How Accurate Are Activity Trackers? EE Data From Omron, Fitbit, Jawbone & Other Devices Reveals 10% Error & More

How Accurate Are Activity Trackers? EE Data From Omron, Fitbit, Jawbone & Other Devices Reveals 10% Error & More

activity activity tracker energy expenditure fitbit fitness health jawbone lose weight omron

Even though the study doesn't provide a straight-forward answer to the question "Which is the best activity tracker?", it is still revealing.

I hope you don't rely on the data from your activity tracker as a basis to decide how much you can, should or may eat on a daily basis. Why? Well, the first and most important result of a recent study from the Human Performance Laboratory at the Ball State University is that "consumer-based PA [physical activity] monitors should be used cautiously for estimating EE [energy expenditure]" (Nelson. 2016) - and this goes for the data from all the devices that were tested by Nelson et al.: The BodyMedia FIT and the NikeFuel armband, the DirectLife monitor, the Omron HJ-720IT, the Fitbit One, the Fitbit Zip, the Fitbit Flex, the Jawbone UP24, the Basis B1 Band Monitor and the ActiGraph.

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In view of the fact that tracking your energy expenditure is only one of the functions activity trackers are supposed to fulfill and considering the fact that you probably use them only to see if you have gotten more or less active (I do at least hope that you don't use them to guide your appetite ;-), it is still worth to take a look at the detailed results of this recent study.

As you will have guessed, the study was designed to "examine the validity of EE estimates from a variety of consumer-based, physical activity monitors under free-living conditions" (Nelson. 2016). To this ends, sixty (26.4 ± 5.7 yr) healthy men (n = 30) and women (n = 30) wore eight different types of activity monitors simultaneously while completing a 69-min protocol.

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"The monitors included the BodyMedia FIT armband worn on the left arm, the DirectLife monitor around the neck, the Fitbit One, the Fitbit Zip, and the ActiGraph worn on the belt, as well as the Jawbone Up and Basis B1 Band monitor on the wrist.

The validity of the EE estimates from each monitor was evaluated relative to criterion values concurrently obtained from a portable metabolic system (i.e., Oxycon Mobile) [which is obviously in itself not 100% exact]. Differences from criterion measures were expressed as a mean absolute percent error and were evaluated using 95% equivalence testing" (Nelson. 2016).

A brief glance at Figure 2 reveals that the accuracy was surprisingly similar among the devices. To be more precise, the mean absolute percent error values (computed as the average absolute value of the group-level errors) were 9.3%, 10.1%, 10.4%, 12.2%, 12.6%, 12.8%, 13.0%, and 23.5% for the BodyMedia FIT, Fitbit Zip, Fitbit One, Jawbone Up, ActiGraph, DirectLife, NikeFuel Band, and Basis B1 Band, respectively (unfortunately, not all data appears to be fully reported in the manuscript version of the study I had access to, so don't ask me about missing data, please ;-).

What did the test protocol look like? Subjects took part in a structured activity protocol consisting of 11 activities (three sedentary, four household, and four ambulatory/exercise) chosen by researchers from a list of 21 activities ranging from lying around on the couch to treadmill jogging. Activities were counterbalanced so that sex and age categories had approximately equal participation in the activities. All subjects began by lying quietly on a bed for 10 min. All other activities were performed for 5 min each, in order of generally increasing intensity. All activities were performed at a self-selected intensity by the subject. Subjects chosen to perform the jogging activity had the option of participating in a brisk walk if unable to jog for 5 min.

As the scientists point out, of all tested devices, only "[t]he results from the equivalence testing showed that the estimates from the BodyMedia FIT, Fitbit Zip, and NikeFuel Band (90% confidence interval = 341.1-359.4) were within the 10% equivalence zone around the indirect calorimetry estimate. If you still insist on trying to match your energy intake "exactly" to your energy expenditure, you should plan for a 10% + X% difference from your actual energetic demands - after all, even the indirect calorimetry that was used as a yardstick to judge the accuracy of the devices is not 100% accurate.

Figure 1: Mean absolute percent error when estimating energy expenditure for selected devices (Nelson. 2016).

In that, it is also worth mentioning that the accuracy of the devices was activity and device dependent. The Fitbit One, for example, produces the least error for stair climbing. For the Jawbone UP24, however, the "activity" for which it predicts your energy expenditure best is sitting around.

Accordingly, you could argue that you'd have to wear a certain device for a certain activity, e.g. (a) the Fitbit One, when sitting around (13%), working in the household (27%), taking the stairs (11%), jogging (22%) or cycling (43%) [note: on absolute terms, the error of the Fitbit for being sedentary is still lower than with the device from Jawbone], and (b) the Jawbone UP24, when you're simply walking around... but let's be honest: Since even that wouldn't be 100% accurate, it would be dumb to buy multiple fitness / activity trackers, wouldn't it?

Figure 2: With the exception of data from cycling and housework, the step count data (this graph) is sign. more accurate than the EE data in Figure 1 | If you want to learn more about what activity trackers are good / not good for and what you can / should make of the results of the study at hand, listen to me discuss this study on Monday's installment Super HumanRadio | click here to download the complete podcast that also includes discussions of the links NSAIDs and satellite cells and BPC-157 for muscle and tendon repair!

With an error of 10% you will always lose or gain weight involuntarily: The idea that a tiny technical device on your arm or belt could exactly tell you how much energy you need is in itself hilarious. And that's not just because the study at hand shows that even the best devices are on average +/-10% off (remember: that's +/-10% off another rough estimate that's never 100% exact). If you were dumb enough to match your diet blindly to the data your activity tracker provides, you would thus never achieve reliable results.

With that being said, our body is no biological machine that works according to a set of several (complex) equations. Therefore, the whole idea of a "quantified self" - as awesome as it may seem for the average control freak - must be seen as a tool to hold yourself accountable; a qualitative or semi-quantitative tool in the sense of "oh, I have been roughly 20% less active this week than last week, maybe I should..."

If the previously described rationale is behind the way you use the data from your activity tracker, congratulations! If not, I have to warn you: The margin between "quantifying yourself" and suffering from obsessive-compulsive disorder (OCD) and/or using the devices to fuel your exercise addiction is narrower than you may think | Do you agree, disagree? Let's discuss. Leave a comment on Facebook!

References

• Nelson, Benjamin N; et al. "Validity of Consumer-Based Physical Activity Monitors for Specific Activity Types ED." Med Sci Sports Exerc (2016): Ahead of print.

BPC-157, the Orally Available Peptide That Repairs Tendon, Muscle, Intestines, Teeth, Bone and More in Vitro & Vivo

BPC-157, the Orally Available Peptide That Repairs Tendon, Muscle, Intestines, Teeth, Bone and More in Vitro & Vivo

bone BPC 157 BPC-157 health IBS injury intestines muscle muscle damage muscle injury muscle repair peptides

BPC is not patentable, and thus not interesting for BigPharma.

In a way this article is a response to a question I got from Ryan on the Faebook Page of the SuppVersity a week ago. He asked, whether I had an article on Pentadecapeptide BPC-157, a substance of which he'd heard that it can accelerate tendon and muscle repair and work all sorts of other healing magic. Now, as a regular at the SuppVersity you may know that I didn't have an article on this agent a week age. So I decided to write one. Not just because Ryan asked, but also because of the practical significance of the healing effects of this peptide from in vitro and in vivo studies (no medical advice here!).

Unlike antioxidants with their anti-hormetic effects, BPC-157 actually promotes healing

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Studies as they were published by Brcic, et al. in the J Physiol Pharmacol  in 2009. A study in cell cultures and living rodents whose crushed muscles and transected muscle and tendons didn't heal magically, but a comparison of the animals who received  BPC 157 at a dosage of 10 µg (human equivalent 5.4 µg/kg) dissolved in saline to those who were treated with an equivalent volume of saline alone (5 ml/kg) showed a sign. accelerated response of the measured cell antigens, FVIII (involved in platelet adhesion and aggregation, present on endothelial cells of mature blood vessels) and CD34 (involved in leukocyte adhesion and endothelial cell migration during angiogenesis, present on capillary endothelial cells), as well as VEGF (Figure 1):

Figure 1: All markers of inflammation and muscle repair were sign. elevated with oral BPC-157(solid live) vs. control treatment with saline (dashed line) treatment in a model of  muscle injury (Brcic. 2009).

These observations clearly suggest an accelerated (or phase-shifted) angiogenic repair process in the crushed tissue of the lab animals. One that stands in line with other scientists like Krivic et al. (2006) had found previously that they promote...

• promote tendon & ligament healing by tendon outgrowth, cell survival, and cell migration as it was observed in a rodent model of Achilles tendon rupture (Chang. 2011), and when administered in the drinking water to rats with experimentally damaged medial collateral ligaments (Cerovecki. 2010)
• direct tendon-to-bone healing so effectivel that they may actually "successfully exchange the present reconstructive surgical methods" (Krivic. 2006), 
• counter the damaging effects of NSAIDs on the gut lining so effectively that scientists call BPC 157 "a NSAIDs antidote" one of which they say that "no other single agent has portrayed a similar array of effects" (Sikiric. 2013), 
• repair the damage that's done by inflammatory bowel disease within days of oral administration in µg or ng doses in a rodent model of IBS (Vuksic. 2007), 
• help cure perdidontitis when it is chronically administered in a rodent model of periodontitis potently enough to have scientists conclude that "BPC 157 may represent a new peptide candidate in the treatment of periodontal disease" (Keremi. 2009), 
• reverse systemic corticosteroid-impaired muscle healing, in a rodent model where it was administered with a front-load of 10µg orally once daily for 14 days to rats w/ crushed gastrocnemius muscle (Pevec. 2010 | similar benefits in a rodent study by Novinscak et al. that was published in Surgery Today in 2008), and
• bone healing in rabbits who suffered an experimental segmental bone defect before being treated with BPC-157 (Šebečić. 1999).

Cool? Well, I guess your next question is: "What's the necessary dosage?" If we use the existing rodent data as a yardstick, the answer to this question is ca. 5µg/kg body weight (Novinscak. 2008; Cerovecki. 2010). That's ~400µg per day for an 80kg man and thus roughly what you will see people on the Internet say they use.

Want to listen to me explain the study? Plus: Update! Download yesterday's installment of the SuppVersity Science-Round-Up at SuperHumanRadio.com | click here to download! On another note, after this article was originally published I received word from someone who claims to know the researchers who did the original studies and cautions against putting to much faith into their results... that is yet not the main argument for me; rather than that I am only skeptically optimistic, because no human studies have confirmed the efficacy of the compound.

Without a human study that would conform that you need that much / that much little is sufficient, it is yet impossible to provide a science-backed recommended dosage for optimal effects at minimal side effects (chronic consumption not suggested, yet | learn why).

Figure 2: Pevec et al. didn't just observe that BPC-157 blocked the ill effects of corticosteroids on muscle healing, they also found that BPC-157 alone super-charged the healing process (Pevec. 2010).

Ah, and before you ask: Yes, the peptide can be administered without a peptidase inhibitor or other agent to increase absorption and reduce breakdown, because it is a gastric juice peptide (Sikirić. 1993), or rather a part of it, namely a 15 amino acid fragment "with apparently no sequence homology with known gut peptides" the effects of which appear to be mediated "at least by the hormones of the adrenal, parathyroid, thyroid and ovarian glands" (Sikiric. 1994).

BPC-157 should stack well with GH as it potentiates its effects on tendon repair (Chang. 2014).

So why didn't my doctor prescribe this? As gastric juice peptides, BPCs - including BPC-157 - are not patentable. Therefore, they are not interesting, and thus not produced or marketed by pharma companies (so your doctor probably doesn't even know about their existence) and thus not available as FDA regulated drugs.

The lack of money one can make from this agent is probably also the reason there's still relatively little research on this compound; and I fear that this is not going to change very soon... it is thus probably more a question of money than one of time when and if we will see the human studies we need to decide if its effective+safe in man | Comment!

References:

• Brcic, L., et al. "Modulatory effect of gastric pentadecapeptide BPC 157 on angiogenesis in muscle and tendon healing." J Physiol Pharmacol 60.Suppl 7 (2009): 191-196.
• Cerovecki, Tomislav, et al. "Pentadecapeptide BPC 157 (PL 14736) improves ligament healing in the rat." Journal of orthopaedic research 28.9 (2010): 1155-1161.
• Chang, Chung-Hsun, et al. "The promoting effect of pentadecapeptide BPC 157 on tendon healing involves tendon outgrowth, cell survival, and cell migration." Journal of Applied Physiology 110.3 (2011): 774-780.
• Chang, Chung-Hsun, et al. "Pentadecapeptide BPC 157 enhances the growth hormone receptor expression in tendon fibroblasts." Molecules 19.11 (2014): 19066-19077.
• Keremi, B., et al. "Antiinflammatory effect of BPC 157 on experimental periodontitis in rats." Journal of physiology and pharmacology 60.7 (2009): 115-122.
• Krivic, Andrija, et al. "Achilles Detachment in Rat and Stable Gastric Pentadecapeptide BPC 157: Promoted Tendon‐to‐Bone Healing and Opposed Corticosteroid Aggravation." Journal of orthopaedic research 24.5 (2006): 982-989.
• Novinscak, Tomislav, et al. "Gastric pentadecapeptide BPC 157 as an effective therapy for muscle crush injury in the rat." Surgery today 38.8 (2008): 716-725.
• Pevec, Danira, et al. "Impact of pentadecapeptide BPC 157 on muscle healing impaired by systemic corticosteroid application." Medical Science Monitor 16.3 (2010): BR81-BR88.
• Šebečić, Božidar, et al. "Osteogenic effect of a gastric pentadecapeptide, BPC-157, on the healing of segmental bone defect in rabbits: a comparison with bone marrow and autologous cortical bone implantation." Bone 24.3 (1999): 195-202.
• Sikirić, Predrag, et al. "A new gastric juice peptide, BPC. An overview of the stomach-stress-organoprotection hypothesis and beneficial effects of BPC." Journal of Physiology-Paris 87.5 (1993): 313-327.
• Sikiric, Predrag, et al. "The beneficial effect of BPC 157, a 15 amino acid peptide BPC fragment, on gastric and duodenal lesions induced by restraint stress, cysteamine and 96% ethanol in rats. A comparative study with H 2 receptor antagonists, dopamine promotors and gut peptides." Life sciences 54.5 (1994): PL63-PL68.
• Sikiric, Predrag, et al. "Toxicity by NSAIDs. Counteraction by stable gastric pentadecapeptide BPC 157." Current pharmaceutical design 19.1 (2013): 76-83.
• Vuksic, Tihomir, et al. "Stable gastric pentadecapeptide BPC 157 in trials for inflammatory bowel disease (PL-10, PLD-116, PL14736, Pliva, Croatia) heals ileoileal anastomosis in the rat." Surgery today 37.9 (2007): 768-777.

Caffeine & Bicarbonate - Individuality is Key: Using Supps That Work for You Make a >90% Performance Difference

Caffeine & Bicarbonate - Individuality is Key: Using Supps That Work for You Make a >90% Performance Difference

bicarbonate caffeine cycling endurance ergogenic ergogenics NAHCO3 natural ergogenic performance sodium bicarbonate time to exhaustion

Right vs. wrong supps can make a victory or defeat difference of >90%.

I've written about the individual response to caffeine and bicarbonate before. To tackle both of these ergogenic supplements I can actually recommend, however, based on a single study that as just been published in the Applied Physiology, Nutrition, and Metabolism is news. The study was conducted at the Derby University's Department of Life Sciences, Sport, Outdoor & Exercise Science (Higgins. 2016) and evaluated the effects of ingesting sodium bicarbonate (NaHCO3) or caffeine individually or in combination on high-intensity cycling capacity.

In a counterbalanced, crossover design, 13 healthy, noncycling trained males (age: 21 ± 3 years, height: 178 ± 6 cm, body mass: 76 ± 12 kg, peak power output (Wpeak): 230 ± 34 W, peak oxygen uptake: 46 ± 8 mL·kg−1·min−1) performed a graded incremental exercise test, 2 familiarisation trials, and 4 experimental trials.

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Trials consisted of cycling to volitional exhaustion at 100% W peak (TLIM) 60 min after ingesting a solution containing either

• 0.3 g·kg−1 body mass sodium bicarbonate (BIC), 
• 5 mg·kg−1 body mass caffeine plus 0.1 g/kg body mass sodium chloride (CAF), 
• 0.3 g·kg−1 body mass sodium bicarbonate plus 5 mg/kg body mass caffeine (BIC-CAF), or 
• 0.1 g·kg−1 body mass sodium chloride (PLA). 

Experimental solutions were (supposedly) administered double-blind (which is difficult imho, because bicarb and salt taste different, but alas).

Figure 1: Tabular overview of the rate of perceived exertion (RPE_L = legs, RPE_O = overall cardiovascular strain | left) and blood pH over time (right) during the four trials (Higgins. 2016).

The first and most obvious effect of treatments (BIC) and (BIC-CAF) was a significant increase in pH, base excess, and bicarbonate ion concentration ([HCO3−]) compared to the CAF and PLA trials.

Another new study supports lower dose (0.3g/kg) bicarbonate for resistance training: The study was conducted by a Bachelor student from the University of Tempa. The purpose of the study was to investigate whether the ingestion of sodium bicarbonate (SB) pre-exercise improved athletic performance during resistance training (RT) and reduced fatigue in male college students. In the study, ,ale college students performed 1RM and endurance tests before their own individualized RT program 4 times a week during the 4 week study. The SB group produced higher increases in mean weight used in each of the 1RM tests (P < 0.05) compared to the placebo group. The SB group also produced a higher amount of repetitions in the IDP, LP, and LPD endurance tests (P < 0.05). There was a significant difference in each self-report scale (P < 0.05) between the SB group and the placebo group. "These findings suggest that the supplementation of SB prior to RT in college male students could enhance performance," (Indorato. 2016) the author concludes.

The effect on TLIM (time to volitional exhaustion) was unfortunately less obvious - for all three active treatments, by the way. When all subjects were considered, ...

• 

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  there was a significant increase in TLIM for CAF (399; 350–415 s; P = 0.039; r = 0.6) and BIC-CAF (367; 333–402 s; P = 0.028; r = 0.6), but only compared with BIC (313: 284–448 s), yet not compared with PLA (358; 290–433 s; P = 0.249, r = 0.3 and P = 0.099 and r = 0.5, respectively), 
• there were no differences between PLA and BIC (P = 0.196; r = 0.4) or between CAF and BIC-CAF (P = 0.753; r = 0.1), and 
• there was no effect whatsoever on the rate of perceived exertion (RPE | Figure 1, left).

The "average" effect does yet not tell you the full truth about the potential ergogenic effects of caffeine and bicarbonate. Why? Higgins et al. found very large inter- and intra-individual variations, when they compared the individual treatments (see Figure 2, right).

Figure 2: Mean +/- SD (left) and individual (right) response to the treatments (Higgins. 2016).

Accordingly, the scientists rightly highlight that optimal supplementation strategies require individualization. Using supplements that work for you can, after all, make a performance difference of 81%, 92% and 63% (max. vs. min responders) for bicarbonate, caffeine and the combination of both (all values relative to T_LIM in the placebo trial).

Caffeine has many benefits, but also potential downsides you should know about to make an educated decision based on science and your individual response to caffeine | learn more

Fine. So shall I use bicarbonate and caffeine or not? I cannot tell you that. Why? Well, it depends on how you react to these proven ergogenics. The only way to find out is to testdrive both - on their own and together. Plus: A study investigating the maximal cycling time at 100% of your peak wattage doesn't tell you sh*t about the effects on your performance during other physical activities like resistance training (the study in the red box, does, though).

Luckily, the new study by Indorato is not the only one to show bicarbonate (example) has, just like caffeine, by the way (example), ergogenic effects . This doesn't mean that either of them will necessarily work for you, but it is a good reason to trial both | Leave a comment on Facebook!

References:

• Higgins, et al. "Evaluating the effects of caffeine and sodium bicarbonate, ingested individually or in combination, and a taste-matched placebo on high-intensity cycling capacity in healthy males." Appl. Physiol. Nutr. Metab. (2016).
• Indorato, Daniel. "Enhanced Resistance Training Performance via the Neutralization of Lactic Acid with Sodium Bicarbonate." Student Pulse 8.03 (2016).

Cure! Diabetes With 8 + 24 Week Diet Intervention: 40% Stay Normo-Glycemic After Switching from VLCD to Normal Diet

Cure! Diabetes With 8 + 24 Week Diet Intervention: 40% Stay Normo-Glycemic After Switching from VLCD to Normal Diet

diabesity diabetes diabetes cure health lose fat obesity T2DM very-low-calorie-diet VLCD

If gaining body fat triggers T2DM, is is not surprising that losing it, cures it.

From the SuppVersity Facebook News you will remember that studies have shown that type II diabetes can be send into remission with "nothing" but a very low energy diet (Steven. 2015). The question scientists still had to answer, though, was whether the astonishing improvements in glycemia and overall health could be maintained on an energy-sufficient diet. In a newstudy from the Newcastle University scientists did now try to confirm just that by combining an 8-week dieting phase with a stepped return to isocaloric diet based on a structured, individualized (isocaloric) program of weight maintenance.

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Glucose control, insulin sensitivity, insulin secretion, and hepatic and pancreas fat content were quantified at baseline, after return to isocaloric diet, and after 6 months to permit the primary comparison of change between post–weight loss and 6 months in responders.

Table 1: Fasting anthropometric and metabolic data in responders and nonresponders at baseline, after VLCD and return to isocaloric eating, and after the 6-month weight maintenance period (Steven. 2016).

To qualify as "responder" and thus patient who successfully reversed his diabetes, the subjects, thirty individuals with T2DM who had been suffering from T2DM for either either short- (<4 years) or long (<8 years)-duration, had to achieve a fasting blood glucose <7 mmol/L - and that not just after the initial 6 weeks, but after return to isocaloric diet.

Figure 1: The weight loss speaks in favor of the efficacy of the diet intervention in both groups; filled responders, open circles non-responders (Steven. 2016).

What did the diet look like? The VLCD consisted of a liquid diet formula (43% carbohydrate, 34% protein, and 19.5% fat; 2.6 MJ/day [624 kcal/day]; OPTIFAST; Nestle Nutrition, Croydon, U.K.) taken as three shakes per day. In addition, up to 240 g of nonstarchy vegetables was consumed, making total energy intake 624–700 kcal/day. Participants were encouraged to drink at least 2 L of calorie-free beverages per day and to maintain their habitual level of physical activity. To maximize adherence, one-to-one support was provided weekly by telephone, e-mail, text message, or face-to-face contact (S.S.).

During stepped food reintroduction, shakes were gradually replaced by solid food over 7 days; with one meal replacing a shake every 3 days. Isocaloric intake was determined from resting energy expenditure measured by indirect calorimetry using an open circuit calorimeter (Quark RMR; COSMED, Rome, Italy) and a canopy hood and ended up ~1/3 below their previous obesogenic food intake - no wonder that they got diabetic before at an energy intake that was ~30% above what they'd needed to stay in a healthy body fat range. Physical activity was encouraged, but food behaviors were the priority.

As the average weight loss in Figure 1 tells you, all but one subject that was excluded after the initial 8-week VLCD phase, achieved a highly significant weight loss. What not all subjects achieved, however, was the desired diabetes remission. To be more precise, only 40% of the participants (12 of 30) achieved the targeted fasting glucose <7.0 mmol/L levels (responders) after return to isocaloric eating (to put that in perspective | even RYGB weight loss surgery achieves only 9% remission rates; albeit measured over 14 vs. 4 months | Wood. 2015). Since that's in spite of similar weight loss, the question is: What is it that made the difference between responders and non-responders? The answer is complex and consists of many factors:

• The responders (n = 12 [8 males, 4 females]) had a shorter diabetes duration (3.8 +/- 1.0 vs. 9.8 +/- 1.6 years, P = 0.007) 
• The responders were also younger (52.0 +/- 2.9 vs. 59.9 +/- 2.1 years, P = 0.032) than nonresponders (n = 17 [7 males, 10 females]). 
• Responders were more likely to suffer from diabetes for a short(er) duration (9 of 15 of the short-duration and 3 of 14 of the long-duration groups).
• At baseline, responders had lower fasting glucose(8.9 +/- 0.7 vs. 13.2 6 0.6 mmol/L, P < 0.001) and HbA1c (7.1 +/- 0.3 vs. 8.4 6 0.3% [55 +/- 4 vs. 68 +/- 3 mmol/mol], P = 0.01). 

In addition, the responders had a lower total fat mass than the nonresponders at baseline (P = 0.04) (see Table 1) and didn't try as many (failed) treatment options, such as diet control (five vs. two); metformin only (six vs. four); metformin and sulfo nylurea (one vs. seven); metformin, sulfonylurea, and insulin (zero vs. two); metformin, sulfonylurea, and thiazolidi nedione (zero vs. one); and insulin only (zero vs. one), as the nonresponders did before participating in the study at hand.

Diabetes can be cured by dieting down below your personal fat threshold! A previous study led by Professor Roy Taylor from 2011, who commented on the study at hand in press release stating that "[t]he study also answered the question that people often ask me - if I lose the weight and keep the weight off, will I stay free of diabetes?" and answering his own question as follows: "The simple answer is yes!" In the same press release from the Newcastle University, Taylor highlights that the results of the study at hand "supports our theory of a Personal Fat Threshold. If a person gains more weight than they personally can tolerate, then diabetes is triggered, but if they then lose that amount of weight then they go back to normal" and adds "[t]he bottom line is that if a person really wants to get rid of their Type 2 diabetes, they can lose weight, keep it off and return to normal."

It is important to point out that the study at hand is part of a growing body of evidence showing that people with Type 2 diabetes who successfully lose weight can reverse their condition (Lim. 211; Steven. 2015)- probably because the fat loss correlates with a reduced fat deposition and increased function in / of the pancreas.

Figure 2: While there were no sign. differences in weight loss, there were other antropometric and related differences between the two groups: BMI, body fat %, triglycrides and the insulin resistance of the liver (Stevens. 2016).

And with a larger trial involving 280 free-living patients is already underway, it may only a question of time before people can no longer ignore that type II diabetes, which is triggered by bad lifestyle choices, can be reversed by healthy ones. This can be "tough" as Allan Tutty, 57, from Sunderland, who transformed his health by taking part in the study and is now

"eat[ing] normal foods though [...] less than [he] used to, and enjoy[ing] takeaways and chocolate but not on a regular basis so [he has] maintained my lower weight [and] changed [his life]completely thanks to this research" (Tutty in press release),

says; and still, I am pretty sure that, just like Tutty who says that, "with [his] diabetes in remission, I haven't looked back", those who are able and willing to follow Tutty's example won't look back either.

The elevated liver enzymes observed in the study point, once again, to the liver - Learn how to help your liver manage your glucose metabolism in this SuppVersity Classic.

Dieting is a diabetes cure, but one that does not work for everyone - yet? While it is not clear whether a longer weight-loss phase that would have brought the non-responders to similarly low bodyfat percentages as the responders wouldn't have changed the results, we have to be honest:  losing weight is easy, but eating 30% less than before, because that's all you need w/ your now normal weight is difficult... too difficult for many, probably.

With that being said, it should be obvious that further research is necessary to determine the factors that distinguish responders from non-responders and whether the latter simply failed to pass their "personal fat threshold" as Professor Taylor's remarks suggest | Comment!

References:

• Lim, Ee Lin, et al. "Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol." Diabetologia 54.10 (2011): 2506-2514.
• Steven, S., and R. Taylor. "Restoring normoglycaemia by use of a very low calorie diet in long‐and short‐duration Type 2 diabetes." Diabetic Medicine 32.9 (2015): 1149-1155.
• Steven, et al. "Very-Low-Calorie Diet and 6 Months of Weight Stability in Type 2 Diabetes: Pathophysiologic Changes in Responders and Nonresponders." Diabetes Care (2016) Accepted Article.
• Wood, G. Craig, et al. "Preoperative use of incretins is associated with increased diabetes remission after RYGB surgery among patients taking insulin: A retrospective cohort analysis." Annals of surgery 261.1 (2015): 125-128.

HIIT vs. Steady-State for Fat Loss: Can EPOC Really Explain the Benefits of Intense Interval Training (HIIT, SIE, HIE)?

HIIT vs. Steady-State for Fat Loss: Can EPOC Really Explain the Benefits of Intense Interval Training (HIIT, SIE, HIE)?

EPOC fat loss fatty acid oxidation HIIT hit LISS; MCT MIT SIE steady state wingate workouts

HIIT has been touted to work its fat burning magic by increasing post-exercise oxygen consumption aka EPOC, a marker of the amount of fat you burn after your workouts. Eventually, however, only the total oxygen consumption and energy expenditure count and this is where the putative mechanism behind the fat loss effects of HIIT lacks scientific backup.

Higher excess postexercise oxygen consumption (EPOC) after high-intensity interval exercise (HIIT / HIE) and sprint interval exercise (SIE) has long been touted to explain the greater fat loss scientists observed in several studies which compared the fat loss effects effects classic "cardio" aka steady-state exercise (SSE) to interval training (HIIT / HIE).

To elucidate whether that's a reasonable and, more importantly, sufficient  (meaning: "Is the increased energy expenditure high enough to explain the fat loss, even if the steady state exercise consumes more energy and fat on total?") explanation for the previously mentioned advantages, researchers from the Healthy Lifestyles Research Center at the Arizona State University conducted a study to compare the EPOC response to the three most common forms of aerobic training: high intensity interval exercise (HIE), sprint interval exercise (SIE), and steady state exercise (SSE).

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Ten recreationally active males (age 24 ± 4 y) participated in this randomized crossover study. On separate days, subjects completed a resting control trial and three exercise conditions on a cycle ergometer:

• HIE (four 4-min intervals at 95% HRpeak, separated by three min of active recovery); and 
• SIE (six 30-s Wingate sprints, separated by four min of active recovery); and 
• SSE (30 min at 80% of peak heart rate (HRpeak)). 

Oxygen consumption (VO2) was measured continuously during and for 3 h after exercise to estimate the actual amount of excess energy / fat that was consumed in the three treatment conditions.

Figure 1: Oxygen consumption and respiratory exchange ratio (higher numbers = higher carbohydrate to fat oxidation ratio) during the first three hours after exercise (Tucker. 2016).

Unsurprisingly, VO2 was initially higher than resting control for all three treatments. The increased oxygen consumption, which is a marker of fatty acid oxidation, however, didn't last long: After only 1 h, it returned to pre-exercise levels.

There's room for "cardio": Even though it is not popular, these days, it would be wrong to assume that classic steady state training is always the inferior choice. For someone who's killing it in the gym regularly, the additional HIIT training may in fact be too much of a sympathetic stimulus. The "boring" classic "cardio" training, on the other hand, is predominantly parasympathetic, which is why walking on an incline treadmill may eventually be a better complement to your 4-5 resistance training sessions per week than HIIT cycling or sprinting.

It is thus not really surprising that both, the complete 3-h EPOC and the total net EE after exercise were not extremely different and that that 3-h EPOC and total net EE after exercise were higher (p=0.01) for SIE (22.0 ± 9.3 L; 110 ± 47 kcal) compared to SSE (12.8 ± 8.5 L; 64 ± 43 kcal).

Figure 2: The total O2 consumption (and thus fat oxidation) and energy expenditure during the workout and the 3h thereafter shows that steady state exercise burns more fat and energy than any of the two HIIT regimen (Tucker. 2016).

What goes against the idea of increased fat oxidation after workouts due to HIIT (i.e. SIE or HIE), however, is the scientists observation that the "total (exercise + postexercise) net O2 consumed and net EE were greater (p=0.03) for SSE (69.5 ± 18.4 L; 348 ± 92 kcal) than for SIE (54.2 ± 12.0 L; 271 ± 60 kcal)" (Tucker. 2016), while those for for HIE were not significantly different from SSE or SIE, so that Tucker et al. rightly conclude that "EPOC after SIE and HIE is unlikely to account for the greater fat loss per unit EE associated with SIE and HIE training reported in the literature" (Tucker. 2016).

Bottom line: As Tucker et al. rightly point out, simple math shows that the increased energy expenditure and O2 consumption during the steady state trial more than compensates the significant, but small increase in energy expenditure and fat oxidation after the workout.

Figure 3: Minute-by-minute energy expenditure during a sedentary day and a day beginning with a single bout of sprint interval training (SIT). Data are mean values (Sevits. 2016).

It is important to know that this does not negate the results of previous studies that found beneficial effects of HIIT on fat loss. What the study does do, however, is to refute the hypothesis that these benefits were a result of an increase in EPOC and thus overall larger total energy expenditure. This, on the other hand, doesn't mean that any effects after the EPOC window of 3h investigated in the study could be responsible for said benefits. As Tucker et al. highlight, "another previously confirmed benefit of intense exercise is that it can increase the resting energy expenditure (REE) [... 17-24 h after exercise ...] in part due to an increase in sympathetic tone " (Tucker. 2016).

In conjunction with increases in the ease of locomotion (16, 17) and increase nonexercise activity thermogenesis (NEAT) (14), these effects could well explain the benefits of HIIT. Studies to confirm that are yet not just lacking, as Tucker et al. highlight, the whole-room calorimeter study of Sevits et al. (32) even suggests that SIE does not elevate REE at 24 h postexercise (see Figure 3). More studies to get to the bottom of the fat loss benefits of HIIT protocols appear warranted | Comment.

References:

• Sevits, Kyle J., et al. "Total daily energy expenditure is increased following a single bout of sprint interval training." Physiological reports 1.5 (2013): e00131.
• Tucker, Wesley J., Siddhartha S. Angadi, and Glenn A. Gaesser. "Excess postexercise oxygen consumption after high-intensity and sprint interval exercise, and continuous steady-state exercise." The Journal of Strength & Conditioning Research (2016).