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).


The mechanism is interesting.

CrossFit Injury Rate Study

Interesting study of CrossFit injury rates (Hak PT, Hodzovic E, Hickey B. The nature and prevalence of injury during CrossFit training. J Strength Cond Res. 2013 Nov 22.). The study reported on an on-line survey so it was probably quite slanted in the results.

An online questionnaire was distributed amongst international CrossFit online forums. Data collected included general demographics, training programs, injury profiles and supplement use. A total of 132 responses were collected with 97 (73.5%) having sustained an injury during CrossFit training. A total of 186 injuries were reported with 9 (7.0%) requiring surgical intervention. An injury rate of 3.1 per 1000 hours trained was calculated.




Protein Before Bed

Here’s an interesting study which indicates that Protein taken before bed stimulates Muscle Protein Synthesis (Tim Snijders, Peter T Res, Joey SJ Smeets, Stephan van Vliet, Janneau van Kranenburg, Kamiel Maase, Arie K Kies, Lex B Verdijk, Luc JC van Loon; Protein Ingestion before Sleep Increases Muscle Mass and Strength Gains during Prolonged Resistance-Type Exercise Training in Healthy Young Men, The Journal of Nutrition, Volume 145, Issue 6, 1 June 2015, Pages 1178–1184).

Methods: Forty-four young men (22 ± 1 y) were randomly assigned to a progressive, 12-wk resistance exercise training program. One group consumed a protein supplement containing 27.5 g of protein, 15 g of carbohydrate, and 0.1 g of fat every night before sleep. The other group received a noncaloric placebo. Muscle hypertrophy was assessed on a whole-body (dual-energy X-ray absorptiometry), limb (computed tomography scan), and muscle fiber (muscle biopsy specimen) level before and after exercise training. Strength was assessed regularly by 1-repetition maximum strength testing.

Results: Muscle strength increased after resistance exercise training to a significantly greater extent in the protein-supplemented (PRO) group than in the placebo-supplemented (PLA) group (+164 ± 11 kg and +130 ± 9 kg, respectively; P < 0.001). In addition, quadriceps muscle cross-sectional area increased in both groups over time (P < 0.001), with a greater increase in the PRO group than in the PLA group (+8.4 ± 1.1 cm2 vs. +4.8 ± 0.8 cm2, respectively; P < 0.05).

Both type I and type II muscle fiber size increased after exercise training (P < 0.001), with a greater increase in type II muscle fiber size in the PRO group (+2319 ± 368 μm2) than in the PLA group (+1017 ± 353 μm2P < 0.05).

Study of Glycogen and Exercise Studies

Thanks to Luis at Ketogains for pointing to a great study which looks at the studies of Glycogen and Exercise (Pim Knuiman, Maria T. E. Hopman, and Marco Mensink. Glycogen availability and skeletal muscle adaptations with endurance and resistance exercise. Nutr Metab (Lond). 2015; 12: 59.).

…Recent research into the effects of glycogen availability sheds new light on the role of the widely accepted energy source for adenosine triphosphate (ATP) resynthesis during endurance exercise.

Indeed, several studies showed that endurance training with low glycogen availability leads to similar and sometimes even better adaptations and performance compared to performing endurance training sessions with replenished glycogen stores.

The study leads with:

…Glycogen is made and stored in cells of the liver (~100 g) and muscles (~350 – 700 g; depending on training status, diet, muscle fibre type composition, sex and bodyweight) and can be reduced by fasting, low intake of dietary carbohydrates and/or by exercise.

Intermittent Fasting, Low Carbs, exercise. Yep, that’s me.

Glycogen is differently distributed within the muscle fibers (subsarcolemmal ~5-15 %, intermyofibrillar ~75 % and intramyofibrillar ~5-15 %)

And here’s the bit about high intensity workouts:

Glycogen is an essential substrate during high intensity exercise by providing a mechanism by which adenosine tri phosphate (ATP) can be resynthesized from adenosine diphosphate (ADP) and phosphate.

The relative use of energy sources during exercise is mainly determined by the intensity and the duration of the exercise bout, as well as the athlete’s training status.

Fat as source of energy is relatively most dominant during moderate intensity (30-65 % of VO2peak), whereas the relative contribution of carbohydrate oxidation to total energy expenditure becomes greater when exercise intensity increases, with muscle glycogen becoming the most important substrate source

…glycogen availability is essential to power ATP resynthesis during high intensity exercise which relies heavily on glycogenolysis.

Furthermore, it has been well documented that the capability of skeletal muscle to exercise is impaired when the glycogen store is reduced to a certain level, even when there is sufficient amount of other fuels available.

To date, few studies have found an improved training-induced performance effect of conducting the exercise bouts with low glycogen levels compared with replenished glycogen levels

On the subject of resistance training:

… a typical resistance exercise session has been shown to reduce glycogen levels by approximately ~24-40 %. This reduction in glycogen content during exercise is determined by the duration, intensity and volume of the performed exercise bout. The largest reductions in glycogen are seen with high repetitions with moderate load training, an effect that mainly occurs in type II fibers.

Remember glycogen is the storage form of glucose.

Yet Another Low Carb Performance Study

Here’s another study which looked a performance on a Low Carb diet (Sawyer, JC, Wood, RJ, Davidson, PW, Collins, SM, Matthews, TD, Gregory, SM, and Paolone, VJ. Effects of a short-term carbohydrate-restricted diet on strength and power performance. J Strength Cond Res 27(8): 2255–2262, 2013).

For this study 16 men and 15 women were tested after a week on their habitual diet (40.7% carbohydrate, 22.2% protein, and 34.4% fat) and then a week later on a Carbohydrate Restricted Diet (CRD – 5.4% carbohydrate, 35.1% protein, and 53.6% fat). The CRD consisted of ≤50 g of carbohydrates per day.

The study was intended to determine if strength is lost with the short diet timeframe. The results were:

Subjects consumed significantly fewer (p < 0.05) total kilocalories during the CRD (2,156.55 ± 126.7) compared with the habitual diet (2,537.43 ± 99.5).

That can be seen here:

That’s less than 400 calories a day or 2800 calories for the seven days. This may be due to the following:

During the CRD, the researcher contacted each subject every 48 hours to answer any questions about the diet. Body weight was measured every 48 hours during the CRD to determine if any body mass changes had occurred. If a reduction in body weight occurred during the CRD, subjects were instructed to consume more calories to maintain body weight.

Continuing with the results.

Body mass decreased significantly (p < 0.05).

Fortunately this study showed the Total body water. This indicates that most of the FFM loss was due to water loss and seemed to be the only significant effect.

Both males and females had improved body fat composition.

Despite a reduction in body mass, strength and power outputs were maintained for men and women during the CRD.

One big advantage of this study was the goal of keeping calories enough to not have losses. That’s relevant to people on keto consuming maintenance calories.

A major weakness was the short duration of the study. We can’t say that seven days isn’t enough time for adaptation in some studies and that it is enough time in other studies, can we?

Another weakness was the lack of a control group. It would have been helpful to have part of the group stay on the habitual diet during the second period.

A third weakness was the same before and after the keto adaptation phase:

Before each testing session, subjects were required to refrain from performing resistance exercise for 48 hours.

A forth weakness was that:

Participants arrived at the Human Performance Laboratory after a 12-hour fast between the hours of 6:00 and 8:00 AM.

They were then fed a fat/protein meal.

The pre-exercise meal was provided to each subject 2 hours before the start of each exercise testing session. The meal consisted of 400 kcal. The meal included 250 ml of water, 2 hard-boiled eggs, 28 g of cheddar cheese, and a protein shake (Advant Edge Whey Protein; EAS, Inc., Abbott Park, IL, USA).

It seems likely that this meal would be more useful to the athletes after keto adaptation than before. Again a control group would have teased out this difference.


Most of the tests were very short duration – One Rep Maximums and short erg bicycles. Only one was to exhaustion and there was a lot of rest between sets (3 minutes). The Keiser power output was lower with the keto diet but judged to not be significant. That is a surprise to me since the change was greater than the error bars.

I would expect the keto athletes to do reasonably well with the short duration of the tests. Without a control group it is difficult to determine if the group should have gotten stronger or not.


MAF and Resistance Training

I’ve spent a little bit of time thinking about the compatibility of MAF Heart Rate Training and weightlifting – generically termed resistance training (RT). Since the activity is relatively short duration and the heart rate isn’t past the MAF Heart Rate it seems on the surface like it would be compatible to do both.

One thing to consider is that VO2max testing is done on a treadmill which increases the speed and angle every couple of minutes. Resistance training lasts for seconds. The Rate of Perceived Exertion (RPE) of the VO2max testing isn’t all that hard until it gets towards the end of the test. The RPE of weightlifting is substantial under significant loads so using RPE as a test this would indicate that there is an issue.

My measurement for whether an activity is aerobic or anaerobic is the Respiratory Exchange Ratio (RER). RER is correlated to heart rate in the VO2max test but rarely considered in RT. There is a study which looked at RER in RT (Scott. Quantifying the Immediate Recovery Energy Expenditure of Resistance Training. The Journal of Strength and Conditioning Research · April 2011) in terms of Excess Postexercise Oxygen Consumption (EPOC). To review:

The respiratory exchange ratio (RER) is calculated as steady-state CO2 produced divided by steady-state O2 consumed and is typically defined from values of 0.70 representing total fat oxidation to 1.00 representing total glucose oxidation.

Here’s the RER data from the study for RT. Note the RER values are all well over 1.0 which indicates anaerobic exercise range.

Another interesting comment helps explain the RER values above 1.0:

During and after exercise, RER values above 1.00 are generally thought to be the result of nonrespiratory CO2 production: The bicarbonate buffering system, for example, involves the removal of hydrogen ions with concomitant CO2 production and hyperventilation blows off ‘‘extra’’ CO2. Yet a true measure of the RER is best found only when the system is in a steady state of gas exchange.

To the subject at hand:

Rapid glycolysis (as part of anaerobic metabolism) ceases when muscle contraction stops so that recovery is considered to be aerobic in nature. If this is true, both fatty acid and lactate oxidation may play a significant role in fueling the immediate energy expenditure needs of recovery. Unfortunately, substrate oxidation immediately postexercise and particularly after anaerobic-type exercise has not been studied well enough to draw specific conclusions. Because of this, it must be assumed here that when muscle contraction immediately stops, glycolysis is limited to the point where fat and lactate are the predominantly oxidized fuels.


Keto Diet and Performance

tl;dr – Don’t expect to do keto, be in a large deficit,
and expect to see performance gains on glycolytic activites.

A good video on lifting and the keto diet. Covers other aspects of performance from the perspective of a real clinician and what he sees in his patient population who does keto. Very truthful even if not totally pro keto at moments (overall it is very supportive of keto so no need to be afraid of watching).


Ultra-Endurance Walking and Running Events

A study looked at the studies on fueling ultra-endurance events. Ultra-endurance is defined as activities (walking and running) which take at least 6 hours. The study was (Eric Williams. Nutritional implications for ultra-endurance walking and running events. Extreme Physiol Med. 2016; 5: 13).

Given that the majority of an ultra-endurance athlete’s training is spent engaged in lengthy durations of aerobic activity, many of these athletes are well adapted to utilizing lipids via oxidative phosphorylation

Fat burners! But during the event itself how hard are they hitting it?

When the athlete is exercising at the standard marathon pace that requires 80–90% of maximal oxygen consumption (VO2 max) or above, carbohydrate will be his or her primary fuel source and could provide up to 96% of the energy being expended.

This is an issue with Low Carbohydrate diets since glycogen stores are reduced greatly. This is also why Phinney’s endurance tests are done at 62% of VO2max.

The paper had a nice graphic which shows the elements involved in performance in marathons.

Each of these would be interesting to look at in detail.


Turmeric and Curcumin for Osteoarthritis and Joint Pain

Here’s a meta-analysis of the use of Turmeric and Curcumin for Osteoarthritis and Joint Pain (Daily James W. , Yang Mini , and Park Sunmin. Efficacy of Turmeric Extracts and Curcumin for Alleviating the Symptoms of Joint Arthritis: A Systematic Review and Meta-Analysis of Randomized Clinical Trials. Journal of Medicinal FoodVol. 19, No. 8.). The study

systemically evaluated all RCTs of turmeric extracts and curcumin for treating arthritis symptoms to elucidate the efficacy of curcuma for alleviating the symptoms of arthritis.

The conclusions were

…meta-analysis of four studies showed a decrease of WOMAC with turmeric/curcumin treatment (mean difference: −15.36 [−26.9, −3.77]; P = .009). Furthermore, there was no significant mean difference in PVAS between turmeric/curcumin and pain medicine in meta-analysis of five studies.

…these RCTs provide scientific evidence that supports the efficacy of turmeric extract (about 1000 mg/day of curcumin) in the treatment of arthritis. However, the total number of RCTs included in the analysis, the total sample size, and the methodological quality of the primary studies were not sufficient to draw definitive conclusions. Thus, more rigorous and larger studies are needed to confirm the therapeutic efficacy of turmeric for arthritis.

I haven’t found any other solution to my shoulder pain and I refuse to use NSAIDs or pain medications so I am trying Turmeric Curcumin.