. Metabolic pathways are interlinked. Coaches and athletes should take notice and training should follow suit. There are no training zones to maximize separate and distinct variables because there are no separate and distinct variables. The bulk of the research shows that low intensity training is not likely to be the best way to improve one's ability to oxidize fat. And high intensity training (above the second ventilatory threshold) does not diminish one's ability to oxidize fat at the expense of carbohydrate - rather, it's the opposite.

Instead of long slow distance, perhaps there is more merit to high intensity training, aimed at increasing VO2max:  Further reading -,


  • Increasing fatty acid oxidation can spare muscle glycogen, potentially improving endurance performance
  • There is an ongoing debate over what type/intensity of training best improves fatty acid oxidation rate
  • Increasing VO2max also increases maximal rate fatty oxidation
  • Low intensity exercise may not not be the best way to maximize fatty acid oxidation. Perhaps athletes should focus on high intensity training (above the second ventilatory threshold). High carbohydrate diets and/or carbohydrate supplementation may enhance high intensity exercise performance.


Achten, J., Gleeson, M., & Jeukendrup, A. E. (2002). Determination of the exercise intensity that elicits maximal fat oxidation. Medicine and Science in Sports and Exercise, 34(1), 92–97.

Achten, J., & Jeukendrup, A. E. (2004). Optimizing fat oxidation through exercise and diet. Nutrition, 20(7), 716–727.

Alkahtani, S. A., King, N. A., Hills, A. P., & Byrne, N. M. (2013). Effect of interval training intensity on fat oxidation, blood lactate and the rate of perceived exertion in obese men. SpringerPlus, 2, 532.

Carey, D. G. (2009). Quantifying differences in the “fat burning” zone and the aerobic zone: implications for training. Journal of Strength and Conditioning Research / National Strength & Conditioning Association, 23(7), 2090–2095.

Margaria, R., Cerretelli, P., Aghemo, P., & Sassi, G. (1963). Energy cost of running. Journal of Applied Physiology, 18(2), 367–370.

Thursday, March 5, 2015

Stressors, Ergogenic Aids and Training Loads

Training Basics

Training always involves balancing stress and recovery. A stress is applied to the system, the stress results in a deviation from homeostasis, acting as a stimulus for cellular signaling that leads to adaptation. This adaptation will leave the system better able to cope with the stimulus in the future (demand for ATP, substrate transport, muscle recruitment, etc).

Generally, there is a dose-response to training so that the more training stress or training load encountered, the greater the signal and response to adapt. For example, if you had two groups of college kids, one group ran 10 miles per week (mpw) and the other group ran 30 mpw - after 10 weeks, the group that ran 30 mpw will likely outperform and/or show greater improvement over the 10 mpw group. Why? Because the 30 mpw group accumulated a greater training load resulting in a greater response.

Of course, that's a very simple example. When it comes to training at a higher level - more is not always better. The athlete who runs or rides the greatest number of miles per week does not always win. Instead, there has to be a balance of stress and recovery - a balance of stimuli contributing to perturbations from homeostasis and factors that can either prevent perturbations in the first place or time to return the system to homeostasis.

Ramping up the Signal
There are several strategies that are being used now to either enhance the signal or increase the training load. What's interesting is that these strategies use entirely different approaches. While training in a hot, high altitude environment will result in a decrease in training load, it may enhance cellular signaling leading to favorable adaptations. Same with training in a glycogen depleted state or with high levels of mental fatigue - training load will be reduced. At least in the acute phase, these strategies are anything but "ergogenic."

Altitude/Heat training
Training is a glycogen depleted or fasted state, low carb diets
Mental fatigue

Increasing the Training Load
Then there are those supplements and strategies that are ergogenic:

Carbohydrate supplementation
Supplemental O2

Yes, there are plenty others - you could consider water an ergogenic aid.

If you think about it, these strategies can help prevent or delay disturbances. Beta-alanine can buffer H+; creatine provides substrate for ATP resynthesis; supplemental O2 prevents declines in O2 saturation at high intensities; carbohydrate prevents declines in muscle glycogen/blood glucose, etc. By preventing disturbances, these strategies and supplements can increase the amount of work an athlete can complete - increasing the training load an athlete experiences.

Balancing the Stressors
On the one hand, the system needs to experience perturbations - and these deviations from the norm can be enhanced by the strategies in the first category. On the other hand, these strategies may decrease the training load that individuals can accumulate. For example, a runner will not be able to complete as many intervals at a given pace in a hot environment while in a glycogen depleted state as a runner in a cool environment, sipping on a CHO beverage a few hours after a high carbohydrate breakfast.

What's more important? Inflating the training load with the help of these "ergogenic strategies" and supplements or maximizing metabolic stress while potentially decreasing training load?

Even if you take every precaution, can you really prevent perturbations from homeostasis and inhibit adaptation? Especially in elite athletes who know how to push themselves to their limits. Even if an athlete supplements with carbohydrate, he/she my still experience glycogen depletion - but after accumulating a greater training load.

And let's not forget that mechanical stress can also be a trigger for adaptation and by limiting training load, you limit mechanical stress.

In my research at Appalachian State, we looked at the effect of different oxygen concentrations on training intensity and performance at simulated altitude. Athletes completed intervals on a cycle ergometer in  either hypoxic or hyperoxic conditions. Predictably, those training under hypoxic conditions cycled at a significantly lower power output (expressed as a percentage of their peak power output). At the end of the 3 week study, those who had trained at greater power outputs, under hyperoxic conditions, improved the most in a time trial at simulated altitude. Why? One reason could be because they were able to accumulate a greater training load by riding at higher intensities. Their muscles would also have experienced greater mechanical stress while training.

From a psychological standpoint, I think it would be best not to train your athletes under additional stress (at least not without lowering their expections). When an athlete sees slow slow splits and struggles to complete the workout or cover the distance, that athlete will be mentally defeated - perhaps that defeat could have been prevented had the coach not been focused on maximizing metabolic stress. Wouldn't you rather have an athlete leave a workout satisfied and feeling as though it came easily?

I'm not here to say one way is right and the other is wrong. Different strategies may be appropriate at different times. Coaches and athletes need to be able to recognize this.

Further reading:

Monday, February 23, 2015

pH Threshold as a Predictor of Endurance Running Performance

Lactate and pH

Lactate threshold as a percentage of VO2max has long been associated with distance running and cycling performance.

But lactate is not a cause of fatigue. Rather, the accumulation of lactate is an indication of what's occurring. Lactate can accumulate without a change in muscle pH. In fact, lactate production prevents or delays changes in pH.

So, could pH threshold be a more sensitive indicator of performance capacity than lactate?

Below is data and a graph from a pH threshold test conducted on a treadmill in a lab.

From the graph, you can see the lactate threshold falls at roughly 9.5 mph or 6:19/mile. Here, we saw an increase from 3.02 mmol/L to 4.78 mmol/L (+1.76 mmol/L). But note that blood pH did not change from 9.5 to 10 mph (7.38 to 7.37). But, pH did fall between 10 and 10.5 mph.

This demonstrates that even though lactate starts accumulating, pH does not necessarily change. In theory, an athlete should be able to maintain a pace in that window above lactate threshold and below pH threshold for a extended amount of time. Here, the cause of fatigue is not likely to be related to lactate or the accumulation of H+ because H+ does not accumulate at this intensity.

If acidosis is not the cause of fatigue, what is?

The issue with maintaining this pace for extended amounts of time (hours) may stem from glucose availability. Glucose is necessary to run glycolysis and glycolysis is a relatively inefficient source of ATP. So, an athlete will be relying heavily on glucose when creating lactate through glycolysis. Plenty of research has demonstrated positive effects of glucose ingestion on exercise performance from sprint intervals to ultra-endurance events.

Take this graph from a fundamental study on carbohydrate consumption and exercise from Coyle, Coggan, Hemmert, and Ivy (1986):

The CHO group ingested a carbohydrate beverage every 20 minutes. The placebo group was given artificially flavored water. Full Text Link Here.

The subjects were asked to cycle to exhaustion at a moderate intensity of ~70% VO2max (well below the pH threshold in trained athletes). CHO supplementation extended the time to exhaustion (TTE) from 3.02 hrs to 4.02 hrs, demonstrating that CHO is an effective ergogenic aid. But, perhaps the most interesting finding from this study is not that CHO maintained blood glucose and extended TTE. Rather, it's that that even in the face of maintained and adequate blood glucose, fatigue still occurs. So, in addition to acidosis and carbohydrate availablity, we have to recognize other potential factors that contribute to fatigue: thermal strain, dehydration and cardiac drift, progressive recruitment, muscle damage, lack of motivation, a central govenor or any combination of these factors.

Just as the accumulation of hydrogen ions was not likely the cause of fatigue in the above experiment, H+ accumulation is not likely to be the culprit behind fatigue during marathon running (unless the effort is very poorly paced) because the marathon will be run at an intensity below pH threshold. Regardless, a relationship between pH threshold and marathon running performance has been established (Zoladz et al., 1993).

VO2max and pH Threshold

Physiological Performance Predictors:
Velocity at VO2max (vVO2) has been cited as a reliable indicator of running performance in a number of studies by a number of authors. But the issue with vVO2max is that it does not take into account changes in blood pH. So while a high vVO2max is generally good, it will not tell you whether a certain pace is sustainable or a certain pace results in acidosis because we cannot predict at what percentage of vVO2max pH threshold will fall.

To address this issue, let's call the velocity at which pH threshold is met, vpH. vpH represents more than velocity and blood pH alone - vpH also encompasses aerobic capacity (VO2max), and running economy. If pH threshold is represented as a percentage of VO2max and running economy is similar between athletes, the greater the VO2max the greater the vpH of the athlete at a given percentage of VO2max. Likewise, if VO2max is similar between athletes, the greater the economy the greater the vpH at a given percentage of VO2max. This model of running performance has been laid out many times; the variables VO2max, running economy and lactate threshold being the key determinants.

By replacing lactate threshold with pH threshold, we have a more definitive point. Here we know, beyond vpH, acidosis will occur and that velocity will not be sustainable for more than ~30:00.

So What?
I say all of this, but in the end performance is still the best predictor of performance:

Noakes et al., 1990
As it turns out, those athletes with the fastest 10K and half marathon times are most likely to have the fastest marathon times.

Then why should anyone care about pH threshold if 10K performance will tell you the same thing?

1) It can be easier to assess pH threshold in the lab than have an athlete nail a 10K at 100%
2) Acidosis is still a performance limiter - it still limits how fast, long, or far an athlete can go

Increasing pH threshold will allow an athlete to accumulate a greater training load. That's why I believe short intervals should supersede longer intervals. By increasing pH threshold, the athlete can then run the longer intervals at a greater velocity and percentage of VO2max.