Jump to content

Recommended Posts

This new study [1] posted by Al (thanks Al!) sheds additional light on the issue of light vs. moderate-vigorous physical activity.


In it, researchers collected physical activity data using an accelerometer over 4 days from 5500 adults (average age 47) from the NHANEs survey, and then followed them for an average of about 7 years to see how deaths correlated with physical activity - particularly focused on Light Intensity Physical Activity (LIPA), since they say Medium-to-Vigorous Physical Activity (MVPA) has previously been shown to reduce mortality.


What they found was that every extra hour per day of LIPA that the subjects engaged in at baseline (the median was 5.66 h/day) was associated with a 16% reduced likelihood of dying during the follow-up period.  But couldn't the subjects have engaged in less LIPA because they were sick, and therefore more likely to die during follow-up? Possibly, but it would have to be due to latent illness, since the researchers controlled for "comorbid illness" - the summed number of morbidities for each participant, based on physician diagnosis of arthritis, coronary artery disease, congestive heart failure, heart attack, stroke, emphysema, chronic bronchitis, and hypertension. In other words, they made sure overt illnesses weren't skewing the data towards better survival for more active participates.


The most interesting thing was that they also controlled for MVPA. So extra time spend in light physical activity was beneficial for survival whether or not subjects also engaged in moderate-to-vigorous physical activity. Given that MVPA has previously been shown to reduce mortality, it seems reasonable to conclude from this study that the combination of moderate-to-vigorous exercise coupled with a relatively large amount of light physical activity will be better for survival than either alone - albeit with the usual caveat that these are people in the general population, not CR practitioners.





[1] Light-Intensity Physical Activity and All-Cause Mortality.
Loprinzi PD.
Am J Health Promot. 2016 Jan 5. [Epub ahead of print]
PMID: 26730555
Purpose . Research demonstrates that moderate-to-vigorous physical activity (MVPA) is associated with a reduced risk of all-cause mortality. Few studies have examined the effects of light-intensity physical activity on mortality. Therefore, the purpose of this study was to examine the association between objectively measured light-intensity physical activity and all-cause mortality risk. Design . Longitudinal. Setting . National Health and Nutrition Examination Survey 2003-2006 with follow-up through December 31, 2011. Subjects . Five thousand five hundred seventy-five U.S. adults. Measures . Participants wore an accelerometer for at least 4 days and completed questionnaires to assess sociodemographics and chronic disease information, with blood samples taken to assess biological markers. Follow-up mortality status was assessed via death certificate data from the National Death Index. Analysis . Cox proportional hazard model. Results . After adjusting for accelerometer-determined MVPA, age, gender, race-ethnicity, cotinine, weight status, poverty level, C-reactive protein, and comorbid illness, for every 60-minute increase in accelerometer-determined light-intensity physical activity, participants had a 16% reduced hazard of all-cause mortality (hazard ratio = .84; 95% confidence interval: .78-.91; p < .001). Conclusion . In this national sample of U.S. adults, light-intensity physical activity was inversely associated with all-cause mortality risk, independent of age, MVPA, and other potential confounders. In addition to MVPA, promotion of light-intensity physical activity is warranted.
Accelerometry, Chronic Disease, Epidemiology, Exercise, Mortality, National Health and Nutrition Examination Survey (NHANES), Prevention Research. Manuscript format: research; Health focus: physical activity; Outcome measure: mortality; Research purpose: modeling/relationship testing; Setting: national; Strategy: education, behavior change; Study design: longitudinal; Target population age: adults; Target population circumstances: education

Share this post

Link to post
Share on other sites



But the sound response could be one with a reversal of your parenthetical: "... to see a couple hundred more calories burned (via long leisurely exercise) improved insulin sensitivity". And that's no big surprise.


Hmm... The only way I can make sense of you not being surprised in the first paragraph (that long/leisurely exercise is better for insulin sensitivity than short/intense exercise) but still wondering about the relative benefits of long/leisurely vs. short/intense exercise for glucose control is the issue of the calorie expenditure. That is, you are unsurprised by the advantage of long/leisurely exercise if/when it also entails burning more calories.




The question for a CR practitioner would typically be, what is the independent effect of different forms of exercise on longevity and health (and, another part of the question: for someone on CR, but that's asking too much of research...). The studies you cite don't answer that question. For me, and many of us, the question is: if we keep our weight constant (yes, this is not the same as keeping energy-intake constant...), what form of exercise is best for longevity (or for particular diseases)?


We have very little to go on here, to find an answer to that question.



Share this post

Link to post
Share on other sites

^^^ yoga. You work your entire body. Nothing escapes. Then you stretch the worked muscles that you didn't know you had until now. Meanwhile, throughout your humbling practice you stay focused on your breath. Which you can't do. But you keep trying anyway. Then again tomorrow you try, and discover that your body feels completely different than it felt yesterday, or last week, or last month, last year, last decade. Then you meditate on all that. And more.

Share this post

Link to post
Share on other sites



This thread has been dormant for a while, so just a reminder - one of the main questions we've been asking here is what type of exercise is best for health & longevity - longer & lower intensity vs. shorter & higher intensity.


These two recent studies [1][2] may shed a modest amount of light on this question - although I stress the word 'modest'. The reason is that they were both done in rats (by two different teams of researchers), and only addressed one aspect of health - namely brain health via measuring adult hippocampal neurogenesis (AHN) - growing new neurons in the hippocampus (an important brain region involved in memory).


OK - I'm going to cut this one short, because I see what I think may be a fatal flaw (maybe two) in both these studies, beyond the rats vs. humans shortcoming. [i'm posting them anyway because I've come this far, and others might find it interesting.]


Basically study [1] found mild exercise resulting in more hippocampal neurogenesis than intense exercise, and study [2] found longer, slower treadmill running resulted in more neurogenesis than did either shorter, more intense treadmill running (HIIT equivalent), or the equivalent of rat resistance training - climbing a wall carrying a weight pouch.


While both these studies would seem to support my preference for longer, milder aerobic exercise, there are several flaws (besides being studies of rats and not humans) that probably prevent drawing any strong conclusions:

  • Both the long, slow treadmill running and the wall climbing resistance training were entirely voluntary. But to get the rats to engage in the high intensity treadmill workouts in both [1] and [2] required electric shocks to "motivate" them if they slipped off the back of the treadmill. The stress of these shocks would seem to call into question the results, since it could have negatively influenced neurogenesis.
  • The authors didn't report the calorie expenditure or weight of the rats in the various groups. So crypto-CR effects as a result of extra energy expenditure in the long, slow exercise group can't be ruled out. 

I think its fair to conclude from [2] that long, slow aerobic exercise is better than resistance training for hippocampal neurogenesis, at least in rats. And perhaps if you dread your HIIT work to the point of being psychologically stressed, it might not be so good for brain health either.


But beyond these modest conclusions, we're still pretty much flying blind on what type of exercise is best.





[1] PLoS One. 2015 Jun 10;10(6):e0128720. doi: 10.1371/journal.pone.0128720.

eCollection 2015.

Long-Term Mild, rather than Intense, Exercise Enhances Adult Hippocampal
Neurogenesis and Greatly Changes the Transcriptomic Profile of the Hippocampus.

Inoue K(1), Okamoto M(2), Shibato J(3), Lee MC(4), Matsui T(4), Rakwal R(5), Soya

Author information:
(1)Laboratory of Exercise Biochemistry & Neuroendocrinology, Faculty of Health
and Sport Sciences, University of Tsukuba, Tsukuba, Ibaraki, 305-8574, Japan;
School of Rehabilitation Science, Health Sciences University of Hokkaido,
Kanazawa, Ishikari-Tobetsu, Hokkaido, 061-0293, Japan.


Free full text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4464753/

Our six-week treadmill running training (forced exercise) model has revealed that
mild exercise (ME) with an intensity below the lactate threshold (LT) is
sufficient to enhance spatial memory, while intense exercise (IE) above the LT
negates such benefits. To help understand the unrevealed neuronal and
signaling/molecular mechanisms of the intensity-dependent cognitive change, in
this rat model, we here investigated plasma corticosterone concentration as a
marker of stress, adult hippocampal neurogenesis (AHN) as a potential contributor
to this ME-induced spatial memory, and comprehensively delineated the hippocampal
transcriptomic profile using a whole-genome DNA microarray analysis approach
through comparison with IE. Results showed that only IE had the higher
corticosterone concentration than control, and that the less intense exercise
(ME) is better suited to improve AHN, especially in regards to the survival and
maturation of newborn neurons. DNA microarray analysis using a 4 × 44 K Agilent
chip revealed that ME regulated more genes than did IE (ME: 604 genes, IE: 415
genes), and only 41 genes were modified with both exercise intensities. The
identified molecular components did not comprise well-known factors related to
exercise-induced AHN, such as brain-derived neurotrophic factor. Rather, network
analysis of the data using Ingenuity Pathway Analysis algorithms revealed that
the ME-influenced genes were principally related to lipid metabolism, protein
synthesis and inflammatory response, which are recognized as associated with AHN.
In contrast, IE-influenced genes linked to excessive inflammatory immune
response, which is a negative regulator of hippocampal neuroadaptation, were
identified. Collectively, these results in a treadmill running model demonstrate
that long-term ME, but not of IE, with minimizing running stress, has beneficial
effects on increasing AHN, and provides an ME-specific gene inventory containing
some potential regulators of this positive regulation. This evidence might serve
in further elucidating the mechanism behind ME-induced cognitive gain.

PMCID: PMC4464753
PMID: 26061528



[2] J Physiol. 2016 Feb 4. doi: 10.1113/JP271552. [Epub ahead of print]

Physical exercise increases adult hippocampal neurogenesis in male rats provided
it is aerobic and sustained.

Nokia MS(1), Lensu S(2), Ahtiainen JP(2), Johansson PP(1,)(2), Koch LG(3),
Britton SL(3,)(4), Kainulainen H(2).

Author information:
(1)University of Jyvaskyla, Department of Psychology, University of Jyvaskyla,
P.O. Box 35, FI-40014, Finland. (2)Department of Biology of Physical Activity,
University of Jyvaskyla, Finland. (3)Department of Anesthesiology, University of
Michigan Medical School, Ann Arbor, Michigan, USA. (4)Department of Molecular &
Integrative Physiology, University of Michigan Medical School, Ann Arbor,
Michigan, USA.


Free full text: http://onlinelibrary.wiley.com/doi/10.1113/JP271552/pdf

KEY POINTS: Aerobic exercise such as running enhances adult hippocampal
neurogenesis (AHN) in rodents. Little is known about the effects of
high-intensity interval training (HIT) or of purely anaerobic resistance training
on AHN. Here, compared to a sedentary lifestyle, we report a very modest effect
of HIT and no effect of resistance training on AHN in adult male rats. We find
most AHN in rats that were selectively bred for an innately high response to
aerobic exercise that also run voluntarily and - increase maximum running
capacity. Our results confirm that sustained aerobic exercise is key in improving
ABSTRACT: Aerobic exercise, such as running, has positive effects on brain
structure and function, for example, adult hippocampal neurogenesis (AHN) and
learning. Whether high-intensity interval training (HIT), referring to
alternating short bouts of very intense anaerobic exercise with recovery periods,
or anaerobic resistance training (RT) has similar effects on AHN is unclear. In
addition, individual genetic variation in the overall response to physical
exercise likely plays a part in the effects of exercise on AHN but is less
studied. Recently, we developed polygenic rat models that gain differentially for
running capacity in response to aerobic treadmill training. Here we subjected
these Low Response Trainer (LRT) and High Response Trainer (HRT) adult male rats
to various forms of physical exercise for 6 to 8 weeks and examined its effects
on AHN. Compared to sedentary animals, the highest number of
doublecortin-positive hippocampal cells was observed in HRT rats that ran
voluntarily on a running wheel while HIT on the treadmill had a smaller,
statistically non-significant effect on AHN. AHN was elevated in both LRT and HRT
rats that endurance trained on a treadmill compared to those that performed RT by
climbing a vertical ladder with weights, despite their significant gain in
strength. Furthermore, RT had no effect on proliferation (Ki67), maturation
(doublecortin) or survival (BrdU) of new adult-born hippocampal neurons in adult
male Sprague-Dawley rats. Our results suggest physical exercise promotes AHN most
if it is aerobic and sustained, and especially when accompanied by a heightened
genetic predisposition for response to physical exercise. This article is
protected by copyright. All rights reserved.

PMID: 26844666

Share this post

Link to post
Share on other sites

Maybe it's time to speed up the game by providing electrical shocks to researchers rather than rats for wasting time and money on meaninglessness.

Share this post

Link to post
Share on other sites

Ha! I'm pretty chill, my skinny friend, no worries on the laid back. But hey now are you posting these studies for honest comments, or would you rather us say wow omg it's so spectacular that rats being tortured with electrical shocks are benefitting our lives so very much?

Share this post

Link to post
Share on other sites



Regarding the study (PMID: 26061528) I discussed above in this post, which tried to compare growth of rat hippocampal neurons as a result of either endurance exercise (voluntary long/slow wheel running), intense HIIT-like training (electric shock-motivated, high-speed, short-duration wheel running) or resistance training (voluntary weighted wall climbing). The national paper of record, the New York Times, did a story on the study, and disappointingly but not surprisingly, it was pretty shallow.


The writer did go so far as to quote the study author about why HIIT might not have the same brain benefits as endurance exercise:


As for high-intensity interval training, its potential brain benefits may be undercut by its very intensity, Dr. Nokia said. It is, by intent, much more physiologically draining and stressful than moderate running, and “stress tends to decrease adult hippocampal neurogenesis,” she said.


So the authors (and the writer) acknowledge stress can reduce growth of new brain cells in the hippocampus. But they fail to mention that the HIIT group of rats in the experiment had to be motivated to get them to run unusually fast by electric shocks, or at least the continuous threat of a shock once they learned if they stopped running they'd be shocked. No possibility of increased stress from that experience... :-(



Share this post

Link to post
Share on other sites



My daily one hour, vigorous exercise on a state-of-the-art Precor elliptical cross-trainer with hand motion:


(1) It's not a "moderate" exercise -- like Dean's long, moderate, runs -- my exercise is a vigorous one, causing a lot of sweating.


(2) I've been a vigorous daily exerciser since graduating college (in 1960) -- originally swimming, about a decade ago switching to the elliptical.


(3) Although my exercise is vigorous and lasts for an hour, it's the opposite of "stressful"; it puts me into a meditative, calm, relaxed state during the exercise.


Dean's posts seem to claim that the kind of moderate exercise that he does is best for relieving stress -- better than regular vigorous exercise -- I find the opposite.

You can't obtain the kind of pleasant relaxation that I get during, and after, my hour of vigorous exercise. (It isn't "intense" -- it's also obviously not an "in short bursts" type of exercise]).


I've seen a couple of articles -- as I recall backed by large studies -- noting the positive effects of such sustained, vigorous (not moderate) aerobic exercise -- including the state of relaxation and stress-reduction

of sustained, regular, lengthy (e.g. one hour) daily aerobic exercise. The kind of pleasant relaxation that I feel during my vigorous exercise has been documented and studied; I can't recall where.

But I definitely have such an effect when -- and after -- I exercise. It has a good, wholesome effect on my whole day.




-- Saul

Edited by Saul

Share this post

Link to post
Share on other sites



This new study [1] (press release) seems to show that strength training in the elderly is associated with decreased all-cause mortality. It polled 30,000 elderly people (>65) on their demographics and exercise habits, and then followed them for 15 years, during which 31% of them died.


On the surface, it appeared the effects of strength training at least twice per week were quite dramatic - a 46% reduction in risk of mortality during the follow-up period relative to people who did strength training less than twice per week. Cancer and cardiovascular mortality were also lower in the iron-pumpers (by 19% and 41% respectively).


But the question is whether their exercising more at baseline simply reflects better health and so a lower likelihood of dying during follow-up. The answer is "yes, partly". Once they adjusted for a bunch of confounders at baseline that one would expect to be associated with both increased mortality and less tendency to exercise (e.g. obesity, prior health conditions, diabetes) they found the protective effects of strength training dropped to 19% for all-cause mortality, and although the trend was still there, strength training was no longer statistically significantly predictive of reduced CVD or cancer mortality.


Obviously it's hard to tease apart cause and effect in a prospective study like this. But it supports something we know already, that trying to maintain muscle mass through strength training, rather than just focusing on cardiovascular fitness, is important for healthy aging. 





[1] Prev Med. 2016 Feb 24;87:121-127. doi: 10.1016/j.ypmed.2016.02.038. [Epub ahead

of print]
Is strength training associated with mortality benefits? A 15year cohort study of
US older adults.
Kraschnewski JL(1), Sciamanna CN(2), Poger JM(3), Rovniak LS(2), Lehman EB(4),
Cooper AB(5), Ballentine NH(3), Ciccolo JT(6).
BACKGROUND: The relationship between strength training (ST) behavior and
mortality remains understudied in large, national samples, although smaller
studies have observed that greater amounts of muscle strength are associated with
lower risks of death. We aimed to understand the association between meeting ST
guidelines and future mortality in an older US adult population.
METHODS: Data were analyzed from the 1997-2001 National Health Interview Survey
(NHIS) linked to death certificate data in the National Death Index. The main
independent variable was guideline-concordant ST (i.e. twice each week) and
dependent variable was all-cause mortality. Covariates identified in the
literature and included in our analysis were demographics, past medical history, 
and other health behaviors (including other physical activity). Given our aim to 
understand outcomes in older adults, analyses were limited to adults age 65years 
and older. Multivariate analysis was conducted using multiple logistic regression
RESULTS: During the study period, 9.6% of NHIS adults age 65 and older (N=30,162)
reported doing guideline-concordant ST and 31.6% died. Older adults who reported 
guideline-concordant ST had 46% lower odds of all-cause mortality than those who 
did not (adjusted odds ratio: 0.64; 95% CI: 0.57, 0.70; p<0.001). The association
between ST and death remained after adjustment for past medical history and
health behaviors.
CONCLUSIONS: Although a minority of older US adults met ST recommendations,
guideline-concordant ST is significantly associated with decreased overall
mortality. All-cause mortality may be significantly reduced through the
identification of and engagement in guideline-concordant ST interventions by
older adults.
Copyright © 2016 Elsevier Inc. All rights reserved.
PMID: 26921660

Share this post

Link to post
Share on other sites

They're back at it. The idea being that 60 seconds - yes, you read that right - 60 seconds of interval training is as good as 45 minutes of moderate aerobic exercise. They did biosamples of muscle cells and blood glucose and so forth, and claim the same benefits for both protocols. Amazing - I mean 60 seconds vs 45 minutes. To think that I could skip my 40 minutes of jogging 4 times a week, and get better results with 4 weekly sessions of 60 seconds each and do better, healthwise, well, that's a time saver if ever there was one. I exercise exclusively because of health benefits - no other reason... I don't enjoy it, and regard it as a waste of time (although I've adjusted by trying to be productive - thinking, and learning, while running). What good is life extension if it's consumed entirely (and then some) by the very activities designed to prolong life (activities I don't enjoy) - the return on investment is poor to say the least, like spending $100 to get $90 in savings. If you jog most of your life, and under the most optimistic scenario (Copenhagen study) you gain 6 years of life, then you can do the math counting the hours spent in misery jogging and adding them up. So this is tempting, no doubt. Of course, this is not a longitudinal study, which is my problem with these kinds of HIIT vs conventional exercise studies - who knows what the end points are in all-cause mortality or even morbidity down the road. For one, I cannot imagine that 60 seconds of HIIT spends anywhere close to the energy 45 minutes of moderate exercise does (in burning calories) - so does all this burning of calories have no impact years down the road - or is it all compensated by more eating? All in all, quite vexing. Here's a pop press account of the study:



Share this post

Link to post
Share on other sites


Amazing - I mean 60 seconds vs 45 minutes. To think that I could skip my 40 minutes of jogging 4 times a week, and get better results with 4 weekly sessions of 60 seconds each and do better, healthwise, well, that's a time saver if ever there was one.


Those are pretty impressive results. Below is the reference and abstract for the study. The only thing that should be noted is that the HIIT workout took 10 minutes - with only 1 minute of it intense. The rest was warmup, cool down, and moderate exercise between 20 sec bouts of extremely intense exercise. So you wouldn't be saving as much time as you suggest.


For a feel for the effort comparison, the 45 minutes of continuous exercise was at an energy burn rate of 110 watts. During the HIIT workout, there were three 20-second sprints at a burn rate of 500 watts, with two minutes between them at 50 watts.


In short, the HIIT subjects spent about 5x less time exercising, but had to exert themselves about 5x harder during the short HIIT sprints. Pick your poison. For me, I rather enjoy extended modest-intensity exercise, like pedalling at my bike desk right now. 





[1] PLoS ONE 11(4): e0154075. doi:10.1371/journal.pone.0154075

Published: April 26, 2016 http://dx.doi.org/10.1371/journal.pone.0154075


Improves Indices of Cardiometabolic Health Similar to Traditional Endurance Training despite a Five-Fold Lower Exercise Volume and Time Commitment. 


Gillen JB, Martin BJ, MacInnis MJ, Skelly LE, Tarnopolsky MA, Gibala MJ (2016) Twelve Weeks of Sprint Interval Training 


Free full text: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0154075


We investigated whether sprint interval training (SIT) was a time-efficient exercise strategy to improve insulin sensitivity and other indices of cardiometabolic health to the same extent as traditional moderate-intensity continuous training (MICT). SIT involved 1 minute of intense exercise within a 10-minute time commitment, whereas MICT involved 50 minutes of continuous exercise per session.
Sedentary men (27±8y; BMI = 26±6kg/m2) performed three weekly sessions of SIT (n = 9) or MICT (n = 10) for 12 weeks or served as non-training controls (n = 6). SIT involved 3x20-second ‘all-out’ cycle sprints (~500W) interspersed with 2 minutes of cycling at 50W, whereas MICT involved 45 minutes of continuous cycling at ~70% maximal heart rate (~110W). Both protocols involved a 2-minute warm-up and 3-minute cool-down at 50W.
Peak oxygen uptake increased after training by 19% in both groups (SIT: 32±7 to 38±8; MICT: 34±6 to 40±8ml/kg/min; p<0.001 for both). Insulin sensitivity index (CSI), determined by intravenous glucose tolerance tests performed before and 72 hours after training, increased similarly after SIT (4.9±2.5 to 7.5±4.7, p = 0.002) and MICT (5.0±3.3 to 6.7±5.0 x 10−4 min-1 [μU/mL]-1, p = 0.013) (p<0.05). Skeletal muscle mitochondrial content also increased similarly after SIT and MICT, as primarily reflected by the maximal activity of citrate synthase (CS; P<0.001). The corresponding changes in the control group were small for VO2peak (p = 0.99), CSI (p = 0.63) and CS (p = 0.97).
Twelve weeks of brief intense interval exercise improved indices of cardiometabolic health to the same extent as traditional endurance training in sedentary men, despite a five-fold lower exercise volume and time commitment.

Share this post

Link to post
Share on other sites

Dean, if you don't mind - what model/make is the "under the desk" exercise bike you are using? Also, I am guessing that your bike exercise under the desk is not designed as "exercise" as such, but rather a "sedentary behavior" countermeasure - correct me if I'm wrong! The idea being is that we should not spend more than 20-30 minutes or so sitting, without breaking it up with at least 1-2 minutes of standing and/or mildly exercising moving-about. That's not really exercise - it's sedentary behavior avoidance. If I am correct in guessing that the bike is meant to allow you to sit for more than 30 minutes at a stretch because you are "moving" - how confident are you in this measure being at least the equivalent of standing up from a health point of view? To me, that is not at all clear. In fact I'm rather skeptical - the kind of mild pedalling happening with your under desk bike (correct me if I'm wrong, and you are doing it vigorously!) does not seem to be much more exertion than in that very old British study of bus drivers vs bus ticket collectors - the bus drivers had much worse all cause mortality; but the thing that I always remembered about that study is that back in those days especially, being a bus driver was not an exertion-free activity equivalent to today's cubicle worker - it was much more active: you were swinging a big steering wheel (without power-assist in old busses) with your arms, turning your body somewhat, in active traffic and curving streets for hours at a time, your legs constantly pumping breaks-gas-clutch. Not at all sitting at a desk tapping on a keyboard or talking on the phone. And yet, even so, despite the bus drivers being much more physically active than a TV-viewer or white-collar cubicle worker, the outcomes for the bus drivers were very dire "sedentary behavior" delta vs ticket collectors who were on their feet walking up and down the bus. Are you sure that as you sit and mildly pedal, you are more active than the bus drivers? I think actually there may be something else at work entirely - it's not just about the exertion or calories spent at a desk - it is something about being vertical and on your feet that mobilizes the physiological response along a different axis than sitting - it may be positional. In fact, a better bet would be a treadmill desk, where you are vertical on your feet and moving - compared to sitting and pumping your feet. Now of course, I suppose there must be some threshold effect of the amount of energy spent, so that if you bike vigorously enough, the position no longer matters, although I would note that given the active involvement of the arms and torso in addition to the legs when you are actually biking in the street is not equivalent to sitting and basically having the entire effort isolated to your leg muscles as in the case of a under the desk bike, no matter how vigorous.  


In any case, I engage in my own "sedentary-behavior-abatement-protocol", which is very simply to have a timer that chimes every 20 minutes letting me know to get up and chimes in again after 2 minutes of my walking about. I'm not crazy about my protocol, so I'm definitely searching for better. If space permitted, I'd go for a treadmill desk, but there are other complications, in that I need to engage in fine motor movements with my hands which make it impractical to walk on a treadmill - I'm thinking that I just might swing it with an under desk bike, as long as my leg pumping is not too disruptive to my hand control; but then, I'm not totally sold on under-the-desk biking being good enough as a sedentary behavior abatement protocol. Have there been any studies wrt. such "in the chair" activities as equivalent to standing up in combatting sedentary behavior health effects (I'm not aware of any)?

Share this post

Link to post
Share on other sites



A simple search on these forums for "bike desk" would do the trick, but let me google that for you to save you the trouble, since Google crawls these forums too1. Oh lookie there - a whole forum thread called Dean's Diet & Exercise Regime, Tips, and Motivation, and a post specifically about my bike desk on the Cool Tools thread. 


Regarding effort, as I describe in that post, the resistance on my bike desk is variable, from very easy to extremely difficult. I have it on an intermediate setting. The bike reports that I'm burning 250 kcal/hr while pedaling, which converts directly to 290 watts - but that is way too high. My understanding is you need to divide that 290 watts by about 4 for cycling, to account for the body's inefficiency at converting calories burned in exercise metabolism to power at the pedals - which would put me at about 73 watts.


That is close to the halfway point between the "warm up/down" power output (50w) and the continuous power output (110w) of the moderate-intensity, 45-minute exercisers in the study you cited. So you can judge for yourself whether this is simply "sedentary behavior avoidance" or actual exercise. But one thing is for sure, it's definitely more than you burn when simply standing up without moving, or even casually walking. As you can see from the first post on the Dean's Diet & Exercise Regime, Tips, and Motivation I get plenty of exercise both at and away from my bike desk - to put it mildly... So I'm not too concerned what how my bike desk pedalling is categorized.


In fact, a better bet would be a treadmill desk...


Oh - let me google that for you too. Oh - lookie there. A post where I talk about my treadmill desk, and another one in that very same thread where I compared my experience with my bike desk and treadmill desk. There is even a post in that thread with an animated GIF showing my bike desk cadence. Amazing what you can find with a little searching...


I need to engage in fine motor movements with my hands which make it impractical to walk on a treadmill - I'm thinking that I just might swing it with an under desk bike, as long as my leg pumping is not too disruptive to my hand control; 


Wow, it just so happens that is exactly the point I address in this post that same thread... 




1Searching the forums with Google is particularly handy when you want to search for a three letter word like "NAD" or "DHA", which the crappy forum search interface barfs on...

Share this post

Link to post
Share on other sites

There was the case of the British popular press self-researcher who tried to quickly exercise himself into shape.  It seems that his genes were unfavorable.



CREB1 is a strong genetic predictor of the variation in exercise heart rate response to regular exercise: the HERITAGE Family Study.
Rankinen T, Argyropoulos G, Rice T, Rao DC, Bouchard C.
Circ Cardiovasc Genet. 2010 Jun;3(3):294-9. doi: 10.1161/CIRCGENETICS.109.925644. Epub 2010 Apr 20.
PMID: 20407090 Free PMC Article
A genome-wide linkage scan identified a quantitative trait locus for exercise training-induced changes in submaximal exercise (50 W) heart rate (DeltaHR50) on chromosome 2q33.3-q34 in the HERITAGE Family Study (n=472).
To fine-map the region, 1450 tag SNPs were genotyped between 205 and 215 Mb on chromosome 2. The strongest evidence of association with DeltaHR50 was observed with 2 single-nucleotide polymorphisms (SNPs) located in the 5' region of the cAMP-responsive element-binding protein 1 (CREB1) gene (rs2253206: P=1.6x10(-5) and rs2360969: P=4.3x10(-5)). The associations remained significant (P=0.01 and P=0.023, respectively) after accounting for multiple testing. Regression modeling of the 39 most significant SNPs in the single-SNP analysis identified 9 SNPs that collectively explained 20% of the DeltaHR50 variance. CREB1 SNP rs2253206 had the strongest effect (5.45% of variance), followed by SNPs in the FASTKD2 (3.1%), MAP2 (2.6%), SPAG16 (2.1%), ERBB4 (3 SNPs approximately 1.4% each), IKZF2 (1.4%), and PARD3B (1.0%) loci. In conditional linkage analysis, 6 SNPs from the final regression model (CREB1, FASTKD2, MAP2, ERBB4, IKZF2, and PARD3B) accounted for the original linkage signal: The log of the odds score dropped from 2.10 to 0.41 after adjusting for all 6 SNPs. Functional studies revealed that the common allele of rs2253206 exhibits significantly (P<0.05) lower promoter activity than the minor allele.
Our data suggest that functional DNA sequence variation in the CREB1 locus is strongly associated with DeltaHR50 and explains a considerable proportion of the quantitative trait locus variance. However, at least 5 additional SNPs seem to be required to fully account for the original linkage signal.

Share this post

Link to post
Share on other sites

Yeah, it didn't occur to me that you could google with someones name attached, but I guess you could! Thanks for the info! And those are interesting threads in their own right. I had a question about the durability of that bike, as I have had several stationary bikes at various price points and none have lasted, I guess I'm too hard on them; but I figure that if you're still using yours, it must mean it's at least durable enough to last 6 months - even if it were to break tomorrow and you had to buy a new one, one can think of it as a $300 yearly expense ($150 + $150). 

Share this post

Link to post
Share on other sites

Lots of Moderate Exercise Beats Equivalent Calories of Intense Exercise for Glucose Control




This new study [1] from researchers at Duke University (press release) contains some interesting results pertaining to the question of which type of exercise is best, how much is necessary, and how does exercise compare with calorie restriction when it comes to maintaining good glucose metabolism - an issue that many of us are concerned about.


The researchers randomly assigned 150 obese/overweight (BMI 25-35) adults (age 45-75) =with elevated fasting glucose (95-125 mg/dl) but without diabetes to one of four conditions:

  1. Diet & Some Moderate Exercise - ~7.5 miles of brisk walking per week (~25min/day) + enough calorie restriction on a 'low-fat' diet to drop 7% of body weight over six months. Considered the "Gold Standard" treatment.
  2. Some Moderate Exercise -     ~7.5 miles of brisk walking per week (~25min/day). No dietary change.
  3. Lots of Moderate Exercise - ~11.5 miles of brisk walking per week (~40min/day). No dietary change.
  4. Lots of Vigorous Exercise -  ~11.5 miles of jogging per week (~30min/day). No dietary change.

Adherence was surprisingly good - with people completing 82-85% of the prescribed exercise minutes at the required intensity as verified by a heart rate monitor as well as supervision by study personnel in the gym where participants worked out at least twice per week.


What they found was interesting. In terms of weight loss, the Diet+Ex group did the best, losing 14lbs on average vs. ~5lbs for the two groups with lots of exercise and around 2lbs in the group with the small amount of moderate exercise.


Fasting glucose and insulin were reduced the most in the Diet+Ex group as well. 


But in terms of glucose tolerance (i.e. performance on an oral glucose tolerance test), which is the best predictor of future diabetes and mortality risk, a large amount (40min/day) of brisk walking was nearly as good (statistically indistinguishable) from the calorie restriction and exercise (Diet+Ex) treatment. 


What's more, the "lots of moderate exercise" group exhibited better glucose tolerance improvements than did the "lots of vigorous exercise" group, who expended the same amount of calories, but engaged in more intense exercise (jogging or equivalent) for a shorter period of time. In fact, the equivalent amount of more vigorous exercise did not significantly improve glucose tolerance at all. Surprisingly, the "some moderate exercise" group (brisk walking ~25min/ day) experienced nearly twice as much improvement on the OGTT as did the "lots of vigorous exercise" group.


The researchers saw this as a win for pre-diabetics patients, who often find compliance to diet + exercise recommendations difficult:


“When faced with the decision of trying to do weight loss, diet, and exercise versus exercise alone, the study indicates you can achieve nearly 80 percent of the effect of doing all three with just a high amount of moderate-intensity exercise,” he said. “I was heartened by the fact that I found out that I can give patients one message and they can get nearly the same effect as when required to exercise, diet and lose weight all at the same time.”


Obvious caveats include:

  • These were overweight/obese & pre-diabetic subjects - not very similar to most of us.
  • The weight loss in the Diet+Ex group, and the amount of exercise in all the groups was pretty modest compared with what most of us do.
  • The best results were seen in the group that lost substantial weight and did some exercise.

But it was nonetheless interesting to see that glucose intolerance could be significantly improved by a moderate amount (~40min/day) of brisk walking, even in the absence of significant weight loss. And most interesting of all was that vigorous exercise (jogging) was inferior to an equivalent number of calories spent in less intense exercise (brisk walking) for combatting glucose intolerance.





[1] Diabetologia. 2016 Jul 15. [Epub ahead of print]

Effects of exercise training alone vs a combined exercise and nutritional
lifestyle intervention on glucose homeostasis in prediabetic individuals: a
randomised controlled trial.
Slentz CA(1), Bateman LA(2,)(3), Willis LH(2), Granville EO(4), Piner LW(2),
Samsa GP(5), Setji TL(6), Muehlbauer MJ(2), Huffman KM(2), Bales CW(4), Kraus
Author information: 
(1)Duke Molecular Physiology Institute, Department of Medicine, Duke University
School of Medicine, 300 North Duke Street, Durham, NC, 27701, USA.
cris.slentz@duke.edu. (2)Duke Molecular Physiology Institute, Department of
Medicine, Duke University School of Medicine, 300 North Duke Street, Durham, NC, 
27701, USA. (3)University of North Carolina at Chapel Hill, Center for Health
Promotion and Disease Prevention, Chapel Hill, NC, USA. (4)Division of
Geriatrics, Duke University School of Medicine, Durham, NC, USA. (5)Department of
Biostatistics and Bioinformatics, Duke University School of Medicine, Durham, NC,
USA. (6)Division of Endocrinology, Duke University School of Medicine, Durham,
NC, USA. (7)Division of Cardiology, Duke University School of Medicine, Durham,, 
AIMS/HYPOTHESIS: Although the Diabetes Prevention Program (DPP) established
lifestyle changes (diet, exercise and weight loss) as the 'gold standard'
preventive therapy for diabetes, the relative contribution of exercise alone to
the overall utility of the combined diet and exercise effect of DPP is unknown;
furthermore, the optimal intensity of exercise for preventing progression to
diabetes remains very controversial. To establish clinical efficacy, we undertook
a study (2009 to 2013) to determine: how much of the effect on measures of
glucose homeostasis of a 6 month programme modelled after the first 6 months of
the DPP is due to exercise alone; whether moderate- or vigorous-intensity
exercise is better for improving glucose homeostasis; and to what extent amount
of exercise is a contributor to improving glucose control. The primary outcome
was improvement in fasting plasma glucose, with improvement in plasma glucose AUC
response to an OGTT as the major secondary outcome.
METHODS: The trial was a parallel clinical trial. Sedentary, non-smokers who were
45-75 year old adults (n = 237) with elevated fasting glucose (5.28-6.94 mmol/l) 
but without cardiovascular disease, uncontrolled hypertension, or diabetes, from 
the Durham area, were studied at Duke University. They were randomised into one
of four 6 month interventions: (1) low amount (42 kJ kg body weight(-1) week(-1) 
[KKW])/moderate intensity: equivalent of expending 42 KKW (e.g. walking ∼16 km
[8.6 miles] per week) with moderate-intensity (50% [Formula: see text]) exercise;
(2) high amount (67 KKW)/moderate intensity: equivalent of expending 67 KKW
(∼22.3 km [13.8 miles] per week) with moderate-intensity exercise; (3) high
amount (67 KKW)/vigorous intensity: equivalent to group 2, but with
vigorous-intensity exercise (75% [Formula: see text]); and (4) diet + 42 KKW
moderate intensity: same as group 1 but with diet and weight loss (7%) to mimic
the first 6 months of the DPP. Computer-generated randomisation lists were
provided by our statistician (G. P. Samsa). The randomisation list was maintained
by L. H. Willis and C. A. Slentz with no knowledge of or input into the
scheduling, whereas all scheduling was done by L. A. Bateman, with no knowledge
of the randomisation list. Subjects were automatically assigned to the next group
listed on the randomisation sheet (with no ability to manipulate the list order) 
on the day that they came in for the OGTT, by L. H. Willis. All plasma analysis
was done blinded by the individuals doing the measurements (i.e. lipids, glucose,
insulin). Subjects and research staff (other than individuals analysing the
blood) were not blinded to the group assignments.
RESULTS: Number randomised, completers and number analysed with complete OGTT
data for each group were: low-amount/moderate-intensity (61, 43, 35);
high-amount/moderate-intensity (61, 44, 40); high-amount/vigorous-intensity (61, 
43, 38); diet/exercise (54, 45, 37), respectively. Only the diet and exercise
group experienced a decrease in fasting glucose (p < 0.001). The means and 95%
CIs for changes in fasting glucose (mmol/l) for each group were:
high-amount/moderate-intensity -0.07 (-0.20, 0.06); high-amount/vigorous 0.06
(-0.07, 0.19); low-amount/moderate 0.05 (-0.05, 0.15); and diet/exercise -0.32
(-0.46, -0.18). The effects sizes for each group (in the same order) were: 0.17, 
0.15, 0.18 and 0.71, respecively. For glucose tolerance (glucose AUC of OGTT),
similar improvements were observed for the diet and exercise (8.2% improvement,
effect size 0.73) and the 67 KKW moderate-intensity exercise (6.4% improvement,
effect size 0.60) groups; moderate-intensity exercise was significantly more
effective than the same amount of vigorous-intensity exercise (p < 0.0207). The
equivalent amount of vigorous-intensity exercise alone did not significantly
improve glucose tolerance (1.2% improvement, effect size 0.21). Changes in
insulin AUC, fasting plasma glucose and insulin did not differ among the exercise
groups and were numerically inferior to the diet and exercise group.
CONCLUSIONS/INTERPRETATION: In the present clinical efficacy trial we found that 
a high amount of moderate-intensity exercise alone was very effective at
improving oral glucose tolerance despite a relatively modest 2 kg change in body 
fat mass. These data, combined with numerous published observations of the strong
independent relation between postprandial glucose concentrations and prediction
of future diabetes, suggest that walking ∼18.2 km (22.3 km prescribed with 81.6% 
adherence in the 67 KKW moderate-intensity group) per week may be nearly as
effective as a more intensive multicomponent approach involving diet, exercise
and weight loss for preventing the progression to diabetes in prediabetic
individuals. These findings have important implications for the choice of
clinical intervention to prevent progression to type 2 diabetes for those at high
TRIAL REGISTRATION: ClinicalTrials.gov NCT00962962 FUNDING: The study was funded 
by National Institutes for Health National Institute of Diabetes and Digestive
and Kidney Diseases (NIH-NDDK) (R01DK081559).
DOI: 10.1007/s00125-016-4051-z 
PMID: 27421729

Share this post

Link to post
Share on other sites

Thank you, Dean for this. We all see how the cohort studies here is different from most readers here. But many people on the CR spectrum don't conform to expectations wrt. glucose tolerance either. Therefore, one wonders if this might actually not be relevant to us insofar as trying for more moderate vs vigorous - I think perhaps this is Dean's approach? Dean, when you had your bout with glucose issues back in the day, what was your exercise regimen then compared to now when you no longer have any glucose issues?

Share this post

Link to post
Share on other sites

Regarding Al's point about genetics having a role in the benefits (or not) of exercise, here's another one:


Resistance to the Beneficial Effects of Exercise in Type 2 Diabetes: Are Some Individuals Programmed to Fail?



Exercise benefits most, but not all, individuals with type 2 diabetes (T2D). The beneficial effects are well studied, but why some individuals do not respond favorably to exercise training is largely unexplored. It is critical to treatment and prevention strategies to identify individuals with T2D that have a blunted metabolic response to exercise and investigate the underlying mechanisms that might predict this “programmed response to fail.”

Evidence Acquisition:

We carried out a systematic review of classic and contemporary primary reports on clinical human and animal exercise studies. We also referenced unpublished data from our previous studies, as well those of collaborators. Genetic and epigenetic components and their associations with the exercise response were also examined.

Evidence Synthesis:

As evidence of the exercise resistance premise, we and others found that supervised exercise training results in substantial response variations in glucose homeostasis, insulin sensitivity, and muscle mitochondrial density, wherein approximately 15–20% of individuals fail to improve their metabolic health with exercise. Classic genetic studies have shown that the extent of the exercise training response is largely heritable, whereas new evidence demonstrates that DNA hypomethylation is linked to the exercise response in skeletal muscle. DNA sequence variation and/or epigenetic modifications may, therefore, dictate the exercise training response.


Studies dedicated to uncovering the mechanisms of exercise resistance will advance the field of exercise and T2D, allowing interventions to be targeted to those most likely to benefit and identify novel approaches to treat those who do not experience metabolic improvements after exercise training.

Seems to me, 20% is quite substantial.

Share this post

Link to post
Share on other sites



Dean, when you had your bout with glucose issues back in the day, what was your exercise regimen then compared to now when you no longer have any glucose issues?


Back then I followed what now I consider silly advice like this by Michael - namely to engage in the minimum amount of exercise to (hopefully) maintain bone and CV health, but avoid doing anything beyond that because it takes too many calories, and according to Michael, longevity is all about "calories, calories, calories".


I wonder if he's changed his tune now - I doubt it. Silly Michael...



Share this post

Link to post
Share on other sites


Back then I followed what now I consider silly advice like this by Michael - namely to engage in the minimum amount of exercise to (hopefully) maintain bone and CV health, but avoid doing anything beyond that because it takes too many calories, and according to Michael, longevity is all about "calories, calories, calories".
I wonder if he's changed his tune now - I doubt it. Silly Michael...

Your charcterization my views here is highly distorted. I would find your glossing of what you call "silly advice like this by Michael" to be an understandable if somewhat sloppy overextrapolation of what I wrote — perhaps in part due to failing to contextualize what I said in the post as a response to the particular questions that they addressed — if you were a noob, but you're not: not only have we been reading each other's posts and engaged in dialog for a decade or so now, but less than two weeks ago you wrote to me with observations that clearly demonstrate that you know better.


Edit, a few minutes after originally posting: Actually, the degree to which you've mischaracterized me here is even more extreme than I had specifically noted in my original post. You say above that I counciled "engag[ing] in the minimum amount of exercise to (hopefully) maintain bone and CV health," when even ignoring the context, the history, and your recent email to me on the subject, the very post that you cite for these comments already clearly extends beyond "exercise to (hopefully) maintain bone and CV health," to "resistance training for your skeletal muscle ..., plus motion throughout the day to avoid "sitting disease.""


So you appear to be both insulting me and publicly and knowingly mischaracterizing my views for no apparent reason, aside from what I might guess is a childish attempt to get me to post by simply provoking me into clarifying your knowing distortion.
I find your comment that "according to Michael, longevity is all about "calories, calories, calories'" to also be misleading in a way that you ought to know better. Now, on the other hand, you did make a similar comment in a previous thread that I did and do think was probably just a case of the usual gestalting oversimplification of memory, to which I drafted a response but didn't post as it was part of a much larger one that I never finished, which I will post here:


it seems relatively well-supported that extra energy expenditure (and therefore calories metabolized) as a result of higher mitochondrial uncoupling doesn't shorten lifespan, as your "calories, calories, calories" mantra would suggest it should. Right?

I know you didn't intend it this way, but that's kind of a "when did you stop beating your wife?" question. You're really misremembering (or greatly misinterpreting!) my long use of this mantram. I've never predicted that simply consuming emore Calories than normal, in the context of energy balance or deficit, would shorten lifespan, and indeed it's very clearly the case that increased energy expenditure (even if counterbalanced by increased Calorie intake) is in general rather good for one, most obviously in the case of exercise, and also in the likely case of cold exposure and various genetic interventions that boost it (tho' many of those also boost exercise). "Calories, Calories, Calories" is about the mechanism of CR: it's about Calorie intake, and not (as people have often postulated) specific sources of energy (protein, carbs, and fat have all been fingered by different people), nor negative energy balance (exercise, UCP-2, etc's uniform failure to extend max LS demonstrates this), or (except to a minimal degree) reduction in adiposity.

The big problem with extra Calories in, of course, is that it normally leads to obesity [sNIP]

... but in that case, as I say, what you said seems to be a reasonable kind of evocation of half-remembered memory of long-past posts and discussions, not an intentional misrepresentation.

Share this post

Link to post
Share on other sites

Create an account or sign in to comment

You need to be a member in order to leave a comment

Create an account

Sign up for a new account in our community. It's easy!

Register a new account

Sign in

Already have an account? Sign in here.

Sign In Now