Author: LCS_Athlete

Exercise and Longevity

There’s a couple of recent studies out that look at the effects of exercise using telomere length as a surrogate for longevity. Our telomeres shorten as we age.

The first study is (Beate Ø Osthus, Ida & Sgura, Antonella & Berardinelli, Francesco & Alsnes, Ingvild & Brønstad, Eivind & Rehn, Tommy & Kristian Støbakk, Per & Hatle, Håvard & Wisløff, Ulrik & Nauman, Javaid. (2012). Telomere Length and Long-Term Endurance Exercise: Does Exercise Training Affect Biological Age? A Pilot Study. PloS one. 7. e52769. 10.1371/journal.pone.0052769). The study:

Older endurance trained athletes had longer telomere length compared with older people with medium activity levels (T/S ratio 1.12±0.1 vs. 0.92±0.2, p = 0.04). Telomere length of young endurance trained athletes was not different than young non-athletes (1.47±0.2 vs. 1.33±0.1, p = 0.12).

A second study looked at the effects of the specific mode of exercise (Christian M Werner, Anne Hecksteden, Arne Morsch, Joachim Zundler, Melissa Wegmann, Jürgen Kratzsch, Joachim Thiery, Mathias Hohl, Jörg Thomas Bittenbring, Frank Neumann, Michael Böhm, Tim Meyer, Ulrich Laufs; Differential effects of endurance, interval, and resistance training on telomerase activity and telomere length in a randomized, controlled study , European Heart Journal, ehy585).

The results were interesting.

This randomized, controlled, and prospective training study shows that specific training protocols lead to differential effects on cellular aging. Aerobic endurance and high-intensive interval training, but not resistance training, increases telomerase activity and telomere length in blood mononuclear cells.

This study was fairly impressively powered with 124 subjects.

One hundred and twenty-four healthy previously inactive individuals completed the 6 months study. Participants were randomized to three different interventions or the control condition (no change in lifestyle): aerobic endurance training (AET, continuous running), high-intensive IT (4 × 4 method), or RT (circle training on 8 devices), each intervention consisting of three 45 min training sessions per week.

The specific results were statistically significant.

Telomerase activity in blood mononuclear cells was up-regulated by two- to three-fold in both endurance exercise groups (AET, IT), but not with RT. In parallel, lymphocyte, granulocyte, and leucocyte TL increased in the endurance-trained groups but not in the RT group. Magnet-activated cell sorting with telomerase repeat-ampliflication protocol (MACS-TRAP) assays revealed that a single bout of endurance training—but not RT—acutely increased telomerase activity in CD14+ and in CD34+ leucocytes.

Things to note is that this is an older (~49 years on average), untrained group of people who were at healthy BMI (~24).

Mechanism

The mechanism is interesting.

Exercise Intensity and Blood Sugar

I’ve come to the conclusion that for me as a diabetic intense exercise (at high heart rates) is not good for my blood sugar control. Here’s a study of Type 1 Diabetics which shows the increase in blood sugar from intense exercise (Vinutha S, Paul F, Raymond D, et al. Effect of exercise intensity and blood glucose level on glucose requirements to maintain stable glycaemia during exercise in individuals with type 1 diabetes. Int J Pediatr Endocrinol. 2015;2015(Suppl 1):O39). The study looked at:

Nine young adults with T1D underwent euglycaemic clamps, whereby stable blood glucose levels between 4.5 to 6mmol/L were maintained during the study at basal insulin levels. Participants performed up to 40 minutes of exercise at four different exercise intensities (35%, 50%, 65% and 80% VO2peak) on four separate days following a randomised counterbalanced design. In a subsequent experiment, eight participants underwent either a euglycaemic or hyperglycaemic (9.5 – 10.5mmol/L) clamp at basal insulin levels, during which they performed 40 minutes of exercise at 50% VO2peak, on two separate days. In both studies, glucose infusion rates (GIR) to maintain stable glycaemia were measured during exercise, constant deuterated glucose was infused to determine glucose kinetics and blood samples were collected for the analysis of glucoregulatory hormones.

The result was:

The average GIR to maintain euglycaemia during exercise was 2.0±0.9, 4.0±1.5, and 4.1±1.7g/h (mean±SEM) at 35%, 50% and 65% VO2peak, respectively. These GIRs were all significantly greater than that at 80% VO2peak where no glucose was required (p<0.05). Exercise at 80% VO2peak was associated with a significant rise in catecholamine levels and endogenous glucose production (p<0.05). The average GIR to maintain stable glycaemia during exercise performed during the second experiment at 50% VO2peak was similar at euglycaemia (4.9±2.1g/h) and hyperglycaemia (5.5±2.5g/h; p>0.05).

 

MAF Plus 20

Peter Defty (of OFM fame) suggests that fat adapted athletes can increase their MAF number from 180 – age (with correction factors added/subtracted) to 200 – age (same correction factors) (Primal Endurance Podcast – #90: Peter Defty Talks Optimized Fat Metabolism).

His reasoning is that the heart rate is 10-15 beats per minute faster in fat adapted athletes (from the FASTER data). He reasoned that Maffetone came up with the number based on non-fat adapted athletes and that once fat adapted the number can be shifted up.

Tempting Idea, but…

I’ve had the same thoughts before and I’d really like to accept Defty’s ideas since I’m getting tired of mostly walking. I’d like to run more. But I’ve also had no injuries in the past few months. Recovery has been so easy that I’m finding myself doing two MAF efforts a day. I’d hate to jeopardize that.

I don’t think I’m getting much faster doing MAF, but I wonder if sticking with MAF and doing intervals would improve my speed. I do feel like I am improving my leg strength at MAF and they are not a limiting factor when I’m out for more than an hour.

The limiting part of MAF is that after 4 or 5 miles I can only run a few steps until I have to start walking again.

MAF is MAF

Of course, Maffetone’s approach is that MAF is MAF. And it’s 180 – age (with correction factors).  The program is fixed and doesn’t need to be changed. The athlete who is not yet fat adapted will burn more carbohydrates at MAF and the athlete who is fat adapted will burn more fat at MAF. This shift away from carbohydrate reliance to fat adaptation is the goal of MAF when done with the recommended lower carbohydrate diet.

20 Beat Shift – VO2 Data

To see what a 20 beat increase would do, take a look at my VO2max fat/carbohydrate oxidation curve. At my MAF (122 bpm) I am currently burning nearly all fat and very little carbohydrates.

Shifting up by 20 bpm from 122 to 142 just happens to be the 50-50 crossover point of calories from fat and carbohydrates. This will cause glycogen depletion which has good and bad aspects. My current view is that staying out of that range is the smartest idea since cycling glycogen doesn’t promote lower glycogen stores since the body responds by over saturating glycogen stores.

Shifting right by 20 bpm could have the advantage of causing a further shift of the curve to the right and increasing my fat oxidation at that same heart rate. If that is the effect then it would be positive since in the end I could have a higher VO2max and improved fitness.

Critique of MAF number

One difficultly of the Maffetone MAF number is that there’s no real explanation of the basis for the number. Maffetone himself says that the number can be adjusted based on actual metabolic tests but he never exactly explains how to adjust the number nor exactly what he based the number on other than observation of a lot of his clients/patients. The number fit the tests within a few beats but Maffetone never explains the derivation of the number in enough details to explain what lab test he used and what the correlation to the tests is. Maffetone has spent a lot of energy explaining what it isn’t (lactic threshold, VO2max, percent of max heart rate, etc) but not a lot explaining what it is. Without tying it to some external metric it’s hard to judge the value of the metric.

Is MAF at the cross-over point for a non-fat adapted athlete but the point of maximum fat burning in a fat adapted athlete? It is true from my data that 122 is the sweet spot. It is literally the peak of fat oxidation (the black theoretical curve fitted line) where no carbohydrates are being burned. Ten beats lower is still in the prime fat burning zone. For me, lower numbers are even ketone burning (evidenced by the RER of less than 0.7).

Rate of Perceived Exertion (RPE)

Mowing my lawn raises my heart rate beyond the MAF range and makes me sweat. MAF makes me sweat when it’s warm outside but it’s a pretty gentle pace. I could do exercises at 142 max and it would be fine. I know because I’ve mowed the lawn (and done CrossFit) at higher rates.

I don’t think I am going to change what I am doing at the moment but I will bear it in mind for the future. I did 5 sessions last week of 5Km or longer and I’d like to keep up the volume.

 

Is it the Low Carb or the High Fat?

Interesting study took a look at the question of whether it is high fat or low carb (Leckey JJ, Hoffman NJ, Parr EB, Devlin BL, Trewin AJ, Stepto NK, Morton JP, Burke LM, Hawley JA. High dietary fat intake increases fat oxidation and reduces skeletal muscle mitochondrial respiration in trained humans. FASEB J. 2018 Jun;32(6):2979-2991.) (Full PDF).

High dietary fat intake increases fat oxidation and reduces skeletal muscle mitochondrial respiration in trained humans.

It’s not a surprise that your body will burn more fat when you consume less carbohydrates. The Food Quotient (Food Quotient) predicts exactly that.

Mitochondria respiration (Mitochondrial Respiration) is:

…the set of metabolic reactions and processes requiring oxygen that takes place in mitochondria to convert the energy stored in macronutrients to  adenosine triphosphate(ATP), the universal energy donor in the cell.

I don’t know enough to know whether or not reduced mitochondrial respiration is good or bad for athletic performance. It seems like reduced rates of ATP would be bad for energy but is that energy made up in other ways? Is the loss offset by the increase in BHOB (ketone bodies)?

 

Fasted Workouts and 24 Hour Fat Oxidation

Fasted workouts cause increased 24 hour fat oxidation (Iwayama K, Kurihara R, Nabekura Y, et al. Exercise Increases 24-h Fat Oxidation Only When It Is Performed Before Breakfast. EBioMedicine. 2015;2(12):2003-2009).

Under energy-balanced conditions, 24-h fat oxidation was increased by exercise only when performed before breakfast. Transient carbohydrate deficits, i.e., glycogen depletion, observed after morning exercise may have contributed to increased 24-h fat oxidation.

These results probably don’t hold true for low carb athletes since our glycogen stores are probably already somewhat depleted.

Energy Expenditure in Hunter Gatherers

We are told that our western lifetyle is to blame and that all we need to eat less and move more. And that sounds intuitively true. The move more part was challenged by a study of the Hadza people (Pontzer H, Raichlen DA, Wood BM, Mabulla AZP, Racette SB, et al. (2012) Hunter-Gatherer Energetics and Human Obesity. PLOS ONE 7(7): e40503.).

…average daily energy expenditure of traditional Hadza foragers was no different than that of Westerners after controlling for body size. The metabolic cost of walking (kcal kg−1 m−1) and resting (kcal kg−1 s−1) were also similar among Hadza and Western groups.

The similarity in metabolic rates across a broad range of cultures challenges current models of obesity suggesting that Western lifestyles lead to decreased energy expenditure.

We hypothesize that human daily energy expenditure may be an evolved physiological trait largely independent of cultural differences.

Interesting article (What a hunter-gatherer diet does to the body in just three days).

My other lasting impression was how little time they spent getting food. It appeared as though it took just a few hours a day — as simple as going round a large supermarket. Any direction you walked there was food — above, on and below ground.

MAF Training And Metabolic Syndrome

There’s an interesting study which looked at two months of training at FATmax to see what the effects on Metabolic Syndrome (Dumortier M, Brandou F, Perez-Martin A, Fedou C, Mercier J, Brun JF. Low intensity endurance exercise targeted for lipid oxidation improves body composition and insulin sensitivity in patients with the metabolic syndrome. Diabetes Metab. 2003 Nov;29(5):509-18). The study showed good improvements from MAF level of training intensity.

The patients exhibited a significant reduction in body weight (- 2.6 +/- 0.7 kg; P=0.002), fat mass (- 1.55 +/- 0.5 kg; P=0.009), waist (- 3.53 +/- 1.3 cm; P<0.05) and hip (- 2.21 +/- 0.9 cm; P<0.05) circumferences, and improved the ability to oxidize lipids at exercise (crossover point: + 31.7 +/- 5.8 W; P<0.0001; LIPOX(max): + 23.5 +/- 5.6 W; P<0.0001; lipid oxidation: + 68.5 +/- 15.4 mg.min(-1); P=0.0001). No clear improvement in either lipid parameters or fibrinogen were observed.

There were significant improvements in the markers of Metabolic Syndrome.

The surrogates of insulin sensitivity evidenced a decrease in insulin resistance: HOMA%S (software): + 72.93 +/- 32.64; p<0.05; HOMA-IR (simplified formula): – 2.42 +/- 1.07; P<0.05; QUICKI: + 0.02 +/- 0.004; P<0.01; SI=40/I: + 3.28 +/- 1.5; P<0.05. Significant correlations were found between changes in body weight and HOMA-IR and between changes in LIPOX(max) and QUICKI.

Here’s a longer term study which shows positive results over a longer time period (Drapier E (2018) Long term (3 years) weight loss after low intensity endurance training targeted at the level of maximal muscular lipid oxidation. Integr Obesity Diabetes 4).

Average weight loss was -2.95 ± 0.37 kg after 3 months, -4.56 ± 0.68 kg after 1 year, -5.31 ± 1.26 kg at 2 years and -8.49 ± 2.39 kg at 3 years.

The beauty of this study was that it compared low intensity exercise to a low fat diet.

This study shows that this low intensity exercise training maintains its weight-reducing effect 3 years while diet is no longer efficient, and that this effect is initially related to muscular ability to oxidize lipids but that metabolic and behavioral adaptations have been further developed and contribute to a long lasting effect.

The results are powerful.

Here’s a third related study (J. O. Holloszy and E. F. Coyle. Adaptations of skeletal muscle to endurance exercise and their metabolic consequences. Journal of Applied Physiology 1984 56:4, 831-838).

The major metabolic consequences of the adaptations of muscle to endurance exercise are a slower utilization of muscle glycogen and blood glucose, a greater reliance on fat oxidation, and less lactate production during exercise of a given intensity.

These adaptations play an important role in the large increase in the ability to perform prolonged strenuous exercise that occurs in response to endurance exercise training.

From the results:

…Probably the most important of these is an increase in mitochondria with an increase in respiratory capacity. One consequence of the adaptations induced in muscle by endurance exercise is that the same work rate requires a smaller percentage of the muscles’ maximum respiratory capacity and therefore results in less disturbance in homeostasis.

A second consequence is increased utilization of fat, with a proportional decrease in carbohydrate utilization, during submaximal exercise.

 

Polar App Zones

The heart rate zones in the Polar Flow app are misleading. Here’s a recent run.

The problem with the Polar app is that the zones are based on assumptions which may not apply for you. More specifically your fuel is a mixture between fat and carbohydrates and the hard edges these applications show don’t reflect a mixture.

I had my own VO2max tested in a lab. I know what my fuel mixture is at a particular heart rate. My Polar app shows me in fat burning below 111 bpm and “fit” above that point. My MAF range is 112-122. My VO2Max test showed my fat/carb burning at 90% / 10% at a heart rate of 124.

But I am fat adapted keto for two years so I am primarily a fat burner. This is why MAF works well for me. My 100% fat burning heart rate is 117 which center of MAF. As long as I am in the MAF zone I’m burning nearly all fat – even though the Polar Flow program says otherwise.

FASTER Study – Three Hour Magic Number

In previous posts I’ve taken a critical look at the FASTER study (FASTER Again – Checking a number on Ben Greenfield’s data). In particular, I took at look at Ben Greenfield’s three hour data (FASTER10 – Ben Greenfield – Three Hour VO2 testing). Ben looked like he still had gas left in his tank after three hours of sub-maximal running.

The Vegan

But what about Damian Stoy (FASTER Subject 43)? He’s a vegan who is not at all fat fueled. He never got more fuel from fat than 50% and that was at 45% of his VO2max.

At 64% of VO2max, Damian was getting nearly zero of his energy from fat. His carbohydrate oxidation rate was ~10 kcal/min. So, in three hours of running, Damian burned ~1800 kcals which has to be close to his entire glycogen stores.

My conclusion? Beyond this time and intensity being carb fueled isn’t a great choice. The reason that marathons are 26 miles is historical and practical. People just can’t run hard for longer times.