Heavy physical activity may significantly reduce heart disease deaths, especially after age 45

Health Correlator: Heavy physical activity may significantly reduce heart disease deaths, especially after age 45

Sunday, April 19, 2015

The idea that heavy physical activity is a main trigger of heart attacks
is widespread. Often endurance running and cardio-type activities are
singled out. Some people refer to this as “death by running”. Others
think that strength training has a higher lethal potential. We know
based on the Oregon Sudden Unexpected Death Study that this is a myth (1)

Here is some evidence that heavy physical activity in fact has a
significant protective effect. The graph below shows the number of
deaths from coronary heart disease, organized by age group, in
longshoremen (dock workers). The shaded bars represent those whose level
of activity at work was considered heavy. The unshaded bars represent
those whose level of activity at work was considered moderate or light
(essentially below the “heavy” level).

The data is based on an old and classic study of 6351 men, aged 35 to 74
years, who were followed either for 22 years, or to death, or to the
age of 75. It shows a significant protective effect of heavy activity,
especially after age 45 (2).

The numbers atop the unshaded bars reflect the relative risk of death
from coronary heart disease in each age group. For example, in the age
group 65-74, the risk among those not in the heavy activity group is 110
percent higher (2.1 times higher) than in the heavy activity group.

It should be noted that this is a cumulative effect, of years of heavy
activity. Based on the description of the types of activities performed,
and the calories spent, I estimate that the heavy activity group
performed the equivalent of a few hours of strength training per week,
plus a lot of walking and other light physical activities. The authors
of the study concluded that “… repeated bursts of high energy output established 
a plateau of protection against coronary mortality.”

Heavy physical activity may not make you lose much weight, but has the potential to make you live longer.

Posted by
Ned Kock at
1:12 PM

DEXA Scans - muscle/fat ratio and bone density theory

W.O.W. 3/20/15-DEXA Scans Have Brought Me More New Clients Than All the Ads I Ever Bought. »



I got a call from a
prospective client.  The call was about one of the most common
issues that brings us new clients….the results of a recent DEXA scan.
 People often become very alarmed when their DEXA results return with
poor scores and their doctor recommends starting bisphosphonates
(medications like Fosamax) to try and reverse their bone loss.  This
usually triggers an internet search on treating and preventing
osteoporosis, which invariably uncovers some article about SuperSlow and
its genesis in the Osteoporosis Research Project at the University of
Florida.  This in return creates some sort of link to Ultimate Exercise
(or many other such facilities).


I have always been a pretty vocal opponent of DEXA scans because I
feel that they alarm patients (a morbidity) and triggers the urge to do
“something”.  That something is usually bisphosphonates, a class of
drugs with some pretty gnarly side-effects. Further, the benefits of
increasing bone mineral density have always been a little oversold by
correlating an absolute increase in bone density with a relative
percentage risk reduction of fractures.  Further, literature suggests
that the real correlate for fracture risk is your starting level of bone
mineral density, NOT the level you improve to.  To me this has always
suggested that bone density was simply a surrogate marker for fracture
risk.  I have always suspected the real marker for risk was muscle mass
and the resultant strength level.

If we look at these images lifted from Skyler Tanner’s post on
bending the aging curve, we must ask ourselves if the sedentary person’s
real risk of a fall and subsequent fracture really dependent on the
bone density of his femur?  Or…is the real problem the atrophy that has
occurred in his thigh muscles and the fact that if he gets the least bit
off of his center of gravity he is going down.  And when he (or she)
does go down, there is not enough shock absorbing skeletal muscle to
protect that frail femur from snapping in two.  If you stuck that frail
bone in the middle of all the muscle in the pictures above or below, do
you think it would stand a much better chance all the way around?

But the situation is actually much better than that.  Because, when
you improve the muscle mass the bone mineral density tracks right along
(as does all other organ mass).  It used to be thought that the bone
mineral density was increasing because of the forces upon the
bone…strain and stress that could also risk a fracture.  But I have seen
too many clients improve bone mineral density without exposure to
dangerous force to believe that.  As it turns out the increase in bone
density, as well as other improvements in organ mass, are related to
muscle to organ cross talk mediated by myokines.  There is even evidence
that myokine exposure can improve bone density in the complete absence
of stress/strain loading.  So when someone tells you that slow cadence,
force-controlled exercise does not sufficiently stress the bone to
improve bone density, you can smile and walk away.  As it turns out,
training in this way gives you all of the upside and none of the down
side of the traditional notion of “load-bearing exercise”.  What the new
research on myokines is demonstrating is that proper strength exercise
is the most profound public health initiative that we have available too
us.  The economic implications of a vibrant and productive aging
populace, as opposed to a debilitated and dependent one is almost too
big to imagine.

This is especially true in light of the collapse of our medical and social entitlement systems.

To get further insight into the issue of muscle-bone cross-talk via myokines, check out the interview linked below:

http://www.nature.com/bonekey/community/2012/05/moving-from-bone-to-muscle-and-back-again-an-interview-with-mark-hamrick/

Muscle loss has little to do with aging | The poor, misunderstood calorie

Sarcopenia has little to do with aging | The poor, misunderstood calorie

Posted on August 9, 2013 | 8 Comments

 

It has to do with the duration of time spent being sedentary.

They say a picture is worth a thousand words, but luckily enough today you get both.
Sarcopenia: “poverty of flesh,” or the age-induced loss of skeletal muscle mass, strength, and function = reduced quality of life.  Sorry old-timers, but I hereby officially revise the definition from “aging-induced” to “sedentary-induced.”  Herein, I present evidence that sarcopenia is not a phenomenon of aging per se, but rather of disuse atrophy.  Dear Webster’s & Britannica, please revise accordingly.
Skeletal muscles: use ‘em or lose ‘em #TPMC

Thanks to Julianne Taylor & Skyler Tanner for directing me to these images.
divide and conquer

Exhibit A. Chronic exercise preserves lean muscle mass in masters athletes (Wroblewski et al., 2011)

This study evaluated “high-level recreational athletes.”  “Masters” just means they were over 40.  And “high-level” doesn’t mean “elite,” it just means they exercised 4-5 times per week.  These weren’t super-obsessed gym rats… it’s probably who I’ll be in 7 years [sigh].


They took a lot of measurements which showed these people were pretty fit, but the money shot was this pic:



It wasn’t a randomized double-blind placebo-controlled intervention trial, but that pic made up for all of that.  Even if they cherry-picked the scans, I find them compelling.  Call it confirmation bias if you like.

Exhibit B.  Knee extensor strength, activation, and size in VERY elderly people following strength training (Harridge et al., 1999)

12 weeks of leg exercises performed in 11 adults 85-97 years of age.  They were recruited from a geriatric hospital, and despite still kicking well beyond their expiration date, they maintained the ability to get strong:

Some of these gains were likely attributable to the novice effect, or the neuromuscular adaptations that occur in untrained individuals during the onset of a new training program, but nonetheless, these data show there are no intrinsic defects caused by being old that hinder the ability to improve muscle strength [and function].

There was no non-exercising control group with which to compare the following figure, but I assure you, non-exercising 90-year old geriatrics aren’t putting on muscle like this guy did:



I’m not recommending retirees to train for a 480-pound deadlift. 

Progress can probably be made carrying a gallon of water around the yard, or up and down a flight of stairs; don’t use handicap parking if your only handicap is being old.  

Sarcopenia is a major reducer of quality of life.  You don’t have to join a gym but you have to get off your ass!

Effective Exercise to Slow Muscle Loss With Aging -- Concepts - Art De Vany on Line

Effective Exercise to Slow Muscle Loss With Aging -- Concepts - Art De Vany on Line

Take a look at the long protein that stretches through the entire sarcomere that is called the giant protein TITIN. It is a sensor of stretch and contraction and passes through the M-band and the Z-band and affects muscle gene expression powerfully.

In this post, I explore the research and theory behind the new form of exercise I have been using now that I am to be 76 this August. It is a combination of standard exercises in some sense, so it is not wholly new and could not be because exercise is simply muscle contraction or stretch.

After looking over the research and using my self-experiment, I have come to a tentative conclusion that targeting TITIN and another sensor in the muscle cell is a useful model of effective exercise. It is a model that can help you and has helped me to design an exercise routine and think about the purpose of exercise.

My basic goals are to

1. stave off sarcopenia (wasting of lean muscle),
2. limit inflammation (but use it as an acute signal),
3. preserve the alpha-motor neurons (they fire the FT fibers) and their signals
4. produce acute signals of BDNF (brain derived neuronal growth factor),
5. preserve mitochondrial density and function, and
6. stimulate (acutely, not chronically) protein synthesis,
7. maintain high anabolic and sex hormone production.

That sounds like a big challenge, but it is not so hard to do since I have spent a lifetime doing that in following Evolutionary Fitness, which I developed in the 1980s and summarized in my book, The New Evolution Diet. The challenge now is to do this without loading my joints or over-loading my adaptive capacity. I find it extraordinary that older people are often put on the same old exercise technology used by body builders and recommended by exercise physiologists --- 3 sets of 10 reps with 80% of the one-repetition maximum, three times a week. The experiments that I have read that track response and stress almost always show that the old-timers experience a rise in stress hormones such as cortisol (so do lots of people who overdo it in the gym) and often experience a rise in inflammation. That they still manage to gain strength and muscle mass is a very strong endorsement of weight lifting, but it could be done much more efficiently in my view. The rise in cortisol and inflammation limit and may even prevent the gains that are sought.

The easiest things to temper the pace of aging are to eat as detailed in my previous post.

In developing my new approach to exercise, I was concerned about the slow rate of force development that occurs with aging, which is attributable to the degeneration of the alpha motor neurons in the spine, and with the imbalance between agonist and antagonist muscles that lead to stiffness, poor balance, and the impaired movement shown in the aged. The muscle cells of the aged take on a disorganized state, with a mixing of fiber types, diffuse signaling of the motor neurons as they diminish in size and signaling strength, intrusion of connective tissue, and lessened density of mitochondria. As the motor neurons diminish in number and firing strength, they fire more broadly over the muscle cells and they become less coordinated. FT fibers are lost and the remaining fibers look like a mass of disorganized, undifferentiated fibers.

The inability of aged muscles to absorb force (such as in landing from a jump) imposes a higher load on the joints and connective tissues. This is partly due to the inability of the agonist muscles to lengthen under load and also due to the excess tone or stiffness of the antagonist muscles. A summary of what follows would be this:

1. Point number one of my exercise is to increase the ability of the agonist muscle to lengthen under load and diminish the resistance from the antagonist muscle.
2. Point number two is to increase the signaling to the FT fibers, which has the side benefit of improving the alpha motor neuron connection, firing, and signal conductance.
3. Point number three is to increase the rate at which I can develop force --- rapid force production is the key.
4. Point number four, and this is a key, is to improve the integrity of the muscle cell to prevent its fall into a disorganized state. I think the alpha motor neuron activation and measures of muscle cell size and stress such as the giant elastic protein titin and dystrophin are big factors here.
5. Point 5, keep the mitochondria in the muscle dense and active, when you lose enough of them the cell goes into a death program.
6. Point 6, hang on to the nuclei of your muscle cells. Lose them and you lose muscle cell size.

The muscle cells diminish through a loss of cell number or a loss of cell size. Disorganized cells may actually be larger than organized ones, but they are lost because disorganized cells are removed. The aging must contend with cell atrophy, which is an active process under genetic control. These atrogenes (atrophy producing genes) promote the activity of the ubiquitin-proteasome pathways that actively destroy the muscle cell. Diabetes, cancer cachexia, renal failure, fasting, and denervation (loss of motor neurons) lead to cell death through activation of the atrogene pathways (atrogin-1/MFb1 and MuFR1 have been identified as the primary atrogenes). The atrogenes seem to be the master genes for muscle wasting.

Insulin, acute insulin, not chronic insulin, and IGF-1 induce Akt action. So, rather than making muscle grow, Akt action primarily works by turning down the muscle-wasting atrogenes. It is simple to activate the Akt (and downstream the mTOR) pathway --- exercise induces muscle-produced IGF-1 and eating protein or consuming BCAAs induces an acute release of insulin. Both activate Akt. Carbohydrates release insulin, which up regulates Akt, but the activation is long-lasting and quickly becomes chronic if excess carbohydrate intake leads to insulin resistance. Note, that diabetics suffer muscle wasting at least partly because they become insulin resistant and fail to activate Akt.

Akt-1 is the important pathway for muscle growth and it is activated by exercise. Passive stretch strongly activates Akt signaling and FT fiber development. Akt expression also up regulates mTOR expression and muscle growth. Protein consumption also increases mTOR expression, which seems to be an energy sensor or nutrient sensor.

Interestingly, blocking myostatin, a limiter of muscle size, seems to produce larger but less effective muscles. The FTb fibers, the ones I prize most, form disorganized tubular structures that do not correlate with force production when myostatin is blocked. A myostatin blocker, the holy grail of body builders, leads to bigger, less functional muscles, a price they may be willing to pay.

The inflammatory pathways, through increased levels of TNF-alpha, the cytokine IL-6, and myostatin, are involved in upregulating the atrogenes that cause muscle atrophy. PGC-1alpha is the master regulatory gene for mitochondrial biogenesis, which is crucial for muscle preservation. A loss of mitochondrial density in muscle not only reduces its effective energy and strength, it leads to either the death of the cell or its atrophy. BCAAs improve PGC-1alpha function and expression so that mitochondrial biogenesis is activated. So does intermittent fasting.

Atrophy is the enemy of aging muscle, more so than a lack of anabolic or growth factors. Aging muscle can grow, but only if the balance of atrophy versus anabolism moves to a positive balance acutely. Chronic expression of an anabolic state, paradoxically to a homeostatic point of view, leads to muscle atrophy. But, unfortunately for the homeostatic model, cell size is not a homeostatic variable under genetic control of the muscle cell. Thus, acute changes in atrophy versus anabolism seem to be essential to preserving or growing muscle cell size. Inhibiting cell turnover does not seem to influence protein breakdown, which primarily occurs in the cell to reduce its size.

Conclusion: sarcopenia, at the current state of knowledge, seems to primarily occur through a loss of muscle cell size rather than number. The cells seem to adjust in size through loss of organelles, cytoplasm, and proteins in such a way as to preserve the size of the nuclear domain, the cell domain surrounding the muscle nuclei. Thus, loss of muscle size occurs through loss of nuclei within the cell. And, we know that nuclei are lost when motorneurons fail to signal the nuclei. Disuse, oxidative damage to the neurons or neural plate junction at the muscle, inflammatory damage, or atrogene expression are factors in the loss of nuclei of muscle cells.

So, the bottom line is: preserve muscle, keep your myonuclei, the nuclei of your muscle cells. Two major points follow:

1. This is primarily linked to the alpha signaling of motorneurons. Evidence comes from experiments that down regulate the opposing beta signals to the motorneurons, which is shown to result in hypertrophy and a conversion from slow to fast fibers. That says, in short, that increasing alpha signaling produces hypertrophy and slow to fast muscle fiber conversion. We know how to do this and my “system” does it very well (more below)
2. The interesting link in muscle signaling is that it depends on mechanical load at the sarcomere, the basic unit of muscle contractive machinery, which is transmitted from there to the nucleus to affect muscle gene expression.

Now, we are really getting somewhere. The giant, elastic protein titin spans half the sarcomere from the Z disk to the M band and interacts with a large number of muscle proteins. Down in the M-band there is a region that alters gene expression that is affected by stretching or contraction of titin. In the absence of stretching or contraction of the titin protein, SRF (serum response factor) a muscle gene expression factor is exported from the muscle cell nucleus.  Without SRF, it seems muscle does not grow. Experimental depletion of SRF genes causes severe muscle hypoplasia.

There is another mechanical sensor in muscle that could play a role in muscle size. Dystrophin glycoprotein complex (DGC) anchors the muscle skeleton to the cell membrane. DGC couples the working part of the cell to its membrane and is essential for translating muscle contraction into force. Dystrophin is lost when muscle atrophies and may even be part of the atrophic signaling. Dystrophin measures the disuse of a muscle and may be an active force in disuse atrophy.

So, we have at least two important mechanical sensors measuring stress on the muscle cell or disuse --- titin (contraction or stretch) and dystrophin (disuse). I don't think one can understand why stretching a muscle causes it to become larger unless you recognize that the TITIN long protein is stretched and dystrophin is stressed. Nor can one understand disuse atrophy without recognizing that dytrophin is a sensor of disuse and functions as a trigger for the atrogenes.

This post has gotten to be too long, so the exercise that I developed with these insights will have to wait for the next post. Hint: the stress sensors and how they alter gene expression play a large part of it.

Too much muscle in his 70's ("Is this really a problem?") - Art De Vany on Line

Is this really a problem? - Art De Vany on Line

 

01/29/2013

26 Comments

 

For about the last month I have been working out pretty steadily. I have not played tennis and have gone into the gym for my activity. I have a couple of old motorcycle racing injuries from about 30 years ago bothering me and tennis is far from good for those injuries. Tennis is very hard on the hips and knees and many elite tennis players (not my problem) go under the knife for hip and knee surgery, including replacement.

The tennis players I see locally are far from healthy specimens and only a few elite players, such as Nadal, Tsonga, and lately Murray, have bodies I admire anyway.

Laying off tennis and hitting the gym more has created my problem --- I am getting too muscular. I have put on muscle like mad but really don't want any more. A lot of people would love to have that problem it seems, but not me. I don't want my shirts getting tight (I am already in an XL shirt) and don't like feeling bulges. I am not even using heavy weights because I do not want my knee or hip to bear the load of a really heavy weight. I just want to be strong, lean and quick and not bulky. I want to maintain my lean muscle mass as I age toward my eighties. You see why if you look at my The Fundamental Dynamic of Life post. In a sense, this little post is a continuation of that series, which will have more posts coming soon.

The point of that post is that, no matter what aspects of diet or exercise you care about or practice, everyone will eventually fall into the aging/death cascade at some point of their life. The cascade revolves around the loss of lean mass. Fat mass has little to do with it, which is why the studies of mortality and BMI find that the older you are the more advantages there are to a higher BMI. The problem is in the way the studies are interpreted. High BMI, such as I have, is more about muscle than fat, unless there is gross obesity (a completely different matter). These mortality studies, as I read them, are really saying that high lean tissue mass is the key to low mortality at advanced age. This is why they find this seeming paradox that high BMI confers some measure of protection. They are really saying that high lean tissue confers protection. BMI does not distinguish between these two possibilities.

Why have I put on so much muscle at my age? It should be hard to do, but it has been effortless.

In thinking about how easy this has been, I have reached a few conclusions that might help you maintain or increase your lean mass as you age. It is the most important thing you can do to stave off or at least temper that slide into aging and, eventually, death.

1. I am not inflamed. My diet is loaded with fresh plants and lean protein. The plants balance the acid in the meat so I am not acidic, which promotes inflammation. Animal products are loaded with important vitamins. Plants are too, but lack complete protein. There is wide spread protein deficiency among the aged since the rate at which they catabolize lean tissue is rather high relative to the rate at which they synthesize it.
2. My insulin is very low. It is at the bottom of the lab range. Everyone says that insulin if anabolic and it is. But, I have finished growing and don't need elevated insulin. Insulin and IGF-1 (insulin like growth factor) at a systemic level are more damaging than beneficial. You want local, muscle activation-derived IGF-1, not systemic. The latter promotes cancer and is more a symptom of elevated insulin than a muscle growth factor. Besides, insulin is even more anabolic with regard to fat than to muscle.
3. I eat relatively low fat compared to many "Paleo-types". Fat in large amounts is inflammatory and damages insulin receptors and beta cells. The combination of inflammation with high circulating blood fats is damaging. Killing insulin receptors is not good and will eventually lead to insulin resistance and diabetes.
4. I lift weights rather than run long distances. I love running, but confine it to sprints interspersed with walks. Lifting weights creates a wholly different metabolic profile than distance running or other long-term aerobic activity. It is better than couch surfing, but still inferior to weight lifting. One of the most important aspects of aging is the loss of the ability to generate force rapidly. Chronic aerobic exercise does not solve this and may even lead to further loss of rapid force development through the loss of FT muscle fibers.
5. The bulk of my calories (they don't count) comes from lean meats and a lot of seafood. Both are anti-inflammatory. It is the progression to inflammaging, the term Fraceschini coined, for the cascade into systemic inflammation and metabolic disease. Your immune system will eventually turn against you because it is "there"  to  keep you alive long enough to let you reproduce and after that your own body's tissues become a target.
6. I eat from one to three meals a day, but more often eat just two meals a day. Spacing meals and eating to hunger seem only to be possible when you eat an evolutionary diet, one based on mimicking what our ancestors ate with no processed foods. Processed foods are loaded with inflammatory chemicals and proteins our ancestors were never exposed to in a chronic fashion.
7. I exercise according to my hierarchical system. No rest between sets and heavier weight and fewer reps with each stage of the hierarchical sequence. Three sets of, say, 15, 8 and 4 reps with heavier weights and fewer reps as I ascend the hierarchy. This is designed to drop out the slower, weaker muscles to get to the FT fibers, our most expensive fibers. 8, 4, 2 with even heavier weights is another form, but I do not use the very heavy weights I used in my past. I go for a bit of a burn, which tells me I am creating a lactic acid load in the muscle, which is a correlate to GH. I am also releasing BDNF, the growth hormone for the brain, adrenalin, glucagon and altering the same metabolic pathways that mimic leptin.
8. I take my own Guardian source of B12 enriched BCAAs. BCAAs promote protein synthesis and leucine is a permissive signal for synthesis. The amino acids provide substrate to keep the energy flow to my brain so I do not get hungry. Eating and releasing insulin  during this post-exercise state, as many promote, kills these hormone responses. Insulin shuts down metabolic pathways because nutrient storage dominated most other demands during the period of time that we evolved to become humans. The BCAAs promote protein synthesis in our mitochondria, our energy furnaces. Without them, we could not be humans.
9. My REDOX state is good because I take Guardian Advanced Glutathione, the same form of Glutathione I have taken for 30 years. I make sure my cells do not tip into an pro-oxidative or oxidized state. In an oxidative state, the cell DNA is damaged, proteins become oxidized and change shape and no longer function properly within the cell. If the shape of these proteins is altered sufficiently, they can not act as signalling or receptor cells and the immune system attacks them as unrecognized foreign proteins. Oxidative damage to the motor neurons seems to be involved in the loss of the ability of the nervous system to activate muscles, particularly the FT fibers, the most important of our muscle fibers. This is the source of the diminishing ability the aged face to rapidly develop force and of the loss of primarily FT fibers as we age. Oxidation strips myelin from the nerves which dampens signal transmission and may even lead to MS. At some stage, I think we all develop a mild form of MS as the insulation that encases our nerves is stripped away.
10. I also think that almost all chronic diseases, at least those that are metabolic or hormonal in origin, that develop in aging are the same as those that have a genetic or epigenetic origin. Aging lays out all the chronic diseases eventually, whatever their genetic component. Aging is an epigenetic process that alters gene expression toward disease right to the end.
11. We do not age the way our ancestors did because of our modern diet and our chronic stresses. We are active genotypes, not the sort of human you see nowadays. Excess energy trapped in all our tissues stacks up the electrons in our mitochondria and they begin to produce far too much oxygen, which tips our cells into the adverse REDOX state, where almost all aging processes lead to. We just age faster, even though we die at an advanced age relative to our ancestors. We do live a longer period of our lives in a state of diminished functional capacity.
12. In the end, it is functional capacity that determines how we age. And, functional capacity is determined by our muscle mass and the composition of our muscle fibers. I have worked out for so long that my genes "know" how to make muscle. That is really the deep explanation, if there is one.

So, in the end the solution to my problem of too much muscle is not a problem. All I have to do is spend more time doing other things and a bit less time in the gym. A nice problem to have.