192 replies to this topic

[Julia36]

So I'm starting to get older and it depresses me. I've heard exercise can slow the rate of biological aging to some extent. True?

I'm into purple at the moment.

japanese purple sweet potato (highest by miles),
red cabbage, blueberries beetrot

Purple (generally) seems to enhance life expectancy

[deadwood]

So I'm starting to get older and it depresses me. I've heard exercise can slow the rate of biological aging to some extent. True?

No I don't believe exercise can slow the rate of aging. You need to do Calorie Restriction to do that.... there is always a chance resveratrol 'might' work though.

BS. No proof calorie restriction works in Humans. Of course eating crap will speed up aging. AGing is all genetics. You either are lucky or you are not.

[johnross47]

Exercise may not counteract aging but it can counteract many of the effects of aging that are commonly treated as just part of the process, such as loss of muscle, general slowing down, loss of appetite and pleasure in food, inflexibility, loss of balance, heart problems and so on. You'll still be grey and wrinkly, speaking for myself, but you can still run up a mountain and back to a very welcome meal. When you go on holiday you don't have to take days off away from the fun to recover. I'm not very old yet, 67, but quite a few of my contemporaries have given things up, such as golf, because they aren't able to do it any more. They aren't fit enough, yet there are other golfers out there in their 80s. You may live a little longer and people might think you are younger than your real age because you look vigorous. It's all win and no lose.

[Mind]

As if we needed anymore evidence that exercise is GREAT for your healthspan: http://www.longecity...n-older-people/ Add this to the growing mountain of positive human data.

[Rocket]

As if we needed anymore evidence that exercise is GREAT for your healthspan: http://www.longecity...n-older-people/ Add this to the growing mountain of positive human data.

I am a gym rat and I will tell you that there is a huge difference in 60 year Olds who are gym rats themselves, especially the weight lifters, and the 60 year Olds at work who obviously don't exercise. The older gym rats move faster and carry themselves the way that younger people do, not to mention that if you ignore everything above the shoulders (looks) you'd think you were looking at someone years and years younger.

[sensei]

Yes -- exercise slows aging

 

"Consistent evidence has shown that exercise is able to retard the onset and impede the progression of aging by modifying mitochondrial oxidant–antioxidant homeostasis. Here we provide a broad overview of the research evidence showing the relationship between mitochondrial redox metabolism, aging and exercise. We address part aspects of mitochondrial reactive oxygen species (ROS) metabolism, from superoxide production to ROS detoxification, especially antioxidant enzymes and uncoupling protein. Furthermore, we describe mitochondrial remodeling response to aging and exercise, which is accompanied by bioenergetics and redox regulation. In addition, potential mechanisms for redox signaling involved in mitochondrial remodeling and redox metabolism regulation are also reviewed."

 

http://www.sciencedi...095254613000288

 

 

 

 

[Mind]

Sitting around on your butt causes vascular dysfunction in as little as 5 days. Until we have rejuvenation therapies or move into a "virtual reality" existence, exercise is the best medication, by far. Doctors should seriously be prescribing exercise instead of "pills" as it is much more powerful. Alas, most people want magic pills, so they can keep sitting around.

[baptized_in_flames]

Sitting around on your butt causes vascular dysfunction in as little as 5 days. Until we have rejuvenation therapies or move into a "virtual reality" existence, exercise is the best medication, by far. Doctors should seriously be prescribing exercise instead of "pills" as it is much more powerful. Alas, most people want magic pills, so they can keep sitting around.

 

 

What's sad is that when people come in to see a doctor and say they're depressed, the first thing a doctor does is point them in the direction of a pamphlet that contains various anti-depressant medications. The reason of this is because big medicine wants these people to get society hooked, so that they have to have some kind of anti-depressant prescription for the rest of their lives. Exercise is free though, and they don't want any part of advertising that. I know a person who has been on that starter anti-depressant med, Wellbutrin, for 4 or 5 years. She's in good shape, but she doesn't exercise - at all - and she used to be an avid gym rat before the meds - because these anti depressants rewire the reward system of your brain to where exercise is seen more as work, and less as reward.

Edited by baptized_in_flames, 02 January 2015 - 04:35 PM.

[Michael]

All:
 
 

Yes -- exercise slows aging
 
"Consistent evidence has shown that exercise is able to retard the onset and impede the progression of aging by modifying mitochondrial oxidant–antioxidant homeostasis [...]"
 
http://www.sciencedi...095254613000288

 
Despite this misleading language (whether repeated in the pop press or the primary literature), it is quite clear that exercise does not slow aging, although many aspects of physiological performance and disease risk are better in exercisers than non-exercisers: because those same parameters worsen with age, there is an illusion in cross-sectional studies that exercise slows or reverses aging, when in fact the age-related decline is similar  and in some indexes and studies faster in exercising vs. sedentary people or rodents. Eg,
 

 

Relation between maximal O₂ uptake (VO_2max) and age in endurance-trained and sedentary men. Absolute rate of decline in VO_2max with age was greater in endurance-trained than in sedentary men (P < 0.001). From (1).

 

See also this post earlier in this thread. As you can see, the exercisers' VO_2maxwas better than that of sedentary people at all ages, but the rate of age-related decline was as fast or even faster.

 

I want to be clear: exercise is good for you, and will delay the onset of frailty and age-related disease, particularly in your fifties through your seventies. But the fact that something is good for you doesn't mean it affects the underlying degenerative aging process.
 
 

What's sad is that when people come in to see a doctor and say they're depressed, the first thing a doctor does is point them in the direction of a pamphlet that contains various anti-depressant medications.. [...] these anti depressants rewire the reward system of your brain to where exercise is seen more as work, and less as reward.

 

I was surprised by the above, since anecdotally I know of a couple of people who cannot motivate themselves to exercise at all unless they're on their antidepressants. Of course, those aren't strictly incompatible. From my initial, superficial dig, it appears that although there is a mechanistic basis in serotonergic metabolism that would lead one to predict greater perceived effort of exercise after SSRI or SNRI use, the actual studies in humans are inconsistent at worst and possibly refutatory overall:

 

The purpose of the experiment was to examine whether selective serotonin (5-HT) re-uptake transporter blockade by paroxetine has any effect on perceived effort (RPE) during exercise or the time to reach volitional fatigue and on the prolactin and cortisol responses during prolonged exercise performed in a warm environment. Eight healthy males performed two cycle rides to exhaustion in a warm (32°C) environment at 60% of maximum oxygen uptake. Paroxetine (20 mg) or placebo was administered 5 h before exercise trials in a randomised double blind fashion. Time to exhaustion was not significantly influenced by administration of paroxetine ... RPE increased over time but was not influenced by paroxetine administration.  [...] In conclusion, acute administration of paroxetine failed to alter RPE, exercise capacity or the response of the determined peripheral hormone markers of central 5-HT activity during prolonged exercise in a warm environment.(2)

 

Nine healthy endurance-trained males were recruited to examine the effect of a dual dopamine/noradrenaline reuptake inhibitor on performance, thermoregulation and the hormonal responses to exercise. Subjects performed four trials, ingesting either a placebo (pla) or 2 × 300 mg bupropion (bup), prior to exercise in temperate (18°C) or warm (30°C) conditions. Trials consisted of 60 min cycle exercise at 55% W_max immediately followed by a time trial (TT). TT performance in the heat was significantly improved by bupropion (pla: 39.8 ± 3.9 min, bup: 36.4 ± 5.7 min; P = 0.046), but no difference between treatments was apparent in temperate conditions (pla: 30.6 ± 2.2 min, bup: 30.6 ± 1.9 min; P = 0.954). While TT power output was consistently lower in the heat when compared to temperate conditions, this decrement was attenuated by bupropion. ... These data indicate that performance in warm conditions is enhanced by acute administration of a dual dopamine/noradrenaline reuptake inhibitor. No such effect was apparent under temperate conditions. It appears that bupropion enabled subjects to maintain a greater TT power output in the heat with the same perception of effort and thermal stress reported during the placebo trial, despite the attainment of a higher core temperature.(3)

 

See detailed discussion in the intro and the "Discussion" section of (2).

 

References

1: Pimentel AE, Gentile CL, Tanaka H, Seals DR, Gates PE. Greater rate of decline in maximal aerobic capacity with age in endurance-trained than in sedentary men. J Appl Physiol (1985). 2003 Jun;94(6):2406-13. Epub 2003 Jan 17. PubMed PMID: 12533496.

 

2: Strachan AT, Leiper JB, Maughan RJ. Paroxetine administration failed [corrected] to influence human exercise capacity, perceived effort or hormone responses during prolonged exercise in a warm environment. Exp Physiol. 2004 Nov;89(6):657-64. Epub 2004 Aug 24. Erratum in: Exp Physiol. 2005 Jan;90(1):151. PubMed PMID: 15328306.

 

3: Watson P, Hasegawa H, Roelands B, Piacentini MF, Looverie R, Meeusen R. Acute dopamine/noradrenaline reuptake inhibition enhances human exercise performance in warm, but not temperate conditions. J Physiol. 2005 Jun 15;565(Pt 3):873-83. Epub 2005 Apr 14. PubMed PMID: 15831540; PubMed Central PMCID: PMC1464564.

[baptized_in_flames]

 

The purpose of the experiment was to examine whether selective serotonin (5-HT) re-uptake transporter blockade by paroxetine has any effect on perceived effort (RPE) during exercise or the time to reach volitional fatigue and on the prolactin and cortisol responses during prolonged exercise performed in a warm environment. Eight healthy males performed two cycle rides to exhaustion in a warm (32°C) environment at 60% of maximum oxygen uptake. Paroxetine (20 mg) or placebo was administered 5 h before exercise trials in a randomised double blind fashion. Time to exhaustion was not significantly influenced by administration of paroxetine ... RPE increased over time but was not influenced by paroxetine administration.  [...] In conclusion, acute administration of paroxetine failed to alter RPE, exercise capacity or the response of the determined peripheral hormone markers of central 5-HT activity during prolonged exercise in a warm environment.(2)

 

Nine healthy endurance-trained males were recruited to examine the effect of a dual dopamine/noradrenaline reuptake inhibitor on performance, thermoregulation and the hormonal responses to exercise. Subjects performed four trials, ingesting either a placebo (pla) or 2 × 300 mg bupropion (bup), prior to exercise in temperate (18°C) or warm (30°C) conditions. Trials consisted of 60 min cycle exercise at 55% W_max immediately followed by a time trial (TT). TT performance in the heat was significantly improved by bupropion (pla: 39.8 ± 3.9 min, bup: 36.4 ± 5.7 min; P = 0.046), but no difference between treatments was apparent in temperate conditions (pla: 30.6 ± 2.2 min, bup: 30.6 ± 1.9 min; P = 0.954). While TT power output was consistently lower in the heat when compared to temperate conditions, this decrement was attenuated by bupropion. ... These data indicate that performance in warm conditions is enhanced by acute administration of a dual dopamine/noradrenaline reuptake inhibitor. No such effect was apparent under temperate conditions. It appears that bupropion enabled subjects to maintain a greater TT power output in the heat with the same perception of effort and thermal stress reported during the placebo trial, despite the attainment of a higher core temperature.(3)

 

 

 

In response to the first paragraph, I was referring to the reward feeling your brain gives you after working out, the afterglow that one experiences for the rest of the day after a good workout, etc. I feel that antidepressants already give this effect to a degree all the time, so it only makes sense that an individual would place working out lower on the agenda, due to the reward being less valuable in that person's mind. 

 

And for your 2nd paragraph, with all due respect, I don't believe it has any bearing on what we're talking about here. Bupropion itself has stimulant qualities. Sure, if you take 9 people who are already very athletic and give them Bupropion before they work out for one day, they're going to perform the same if not maybe a little bit better, since it has stimulant qualities. But it's irrelevant because what was being discussed was the chronic effect of antidepressants on the brain, and how it affects the reward system. Not a trial run of 9 athletes given Bupropion for 1 day.

 

[Edit: trimmed to remove  BIF's comments from quote-box for material quoted by MR -MR]

Edited by Michael, 03 January 2015 - 05:45 PM.

[sensei]

 

Yes -- exercise slows aging
 
"Consistent evidence has shown that exercise is able to retard the onset and impede the progression of aging by modifying mitochondrial oxidant–antioxidant homeostasis [...]"
 
http://www.sciencedi...095254613000288

 
Despite this misleading language (whether repeated in the pop press or the primary literature), it is quite clear that exercise does not slow aging, although many aspects of physiological performance and disease risk are better in exercisers than non-exercisers: because those same parameters worsen with age, there is an illusion in cross-sectional studies that exercise slows or reverses aging, when in fact the age-related decline is similar  and in some indexes and studies faster in exercising vs. sedentary people or rodents. [SNIP]

 

The rate of Aerobic decline is not a marker for  aging.
 
The action of exercise on mitochondrial function is unequivocal.  More efficient mitochondrial function has been shown to lengthen the time between cellular replication -- as aging is tied to cellular doubling Hayflick Limit, lengthening the time between cellular replication SLOWS AGING.

 

[Edit: redundant full-post quotation trimmed -MR]

Edited by Michael, 03 January 2015 - 01:01 AM.

[Michael]

Yes -- exercise slows aging

"Consistent evidence has shown that exercise is able to retard the onset and impede the progression of aging by modifying mitochondrial oxidant–antioxidant homeostasis [...]"

http://www.sciencedi...095254613000288

Despite this misleading language (whether repeated in the pop press or the primary literature), it is quite clear that exercise does not slow aging, although many aspects of physiological performance and disease risk are better in exercisers than non-exercisers: because those same parameters worsen with age, there is an illusion in cross-sectional studies that exercise slows or reverses aging, when in fact the age-related decline is similar and in some indexes and studies faster in exercising vs. sedentary people or rodents.[SNIP]

The rate of Aerobic decline is not a marker for aging.

Er ... of course it is!
 

The action of exercise on mitochondrial function is unequivocal. More efficient mitochondrial function has been shown to lengthen the time between cellular replication -- as aging is tied to cellular doubling Hayflick Limit, lengthening the time between cellular replication SLOWS AGING.

That's a nice mechanistic hypothesis, but it doesn't pan out at the level of function or lifespan. And aging is not really tied to the Hayflick limit under physiological conditions.
 

In response to the first [SSRI study], I was referring to the reward feeling your brain gives you after working out, the afterglow that one experiences for the rest of the day after a good workout, etc. I feel that antidepressants already give this effect to a degree all the time, so it only makes sense that an individual would place working out lower on the agenda, due to the reward being less valuable in that person's mind.

But, to be clear, do you have any actual evidence that this is so, or are you speculating from the above reasonable-sounding hypothesis and what "makes sense"?
 

And for your 2nd [study, in Bupropion], ... Bupropion itself has stimulant qualities. Sure, if you take 9 people who are already very athletic and give them Bupropion before they work out for one day, they're going to perform the same if not maybe a little bit better, since it has stimulant qualities. But it's irrelevant because what was being discussed was the chronic effect of antidepressants on the brain, and how it affects the reward system. Not a trial run of 9 athletes given Bupropion for 1 day.

Again, reasonable-sounding. Do you have any empirical evidence from controlled human or rodent studies to back it up?

[Michael]

Sitting around on your butt causes vascular dysfunction in as little as 5 days. Until we have rejuvenation therapies or move into a "virtual reality" existence, exercise is the best medication, by far. Doctors should seriously be prescribing exercise instead of "pills" as it is much more powerful. Alas, most people want magic pills, so they can keep sitting around.

 

Someone at the University of Missouri  Office of Communications appears to have screwed up the reporting of an interesting study rather badly. When you look at the actual study, what they really find is that "Femoral and brachial artery blood flow increased during the OGTT but neither was significantly impacted by changes in physical activity (p>0.05). However, insulin sensitivity was decreased by [the "acute reduction in daily activity (from >10,000 to <5,000 steps/day) for 5 days (RA5)] (11.3+/-1.5 to 8.0+/-1.0; p<0.05). Likewise, free living [glycemic control] measures of peak post prandial blood glucose (113+/-3 to 123+/-5 mg/dL; p<0.05) was significantly increased at RA5. Interestingly, insulin sensitivity and GC as assessed by peak PPG were not restored after RTA1 (p>0.05)."

[sensei]

 

The action of exercise on mitochondrial function is unequivocal. More efficient mitochondrial function has been shown to lengthen the time between cellular replication -- as aging is tied to cellular doubling Hayflick Limit, lengthening the time between cellular replication SLOWS AGING.

That's a nice mechanistic hypothesis, but it doesn't pan out at the level of function or lifespan. And aging is not really tied to the Hayflick limit under physiological conditions.

 

 

Yes, I have to go find the papers. I posted them on the C60 health forum. 

 

And actually, aging is tied to the Hayflick limit under physiological conditions.

 

Cellular stress causes the time between replications to decrease. Aging is a direct result of cellular senescence. Even though there is some variation among humans for the Hayflick limit, mathematically, if the time between doublings is shortened, senescence of any particular cell is hastened, hence the organism ages faster.

Edited by sensei, 03 January 2015 - 02:14 AM.

[Mind]

 

Sitting around on your butt causes vascular dysfunction in as little as 5 days. Until we have rejuvenation therapies or move into a "virtual reality" existence, exercise is the best medication, by far. Doctors should seriously be prescribing exercise instead of "pills" as it is much more powerful. Alas, most people want magic pills, so they can keep sitting around.

 

Someone at the University of Missouri  Office of Communications appears to have screwed up the reporting of an interesting study rather badly. When you look at the actual study, what they really find is that "Femoral and brachial artery blood flow increased during the OGTT but neither was significantly impacted by changes in physical activity (p>0.05). However, insulin sensitivity was decreased by [the "acute reduction in daily activity (from >10,000 to <5,000 steps/day) for 5 days (RA5)] (11.3+/-1.5 to 8.0+/-1.0; p<0.05). Likewise, free living [glycemic control] measures of peak post prandial blood glucose (113+/-3 to 123+/-5 mg/dL; p<0.05) was significantly increased at RA5. Interestingly, insulin sensitivity and GC as assessed by peak PPG were not restored after RTA1 (p>0.05)."

 

 

You are right...and it seems pretty obvious from the title:

 

Acute Inactivity Impairs Glycemic Control but Not Blood Flow to Glucose Ingestion.

 

[sensei]

 

The rate of Aerobic decline is not a marker for aging.

Er ... of course it is!

 
SO then, if a 70 year old that has been sedentary, starts to exercise; and through such aerobic exercise they increase their aerobic capacity -- they have de-aged?
 
Or, if an adult acquires adult onset asthma, and their aerobic capacity drops, they have begun to age faster?
 

[Edit: trimming redundant quote boxes -MR]

Edited by Michael, 09 January 2015 - 11:53 PM.

[Michael]

The rate of Aerobic decline is not a marker for aging.

Er ... of course it is!

 
SO then, if a 70 year old that has been sedentary, starts to exercise; and through such aerobic exercise they increase their aerobic capacity -- they have de-aged?
 
Or, if an adult acquires adult onset asthma, and their aerobic capacity drops, they have begun to age faster?

Those are intelligent examples of the slipperiness of all of this — but of course, any decline physiological function, form of cellular or molecular damage, or disease process driven by or driving degenerative aging can be further exacerbated by disease processes or environmental or lifestyle influences. Even the stronger of your two cases (the sedentary person who becomes active late in life) is only transient: as the graph I showed illustrates, while s/he will doubtless enjoy an acute boost of VO_2max, but from that new the decline with age will continue inexorably. Cf. the standard survival curve, which has both an the age-independent (Makeham) mortality component that varies with things like sanitation, nutrition, and medical intervention, while the age-dependent (Gompertz) mortality component keeps dragging us down at an exponentially-accelerating rate.

 

(By the way, 'sensei,' it looks like you were having some trouble trimming your reply post; if you can tell me what you were trying to do (by PM?), I can use my moderator access to fix it for you. Thanks for trimming!).

Edited by Michael, 03 January 2015 - 05:42 PM.

[sensei]

say i agree and : a priori a decline in Aerobic capacity is a marker of aging

 

Does it follow that the decline is due to a corresponding decline in mitochondrial function; and SOD and glutathione peroxidase production in the body?

 

If so, that line of thought lends itself to the " mitochondrial damage and oxidation as the cause of aging" theory

[Mind]

Exercise keeps you healthier into old age: http://www.kcl.ac.uk...-optimally.aspx

 

 

Cyclists were recruited to exclude the effects of a sedentary lifestyle, which can aggravate health problems and cause changes in the body, which might appear to be due to the ageing process. Men and women had to be able to cycle 100 km in under 6.5 hours and 60 km in 5.5 hours, respectively, to be included in the study. Smokers, heavy drinkers and those with high blood pressure or other health conditions were excluded from the study.

Participants underwent two days of laboratory testing at King’s. For each participant, a physiological profile was established which included measures of cardiovascular, respiratory, neuromuscular, metabolic, endocrine and cognitive functions, bone strength, and health and well-being. Volunteers’ reflexes, muscle strength, oxygen uptake during exercise and peak explosive cycling power were determined. 

The results of the study showed that in these individuals, the effects of ageing were far from obvious. Indeed, people of different ages could have similar levels of function such as muscle strength, lung power and exercise capacity. The maximum rate of oxygen consumption showed the closest association with age, but even this marker could not identify with any degree of accuracy the age of any given individual, which would be the requirement for any useful biomarker of ageing.

 

[sensei]

 

Exercise keeps you healthier into old age: http://www.kcl.ac.uk...-optimally.aspx

 

 

Cyclists were recruited to exclude the effects of a sedentary lifestyle, which can aggravate health problems and cause changes in the body, which might appear to be due to the ageing process. Men and women had to be able to cycle 100 km in under 6.5 hours and 60 km in 5.5 hours, respectively, to be included in the study. Smokers, heavy drinkers and those with high blood pressure or other health conditions were excluded from the study.

Participants underwent two days of laboratory testing at King’s. For each participant, a physiological profile was established which included measures of cardiovascular, respiratory, neuromuscular, metabolic, endocrine and cognitive functions, bone strength, and health and well-being. Volunteers’ reflexes, muscle strength, oxygen uptake during exercise and peak explosive cycling power were determined. 

The results of the study showed that in these individuals, the effects of ageing were far from obvious. Indeed, people of different ages could have similar levels of function such as muscle strength, lung power and exercise capacity. The maximum rate of oxygen consumption showed the closest association with age, but even this marker could not identify with any degree of accuracy the age of any given individual, which would be the requirement for any useful biomarker of ageing.

 

Michael THIS  citation even states that V02 max is NOT a biomarker for aging

 

"he maximum rate of oxygen consumption showed the closest association with age, but even this marker could not identify with any degree of accuracy the age of any given individual, which would be the requirement for any useful biomarker of ageing."

Edited by sensei, 09 January 2015 - 06:16 PM.

[Michael]

 

Exercise keeps you healthier into old age: http://www.kcl.ac.uk...-optimally.aspx

Cyclists were recruited to exclude the effects of a sedentary lifestyle ... Smokers, heavy drinkers and those with high blood pressure or other health conditions were excluded from the study. ...

in these individuals, the effects of ageing were far from obvious. Indeed, people of different ages could have similar levels of function such as muscle strength, lung power and exercise capacity. The maximum rate of oxygen consumption showed the closest association with age, but even this marker could not identify with any degree of accuracy the age of any given individual, which would be the requirement for any useful biomarker of ageing.

Michael THIS  citation even states that V02 max is NOT a biomarker for aging
 
"he maximum rate of oxygen consumption showed the closest association with age, but even this marker could not identify with any degree of accuracy the age of any given individual, which would be the requirement for any useful biomarker of ageing.

 
Sensei, everyone on Longecity knows how to adjust the font size on their device display: there's no need to shout.
 
I didn't claim that VO_2max was a biomarker of aging: at present, there are no known biomarkers of aging, despite all the "anti-aging" medical quacks trying to sell you their custom biomarker tests and profiles. There's too much intra- and interindividual variability for it to be used for that purpose. None the less, the age-related decline is clear. To contextualize the phrase you quote from the press release states, "in these individuals, the effects of ageing were far from obvious [not nonexistant -MR] ... The maximum rate of oxygen consumption showed the closest association with age, but even this marker could not identify with any degree of accuracy the age of any given individual, which would be the requirement for any useful biomarker of ageing."
 
To quote from the abstract of the actual scientific report, "Significant associations between age and function were observed for many functions. The maximal rate of oxygen consumption (VO_2max) showed the closest association with age (r = −0.443 to −0.664; P < 0.001), but even here the variance in age for any given level was high, precluding the clear identification of the age of any individual."
 
This new study is very useful in doing its best to exclude confounding lifestyle factors. It was not, unfortunately, prospective, which would have been required in any case to reliably identify biomarkers of aging.

Edited by Michael, 09 January 2015 - 06:51 PM.

[sensei]

 

 

 
Sensei, everyone on Longecity knows how to adjust the font size on their device display: there's no need to shout.
 
I didn't claim that VO_2max was a biomarker of aging: at present, there are no known biomarkers of aging, despite all the "anti-aging" medical quacks trying to sell you their custom biomarker tests and profiles. There's too much intra- and interindividual variability for it to be used for that purpose. None the less, the age-related decline is clear. To contextualize the phrase you quote from the press release states, "in these individuals, the effects of ageing were far from obvious [not nonexistant -MR] ... The maximum rate of oxygen consumption showed the closest association with age, but even this marker could not identify with any degree of accuracy the age of any given individual, which would be the requirement for any useful biomarker of ageing."
 
To quote from the abstract of the actual scientific report, "Significant associations between age and function were observed for many functions. The maximal rate of oxygen consumption (VO_2max) showed the closest association with age (r = −0.443 to −0.664; P < 0.001), but even here the variance in age for any given level was high, precluding the clear identification of the age of any individual."
 
This new study is very useful in doing its best to exclude confounding lifestyle factors. It was not, unfortunately, prospective, which would have been required in any case to reliably identify biomarkers of aging.

 

You specifically argued "rate of aerobic is a biomarker of aging" by stating err.. of course it is.

 

1. I can falsify your premise by showing an anti-decline in aged persons that start to exercise

2. The best you can state is that there is an association, but with a high variance in age for any given level its useless.

3. Furthermore, if an individual can maintain VO2 max for any length of time -- you are stating that they are not aging -- 

 

I propose that it is unequivocal that a 50 year old could maintain (a rate of decline that approaches zero) their VO2 max for a decade by steadily increasing their level of aerobic exercise.

 

This means either 1 of 2 things 

 

A - the rate of decline in VO2 max is not a biomarker for aging

or

B - exercise slows aging

[Michael]

 

I didn't claim that VO_2max was a biomarker of aging: at present, there are no known biomarkers of aging ...
 
To quote from the abstract of the actual scientific report, "Significant associations between age and function were observed for many functions. The maximal rate of oxygen consumption (VO_2max) showed the closest association with age (r = −0.443 to −0.664; P < 0.001), but even here the variance in age for any given level was high, precluding the clear identification of the age of any individual."
 
This new study is very useful in doing its best to exclude confounding lifestyle factors. It was not, unfortunately, prospective, which would have been required in any case to reliably identify biomarkers of aging.

 
You specifically argued "rate of aerobic is a biomarker of aging" by stating err.. of course it is.

No, I didn't. I was responding to your statement that "The rate of Aerobic decline is not a marker for aging" — a marker, not a biomarker. A biomarker is a contested but scientifically understood technical term, which could be used clinically for identification of the biological age of an individual and the effects of anti-aging interventions; if you had said "biomarker," I wouldn't have asserted that it was one, although I would still have disagreed with some of the things you have gone on to say in the post.
 

1. I can falsify your premise by showing an anti-decline in aged persons that start to exercise

That doesn't falsify my premise (see comments above), although I'd certainly agree that it is one reason it won't work as a biomarker.
 

2. The best you can state is that there is an association, but with a high variance in age for any given level its useless.

Useless as a biomarker of aging, sure: no argument. At no time did I say that it could be used thus. What I said in the original post to which you were responding was, "Despite this misleading language [...] it is quite clear that exercise does not slow aging, although many aspects of physiological performance and disease risk are better in exercisers than non-exercisers: because those same parameters worsen with age, there is an illusion in cross-sectional studies that exercise slows or reverses aging, when in fact the age-related decline is similar  and in some indexes and studies faster in exercising vs. sedentary people or rodents."
 

3. Furthermore, if an individual can maintain VO2 max for any length of time -- you are stating that they are not aging --

 
Nope — not saying that either .
 

I propose that it is unequivocal that a 50 year old could maintain (a rate of decline that approaches zero) their VO2 max for a decade by steadily increasing their level of aerobic exercise.

I wouldn't say "unequivocal," though I'd agree that probably many 50-y.os could do it. Again, that makes it useless as a diagnostic for individual biological age (ie, as a biomarker of aging). That doesn't mean that the underlying cellular and molecular structures aren't suffering progressive degradation with age. The decline in VO_2max with age is a surrogate marker for a these processes, but it is also affected by many other things (including changes in the amount of training one does, as well as individual genetics, traumatic injuries, etc), and increasing training can affect some but not all of them — amongst which is not the underlying rate of aging. Hence, exercise does not slow aging.
 

This means either 1 of 2 things 
 
A - the rate of decline in VO2 max is not a biomarker for aging
or
B - exercise slows aging

It means A, and not B.

[sensei]

 

The rate of Aerobic decline is not a marker for aging.

Er ... of course it is!

 
There is where you said it is a marker of aging.
 
If the rate of decline is a marker of aging, and exercise can slow that rate of decline (to any degree at all in any individual) - then exercise slows aging.

[Edit: cleaning up redundant quote boxes -MR]

Edited by Michael, 09 January 2015 - 11:50 PM.

[Michael]

 

 

The rate of Aerobic decline is not a marker for aging.

Er ... of course it is!

 
There is where you said it is a marker of aging.
 
If the rate of decline is a marker of aging, and exercise can slow that rate of decline (to any degree at all in any individual) - then exercise slows aging.

Exercise does not slow aging; exercise does not slow the rate of decline of VO_2max as a "marker" of aging, as the two studies (the one I cited and the one for which Mind identified a press release) demonstrate. I agree that you can game the test with the artifacts you suggest; these studies were designed to avoid such artifacts. My study was in lifelong master athletes, and Mind's in people with existing high levels of fitness, not untrained or grossly undertrained people who suddenly boost their exercise levels and thus experience a transient increase in capacity.

[Maecenas]

In my opinion, you don't need any scientific studies to see the evident - regular aerobic excercise significantly slows down the aging process. I see dozens of 60-70 years folks on a daily basis who have been running all their lives and most of whom can still run a marathon in under 4 hours.

Every time after my running session of 10 to 15 km I feel rejuvenated and I have twice the amount of energy next morning compared to the days i don't run.

[Iporuru]

This might be relevant for the discussion:

 

http://onlinelibrary...282863/abstract

 

Key Points

• The relationship between age and physiological function remains poorly defined and there are no physiological markers that can be used to reliably predict the age of an individual.
• This could be due to a variety of confounding genetic and lifestyle factors, and in particular to ill-defined and low levels of physical activity.
• This study assessed the relationship between age and a diverse range of physiological functions in a cohort of highly active older individuals (cyclists) aged 55–79 years in whom the effects of lifestyle factors would be ameliorated.
• Significant associations between age and function were observed for many functions. was most closely associated with age, but even here the variance in age for any given level was high, precluding the clear identification of the age of any individual.
• The data suggest that the relationship between human ageing and physiological function is highly individualistic and modified by inactivity.

Abstract

Despite extensive research, the relationship between age and physiological function remains poorly characterised and there are currently no reliable markers of human ageing. This is probably due to a number of confounding factors, particularly in studies of a cross-sectional nature. These include inter-subject genetic variation, as well as inter-generational differences in nutrition, healthcare and insufficient levels of physical activity as well as other environmental factors. We have studied a cohort of highly and homogeneously active older male (n = 84) and female (n = 41) cyclists aged 55–79 years who it is proposed represent a model for the study of human ageing free from the majority of confounding factors, especially inactivity. The aim of the study was to identify physiological markers of ageing by assessing the relationship between function and age across a wide range of indices. Each participant underwent a detailed physiological profiling which included measures of cardiovascular, respiratory, neuromuscular, metabolic, endocrine and cognitive functions, bone strength, and health and well-being. Significant associations between age and function were observed for many functions. The maximal rate of oxygen consumption ( showed the closest association with age (r = −0.443 to −0.664; P < 0.001), but even here the variance in age for any given level was high, precluding the clear identification of the age of any individual. The results of this cross-sectional study suggest that even when many confounding variables are removed the relationship between function and healthy ageing is complex and likely to be highly individualistic and that physical activity levels must be taken into account in ageing studies.

 

[Michael]

 

This might be relevant for the discussion:

 

Despite extensive research, the relationship between age and physiological function remains poorly characterised and there are currently no reliable markers of human ageing. This is probably due to a number of confounding factors, ...  includ[ing] inter-subject genetic variation, as well as inter-generational differences in nutrition, healthcare and insufficient levels of physical activity as well as other environmental factors. We have studied a cohort of highly and homogeneously active older male (n = 84) and female (n = 41) cyclists aged 55–79 years who it is proposed represent a model for the study of human ageing free from the majority of confounding factors, especially inactivity.  [...]

 

Each participant underwent a detailed physiological profiling which included measures of cardiovascular, respiratory, neuromuscular, metabolic, endocrine and cognitive functions, bone strength, and health and well-being. Significant associations between age and function were observed for many functions. The maximal rate of oxygen consumption (VO_2max) showed the closest association with age (r = −0.443 to −0.664; P < 0.001), but even here the variance in age for any given level was high, precluding the clear identification of the age of any individual. The results of this cross-sectional study suggest that even when many confounding variables are removed the relationship between function and healthy ageing is complex and likely to be highly individualistic and that physical activity levels must be taken into account in ageing studies.

 

http://onlinelibrary...014.282863/full

 

Right: this is the study for which Mind identified the press release, and which I discussed further with Sensei.
 

 

 

Figure 1. Maximal aerobic capacity relationships with age

The relationship of age with maximal aerobic capacity (in absolute terms, A; relative to body weight, B; and fat free mass (FFM)) (C?) and maximum heart rate (D). Data are from females (● and continuous line) and males (∇ and dashed line). [Note: "Age (years)" on the right is accidentally looped in from another set of graphs on functional equivalence: the proper metrics on these graphs are labeled on the left (y-axis) and right (x-axis) as usual].

 

Edited by Michael, 11 January 2015 - 08:12 PM.

[proileri]

Unfortunately, VO_2max and O₂pulse_max seem to be highly dependant on exercise minutes. In addition, VO_2max depends on HR_max that declines over age. These factors, in addition to the high variability, make them pretty much useless as markers.

 

However, it's nice to see that aerobic exercise can be said to be rather effective in any age group, at least to the point that you maintain the levels of sedentary young people. I would expect that we will get better data in the age group 70-100 in the future, as the number of active seniors seems to be constantly rising. 

[pone11]

Unfortunately, VO_2max and O₂pulse_max seem to be highly dependant on exercise minutes. In addition, VO_2max depends on HR_max that declines over age. These factors, in addition to the high variability, make them pretty much useless as markers.

 

 

I think that is not a complete view of the use cases.   At the high end, among endurance trained and genetically capable individuals, their aerobic metabolism is limited by their ability to deliver O2 to the mitochondria, which is in turn related to mechanical limitations in breathing and heart pumping of blood.

 

At the low end, there are people with cardiomyopathy or type 2 diabetes who are effectively hypoxic and cannot deliver sufficient oxygen.

 

But in the middle of the data are people with impaired aerobic metabolism.   If the electron transport chain (ETC) just does not work well, it won't matter that your heart can go faster and that you can breath more oxygen.   This includes people with:

 

* genetic defects in mitochondria or metabolism feeding the ETC

* chronic fatigue syndromes that are not tied to hypoxia

* heavy metal poisoning, like mercury which replaces iron sulphate complexes in the electron transport chain and neutralizes them

* heavy mitochondrial damage from ROS, more typically seen as people age

 

There is a very muddy middle between the end points, where the limiting factor is metabolism not oxygen.