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I recall Edison didn't think exercise was good. He lived to 96, I think. If exercise is all important why don't we have a preponderance of jocks in the 100yo group?

The more we exercise the more cals we have to eat.

Regards.

----- Original Message -----

From: old542000

Sent: Thursday, January 20, 2005 2:10 PM

Subject: [ ] Exercise benefit for some questioned

Hi All, Some CRers have higher levels of lipids thought to beassociated with better health than others. A good exampleis Saul, who does not CR as much as many of us do. Thisappears not to be due to any particular unique feature ofhis CRON diet. Do our benefits from exercise depend on our genes? Exercise increases levels of high density lipoprotein(HDL) and an enzyme called angiotensin-converting enzyme (ACE). The article from Nature not in Medlineyet indicates that our benefits from exercise aredictated by genes regulating the level of these molecules. Nature 433, 188 - 189 (20 January 2005)Alison Abbott All pain, no gain? Exercise is good for you, or so we always thought. But, as Alison Abbott learns, your genes don't always cooperate. When Claude Bouchard set out to see whether genes play a role in physical fitness, he assumed, like most people, that exercise training makes everyone fitter. Although he expected genes to modulate some individual responses to diet and exercise, he also anticipated that regular workouts would improve fitness indicators such as lung efficiency and blood cholesterol for everybody. Some 20 years later, it has become clear from the work of Bouchard and others that this is not the case. Looking at certain measures of fitness, some people actually fare worse after exercise, whereas others show little or no improvement. But this isn't vindication for couch potatoes. Everyone's health improves in some way or other from exercise, but just how it improves is largely dependent on genes. Now, the growing field of fitness genetics is attempting to tease those genetic components apart, and the studies are generating fresh insights into the benefits of exercise as well as unexpected pay-offs for medicine. Bouchard's attempts to track fitness genes began in the mid-1980s at Laval University in Quebec, Canada. He and his colleagues focused on the maximum amount of oxygen absorbed by the body from a lungful of air — a standard measure of aerobic fitness, usually abbreviated as VO2max. They found that most people can get more oxygen out of each breath after training but that a minority were no better off, regardless of how efficient their lungs were at the start. Because the variation was much less extreme within pairs of identical twins, Bouchard concluded that the effect was largely dictated by genes1. "Our work on athletes is feeding back into the clinic. How efficiently we use oxygen is decisive when we are desperately sick." That initial study was fairly small, so Bouchard extended the work in 1992 by helping to set up a multicentre research effort called the HERITAGE Family Study, which is still running today. Now based — together with Bouchard — at the Pennington Biomedical Research Center in Baton Rouge, Louisiana, the study's main data set comes from some 740 sedentary adults who were subjected to an intense exercise regime in the lab. The researchers monitored changes in the participants' blood pressure, heart rate, blood chemistry and VO2max over 20 weeks. Survival of the fittest The study's main aim was to determine how exercise reduces risk factors for cardiovascular disease and diabetes, but Bouchard and researchers at the four other collaborating institutions also took blood samples for genetic analysis. "We were trying to find as many genes as possible that influence fitness and performance," Bouchard says. The resulting reams of data and frozen blood samples are still being analysed, but the results so far confirm Bouchard's earlier studies. The average increase in VO2max after the training programme was 19%. But 5% of the subjects had virtually no change, and another 5% had improved by more than twice the average amount. Similarly, most people had lower exercising heart rates and blood pressure after the training programme — an indication of improved fitness — but the extent of the reduction was extremely variable. In a few people there was even a small rise in these numbers2. Much of this variability seems to be attributable to genes. The researchers found more variation between than within families, suggesting at least a portion of a person's ability to benefit from exercise is inherited. "We concluded that just about half of the difference in trainability was heritable," says Tuomo Rankinen, the study's project manager. It is unclear to what extent fitness parameters such as VO2max are indicative of long-term health prospects, but even presumed health indicators such as cholesterol, a factor in heart disease, did not follow the expected pattern of more exercise is better. Conventional wisdom has it that regular exercise reduces the risk of heart disease by raising blood levels of high-density lipoprotein (HDL) cholesterol, a complex that helps prevent cholesterol from forming fatty deposits on blood-vessel walls. This is considered one of the key benefits of taking up sports such as running. But the HERITAGE data show that training does not inevitably increase levels of HDL cholesterol. In fact, in about one-third of exercisers, the level of the complex fell. Does this all mean that exercise could actually be bad for those of us with the 'wrong genes'? Not at all, insists Rankinen. "We found not a single 'universal non-responder'," he says. In other words, everyone improved on some score. Even those who could not raise their VO2max through exercise were still getting some other health benefit such as higher HDL cholesterol levels or lower blood pressure. And overall, the HERITAGE data show that the risk of cardiovascular disease and type 2 diabetes falls in those who exercise regularly, Rankinen says. One way to begin to untangle these apparently contradictory effects is to go after the genes involved. This could ultimately reveal a great deal about how exercise produces health benefits, and may lead to treatments for diseases of metabolism and physiology. To this end, scientists at the HERITAGE study are scanning the genomes of participants for gene variants that occur more frequently in association with different fitness responses. Although some metabolism genes have been identified that may play a role, the most strongly linked gene so far is Titin. This produces protein fibres that contribute to the elasticity of heart muscle cells. It may be that some forms of the gene allow the heart to pump larger volumes of blood than others3. Physical attractions Other teams are also on the hunt for fitness genes. , a health researcher at the Lawrence Berkeley National Laboratory in Berkeley, California, for instance, suspects that a gene related to the synthesis of HDL cholesterol might be involved. Ten years ago, he found that people who have an easier time taking up running after leading sedentary lives also started out with higher levels of HDL cholesterol in their blood — and increased those levels more quickly —than those who find running difficult4. It turns out that an enzyme that boosts HDL cholesterol is found in 'slow-twitch' muscle fibre, the type that takes longer to fatigue and so makes distance running easier. is now beginning a large-scale genetic study to see whether differences in that enzyme are associated with differences in lifestyle choice. Meanwhile, Gaston Beunen, a sports scientist at the Catholic University of Leuven in Belgium, is looking at the half-dozen or so key genes that contribute to the synthesis of myostatin, a protein that blocks new muscle growth. His study of some 300 young sibling males, published in May last year, hints that three of these genes may help to determine a person's physical strength5. In the end, the number of fitness-linked genes is expected to be large. So far, more than 100 appear in the literature, most of which have been identified in the past four years6, although in many cases more work is needed to confirm the link. And some of these now seem likely to prove their worth in the clinic. One gene drawing a lot of attention encodes an enzyme called ACE, or angiotensin-converting enzyme. ACE activates the hormone angiotensin, which helps to maintain blood pressure and promotes the growth of the heart in response to exercise. One common gene variant, known as ACE D, makes more ACE than the other common version, ACE I. And athletes who have inherited ACE D from both parents experience about three times more heart growth in response to exercise than those who have inherited two ACE I genes7. They also seem to perform better in sports that rely on sheer strength and power, such as weight-lifting or sprinting. The I variant, in contrast, is more common among élite athletes in endurance sports such as long-distance running and swimming, which require more efficient metabolic use of energy and oxygen8, 9. As the lower levels of ACE associated with ACE I improve endurance, Hugh Montgomery, a cardiovascular geneticist at University College London, wondered whether ACE I might also be advantageous to those suffering serious illness. He found that children with potentially deadly meningitis were more likely to require intensive care or to die if they had two copies of the ACE D gene rather than two copies of ACE I10. His team also found that premature babies with ACE I fare better11. "Our work on athletes is feeding back into the clinic," says Montgomery. "How efficiently we use oxygen is decisive when we are desperately sick." It may eventually be possible to help such patients with drugs that slow down ACE activity. Already, in unpublished work, ACE inhibitors have been shown to reduce muscle wasting in mice. And London-based drug company Ark Therapeutics is currently running final-stage clinical trials on the use of the ACE inhibitor imidapril to treat severe muscle wasting in cancer patients. "Genetic destiny should not become a new excuse for couch potatoes — everyone gets at least some benefit from regular exercise." Fitness genetics may be feeding ideas into the clinic, but could genetic destiny become a new excuse for couch potatoes? "If they think their performance is limited by their genes, people tend to give up," says Montgomery. "People are afraid of trying and failing — it's part of the human condition." Nevertheless, his advice to those who long to be fitter is to do serious exercise come what may. For everyone, it seems, there is at least some benefit. References 1. Bouchard, C., Dionne, F. T., Simoneau, J. A. & Boulay, M. R. Exerc. Sport Sci. Rev. 20, 27-58 (1992). | PubMed | ChemPort | 2. Bouchard, C. & Rankinen, T. Med. Sci. Sports Exerc. 33 (Suppl.), S446-S451 (2001). | PubMed | ChemPort | 3. Rankinen, T. et al. Physiol. Genom. 15, 27-33 (2003). | ChemPort | 4. , P. T., Stefanick, M. L., Vranizan, K. M. & Wood, P. D. Metabolism 43, 917-924 (1994). | Article | PubMed | ChemPort | 5. Huygens, W. et al. Physiol. Genom. 17, 264-279 (2004). | ChemPort | 6. Perusse, L. et al. Med. Sci. Sports Exerc. 35, 1248-1264 (2003). | PubMed | ChemPort | 7. Myerson, S. G. et al. Circulation 103, 226-230 (2001). | PubMed | ChemPort | 8. Nazarov, I. B. et al. Eur. J. Hum. Genet. 9, 797-801 (2001). | Article | PubMed | ChemPort | 9. Tsianos, G. et al. Eur. J. Appl. Physiol. 92, 360-362 (2004). | PubMed | ChemPort | 10. Harding, D. et al. Am. J. Respir. Crit. Care Med. 165, 1103-1106 (2002). | PubMed | 11. Harding, D. et al. J. Pediatr. 143, 746-749 (2003).Cheers, Al Pater

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Jack Lalanne is 90 year old. He born 09/26/1914.

http://www.jacklalanne.com/

Avg life span of people and rats that exercise is extended. Exercise

increase avg lifespan, study proving this post here several time. Look

back! Why you insist on this opinion??

> I recall Edison didn't think exercise was good. He lived to

96, I think. If exercise is all important why don't we have a

preponderance of jocks in the 100yo group?

> The more we exercise the more cals we have to eat.

>

> Regards.

>

> ----- Original Message -----

> From: old542000

>

> Sent: Thursday, January 20, 2005 2:10 PM

> Subject: [ ] Exercise benefit for some questioned

>

>

>

> Hi All,

>

> Some CRers have higher levels of lipids thought to be

> associated with better health than others. A good example

> is Saul, who does not CR as much as many of us do. This

> appears not to be due to any particular unique feature of

> his CRON diet.

>

> Do our benefits from exercise depend on our genes?

>

> Exercise increases levels of high density lipoprotein

> (HDL) and an enzyme called angiotensin-converting

> enzyme (ACE). The article from Nature not in Medline

> yet indicates that our benefits from exercise are

> dictated by genes regulating the level of these molecules.

>

> Nature 433, 188 - 189 (20 January 2005)

> Alison Abbott

> All pain, no gain?

>

> Exercise is good for you, or so we always thought. But, as Alison

> Abbott learns, your genes don't always cooperate.

> When Claude Bouchard set out to see whether genes play a role in

> physical fitness, he assumed, like most people, that exercise

> training makes everyone fitter. Although he expected genes to

> modulate some individual responses to diet and exercise, he also

> anticipated that regular workouts would improve fitness indicators

> such as lung efficiency and blood cholesterol for everybody.

> Some 20 years later, it has become clear from the work of Bouchard

> and others that this is not the case. Looking at certain measures of

> fitness, some people actually fare worse after exercise, whereas

> others show little or no improvement.

> But this isn't vindication for couch potatoes. Everyone's health

> improves in some way or other from exercise, but just how it improves

> is largely dependent on genes. Now, the growing field of fitness

> genetics is attempting to tease those genetic components apart, and

> the studies are generating fresh insights into the benefits of

> exercise as well as unexpected pay-offs for medicine.

> Bouchard's attempts to track fitness genes began in the mid-1980s

> at Laval University in Quebec, Canada. He and his colleagues focused

> on the maximum amount of oxygen absorbed by the body from a lungful

> of air - a standard measure of aerobic fitness, usually abbreviated

> as VO2max. They found that most people can get more oxygen out of

> each breath after training but that a minority were no better off,

> regardless of how efficient their lungs were at the start. Because

> the variation was much less extreme within pairs of identical twins,

> Bouchard concluded that the effect was largely dictated by genes1.

> " Our work on athletes is feeding back into the clinic. How

> efficiently we use oxygen is decisive when we are desperately sick. "

> That initial study was fairly small, so Bouchard extended the

> work in 1992 by helping to set up a multicentre research effort

> called the HERITAGE Family Study, which is still running today. Now

> based - together with Bouchard - at the Pennington Biomedical

> Research Center in Baton Rouge, Louisiana, the study's main data set

> comes from some 740 sedentary adults who were subjected to an intense

> exercise regime in the lab. The researchers monitored changes in the

> participants' blood pressure, heart rate, blood chemistry and VO2max

> over 20 weeks.

>

> Survival of the fittest

> The study's main aim was to determine how exercise reduces risk

> factors for cardiovascular disease and diabetes, but Bouchard and

> researchers at the four other collaborating institutions also took

> blood samples for genetic analysis. " We were trying to find as many

> genes as possible that influence fitness and performance, " Bouchard

> says.

> The resulting reams of data and frozen blood samples are still

> being analysed, but the results so far confirm Bouchard's earlier

> studies. The average increase in VO2max after the training programme

> was 19%. But 5% of the subjects had virtually no change, and another

> 5% had improved by more than twice the average amount. Similarly,

> most people had lower exercising heart rates and blood pressure after

> the training programme - an indication of improved fitness - but the

> extent of the reduction was extremely variable. In a few people there

> was even a small rise in these numbers2.

> Much of this variability seems to be attributable to genes. The

> researchers found more variation between than within families,

> suggesting at least a portion of a person's ability to benefit from

> exercise is inherited. " We concluded that just about half of the

> difference in trainability was heritable, " says Tuomo Rankinen, the

> study's project manager.

> It is unclear to what extent fitness parameters such as VO2max are

> indicative of long-term health prospects, but even presumed health

> indicators such as cholesterol, a factor in heart disease, did not

> follow the expected pattern of more exercise is better. Conventional

> wisdom has it that regular exercise reduces the risk of heart disease

> by raising blood levels of high-density lipoprotein (HDL)

> cholesterol, a complex that helps prevent cholesterol from forming

> fatty deposits on blood-vessel walls. This is considered one of the

> key benefits of taking up sports such as running. But the HERITAGE

> data show that training does not inevitably increase levels of HDL

> cholesterol. In fact, in about one-third of exercisers, the level of

> the complex fell.

> Does this all mean that exercise could actually be bad for those

> of us with the 'wrong genes'? Not at all, insists Rankinen. " We found

> not a single 'universal non-responder', " he says. In other words,

> everyone improved on some score. Even those who could not raise their

> VO2max through exercise were still getting some other health benefit

> such as higher HDL cholesterol levels or lower blood pressure. And

> overall, the HERITAGE data show that the risk of cardiovascular

> disease and type 2 diabetes falls in those who exercise regularly,

> Rankinen says.

> One way to begin to untangle these apparently contradictory

> effects is to go after the genes involved. This could ultimately

> reveal a great deal about how exercise produces health benefits, and

> may lead to treatments for diseases of metabolism and physiology.

> To this end, scientists at the HERITAGE study are scanning the

> genomes of participants for gene variants that occur more frequently

> in association with different fitness responses. Although some

> metabolism genes have been identified that may play a role, the most

> strongly linked gene so far is Titin. This produces protein fibres

> that contribute to the elasticity of heart muscle cells. It may be

> that some forms of the gene allow the heart to pump larger volumes of

> blood than others3.

>

> Physical attractions

> Other teams are also on the hunt for fitness genes. ,

> a health researcher at the Lawrence Berkeley National Laboratory in

> Berkeley, California, for instance, suspects that a gene related to

> the synthesis of HDL cholesterol might be involved. Ten years ago, he

> found that people who have an easier time taking up running after

> leading sedentary lives also started out with higher levels of HDL

> cholesterol in their blood - and increased those levels more quickly -

> than those who find running difficult4. It turns out that an enzyme

> that boosts HDL cholesterol is found in 'slow-twitch' muscle fibre,

> the type that takes longer to fatigue and so makes distance running

> easier. is now beginning a large-scale genetic study to see

> whether differences in that enzyme are associated with differences in

> lifestyle choice.

> Meanwhile, Gaston Beunen, a sports scientist at the Catholic

> University of Leuven in Belgium, is looking at the half-dozen or so

> key genes that contribute to the synthesis of myostatin, a protein

> that blocks new muscle growth. His study of some 300 young sibling

> males, published in May last year, hints that three of these genes

> may help to determine a person's physical strength5.

> In the end, the number of fitness-linked genes is expected to be

> large. So far, more than 100 appear in the literature, most of which

> have been identified in the past four years6, although in many cases

> more work is needed to confirm the link. And some of these now seem

> likely to prove their worth in the clinic.

> One gene drawing a lot of attention encodes an enzyme called ACE,

> or angiotensin-converting enzyme. ACE activates the hormone

> angiotensin, which helps to maintain blood pressure and promotes the

> growth of the heart in response to exercise. One common gene variant,

> known as ACE D, makes more ACE than the other common version, ACE I.

> And athletes who have inherited ACE D from both parents experience

> about three times more heart growth in response to exercise than

> those who have inherited two ACE I genes7. They also seem to perform

> better in sports that rely on sheer strength and power, such as

> weight-lifting or sprinting. The I variant, in contrast, is more

> common among élite athletes in endurance sports such as long-distance

> running and swimming, which require more efficient metabolic use of

> energy and oxygen8, 9.

> As the lower levels of ACE associated with ACE I improve

> endurance, Hugh Montgomery, a cardiovascular geneticist at University

> College London, wondered whether ACE I might also be advantageous to

> those suffering serious illness. He found that children with

> potentially deadly meningitis were more likely to require intensive

> care or to die if they had two copies of the ACE D gene rather than

> two copies of ACE I10. His team also found that premature babies with

> ACE I fare better11. " Our work on athletes is feeding back into the

> clinic, " says Montgomery. " How efficiently we use oxygen is decisive

> when we are desperately sick. "

> It may eventually be possible to help such patients with drugs

> that slow down ACE activity. Already, in unpublished work, ACE

> inhibitors have been shown to reduce muscle wasting in mice. And

> London-based drug company Ark Therapeutics is currently running final-

> stage clinical trials on the use of the ACE inhibitor imidapril to

> treat severe muscle wasting in cancer patients.

> " Genetic destiny should not become a new excuse for couch

> potatoes - everyone gets at least some benefit from regular

> exercise. "

> Fitness genetics may be feeding ideas into the clinic, but could

> genetic destiny become a new excuse for couch potatoes? " If they

> think their performance is limited by their genes, people tend to

> give up, " says Montgomery. " People are afraid of trying and failing -

> it's part of the human condition. " Nevertheless, his advice to those

> who long to be fitter is to do serious exercise come what may. For

> everyone, it seems, there is at least some benefit.

>

> References

> 1. Bouchard, C., Dionne, F. T., Simoneau, J. A. & Boulay, M. R.

> Exerc. Sport Sci. Rev. 20, 27-58 (1992). | PubMed | ChemPort |

> 2. Bouchard, C. & Rankinen, T. Med. Sci. Sports Exerc. 33 (Suppl.),

> S446-S451 (2001). | PubMed | ChemPort |

> 3. Rankinen, T. et al. Physiol. Genom. 15, 27-33 (2003). | ChemPort |

> 4. , P. T., Stefanick, M. L., Vranizan, K. M. & Wood, P. D.

> Metabolism 43, 917-924 (1994). | Article | PubMed | ChemPort |

> 5. Huygens, W. et al. Physiol. Genom. 17, 264-279 (2004). | ChemPort

> |

> 6. Perusse, L. et al. Med. Sci. Sports Exerc. 35, 1248-1264 (2003). |

> PubMed | ChemPort |

> 7. Myerson, S. G. et al. Circulation 103, 226-230 (2001). | PubMed |

> ChemPort |

> 8. Nazarov, I. B. et al. Eur. J. Hum. Genet. 9, 797-801 (2001). |

> Article | PubMed | ChemPort |

> 9. Tsianos, G. et al. Eur. J. Appl. Physiol. 92, 360-362 (2004). |

> PubMed | ChemPort |

> 10. Harding, D. et al. Am. J. Respir. Crit. Care Med. 165, 1103-1106

> (2002). | PubMed |

> 11. Harding, D. et al. J. Pediatr. 143, 746-749 (2003).

>

>

> Cheers, Al Pater

>

>

>

>

>

>

------------------------------------------------------------------------------

>

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" This study suggests that circulating CRP concentrations can be

markedly suppressed, independently of total adiposity or indeed fat

mass, by intense regular physical exercise. "

Exercise important:

http://atvb.ahajournals.org/cgi/content/full/23/9/1640

> I recall Edison didn't think exercise was good. He lived to

96, I think. If exercise is all important why don't we have a

preponderance of jocks in the 100yo group?

> The more we exercise the more cals we have to eat.

>

> Regards.

>

> ----- Original Message -----

> From: old542000

>

> Sent: Thursday, January 20, 2005 2:10 PM

> Subject: [ ] Exercise benefit for some questioned

>

>

>

> Hi All,

>

> Some CRers have higher levels of lipids thought to be

> associated with better health than others. A good example

> is Saul, who does not CR as much as many of us do. This

> appears not to be due to any particular unique feature of

> his CRON diet.

>

> Do our benefits from exercise depend on our genes?

>

> Exercise increases levels of high density lipoprotein

> (HDL) and an enzyme called angiotensin-converting

> enzyme (ACE). The article from Nature not in Medline

> yet indicates that our benefits from exercise are

> dictated by genes regulating the level of these molecules.

>

> Nature 433, 188 - 189 (20 January 2005)

> Alison Abbott

> All pain, no gain?

>

> Exercise is good for you, or so we always thought. But, as Alison

> Abbott learns, your genes don't always cooperate.

> When Claude Bouchard set out to see whether genes play a role in

> physical fitness, he assumed, like most people, that exercise

> training makes everyone fitter. Although he expected genes to

> modulate some individual responses to diet and exercise, he also

> anticipated that regular workouts would improve fitness indicators

> such as lung efficiency and blood cholesterol for everybody.

> Some 20 years later, it has become clear from the work of Bouchard

> and others that this is not the case. Looking at certain measures of

> fitness, some people actually fare worse after exercise, whereas

> others show little or no improvement.

> But this isn't vindication for couch potatoes. Everyone's health

> improves in some way or other from exercise, but just how it improves

> is largely dependent on genes. Now, the growing field of fitness

> genetics is attempting to tease those genetic components apart, and

> the studies are generating fresh insights into the benefits of

> exercise as well as unexpected pay-offs for medicine.

> Bouchard's attempts to track fitness genes began in the mid-1980s

> at Laval University in Quebec, Canada. He and his colleagues focused

> on the maximum amount of oxygen absorbed by the body from a lungful

> of air - a standard measure of aerobic fitness, usually abbreviated

> as VO2max. They found that most people can get more oxygen out of

> each breath after training but that a minority were no better off,

> regardless of how efficient their lungs were at the start. Because

> the variation was much less extreme within pairs of identical twins,

> Bouchard concluded that the effect was largely dictated by genes1.

> " Our work on athletes is feeding back into the clinic. How

> efficiently we use oxygen is decisive when we are desperately sick. "

> That initial study was fairly small, so Bouchard extended the

> work in 1992 by helping to set up a multicentre research effort

> called the HERITAGE Family Study, which is still running today. Now

> based - together with Bouchard - at the Pennington Biomedical

> Research Center in Baton Rouge, Louisiana, the study's main data set

> comes from some 740 sedentary adults who were subjected to an intense

> exercise regime in the lab. The researchers monitored changes in the

> participants' blood pressure, heart rate, blood chemistry and VO2max

> over 20 weeks.

>

> Survival of the fittest

> The study's main aim was to determine how exercise reduces risk

> factors for cardiovascular disease and diabetes, but Bouchard and

> researchers at the four other collaborating institutions also took

> blood samples for genetic analysis. " We were trying to find as many

> genes as possible that influence fitness and performance, " Bouchard

> says.

> The resulting reams of data and frozen blood samples are still

> being analysed, but the results so far confirm Bouchard's earlier

> studies. The average increase in VO2max after the training programme

> was 19%. But 5% of the subjects had virtually no change, and another

> 5% had improved by more than twice the average amount. Similarly,

> most people had lower exercising heart rates and blood pressure after

> the training programme - an indication of improved fitness - but the

> extent of the reduction was extremely variable. In a few people there

> was even a small rise in these numbers2.

> Much of this variability seems to be attributable to genes. The

> researchers found more variation between than within families,

> suggesting at least a portion of a person's ability to benefit from

> exercise is inherited. " We concluded that just about half of the

> difference in trainability was heritable, " says Tuomo Rankinen, the

> study's project manager.

> It is unclear to what extent fitness parameters such as VO2max are

> indicative of long-term health prospects, but even presumed health

> indicators such as cholesterol, a factor in heart disease, did not

> follow the expected pattern of more exercise is better. Conventional

> wisdom has it that regular exercise reduces the risk of heart disease

> by raising blood levels of high-density lipoprotein (HDL)

> cholesterol, a complex that helps prevent cholesterol from forming

> fatty deposits on blood-vessel walls. This is considered one of the

> key benefits of taking up sports such as running. But the HERITAGE

> data show that training does not inevitably increase levels of HDL

> cholesterol. In fact, in about one-third of exercisers, the level of

> the complex fell.

> Does this all mean that exercise could actually be bad for those

> of us with the 'wrong genes'? Not at all, insists Rankinen. " We found

> not a single 'universal non-responder', " he says. In other words,

> everyone improved on some score. Even those who could not raise their

> VO2max through exercise were still getting some other health benefit

> such as higher HDL cholesterol levels or lower blood pressure. And

> overall, the HERITAGE data show that the risk of cardiovascular

> disease and type 2 diabetes falls in those who exercise regularly,

> Rankinen says.

> One way to begin to untangle these apparently contradictory

> effects is to go after the genes involved. This could ultimately

> reveal a great deal about how exercise produces health benefits, and

> may lead to treatments for diseases of metabolism and physiology.

> To this end, scientists at the HERITAGE study are scanning the

> genomes of participants for gene variants that occur more frequently

> in association with different fitness responses. Although some

> metabolism genes have been identified that may play a role, the most

> strongly linked gene so far is Titin. This produces protein fibres

> that contribute to the elasticity of heart muscle cells. It may be

> that some forms of the gene allow the heart to pump larger volumes of

> blood than others3.

>

> Physical attractions

> Other teams are also on the hunt for fitness genes. ,

> a health researcher at the Lawrence Berkeley National Laboratory in

> Berkeley, California, for instance, suspects that a gene related to

> the synthesis of HDL cholesterol might be involved. Ten years ago, he

> found that people who have an easier time taking up running after

> leading sedentary lives also started out with higher levels of HDL

> cholesterol in their blood - and increased those levels more quickly -

> than those who find running difficult4. It turns out that an enzyme

> that boosts HDL cholesterol is found in 'slow-twitch' muscle fibre,

> the type that takes longer to fatigue and so makes distance running

> easier. is now beginning a large-scale genetic study to see

> whether differences in that enzyme are associated with differences in

> lifestyle choice.

> Meanwhile, Gaston Beunen, a sports scientist at the Catholic

> University of Leuven in Belgium, is looking at the half-dozen or so

> key genes that contribute to the synthesis of myostatin, a protein

> that blocks new muscle growth. His study of some 300 young sibling

> males, published in May last year, hints that three of these genes

> may help to determine a person's physical strength5.

> In the end, the number of fitness-linked genes is expected to be

> large. So far, more than 100 appear in the literature, most of which

> have been identified in the past four years6, although in many cases

> more work is needed to confirm the link. And some of these now seem

> likely to prove their worth in the clinic.

> One gene drawing a lot of attention encodes an enzyme called ACE,

> or angiotensin-converting enzyme. ACE activates the hormone

> angiotensin, which helps to maintain blood pressure and promotes the

> growth of the heart in response to exercise. One common gene variant,

> known as ACE D, makes more ACE than the other common version, ACE I.

> And athletes who have inherited ACE D from both parents experience

> about three times more heart growth in response to exercise than

> those who have inherited two ACE I genes7. They also seem to perform

> better in sports that rely on sheer strength and power, such as

> weight-lifting or sprinting. The I variant, in contrast, is more

> common among élite athletes in endurance sports such as long-distance

> running and swimming, which require more efficient metabolic use of

> energy and oxygen8, 9.

> As the lower levels of ACE associated with ACE I improve

> endurance, Hugh Montgomery, a cardiovascular geneticist at University

> College London, wondered whether ACE I might also be advantageous to

> those suffering serious illness. He found that children with

> potentially deadly meningitis were more likely to require intensive

> care or to die if they had two copies of the ACE D gene rather than

> two copies of ACE I10. His team also found that premature babies with

> ACE I fare better11. " Our work on athletes is feeding back into the

> clinic, " says Montgomery. " How efficiently we use oxygen is decisive

> when we are desperately sick. "

> It may eventually be possible to help such patients with drugs

> that slow down ACE activity. Already, in unpublished work, ACE

> inhibitors have been shown to reduce muscle wasting in mice. And

> London-based drug company Ark Therapeutics is currently running final-

> stage clinical trials on the use of the ACE inhibitor imidapril to

> treat severe muscle wasting in cancer patients.

> " Genetic destiny should not become a new excuse for couch

> potatoes - everyone gets at least some benefit from regular

> exercise. "

> Fitness genetics may be feeding ideas into the clinic, but could

> genetic destiny become a new excuse for couch potatoes? " If they

> think their performance is limited by their genes, people tend to

> give up, " says Montgomery. " People are afraid of trying and failing -

> it's part of the human condition. " Nevertheless, his advice to those

> who long to be fitter is to do serious exercise come what may. For

> everyone, it seems, there is at least some benefit.

>

> References

> 1. Bouchard, C., Dionne, F. T., Simoneau, J. A. & Boulay, M. R.

> Exerc. Sport Sci. Rev. 20, 27-58 (1992). | PubMed | ChemPort |

> 2. Bouchard, C. & Rankinen, T. Med. Sci. Sports Exerc. 33 (Suppl.),

> S446-S451 (2001). | PubMed | ChemPort |

> 3. Rankinen, T. et al. Physiol. Genom. 15, 27-33 (2003). | ChemPort |

> 4. , P. T., Stefanick, M. L., Vranizan, K. M. & Wood, P. D.

> Metabolism 43, 917-924 (1994). | Article | PubMed | ChemPort |

> 5. Huygens, W. et al. Physiol. Genom. 17, 264-279 (2004). | ChemPort

> |

> 6. Perusse, L. et al. Med. Sci. Sports Exerc. 35, 1248-1264 (2003). |

> PubMed | ChemPort |

> 7. Myerson, S. G. et al. Circulation 103, 226-230 (2001). | PubMed |

> ChemPort |

> 8. Nazarov, I. B. et al. Eur. J. Hum. Genet. 9, 797-801 (2001). |

> Article | PubMed | ChemPort |

> 9. Tsianos, G. et al. Eur. J. Appl. Physiol. 92, 360-362 (2004). |

> PubMed | ChemPort |

> 10. Harding, D. et al. Am. J. Respir. Crit. Care Med. 165, 1103-1106

> (2002). | PubMed |

> 11. Harding, D. et al. J. Pediatr. 143, 746-749 (2003).

>

>

> Cheers, Al Pater

>

>

>

>

>

>

------------------------------------------------------------------------------

>

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Is it not a FACT that we burn more calories when we exercise?

Jack Lalanne is not my idea of a fitness person of today. He did calisthenics and was not a jock, rather an actor. 90 yo is not old.

I'm not a rat - rats don't build high rise buildings.

A rat study doesn't "PROVE" anything for humans.

How many >100 yo are bodybuilders, etc? Please, the data.

We have many human experiments that would show whether excess exercise extended lifespan in humans. Compile the data of footballers, basketballers, weightlifters, etc.

Regards.

----- Original Message -----

From: chuinyun

Sent: Thursday, January 20, 2005 4:02 PM

Subject: [ ] Re: Exercise benefit for some questioned

Jack Lalanne is 90 year old. He born 09/26/1914.http://www.jacklalanne.com/Avg life span of people and rats that exercise is extended. Exerciseincrease avg lifespan, study proving this post here several time. Lookback! Why you insist on this opinion??> I recall Edison didn't think exercise was good. He lived to96, I think. If exercise is all important why don't we have apreponderance of jocks in the 100yo group?> The more we exercise the more cals we have to eat.> > Regards.

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Of course it's all relative but by most measures 90yo is not considered young.

This is an old topic long discussed, and discussion is sure to be colored by personal preferences.

No, AFAIK exercise alone doesn't appear to extend maximum "lifespan" (in experimental animal studies),

but it may improve your quality of life (in real humans) and may even prevent you from dying too soon.

Two different things.

JR

-----Original Message-----From: jwwright [mailto:jwwright@...]Sent: Thursday, January 20, 2005 4:12 PM Subject: Re: [ ] Re: Exercise benefit for some questioned

Is it not a FACT that we burn more calories when we exercise?

Jack Lalanne is not my idea of a fitness person of today. He did calisthenics and was not a jock, rather an actor. 90 yo is not old.

I'm not a rat - rats don't build high rise buildings.

A rat study doesn't "PROVE" anything for humans.

How many >100 yo are bodybuilders, etc? Please, the data.

We have many human experiments that would show whether excess exercise extended lifespan in humans. Compile the data of footballers, basketballers, weightlifters, etc.

Regards.

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Hi folks:

At the time of a previous discussion here on exercise, with Freebird

I believe, I emailed the New England Centenarian Study and asked them

why exercise was not on their list of behaviours common to the

centenarians they have studied (all of the centenarians resident in

New England, as well as many elsewhere).

Their reply, which I posted here in full at the time, was,

approximately: " because we do not see a lifetime of exercise as a

characteristic common to the centenarians we study " .

If someone really wants to see that response it is sitting in the

archives. If I had to guess I would say perhaps around post

#10,000. But that is just a guess.

Rodney.

--- In , " " <crjohnr@b...>

wrote:

> Of course it's all relative but by most measures 90yo is not

considered

> young.

>

> This is an old topic long discussed, and discussion is sure to be

colored by

> personal preferences.

>

> No, AFAIK exercise alone doesn't appear to extend

maximum " lifespan " (in

> experimental animal studies),

> but it may improve your quality of life (in real humans) and may

even

> prevent you from dying too soon.

>

> Two different things.

>

> JR

>

> -----Original Message-----

> From: jwwright [mailto:jwwright@e...]

> Sent: Thursday, January 20, 2005 4:12 PM

>

> Subject: Re: [ ] Re: Exercise benefit for some

questioned

>

>

> Is it not a FACT that we burn more calories when we exercise?

>

> Jack Lalanne is not my idea of a fitness person of today. He did

> calisthenics and was not a jock, rather an actor. 90 yo is not old.

> I'm not a rat - rats don't build high rise buildings.

> A rat study doesn't " PROVE " anything for humans.

> How many >100 yo are bodybuilders, etc? Please, the data.

>

> We have many human experiments that would show whether excess

exercise

> extended lifespan in humans. Compile the data of footballers,

basketballers,

> weightlifters, etc.

>

> Regards.

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Share on other sites

Hi folks:

At the time of a previous discussion here on exercise, with Freebird

I believe, I emailed the New England Centenarian Study and asked them

why exercise was not on their list of behaviours common to the

centenarians they have studied (all of the centenarians resident in

New England, as well as many elsewhere).

Their reply, which I posted here in full at the time, was,

approximately: " because we do not see a lifetime of exercise as a

characteristic common to the centenarians we study " .

If someone really wants to see that response it is sitting in the

archives. If I had to guess I would say perhaps around post

#10,000. But that is just a guess.

Rodney.

--- In , " " <crjohnr@b...>

wrote:

> Of course it's all relative but by most measures 90yo is not

considered

> young.

>

> This is an old topic long discussed, and discussion is sure to be

colored by

> personal preferences.

>

> No, AFAIK exercise alone doesn't appear to extend

maximum " lifespan " (in

> experimental animal studies),

> but it may improve your quality of life (in real humans) and may

even

> prevent you from dying too soon.

>

> Two different things.

>

> JR

>

> -----Original Message-----

> From: jwwright [mailto:jwwright@e...]

> Sent: Thursday, January 20, 2005 4:12 PM

>

> Subject: Re: [ ] Re: Exercise benefit for some

questioned

>

>

> Is it not a FACT that we burn more calories when we exercise?

>

> Jack Lalanne is not my idea of a fitness person of today. He did

> calisthenics and was not a jock, rather an actor. 90 yo is not old.

> I'm not a rat - rats don't build high rise buildings.

> A rat study doesn't " PROVE " anything for humans.

> How many >100 yo are bodybuilders, etc? Please, the data.

>

> We have many human experiments that would show whether excess

exercise

> extended lifespan in humans. Compile the data of footballers,

basketballers,

> weightlifters, etc.

>

> Regards.

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Share on other sites

Hi Chuiyun:

That is a very interesting study. It does appear to show that

exercise reduces CRP, which is good to know. Thank you.

However, to go to the trouble of running ultra-marathons (I don't

even know how far that is, but presumably it is more than 26 miles)

in order to drop your CRP by 50% seems to be an awful lot of effort,

especially when you consider that the WUSTL CRON subjects had an 81%

reduction in CRP without having to take a single extra step - just by

eating less of a very healthy diet.

I am in favor of taking more than average exercise. But I am still

very uncertain as to whether it will materially extend my lifespan.

Rodney.

--- In , " chuinyun " <chuinyun@a...>

wrote:

>

>

> " This study suggests that circulating CRP concentrations can be

> markedly suppressed, independently of total adiposity or indeed fat

> mass, by intense regular physical exercise. "

>

> Exercise important:

>

> http://atvb.ahajournals.org/cgi/content/full/23/9/1640

>

> --- In , " jwwright " <jwwright@e...>

wrote:

> > I recall Edison didn't think exercise was good. He lived to

> 96, I think. If exercise is all important why don't we have a

> preponderance of jocks in the 100yo group?

> > The more we exercise the more cals we have to eat.

> >

> > Regards.

> >

> > ----- Original Message -----

> > From: old542000

> >

> > Sent: Thursday, January 20, 2005 2:10 PM

> > Subject: [ ] Exercise benefit for some questioned

> >

> >

> >

> > Hi All,

> >

> > Some CRers have higher levels of lipids thought to be

> > associated with better health than others. A good example

> > is Saul, who does not CR as much as many of us do. This

> > appears not to be due to any particular unique feature of

> > his CRON diet.

> >

> > Do our benefits from exercise depend on our genes?

> >

> > Exercise increases levels of high density lipoprotein

> > (HDL) and an enzyme called angiotensin-converting

> > enzyme (ACE). The article from Nature not in Medline

> > yet indicates that our benefits from exercise are

> > dictated by genes regulating the level of these molecules.

> >

> > Nature 433, 188 - 189 (20 January 2005)

> > Alison Abbott

> > All pain, no gain?

> >

> > Exercise is good for you, or so we always thought. But, as

Alison

> > Abbott learns, your genes don't always cooperate.

> > When Claude Bouchard set out to see whether genes play a

role in

> > physical fitness, he assumed, like most people, that exercise

> > training makes everyone fitter. Although he expected genes to

> > modulate some individual responses to diet and exercise, he

also

> > anticipated that regular workouts would improve fitness

indicators

> > such as lung efficiency and blood cholesterol for everybody.

> > Some 20 years later, it has become clear from the work of

Bouchard

> > and others that this is not the case. Looking at certain

measures of

> > fitness, some people actually fare worse after exercise,

whereas

> > others show little or no improvement.

> > But this isn't vindication for couch potatoes. Everyone's

health

> > improves in some way or other from exercise, but just how it

improves

> > is largely dependent on genes. Now, the growing field of

fitness

> > genetics is attempting to tease those genetic components apart,

and

> > the studies are generating fresh insights into the benefits of

> > exercise as well as unexpected pay-offs for medicine.

> > Bouchard's attempts to track fitness genes began in the mid-

1980s

> > at Laval University in Quebec, Canada. He and his colleagues

focused

> > on the maximum amount of oxygen absorbed by the body from a

lungful

> > of air - a standard measure of aerobic fitness, usually

abbreviated

> > as VO2max. They found that most people can get more oxygen out

of

> > each breath after training but that a minority were no better

off,

> > regardless of how efficient their lungs were at the start.

Because

> > the variation was much less extreme within pairs of identical

twins,

> > Bouchard concluded that the effect was largely dictated by

genes1.

> > " Our work on athletes is feeding back into the clinic. How

> > efficiently we use oxygen is decisive when we are desperately

sick. "

> > That initial study was fairly small, so Bouchard extended

the

> > work in 1992 by helping to set up a multicentre research effort

> > called the HERITAGE Family Study, which is still running today.

Now

> > based - together with Bouchard - at the Pennington Biomedical

> > Research Center in Baton Rouge, Louisiana, the study's main

data set

> > comes from some 740 sedentary adults who were subjected to an

intense

> > exercise regime in the lab. The researchers monitored changes

in the

> > participants' blood pressure, heart rate, blood chemistry and

VO2max

> > over 20 weeks.

> >

> > Survival of the fittest

> > The study's main aim was to determine how exercise reduces

risk

> > factors for cardiovascular disease and diabetes, but Bouchard

and

> > researchers at the four other collaborating institutions also

took

> > blood samples for genetic analysis. " We were trying to find as

many

> > genes as possible that influence fitness and performance, "

Bouchard

> > says.

> > The resulting reams of data and frozen blood samples are

still

> > being analysed, but the results so far confirm Bouchard's

earlier

> > studies. The average increase in VO2max after the training

programme

> > was 19%. But 5% of the subjects had virtually no change, and

another

> > 5% had improved by more than twice the average amount.

Similarly,

> > most people had lower exercising heart rates and blood pressure

after

> > the training programme - an indication of improved fitness -

but the

> > extent of the reduction was extremely variable. In a few people

there

> > was even a small rise in these numbers2.

> > Much of this variability seems to be attributable to genes.

The

> > researchers found more variation between than within families,

> > suggesting at least a portion of a person's ability to benefit

from

> > exercise is inherited. " We concluded that just about half of

the

> > difference in trainability was heritable, " says Tuomo Rankinen,

the

> > study's project manager.

> > It is unclear to what extent fitness parameters such as

VO2max are

> > indicative of long-term health prospects, but even presumed

health

> > indicators such as cholesterol, a factor in heart disease, did

not

> > follow the expected pattern of more exercise is better.

Conventional

> > wisdom has it that regular exercise reduces the risk of heart

disease

> > by raising blood levels of high-density lipoprotein (HDL)

> > cholesterol, a complex that helps prevent cholesterol from

forming

> > fatty deposits on blood-vessel walls. This is considered one of

the

> > key benefits of taking up sports such as running. But the

HERITAGE

> > data show that training does not inevitably increase levels of

HDL

> > cholesterol. In fact, in about one-third of exercisers, the

level of

> > the complex fell.

> > Does this all mean that exercise could actually be bad for

those

> > of us with the 'wrong genes'? Not at all, insists Rankinen. " We

found

> > not a single 'universal non-responder', " he says. In other

words,

> > everyone improved on some score. Even those who could not raise

their

> > VO2max through exercise were still getting some other health

benefit

> > such as higher HDL cholesterol levels or lower blood pressure.

And

> > overall, the HERITAGE data show that the risk of cardiovascular

> > disease and type 2 diabetes falls in those who exercise

regularly,

> > Rankinen says.

> > One way to begin to untangle these apparently contradictory

> > effects is to go after the genes involved. This could

ultimately

> > reveal a great deal about how exercise produces health

benefits, and

> > may lead to treatments for diseases of metabolism and

physiology.

> > To this end, scientists at the HERITAGE study are scanning

the

> > genomes of participants for gene variants that occur more

frequently

> > in association with different fitness responses. Although some

> > metabolism genes have been identified that may play a role, the

most

> > strongly linked gene so far is Titin. This produces protein

fibres

> > that contribute to the elasticity of heart muscle cells. It may

be

> > that some forms of the gene allow the heart to pump larger

volumes of

> > blood than others3.

> >

> > Physical attractions

> > Other teams are also on the hunt for fitness genes.

,

> > a health researcher at the Lawrence Berkeley National

Laboratory in

> > Berkeley, California, for instance, suspects that a gene

related to

> > the synthesis of HDL cholesterol might be involved. Ten years

ago, he

> > found that people who have an easier time taking up running

after

> > leading sedentary lives also started out with higher levels of

HDL

> > cholesterol in their blood - and increased those levels more

quickly -

> > than those who find running difficult4. It turns out that an

enzyme

> > that boosts HDL cholesterol is found in 'slow-twitch' muscle

fibre,

> > the type that takes longer to fatigue and so makes distance

running

> > easier. is now beginning a large-scale genetic study

to see

> > whether differences in that enzyme are associated with

differences in

> > lifestyle choice.

> > Meanwhile, Gaston Beunen, a sports scientist at the

Catholic

> > University of Leuven in Belgium, is looking at the half-dozen

or so

> > key genes that contribute to the synthesis of myostatin, a

protein

> > that blocks new muscle growth. His study of some 300 young

sibling

> > males, published in May last year, hints that three of these

genes

> > may help to determine a person's physical strength5.

> > In the end, the number of fitness-linked genes is expected

to be

> > large. So far, more than 100 appear in the literature, most of

which

> > have been identified in the past four years6, although in many

cases

> > more work is needed to confirm the link. And some of these now

seem

> > likely to prove their worth in the clinic.

> > One gene drawing a lot of attention encodes an enzyme called

ACE,

> > or angiotensin-converting enzyme. ACE activates the hormone

> > angiotensin, which helps to maintain blood pressure and

promotes the

> > growth of the heart in response to exercise. One common gene

variant,

> > known as ACE D, makes more ACE than the other common version,

ACE I.

> > And athletes who have inherited ACE D from both parents

experience

> > about three times more heart growth in response to exercise

than

> > those who have inherited two ACE I genes7. They also seem to

perform

> > better in sports that rely on sheer strength and power, such as

> > weight-lifting or sprinting. The I variant, in contrast, is

more

> > common among élite athletes in endurance sports such as long-

distance

> > running and swimming, which require more efficient metabolic

use of

> > energy and oxygen8, 9.

> > As the lower levels of ACE associated with ACE I improve

> > endurance, Hugh Montgomery, a cardiovascular geneticist at

University

> > College London, wondered whether ACE I might also be

advantageous to

> > those suffering serious illness. He found that children with

> > potentially deadly meningitis were more likely to require

intensive

> > care or to die if they had two copies of the ACE D gene rather

than

> > two copies of ACE I10. His team also found that premature

babies with

> > ACE I fare better11. " Our work on athletes is feeding back into

the

> > clinic, " says Montgomery. " How efficiently we use oxygen is

decisive

> > when we are desperately sick. "

> > It may eventually be possible to help such patients with

drugs

> > that slow down ACE activity. Already, in unpublished work, ACE

> > inhibitors have been shown to reduce muscle wasting in mice.

And

> > London-based drug company Ark Therapeutics is currently running

final-

> > stage clinical trials on the use of the ACE inhibitor imidapril

to

> > treat severe muscle wasting in cancer patients.

> > " Genetic destiny should not become a new excuse for couch

> > potatoes - everyone gets at least some benefit from regular

> > exercise. "

> > Fitness genetics may be feeding ideas into the clinic, but

could

> > genetic destiny become a new excuse for couch potatoes? " If

they

> > think their performance is limited by their genes, people tend

to

> > give up, " says Montgomery. " People are afraid of trying and

failing -

> > it's part of the human condition. " Nevertheless, his advice to

those

> > who long to be fitter is to do serious exercise come what may.

For

> > everyone, it seems, there is at least some benefit.

> >

> > References

> > 1. Bouchard, C., Dionne, F. T., Simoneau, J. A. & Boulay, M. R.

> > Exerc. Sport Sci. Rev. 20, 27-58 (1992). | PubMed | ChemPort |

> > 2. Bouchard, C. & Rankinen, T. Med. Sci. Sports Exerc. 33

(Suppl.),

> > S446-S451 (2001). | PubMed | ChemPort |

> > 3. Rankinen, T. et al. Physiol. Genom. 15, 27-33 (2003). |

ChemPort |

> > 4. , P. T., Stefanick, M. L., Vranizan, K. M. & Wood,

P. D.

> > Metabolism 43, 917-924 (1994). | Article | PubMed | ChemPort |

> > 5. Huygens, W. et al. Physiol. Genom. 17, 264-279 (2004). |

ChemPort

> > |

> > 6. Perusse, L. et al. Med. Sci. Sports Exerc. 35, 1248-1264

(2003). |

> > PubMed | ChemPort |

> > 7. Myerson, S. G. et al. Circulation 103, 226-230 (2001). |

PubMed |

> > ChemPort |

> > 8. Nazarov, I. B. et al. Eur. J. Hum. Genet. 9, 797-801 (2001).

|

> > Article | PubMed | ChemPort |

> > 9. Tsianos, G. et al. Eur. J. Appl. Physiol. 92, 360-362

(2004). |

> > PubMed | ChemPort |

> > 10. Harding, D. et al. Am. J. Respir. Crit. Care Med. 165, 1103-

1106

> > (2002). | PubMed |

> > 11. Harding, D. et al. J. Pediatr. 143, 746-749 (2003).

> >

> >

> > Cheers, Al Pater

> >

> >

> >

> >

> >

> >

> --------------------------------------------------------------------

----------

> >

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Does the article consider a person could have lower fat mass just from eating less?

Regards.

----- Original Message -----

From: chuinyun

Sent: Thursday, January 20, 2005 4:06 PM

Subject: [ ] Re: Exercise benefit for some questioned

"This study suggests that circulating CRP concentrations can bemarkedly suppressed, independently of total adiposity or indeed fatmass, by intense regular physical exercise."Exercise important:http://atvb.ahajournals.org/cgi/content/full/23/9/1640

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Hi All,

Thank you, Rodney for that heads-up. It brought to my attention the

pdf-available to all:

>2: Perls T.

>>>> Centenarians who avoid dementia.

>Trends Neurosci. 2004 Oct;27(10):633-636.

>PMID: 15374676 [PubMed - as supplied by publisher]

>

>http://tinyurl.com/7yq46

>

> There was brief mention made of CR in:

>

> ... Discovering genes that could impart the ability to live

>to old age while compressing the period of disability

>toward the end of life should yield important insight into

>how the aging process increases susceptibility to diseases

>associated with aging, and into how this susceptibility

>might be modulated [8]. Human longevity-enabling genes

>are likely to influence aging at its most basic levels, thus

>affecting a broad spectrum of genetic and cellular path-ways

>synchronously. The centenarian genome should also

>be an efficient tool for ferreting out disease genes.

>Comparing SNP frequencies implicated in disease in

>centenarians with frequencies in persons with the disease

>should show clinically relevant polymorphisms. Another

>approach that researchers are in the early stages of

>understanding is differential gene expression in models

>known to slow the aging process, such as caloric restriction

>[55]. This might prove to be another potent tool for

>discovering longevity-enabling genes. The hope, of course,

>is that these gene discoveries will help in identification of

>drug targets and creation of drugs to allow persons to

>become more `centenarian-like' by maximizing the period

>of their lives spent in good health.

>

>

This article is now pdf-available at:

http://www.bumc.bu.edu/www/BUSM/Cen/articles/trends_in_NP.pdf

http://tinyurl.com/4hoko

> > Of course it's all relative but by most measures 90yo is not

> considered

> > young.

> >

> > This is an old topic long discussed, and discussion is sure to be

> colored by

> > personal preferences.

> >

> > No, AFAIK exercise alone doesn't appear to extend

> maximum " lifespan " (in

> > experimental animal studies),

> > but it may improve your quality of life (in real humans) and may

> even

> > prevent you from dying too soon.

> >

> > Two different things.

> >

> > JR

> >

> > -----Original Message-----

> > From: jwwright [mailto:jwwright@e...]

> > Sent: Thursday, January 20, 2005 4:12 PM

> >

> > Subject: Re: [ ] Re: Exercise benefit for some

> questioned

> >

> >

> > Is it not a FACT that we burn more calories when we exercise?

> >

> > Jack Lalanne is not my idea of a fitness person of today. He did

> > calisthenics and was not a jock, rather an actor. 90 yo is not

old.

> > I'm not a rat - rats don't build high rise buildings.

> > A rat study doesn't " PROVE " anything for humans.

> > How many >100 yo are bodybuilders, etc? Please, the data.

> >

> > We have many human experiments that would show whether excess

> exercise

> > extended lifespan in humans. Compile the data of footballers,

> basketballers,

> > weightlifters, etc.

> >

> > Regards.

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I once knew a retired footballer from the Chi Bears, a retired executive 85yo. That was about 1982, and he died not long after. But that's my only recollection of any old person being let's say, more than walking a lot. The old people I see now, are definitely not walking much and it's hard to get them to walk.

What really strikes me, is that a guy can be very active at work, going between meetings, etc. and yet acquire a D shape at about 50. Even golfing, swimming, racquet ball, handball. My gardener, I've seen grow from a healthy hard working yard man to a fat slob, in the 14 yrs I've known him. He used to do 8 to 10 lawns per day, now he does 1 or 2 and he suffers in the heat. I could use that as an example of what exercise not to do, but it's a metabolic thing we don't understand yet.

Hey, I can get that gut back if I want to eat too much. And I can outeat any exercise I can do. Question is what's the relationship between aging and calories. I think we found it.

regards.

----- Original Message -----

From: Rodney

Sent: Thursday, January 20, 2005 4:48 PM

Subject: [ ] Re: Exercise benefit for some questioned

Hi folks:At the time of a previous discussion here on exercise, with Freebird I believe, I emailed the New England Centenarian Study and asked them why exercise was not on their list of behaviours common to the centenarians they have studied (all of the centenarians resident in New England, as well as many elsewhere).Their reply, which I posted here in full at the time, was, approximately: "because we do not see a lifetime of exercise as a characteristic common to the centenarians we study".If someone really wants to see that response it is sitting in the archives. If I had to guess I would say perhaps around post #10,000. But that is just a guess.Rodney.

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>>>

From: " Rodney " <perspect1111@y...>

Date: Thu Jan 20, 2005 5:48 pm

Subject: Re: Exercise benefit for some questioned

.... I emailed the New England Centenarian Study and asked them

why exercise was not on their list of behaviours common to the

centenarians they have studied (all of the centenarians resident in

New England, as well as many elsewhere).

Their reply, which I posted here in full at the time, was,

approximately: " because we do not see a lifetime of exercise as a

characteristic common to the centenarians we study " .

>>>

Exercise is positively correlated with longevity and/or reduced

mortality. However, I have read somewhere that if you do not exercise

for about two or three months, it is as if you had never exercised.

You need to exercise regularly to obtain any benefits, but PMID

14615275, below, suggests that exercise in old age does not help

(whatever " old " is). Maybe when we reach an age of 95 we don't need

to exercise any more.

A search in Pubmed for " exercise " and " longevity " provided over 200

hits. Below is a sample. Interestingly, I did not find any articles

that said that exercise reduced lifespan. So, exercise is good

overall.

Tony

====

J Gerontol. 1993 May;48(3):B97-100.

Exercise increases average longevity of female rats despite

increased food intake and no growth retardation.

Holloszy JO.

These results show that exercise improves average longevity of rats

independent of decreased availability of energy for cell proliferation

and growth. They also provide evidence that an increase in food intake

is not harmful when balanced by an increase in energy expenditure.

PMID: 8482812

JAMA. 1995 Apr 19;273(15):1179-84.

Exercise intensity and longevity in men. The Harvard Alumni Health

Study.

Lee IM, Hsieh CC, Paffenbarger RS Jr.

CONCLUSIONS--These data demonstrate a graded inverse relationship

between total physical activity and mortality. Furthermore, vigorous

activities but not nonvigorous activities were associated with

longevity. These findings pertain only to all-cause mortality;

nonvigorous exercise has been shown to benefit other aspects of

health.

PMID: 7707624

Mech Ageing Dev. 2005 Feb;126(2):327-31.

Strategies to enhance longevity and independent function: the

Jerusalem Longitudinal Study.

Stessman J, Hammerman-Rozenberg R, Maaravi Y, Azoulai D, Cohen A.

CONCLUSIONS: : These findings highlight the ability of social,

economic and functional factors to modify genetic influence on

survival and function. Increased physical and social activity is an

important tool to lengthen the span of robust function. The role of

heredity in determining function and mortality may be expressed

through diverse pathways.

PMID: 15621214

Ann Epidemiol. 2004 Jul;14(6):391-8.

Leisure time physical activity and mortality in Hong Kong:

case-control study of all adult deaths in 1998.

Lam TH, Ho SY, Hedley AJ, Mak KH, Leung GM.

Using a case-control study, past (10 years prior) levels of LTPA were

ascertained via proxy informants for 24,079 dead cases (81% of all

registered deaths) and 13,054 live controls aged #10878;35 years and

were analyzed by unmatched logistic regression to determine their

association with all-cause and cause-specific mortality. RESULTS:

Compared with an exercise frequency of <1 episode per month, > or = 1

episode of LTPA per month was inversely associated with all-cause

mortality [multivariable odds ratio (OR)=0.63, 95% confidence interval

(CI), 0.59, 0.68 for males; OR=0.75, 95% CI, 0.70, 0.80 for females;

adjusted for age, education, smoking status, alcohol consumption, and

physical demand at work]. Each activity level above the reference

level of <1 episode per month (i.e., 1 episode per month to 1-3

episodes per week, > or = 4 episodes per week) had approximately the

same level of risk reduction and no dose-response gradient was

observed.

PMID: 15246327

Am J Physiol Regul Integr Comp Physiol. 2004 Mar;286(3):R505-11. Epub

2003 Nov 13.

Beneficial effects of moderate exercise on mice aging: survival,

behavior, oxidative stress, and mitochondrial electron transfer.

Navarro A, Gomez C, -Cepero JM, Boveris A.

Moderate exercise, started at young age in mice, increased life span,

decreased oxidative stress, and prevented the decline of cytochrome

oxidase activity and behavioral performance at middle age but not at

old age.

PMID: 14615275

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Not to argue against exercise (whatever that is),

What is "exercise"?

Calories per day____________ % of total calories____________

Best type - manual labor versus jogging, eg.____________

Recognize that longevity is often correlated to education level ( I guess that means less manual labor); income (better medical care); social status/support (less stress perhaps)?

If I expand the search with "OR exercise and lifespan", I get 292 for humans only, and several interesting sounding titles have no abstract.

Your post is interesting:

Ann Epidemiol. 2004 Jul;14(6):391-8.

Leisure time physical activity and mortality in Hong Kong: case-control study of all adult deaths in 1998.

{BUT, recognize these were people who COULD exercise. How can anyone alive do less than one per month? I exercise more than the people around me, but is it enough, is it optimal?}

At present, however, there is no definite evidence that "frail" elderly subjects really benefit from restoring GH and IGF-I levels within the young adult range by treatment with rhGH, rhlGF-I, GHRH or GHS. In this article the alteration of the GH/IGF-I axis activity during ageing is revised taking into account the role of physical activity as a regulator of the axis function and considering the effects of the restoration of GH and IGF-I circulating levels on body composition and physical performance. PMID: 14964439

I liked this:

Adv Gerontol. 2003;12:57-76.

[biochemistry of lifespan extension]Golubev AG.When these conclusions are compared with demographic data, it comes out that virtually all advances in gerontology may be reduced to maxims of healthy ageing known from extreme antiquity. Under optimal socioeconomic conditions, the chances to approach the documented world record of human longevity (122 years) may be increased by (not to mention getting rid of smoking and other abuses) high physical activity, adequate nutrition enriched in fresh fruits, optimism, and timely treatment of specific diseases. The most important bottleneck in the realization of these reserves is currently the public consciousness rather than the science. PMID: 14743602

Regards.

----- Original Message -----

From: citpeks

Sent: Thursday, January 20, 2005 9:59 PM

Subject: [ ] Re: Exercise benefit for some questioned

>>>From: "Rodney" <perspect1111@y...>Date: Thu Jan 20, 2005 5:48 pmSubject: Re: Exercise benefit for some questioned... I emailed the New England Centenarian Study and asked themwhy exercise was not on their list of behaviours common to thecentenarians they have studied (all of the centenarians resident inNew England, as well as many elsewhere).Their reply, which I posted here in full at the time, was,approximately: "because we do not see a lifetime of exercise as acharacteristic common to the centenarians we study".>>>Exercise is positively correlated with longevity and/or reducedmortality. However, I have read somewhere that if you do not exercisefor about two or three months, it is as if you had never exercised. You need to exercise regularly to obtain any benefits, but PMID14615275, below, suggests that exercise in old age does not help(whatever "old" is). Maybe when we reach an age of 95 we don't needto exercise any more.A search in Pubmed for "exercise" and "longevity" provided over 200hits. Below is a sample. Interestingly, I did not find any articlesthat said that exercise reduced lifespan. So, exercise is goodoverall.TonyJAMA. 1995 Apr 19;273(15):1179-84. Exercise intensity and longevity in men. The Harvard Alumni HealthStudy. Lee IM, Hsieh CC, Paffenbarger RS Jr.CONCLUSIONS--These data demonstrate a graded inverse relationshipbetween total physical activity and mortality. Furthermore, vigorousactivities but not nonvigorous activities were associated withlongevity. These findings pertain only to all-cause mortality;nonvigorous exercise has been shown to benefit other aspects ofhealth.PMID: 7707624Mech Ageing Dev. 2005 Feb;126(2):327-31. Strategies to enhance longevity and independent function: theJerusalem Longitudinal Study. Stessman J, Hammerman-Rozenberg R, Maaravi Y, Azoulai D, Cohen A.CONCLUSIONS: : These findings highlight the ability of social,economic and functional factors to modify genetic influence onsurvival and function. Increased physical and social activity is animportant tool to lengthen the span of robust function. The role ofheredity in determining function and mortality may be expressedthrough diverse pathways.PMID: 15621214Ann Epidemiol. 2004 Jul;14(6):391-8. Leisure time physical activity and mortality in Hong Kong:case-control study of all adult deaths in 1998. Lam TH, Ho SY, Hedley AJ, Mak KH, Leung GM.Using a case-control study, past (10 years prior) levels of LTPA wereascertained via proxy informants for 24,079 dead cases (81% of allregistered deaths) and 13,054 live controls aged #10878;35 years andwere analyzed by unmatched logistic regression to determine theirassociation with all-cause and cause-specific mortality. RESULTS:Compared with an exercise frequency of <1 episode per month, > or = 1episode of LTPA per month was inversely associated with all-causemortality [multivariable odds ratio (OR)=0.63, 95% confidence interval(CI), 0.59, 0.68 for males; OR=0.75, 95% CI, 0.70, 0.80 for females;adjusted for age, education, smoking status, alcohol consumption, andphysical demand at work]. Each activity level above the referencelevel of <1 episode per month (i.e., 1 episode per month to 1-3episodes per week, > or = 4 episodes per week) had approximately thesame level of risk reduction and no dose-response gradient wasobserved.PMID: 15246327

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