More of my VO2Max Test Results

Here’s some more data from my VO2Max Testing (Part 1 is here). The test was done fasted at about 9AM. Part 3 follows where I look at the graphs for this data.

Respiratory Exchange Ratio (RER)

One of the things I wanted to know was how much I am fat fueled. The RER is a measure of carb vs fat fuel utilization.

My initial RER at rest was 0.73. The RER number went down as the exercise started and bottomed out at 0.59. At about 7 minutes in the number started to increase and finally peaked when I tapped out at a value of 1.09. From Wikipedia:

An RER of 0.70 indicates that fat is the predominant fuel source, RER of 0.85 suggests a mix of fat and carbohydrates, and a value of 1.00 or above is indicative of carbohydrate being the predominant fuel source.

Not sure how I got RER numbers below 0.7. Clearly I am a fat burner.  Ben Greenfield say that is indicative of burning more than 100% fat (no clue what that actually means) and the machine is not calibrated to measure that. Being at a low body fat amount probably played into my inability to go longer and deeper into fat stores.

As the exercise continued my body moved to burning carbs (which I have very few of since I would have a minimal glycogen stores and the liver can only produce so much glucose at any rate).

The high RER value of 1.09 was exceeded when I was cooling down when it reached 1.11. From Wikipedia:

Calculation of RER is commonly done in conjunction with exercise tests such as the VO2 max test and can be used as an indicator that the participants are nearing exhaustion and the limits of their cardio-respiratory system.

An RER greater than or equal to 1.15 is often used as a secondary endpoint criterion of a VO2 max test.

They stop the test at 1.15 because that’s the end of where they will take you. So I was a few seconds from that time. I felt like a wimp for stopping but I can see from the numbers I was actually very close to my physiological limit. Being low carb I have very little carbohydrate (glycogen) stores to draw from so that’s another reason for my limited performance.

They will let the systolic blood pressure go up to 250 and mine peaked at 210. Incidentally, it started high. My white coat flight or fight syndrome was in full bore for much of this. Interestingly, diastolic pressure drops during exercise (for most people) and mine did as well.

Study on RER in Low Carbers

From (Nutrition, Published Online:1 Apr 2014. Effect of a very low carbohydrate diet followed by incremental increases in carbohydrate on respiratory exchange ratio (LB444). Laura Kunces, Brittanie Volk, Daniel Freidenreich, Catherine Saenz, Maria Luz Fernandez, Carl Maresh, William Kraemer, Stephen Phinney, and Jeff Volek):

Low carbohydrate diets are associated with increases in fat oxidation, but the extent to which substrate utilization is altered as individuals reintroduce carbohydrate into the diet has not been studied under controlled conditions.

We therefore examined postabsorptive respiratory exchange ratio (RER) across a broad range of dietary carbohydrate and fat levels in adults with metabolic syndrome.

After an initial 3-wk run-in low-carbohydrate diet, 16 adults (age 55 ± 10 yr, BMI 37.9 ± 6.3 kg/m2) were fed six sequential moderately hypocaloric 3-wk diets that progressively increased carbohydrae (47, 82, 131, 179, 250, 344 g/day) with parallel decreases in fat.

Resting RER was lowest after the very low carbohydrate diet and increased in a linear manner as carbohydrate increased (0.75 ± 0.04, 0.77 ± 0.03, 0.79 ± 0.04, 0.80 ± 0.04, 0.82 ± 0.03, 0.84 ± 0.05, respectively).

These findings indicate that very low carbohydrate diets accelerate fat oxidation and that progressive increases in carbohydrate track linearly with decreased fat oxidation.

Another Low Carb Athlete’s Results

Here’s Ben Greefield‘s Vo2max test results. His number stayed above 0.70 and for some odd reason I can’t explain or understand my number dropped below 0.70. That’s not supposed to happen as far as I can tell. My RER reached a low of 0.59 during the test.

 

Pre-exercise carbohydrate loading

Contrary to common wisdom pre-loading carbohydrates does not improve performance. From this study (Medicine and Science in Sports [01 Jan 1979, 11(1):1-5]. Effects of preexercise feedings on endurance performance. Foster C , Costill DL , Fink WJ.):

Eight male and female students were studied during exercise to exhaustion on a bicycle ergometer at 80 and 100% of Vo2max following the ingestion of water (W), 75 g of glucose (G) or a liquid meal (M) (10 g protein, 12.5 g fat, 15 g CHO).

When compared to the endurance ride (80% Vo2max) in the W treatment, endurance performance time was reduced by 19%, (p less than .05) (53.2 to 43.2 min) as a result of the preexercise glucose feeding (Trial G).

No difference in performance at 80% Vo2max was found between the W and M trials. The preexercise feedings had no effect on exercise time to exhaustion at 100% Vo2max.

During the G and M trials at 80% Vo2max, most of the subjects demonstrated a transient decline in serum glucose (less than 3.5 mM). After 30-40 min. of exercise, however, serum glucose returned to normal and was seldom low at the time of exhaustion.

Serum free fatty acids (FFA) were depressed throughout the G trial.

The results of these experiments indicate impaired lipid mobilization following CHO ingestion. The present data support our earlier findings (11) which demonstrate that glucose feedings 30-45 minutes before endurance exercise increase the rate of CHO oxidation and impede the mobilization of FFA, thereby reducing exercise time to exhaustion.

 

Exogenous Ketones – Part 1

Taking ketones may reduce your own body’s production of ketones (Metabolism, Volume 24, Issue 9, September 1975, Pages 999-1007. Inhibition of ketogenesis by ketone bodies in fasting humans. E.O. Balasseab, M.A.Neefab):

The administration of exogenous ketones during the second phase of the study induced a 47%–92% increase in total ketone levels. During this period, the endogenous production of ketones (calculated as the difference between total inflow rate and acetoacetate infusion rate) amounted only to 67%–90% of control values. Among other factors, this inhibition of ketogenesis was probably partially related to the direct antilipolytic effect of infused ketones. Indeed, there was a concomitant fall in FFA and in glycerol levels averaging respectively 13.5% and 17.3%, without significant changes in peripheral insulin concentrations.

Our results demonstrate that during fasting, circulating ketone bodies exert an inhibitory influence on the rate of ketogenesis. This mechanism might play an important role in preventing the development of uncontrolled hyperketonemia during starvation.

Second Study

Another study (Physiol., 30 October 2017. On the Metabolism of Exogenous Ketones in Humans. Brianna J. Stubbs, Pete J. Cox, Rhys D. Evans, Peter Santer, Jack J. Miller, Olivia K. Faull, Snapper Magor-Elliott, Satoshi Hiyama, Matthew Stirling and Kieran Clarke):

Drinks containing exogenous ketones, in either ester or salt form, can raise concentrations of blood βHB in humans, although elevation of L-βHB lasts longer after racemic KS consumption. Both KE and KS drinks mildly altered acid-base balance. Exogenous ketones lowered blood glucose and lipids without inhibiting endogenous insulin secretion. The KE delivered highly repeatable blood concentrations of D-βHB, although ketosis was decreased by a meal. Uptake and elimination of D-βHB were similar when several drinks were consumed in succession. The dietary KE could maintain ketosis using drinks taken regularly around a normal meal pattern, or using a continuous infusion via a nasogastric tube. Therefore, ketone drinks are a viable and practical alternative to dietary strategies to achieve ketosis.

Third Study

From a study by a guy I respect (Cell Metabolism, Volume 24, Issue 3, 13 September 2016, Pages 373-375. Fueling Performance: Ketones Enter the Mix. (PDF) Brendan Egan, Dominic P.D’Agostino.)

…exogenous ketones can confer a performance benefit to elite athletes through a combination of fuel sparing and improved energetic efficiency.

…the often-cited higher energetic efficiency of exogenous ketones may provide thermodynamic advantages over CHO and fat given the greater free energy of ATP hydrolysis (ΔG′ATP) and less oxygen required per mole of carbon. In practical terms, this would translate as a higher power output for the same oxygen consumption (i.e., improved muscular efficiency) during exercise, and thereby confer a performance benefit as observed.

A Fourth Study

Another study (Cell Metabolism 24, 256–268. Nutritional Ketosis Alters Fuel Preference and Thereby Endurance Performance in Athletes. Pete J. Cox, Tom Kirk,  Tom Ashmore, Kristof Willerton, Rhys Evans, Alan Smith, Andrew J. Murray, Brianna Stubbs, James West, Stewart W. McLure, M. Todd King, Michael S. Dodd, Cameron Holloway, Stefan Neubauer, Scott Drawer, Richard L. Veech, Julian L. Griffin, and Kieran Clarke).

We have demonstrated the metabolic effects of elevated circulating
ketone bodies as a fuel and biological signal to create a
unique physiological condition. Ketosis may alter substrate
competition for respiration, while improving oxidative energy
transduction under certain conditions, such as endurance exercise.
Consequently, nutritional ketosis may help to unlock
greater human metabolic potential.

A Fifth Study

Another study looked at the safety of exogenous ketones (Regul. Toxicol. Pharmacol., 63 (2012), pp. 401-408. Kinetics, safety and tolerability of (R)-3-hydroxybutyl (R)-3-hydroxybutyrate in healthy adult subjects. Clarke et al., 2012. K. Clarke, K. Tchabanenko, R. Pawlosky, E. Carter, M. Todd King, K. Musa-Veloso, M. Ho, A. Roberts, J. Robertson, T.B. Vanitallie, R.L. Veech):

…the pharmacokinetic properties and safety of a synthetic ketone monoester was evaluated in healthy adult humans. The ketone monoester was completely hydrolyzed to its components (D-β-hydroxybutyrate and R-1,3-butanediol), resulting in increased plasma levels of the ketones, D-β-hydroxybutyrate and acetoacetate. Ingestion of the ketone monoester over a period of 5 days was generally well tolerated. Some gastrointestinal disturbances were observed in individuals who consumed the highest dose (2142 mg/kg bw/day taken in three divided doses of 714 mg/kg bw/day daily), though these were considered to be related to the large volumes (>1 l) of a milk-based drink consumed in a short period, rather than effects caused by the ketone monoester.

So… I Ordered This Item

I ordered this item from Perfect Keto. It’s a keto supplement with a lot of βHB (Beta hydroxybutyrate).

Nutritional Facts

Here’s the nutritional facts for this product:

I have to wonder if the people who liked the energy from this were getting energy from the extra salt? Looks like it provides a good amount of Magnesium as well.

Expectations?

I don’t have high expectations for the result since I have been in ketosis for around 20 months). It will be interesting to see if I get the tingles that are described by some people.

Expensive Stuff

The cost was not cheap at $60 for 15 servings ($4 a serving seems like a whole lot of money).

 

Ketogenic Diet and Moderate Exercise

Here’s another study (J Clin Invest. 1980;66(5):1152–1161. Capacity for Moderate Exercise in Obese Subjects after Adaptation to a Hypocaloric, Ketogenic Diet. Stephen D. Phinney, Edward S. Horton, Ethan A. H. Sims, John S. Hanson, Elliot Danforth Jr., and Betty M. Lagrange.) on exercise while in ketosis.

To study the capacity for moderate endurance exercise and change in metabolic fuel utilization during adaptation to a ketogenic diet, six moderately obese, untrained subjects were fed a eucaloric, balanced diet (base line) for 2 wk, followed by 6 wk of a protein-supplemented fast (PSF), which provided 1.2 g of protein/kg ideal body wt, supplemented with minerals and vitamins. The mean weight loss was 10.6 kg.

The duration of treadmill exercise to subjective exhaustion was 80% of base line after 1 wk of the PSF, but increased to 155% after 6 wk. Despite adjusting up to base line, with a backpack, the subjects’ exercise weight after 6 wk of dieting, the final exercise test was performed at a mean of 60% of maximum aerobic capacity, whereas the base-line level was 76%. Resting vastus lateralis glycogen content fell to 57% of base line after 1 wk of the PSF, but rose to 69% after 6 wk, at which time no decrement in muscle glycogen was measured after >4 h of uphill walking. The respiratory quotient (RQ) during steady-state exercise was 0.76 during base line, and fell progressively to 0.66 after 6 wk of the PSF. Blood glucose was well maintained during exercise in ketosis. The sum of acetoacetate and beta hydroxybutyrate rose from 3.28 to 5.03 mM during exercise after 6 wk of the PSF, explaining in part the low exercise RQ.

The low RQ and the fact that blood glucose and muscle glycogen were maintained during exhausting exercise after 6 wk of a PSF suggest that prolonged ketosis results in an adaptation, after which lipid becomes the major metabolic fuel, and net carbohydrate utilization is markedly reduced during moderate but ultimately exhausting exercise.

 

Fasted Resistance Training

This study (Deldicque L1, De Bock K, Maris M, Ramaekers M, Nielens H, Francaux M, Hespel P. Increased p70s6k phosphorylation during intake of a protein-carbohydrate drink following resistance exercise in the fasted state. Eur J Appl Physiol. 2010 Mar;108(4):791-800.) found that  subjects who lifted weights in a fasted state had a greater anabolic response to a postworkout meal). This was indicated by levels of p70S6 kinase, a muscle protein synthesis-­signaling mechanism that acts as an indicator of muscle growth, doubling in the fasted group compared with the fed group.

Interesting.

 

Low Carb and Athletic Performance

Lots of people complain that their athletic performance is reduced with a Low Carbohydrate diet. Dr Volek contends that these issues are due to various reasons:

  1. Insufficient adaption time – it can take between weeks to months to fully adapt to the ketogenic diet. That is because the body is fueled by ketones rather than glucose.
  2. Electrolyte Imbalances – The ketogenic diet causes a shift in the body’s electrolytes and requires supplementation. This is even more the case with athletes who sweat a lot.
  3. Incorrect Amount of Protein – Too little or too much is a problem (between 15% and 25% of calories per day from Protein seems optimal).

See also, the book “The Art and Science of Low Carbohydrate Performance“.

Note that this may be limited to endurance activities rather than higher intensity activities.

…one caveat that anaerobic (ie, weight lifting or sprint) performance is limited by the low muscle glycogen levels induced by a ketogenic diet, and this would strongly discourage its use under most conditions of competitive athletics.

[Added the following studies 2018-02-22]

Here’s another study which has fairly positive results (Nutr Metab (Lond). 2017 Feb 20;14:17. doi: 10.1186/s12986-017-0175-5. eCollection 2017. Impact of a 6-week non-energy-restricted ketogenic diet on physical fitness, body composition and biochemical parameters in healthy adults. Urbain P, Strom L, Morawski L, Wehrle A, Deibert P, Bertz H.). They concluded:

We detected a mildly negative impact from this 6-week non-energy-restricted KD on physical performance (endurance capacity, peak power and faster exhaustion). Our findings lead us to assume that a KD does not impact physical fitness in a clinically relevant manner that would impair activities of daily living and aerobic training. However, a KD may be a matter of concern in competitive athletes.

Another study (J Int Soc Sports Nutr. 2017 Jul 12;14:22. doi: 10.1186/s12970-017-0180-0. eCollection 2017. Ketogenic diet benefits body composition and well-being but not performance in a pilot case study of New Zealand endurance athletes. Zinn C, Wood M, Williden M, Chatterton S, Maunder E.) concluded:

All athletes increased their ability to utilize fat as a fuel source, including at higher exercise intensities. Mean body weight was reduced by 4 kg ± SD 3.1 (p = 0.046; effect size (ES):0.62), and sum of 8 skinfolds by 25.9 mm ± SD 6.9; ES: 1.27; p = 0.001). Mean time to exhaustion dropped by ~2 min (±SD 0.7; p = 0.004; ES: 0.53). Other performance outcomes showed mean reductions, with some increases or unchanged results in two individuals (VO2 Max: -1.69 ml.kg.min ± SD 3.4 (p = 0.63); peak power: -18 W ± SD 16.4 (p = 0.07), and VT2: -6 W ± SD 44.5 (p = 0.77). Athletes reported experiencing reduced energy levels initially, followed by a return of high levels thereafter, especially during exercise, but an inability to easily undertake high intense bouts. Each athlete reported experiencing enhanced well-being, included improved recovery, improvements in skin conditions and reduced inflammation.

 

Types of Exercise and Glycogen

I have been trying to tease out the limits of low carb performance. Here is a key paper (Metabolism. 1983 Aug;32(8):769-76. The human metabolic response to chronic ketosis without caloric restriction: preservation of submaximal exercise capability with reduced carbohydrate oxidation. Phinney SD, Bistrian BR, Evans WJ, Gervino E, Blackburn GL).  Buried within the paper is:

In agreement with this were a three-fold drop in glucose oxidation (from 15.1 to 5.1 mg/kg/min, P less than 0.05) and a four-fold reduction in muscle glycogen use (0.61 to 0.13 mmol/kg/min, P less than 0.01).

This seems buried because of the units used. Another site (September 13, 2017. Why Am I Getting Low Ketone Readings on a Ketogenic Diet? By Mark Sisson) translates these units as:

During the high-carb arm, the group began the workout with 150 grams of glycogen and ended it with 50 grams. While eating ketogenic, the group began the workout with 75 grams and also ended it with 50 grams.

The time of this test was approx 150 minutes.

 

Glycogen Stores – Why does it matter?

From the study (K J Acheson Y Schutz T Bessard K Anantharaman J P Flatt E Jéquier. Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man. The American Journal of Clinical Nutrition, Volume 48, Issue 2, 1 August 1988, Pages 240–247):

Glycogen storage capacity in man is approximately 15 g/kg body weight and can accommodate a gain of approximately 500 g before net lipid synthesis contributes to increasing body fat mass.

The question then comes up – what happens when you fill up the glycogen stores from carbohydrate consumption? That’s exactly the question that the study asked. And the answer they got was:

When the glycogen stores are saturated, massive intakes of carbohydrate are disposed of by high carbohydrate-oxidation rates and substantial de novo lipid synthesis (150 g lipid/d using approximately 475 g CHO/d) without postabsorptive hyperglycemia.

Some of it burns off (the “high carbohydrate-oxidation rates”) but a lot of it gets stored as fat via DNL (de novo lipogenesis). And the storage efficiency is pretty darned good. 150g of lipids are 1350 calories of fat. The 475g of carbs provides 1900 calories. So the efficiency is 71%.

Without High Blood Sugar Levels

The most amazing part is that all of this happens, per the study “without postabsorptive hyperglycemia”. In other words, the blood sugar doesn’t go high. It all happens within the liver.

The Test Subjects were young and their livers weren’t fat to begin with.

Second Study

Another study (Increased liver fat and glycogen stores after consumption of high versus low glycaemic index food: A randomized crossover study.
Stephen Bawden PhD Mary Stephenson PhD Yirga Falcone Melanie Lingaya Elisabetta Ciampi PhD Karl Hunter PhD Frances Bligh PhD Jörg Schirra PhD Moira Taylor. 4 September 2016).

Results
Plasma glucose and insulin peak values and area under the curve were significantly greater after the HGI test meal compared with the LGI test meal, as expected. Hepatic glycogen concentrations increased more after the HGI test meal ( P < .05) and peak levels were significantly greater after 7 days of HGI dietary intervention compared with those at the beginning of the intervention ( P < .05). Liver fat fractions increased significantly after the HGI dietary intervention compared with the LGI dietary intervention (two‐way repeated‐measures analysis of variance P ≤ .05).

Conclusions
Compared with an LGI diet, a 1‐week HGI diet increased hepatic fat and glycogen stores. This may have important clinical relevance for dietary interventions in the prevention and management of non‐alcoholic fatty liver disease.

A Third Study

In this paper (Int J Sports Med. 1982 Feb;3(1):22-4. Muscle glycogen storage and its relationship with water. Sherman WM, Plyley MJ, Sharp RL, Van Handel PJ, McAllister RM, Fink WJ, Costill DL.):

This study examined the relationship between muscle glycogen and muscle water content. Exercise dietary manipulations were used to vary skeletal muscle glycogen levels in four groups of rodents: (1) eight animals were sedentary controls (SC); (2) ten animals were treadmill familiarized and allowed to recover 24 h before sacrifice (F); (3) ten animals were treadmill familiarized and exercised to exhaustion (E); (4) ten animals were treadmill familiarized, exercised to exhaustion, and allowed to recover with food and water ad libitum for 72 h (ER).

All animals were sacrificed in a resting state to normalize intracellular, extracellular, and interstitial water compartments; thus, the E group was sacrificed 45 m in following their run. The treatments altered skeletal muscle glycogen to values ranging from 10.0 to 30.2 mumol glucosyl units/g wet tissue weight. Neither muscle triglyceride nor protein levels were affected by the treatments.

Muscle water content expressed as mumol H2O lost/g wet tissue weight or made relative to protein content showed no consistent relationship to the glycogen content.

These data, therefore, do not support the commonly accepted muscle glycogen-to-water ratio of 1.0:2.7 (g:g). Further work is necessary to quantify the exact amount of water that is actually associated with the glycogen complex.

 Impressive Fourth Study

From (Eur J Appl Physiol. 2015 Sep;115(9):1919-26. doi: 10.1007/s00421-015-3175-z. Epub 2015 Apr 25. Relationship between muscle water and glycogen recovery after prolonged exercise in the heat in humans. Fernández-Elías VE1, Ortega JF, Nelson RK, Mora-Rodriguez R.):

METHODS:

On two occasions, nine aerobically trained subjects ([Formula: see text] = 54.4 ± 1.05 mL kg(-1) min(-1); mean ± SD) dehydrated 4.6 ± 0.2 % by cycling 150 min at 65 % [Formula: see text] in a hot-dry environment (33 ± 4 °C). One hour after exercise subjects ingested 250 g of carbohydrates in 400 mL of water (REHLOW) or the same syrup plus water to match fluid losses (i.e., 3170 ± 190 mL; REHFULL). Muscle biopsies were obtained before, 1 and 4 h after exercise.

RESULTS:

In both trials muscle water decreased from pre-exercise similarly by 13 ± 6 % and muscle glycogen by 44 ± 10 % (P < 0.05). After recovery, glycogen levels were similar in both trials (79 ± 15 and 87 ± 18 g kg(-1) dry muscle; P = 0.20) while muscle water content was higher in REHFULL than in REHLOW (3814 ± 222 vs. 3459 ± 324 g kg(-1) dm, respectively; P < 0.05; ES = 1.06). Despite the insufficient water provided during REHLOW, per each gram of glycogen, 3 g of water was stored in muscle (recovery ratio 1:3) while during REHFULL this ratio was higher (1:17).

CONCLUSIONS:

Our findings agree with the long held notion that each gram of glycogen is stored in human muscle with at least 3 g of water. Higher ratios are possible (e.g., during REHFULL) likely due to water storage not bound to glycogen.

Fifth Study
Another study (J. Bergström & E. Hultman (1967) A Study of the Glycogen Metabolism during Exercise in Man, Scandinavian Journal of Clinical and Laboratory Investigation, 19:3, 218-228).

The following inferences can be drawn from the results:

1. During work, the muscle glycogen falls successively to values approaching zero, and the working capacity decreases when the glycogen store is depleted.

2. The glycogen concentration in resting muscle remains unchanged when other muscle groups in the same subject have been emptied of glycogen by exercise.

3. If glucose is infused continuously during muscular work, the glycogen consumption is significantly lower than when no glucose is administered. The difference is nevertheless small, and the consumption of muscle glycogen is responsible for the greater part of the energy production, even when the blood sugar level is high.

4. The glucose production by the liver increases towards the end of continuous muscular work, but is of relatively small magnitude in comparison to the total carbohydrate metabolism.

Shorter Study Problems

Short studies have the problem that it takes time to saturate the body’s glycogen stores. For instance a four day long carbohydrate overfeed showed the phenomenon of glycogen fill (Minehira, et.al. Effect of Carbohydrate Overfeeding on Lipogenesis. OBESITY RESEARCH Vol. 11 No. 9 September 2003, p 1096).
Under standard isocaloric conditions, 42% of the ingested glucose was oxidized over the 5-hour postingestive period. The remaining 58% was essentially stored as glycogen (54%), with very little net de novo lipogenesis (4% of the glucose load).
After overfeeding:
Net nonoxidative glucose disposal was consequently reduced and represented only 43% of the glucose load. Simultaneously, net glycogen synthesis was reduced and represented only 30% of ingested glucose, whereas net de novo lipogenesis increased by 296% and corresponded to 13% of ingested glucose. There was also a marked increase in fasting and postprandial plasma TG concentrations after carbohydrate overfeeding together with suppressed plasma FFA concentrations. This increase in plasma TGs may be caused by both stimulation of hepatic de novo lipogenesis (18) and a decreased clearance of very-low-density lipoprotein-TGs.
Even that study shows increased DNL.
In conclusion, the present data indicate that whole body
de novo lipogenesis after glucose ingestion was markedly
enhanced by a 4-day carbohydrate overfeeding and that the
amount of lipid newly synthesized markedly exceeded the
maximal reported rates for hepatic de novo lipogenesis.
A Useful Strategy

So the useful strategy is to lower the glycogen stores via low carbohydrate diet and exercise. Both of these lower glycogen quickly and can begin to drop the fat in the liver. The fat around the pancreas can then begin to drop and diabetes gets reversed.

 

We All Are Hybrid Engines

A hybrid engine can run on more than one fuel. Hybrid cars run on electricity (from a battery) or gasoline (which charges the battery).

Turns out the human body is a hybrid engine. We can run on carbohydrates or fat. We can also run on Protein but it’s not efficient as a fuel (Glycogen Replenishment After Exhaustive Exercise).

The ability to switch between fuel sources is key to the ketogenic diet. Someone who is not fat fueled takes days to fully make the switch between fuel sources. But it turns out we are always running on a hybrid system regardless of whether or not we are ketogenic. For instance, overnight we are fasting until we eat and the carbohydrates in our system are depleted.

Similarly in exercise we switch from the various fuel systems in our body.  Athletes on High Carb (HC) and Low Carb (LC) diets were put onto a treadmill and run for hours. These curves show the metabolic flexibility of the LC diet.

The top graph is the rate that fat is oxidized (burned). The LC diet provides fat as a fuel very quickly and at a much higher level than the HC diet.

The bottom graph is the rate of carbohydrate oxidation. The LC diet doesn’t have the carb repositories (glycogen stores) that the HC diet has so they don’t get much energy from glycogen stores. However, unlike the HC diet the LC diet provides consistent amount of carb energy throughout the workout.The HC diet has a high level at the beginning but drops over time which results in the characteristic bonk of the long distance runner.

Note that even the HC diet eventually requires body fat for fuel. It just doesn’t have instant access to the fat like the LC diet.

What I Observe In the Gym

I do CrossFit for exercise. CrossFit is commonly viewed as a glycogen intensive sport (J Physiol. 2013 Sep 15; 591(Pt 18): 4405–4413. Muscle glycogen stores and fatigue. Niels Ørtenblad, Håkan Westerblad, and Joachim Nielsen).

A Typical CrossFit Workout

Today’s Workout of the Day (WOD) was:

That’s 21 minutes of Box Jumping, Push-ups, Burpees, Back Squats, Hang Cleans, and Up-Downs (Burpees without pushups). That’s fairly short (not like running a marathon. It also includes 3 sets of 30 Wall balls. Quite a good workout.

Why Do CrossFit?

Note, I said I do CrossFit for exercise – not for sport. I don’t care what my exercise times are at CrossFit. I care if I get an effective workout. And I measure effectiveness by the accepted standard of heart rate .

Heart Rate as Metric of Effectiveness of a Workout

From the Mayo Clinic Website:

Gauging intensity using your heart rate

Another way to gauge your exercise intensity is to see how hard your heart is beating during physical activity. To use this method, you first have to figure out your maximum heart rate — the upper limit of what your cardiovascular system can handle during physical activity.

The basic way to calculate your maximum heart rate is to subtract your age from 220. For example, if you’re 45 years old, subtract 45 from 220 to get a maximum heart rate of 175. This is the maximum number of times your heart should beat per minute during exercise.

Once you know your maximum heart rate, you can calculate your desired target heart rate zone — the level at which your heart is being exercised and conditioned but not overworked.

The American Heart Association and the Centers for Disease Control and Prevention recommend a general target heart rate of:

  • Moderate exercise intensity: 50 to about 70 percent of your maximum heart rate

  • Vigorous exercise intensity: 70 to about 85 percent of your maximum heart rate

My Own Results

Here’s my heart rate as recorded by my Samsung Gear Sport watch:

The first part (0-30 minutes) was a chipper (the coach tells you what to do) which included a whole lot of stuff (pushups, jumping jacks, forward lunges, PVC work, sit-ups, squats). That got my heat rate as high as 160 near the end. The rest period then let my heart drop to “normal” range. Then the WOD…

I am 57-years old. To calculate max heart rate the standard way is to subtract your age from 220. So my max heart rate is 163. I hit that rate during the workout and I felt it. I had to stop and breath/rest at spots.

At the end I had spent most of my time at 85% (138 in my case) or more of my max heart rate. But I had energy left to clean up and started cleaning up immediately. It wasn’t that I didn’t work out hard. It’s that I am not glycogen dependent.  (Heart Rate Calculator).

The different oxidation rates of carbs and fat may provide the reason why I  can work out at a high heart rate but not be depleted at the end of the workout.

Both oxidation charts are in grams but remember that a gram of fat contains 9 calories of energy and a gram of carbohydrates contains 4 calories of energy. And the repositories of glycogen are in the hundreds of grams total. That’s a calorie repository of around 1600 calories, give or take. And it starts to drop quickly over time.

The repositories of fat are in the many thousands of grams. If you have just 22 lbs of fat, that’s 10 kg of fat or 90,000 calories available. Fat energy stays pretty constant. That may explain why I can keep moving after the WOD ends.

I work out for the express purpose of depleting my glycogen stores.

 

STRRIDE-AT/RT – Exercise Study

I was considering dropping CrossFit in favor of a strength program when I came across an interesting study which compared Aerobic Training (AT) to Resistance Training (RT) for impact on Metabolic Syndrome (MS). (September 15, 2011, Volume 108, Issue 6, Pages 838–844. Comparison of Aerobic Versus Resistance Exercise Training Effects on Metabolic Syndrome (from the Studies of a Targeted Risk Reduction Intervention Through Defined Exercise – STRRIDE-AT/RT. Lori A. Bateman, Cris A. Slentz, PhD, Leslie H. Willis, MS, A. Tamlyn Shields, MS, Lucy W. Piner, MS, Connie W. Bales, PhD, RD, Joseph A. Houmard, PhD, William E. Kraus, MD.)

AT/RT induced a significant improvement in the MS z score (p = 0.004) and AT alone exhibited a trend toward improvement (p <0.07). However, RT alone failed to significantly alter the MS z score.

My conclusion is to stick with CrossFit and work in the resistance training as often as reasonable as an accessory to CrossFit.

Another view of the same data (J Appl Physiol (1985). 2015 Jun 15;118(12):1474-82. The effects of aerobic, resistance, and combination training on insulin sensitivity and secretion in overweight adults from STRRIDE AT/RT: a randomized trial. Abou Assi H, Slentz CA, Mikus CR, Tanner CJ, Bateman LA, Willis LH, Shields AT, Piner LW, Penry LE, Kraus EA, Huffman KM, Bales CW, Houmard JA, Kraus WE.). Conclusion:

AT/RT resulted in greater improvements in insulin sensitivity, β-cell function (disposition index), and glucose effectiveness than either AT or RT alone (all P < 0.05). Approximately 52% of the improvement in insulin sensitivity by AT/RT was retained 14 days after the last exercise training bout. Neither AT or RT led to acute or chronic improvement in sensitivity index. In summary, only AT/RT (which required twice as much time as either alone) led to significant acute and sustained benefits in insulin sensitivity.

Yet another look at the same data (Am J Physiol Endocrinol Metab. 2011 Nov;301(5):E1033-9. doi: 10.1152/ajpendo.00291.2011. Epub 2011 Aug 16.
Effects of aerobic vs. resistance training on visceral and liver fat stores, liver enzymes, and insulin resistance by HOMA in overweight adults from STRRIDE AT/RT. Slentz CA, Bateman LA, Willis LH, Shields AT, Tanner CJ, Piner LW, Hawk VH, Muehlbauer MJ, Samsa GP, Nelson RC, Huffman KM, Bales CW, Houmard JA, Kraus WE.) concluded:

AT was more effective than RT at improving visceral fat, liver-to-spleen ratio, and total abdominal fat (all P < 0.05) and trended toward a greater reduction in liver fat score (P < 0.10). The effects of AT/RT were statistically indistinguishable from the effects of AT. These data show that, for overweight and obese individuals who want to reduce measures of visceral fat and fatty liver infiltration and improve HOMA and alanine aminotransferase, a moderate amount of aerobic exercise is the most time-efficient and effective exercise mode.

Yet another view (Arch Intern Med. 2004 Jan 12;164(1):31-9. Effects of the amount of exercise on body weight, body composition, and measures of central obesity: STRRIDE–a randomized controlled study. Slentz CA1, Duscha BD, Johnson JL, Ketchum K, Aiken LB, Samsa GP, Houmard JA, Bales CW, Kraus WE.):

In nondieting, overweight subjects, the controls gained weight, both low-amount exercise groups lost weight and fat, and the high-amount group lost more of each in a dose-response manner. These findings strongly suggest that, absent changes in diet, a higher amount of activity is necessary for weight maintenance and that the positive caloric imbalance observed in the overweight controls is small and can be reversed by a modest amount of exercise. Most individuals can accomplish this by walking 30 minutes every day.

Note none of the results were comparable to the effect on the metabolic syndrome from the Low Carb High Fat diet.