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Dean Pomerleau

Metabolism, Aging, CR & Exercise

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I found this new paper %5B1%5D posted by Al Pater to the now defunct (RIP) CR mailing list to be a very interesting model of aging and how it relates to metabolism. I was particularly interested in how the authors explained the benefit (or at least, the non-harm) of exercise when it comes to lifespan, despite the fact that a naive interpretation, based on the Rate-of-Living Theory, would suggest that exercise requires more calories which will inevitably result in greater metabolic damage (e.g. via reactive oxygen species (ROS) generation), and thus faster aging.

 

 

They offer a theory which compartmentalizes metabolism into several components, illustrated schematically in Fig 4:

 

1-s2.0-S0047637415000846-gr4.jpg

 

The black (outside) box represents the total metabolism of an organism, either being fed ad lib (left bar) vs. CR (middle bar). In order for the organism to grow (i.e. deposition of new biomass), it must not only sequester matter into new tissue which stores energy and therefore requires ingested calories (green box), but also active expenditure of energy to convert the food into living (muscle, fat or bone) tissue, which they call biosynthesis (blue box).

 

With dietary restriction, the total metabolic budget is lower (middle bar shorter than left bar). With fewer calories to go around, the body decides to create less new tissue, cutting down on the green box to stay "within budget". With less tissue to create, the active cost of biosynthesis that would be required to create that tissue is also reduced (blue box) in the CR condition. That leaves more net energy available for "protection (scavaging and repair)" (yellow box) in the CR condition than in the AL condition, leading to better health maintenance and increased longevity.

 

In the bulk of the paper, the authors develop equations to quantify these relationships, explain known (sometimes paradoxical) observations about the relationship between metabolism and longevity, and to make predictions.  

 

What it seems to boil down to is that if an organism stays small (relative to the 'normal' size for its species), it will tend to live longer. They show an interesting graph (Fig 5) to support this hypothesis, which illustrates how lifespan extension appears linearly related to the degree of body mass reduction induced by either CR or genetic manipulation of growth hormone:

 

 

1-s2.0-S0047637415000846-gr5.jpg

 

What I found most interesting personally was their discussion of the impact of exercise on metabolism and lifespan. Here is a quote from that section of the paper:

 

 

[T]he model can be generalized to include the variation in activity level. As shown in Fig. 4, with a limited food supply, an increase in activity would further suppress growth. Thus, depending on the degree of the increase in activity, the adult mass of DR animals (MDR) will be even smaller. In Eq. (3), lifespan extension is proportional to the body mass reduction (M/MDR − 1). So, if MDR is smaller due to the increase in activity, the lifespan extension will be larger.

 

There is no empirical data to test this prediction directly and quantitatively, because most studies did not measure the energy cost of the increased activity level. But the results from Holloszy (1997) [2] support this prediction indirectly by showing that the major determinant of lifespan extension is the body mass reduction even if activity level varies [my emphasis]. Holloszy (1997) reported the lifespan, food consumption, and body mass of four groups of male Long-Evans rats reared at different levels of food supply and exercises: ad libitum (AL)-runner, AL-sedentary, DR-runner, and DR-sedentary. The peak body mass (M and MDR) of these four groups rank in such an order: AL-sedentary (597 g) > AL-runner (420 g) > DR-runner (333 g) = DR-sedentary (330 g).

 

Equation (3) predicts that their lifespan will be in the opposite order. The data supports this prediction: AL-sedentary (858 days) < AL-runner (973 days) < DR-runner (1058 days) = DR-sedentary (1051 days). Note, in this study, although they are both under DR, DR-runners consumed more food (13.4 g/day) than DR-sedentary group (10 g/day). So the runner and sedentary groups ended up with the same body mass (∼330 g). The interesting result is that despite the different exercise and food levels, the same body mass led to the same lifespan (∼1050 days) in these two groups, exactly as our model predicts [my emphasis].

 

We postulate that if DR-runner and DR-sedentary were fed with the same level of food, then the runners will be have a smaller body mass, and therefore a longer lifespan.

 

So the calorie-restricted running rats ate 34% more calories than the sedentary calorie-restricted rats, but as a result of their extra energy expenditure, weighed the same, and lived just as long as the sedentary CR rats.

 

The authors point out that while burning more calories will usually generate more damaging free radicals, when calories are burned in exercise they are burned "more cleanly", and hence don't generate as many ROS's as when burned under sedentary conditions. To quote the paper again:

 

The percentage of electron leak can also vary during exercises, where the mitochondrial respiration transits from state 4 to state 3 (Barja, 2007 and Barja, 2013). Under state 4 (resting respiration), oxygen consumption is low, proton-motive force is high, and ROS production is high (Barja, 2013 and Harper et al., 2004), whereas under state 3 (active respiration), ROS production reduces rapidly (Boveris and Chance, 1973, Boveris et al., 1972 and Loschen et al., 1971). 

 

So if exercise trains mitochondria to operate in state 3 both during exercise and (possibly) during rest as well, the net effect of exercise on free radical production may not be very significant. And if exercise also induces a hormetic effect that increases free radical scavenging (which there is quite a bit of evidence to support), the net result could be less damage from free radicals despite more calories burned as a result of exercise.

 

This seems to contradict the oft-cited mantra among some human CR practitioners of "calories, calories, calories" - i.e. its reducing calories that matters, whether or not it leads to weight loss, and attaining a low weight as a result of extra activity/exercise won't be equivalently beneficial for longevity as a higher degree of (semi-sedentary) CR.

 

Given that Holloszy's paper [2] is from 1997, I'm sure we hashed all this out on the old CR mailing list many years ago, and perhaps MR will point to that old thread :). But I thought it was interesting (and encouraging) given my recent disclosure that lately I've been eating more calories but exercising a lot more to maintain a very CR-like weight (BMI ~17.5).

 

--Dean

 

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

[1] On the complex relationship between energy expenditure and longevity: Reconciling the contradictory empirical results with a simple theoretical model.

Hou C, Amunugama K.[/size]

 

Mech Ageing Dev. 2015 Jun 15;149:50-64. doi: 10.1016/j.mad.2015.06.003. [Epub ahead of print]

PMID:26086438 

 

http://www.sciencedirect.com/science/article/pii/S0047637415000846

http://ac.els-cdn.com/S0047637415000846/1-s2.0-S0047637415000846-main.pdf?_tid=e680437e-1d32-11e5-8323-00000aacb361&acdnat=1435454195_8ec497f0141d9e67cb89cf2909758cd4

 

Abstract

 

The relationship between energy expenditure and longevity has been a central theme in aging studies. Empirical studies have yielded controversial results, which cannot be reconciled by existing theories.

 

In this paper, we present a simple theoretical model based on first principles of energy conservation and allometric scaling laws.

 

The model takes into considerations the energy tradeoffs between life history traits and the efficiency of the energy utilization, and offers quantitative and qualitative explanations for a set of seemingly contradictory empirical results. We show that oxidative metabolism can affect cellular damage and longevity in different ways in animals with different life histories and under different experimental conditions. Qualitative data and the linearity between energy expenditure, cellular damage, and lifespan assumed in previous studies are not sufficient to understand the complexity of the relationships. Our model provides a theoretical framework for quantitative analyses and predictions. The model is supported by a variety of empirical studies, including studies on the cellular damage profile during ontogeny; the intra- and inter-specific correlations between body mass, metabolic rate, and lifespan; and the effects on lifespan of (1) diet restriction and genetic modification of growth hormone, (2) the cold and exercise stresses, and (3) manipulations of antioxidant.

 

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

[2] J.O. Holloszy

 

Mortality rate and longevity of food-restricted exercising male rats: a reevaluation

 

J. Appl. Physiol., 82 (1997), pp. 399–403

 

Abstract

 

Food restriction increases the maximal longevity of rats. Male rats do not increase their food intake to compensate for the increase in energy expenditure in response to exercise. However, a decrease in the availability of energy for growth and cell proliferation that induces an increase in maximal longevity in sedentary rats only results in an improvement in average survival, with no extension of maximal life span, when caused by exercise. In a previous study (J. O. Holloszy and K. B. Schechtman. J. Appl. Physiol. 70: 1529-1535, 1991), to test the possibility that exercise prevents the extension of life span by food restriction, wheel running and food restriction were combined. The food-restricted runners showed the same increase in maximal life span as food-restricted sedentary rats but had an increased mortality rate during the first one-half of their mortality curve. The purpose of the present study was to determine the pathological cause of this increased early mortality. However, in contrast to our previous results, the food-restricted wheel-running rats in this study showed no increase in early mortality, and their survival curves were virtually identical to those of sedentary animals that were food restricted so as to keep their body weights the same as those of the runners. Thus it is possible that the rats in the previous study had a health problem that had no effect on longevity except when both food restriction and exercise were superimposed on it. Possibly of interest in this regard, the rats in this study did considerably more voluntary running than those in the previous study. It is concluded that 1) moderate caloric restriction combined with exercise does not normally increase the early mortality rate in male rats, 2) exercise does not interfere with the extension of maximal life span by food restriction, and 3) the beneficial effects of food restriction and exercise on survival are not additive or synergistic.

Edited by Michael R
http-->https doesn't work; reverting

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I created a modified Fig 4 from the paper to illustrate how the authors would characterize the metabolic allocation for extra exercise, and their model's prediction on its impact on health/longevity:

 

gFUZdOB.jpg

 

The (new) third column shows increased total metabolic activity as a result of exercise (increased pink area of "Activities") and therefore greater "calories in" - as high as ad libidum in the first column. Because there aren't extra calories to spare, the body decides it can't afford to deposit much new biomass (i.e. create more fat, muscle or bone). With little additional biomass being created, biosynthesis is also reduced (blue box smaller in third column than first). That leaves extra calories for "Protection (scavenging and repair)", so the yellow box is as large in the third (exercise) column as the second (CR) column.

 

Of course at some point, the calories burned via extra exercise could require too many calories, cutting into the calories available for protection, or resulting in catabolism of existing biomass.

 

--Dean

Edited by Michael R

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Hi Dean!

I'm an exerciser too -- but I my exercise is cardio, not strengthening -- I use the latest model Precor Elliptical with hand motion, in my local gym. I exercise for an hour daily. Cardio exercise burns very few calories -- I remember an old post by AL Pater that indicated that calories burned in exercising on Precor ellipticals is less than claimed by the manufacturer.

 

I realize that some strengthening exercise is "de rigour" with heavy CRON -- so I do my exercise with the maximum resistance (20) set, and accomplish more than 5.1 miles of foot motion (a fast speed at that resistance), which (I hope) results in some minimal muscle strengthening.

However, I'm not optimistic about your pictured model of exercise -- IMO, it may be wishful thinking.

(:

I think that there are many unknowns on this subject.

I know that Luigi divides tested groups by many criteria -- one is whether or not the individual is an exerciser.

Luigi might have some preliminary evidence on this subject

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Hi Saul,

 

However, I'm not optimistic about your pictured model of exercise -- IMO, it may be wishful thinking.

 

Is your opinion based on evidence, or just a hunch?

 

I know that Luigi divides tested groups by many criteria -- one is whether or not the individual is an exerciser.

Luigi might have some preliminary evidence on this subject

 

You prompted me to do a search on "Fontana Exercise PMID" and came across a very relevant paper [1] by Luigi that I don't remember seeing before. In this paper, Luigi, Holloszy et al tested a 20% energy deficit resulting from eating fewer calories (CR) vs. a 20% energy deficit from increased exercising (EX) in normal and overweight people for one year. 

 

It basically found that the two interventions resulted in similar weight loss (about 6kg in fat mass) and a similar reduction in cardiovascular risk factors.  Here are some quotes from the paper:

 

Two studies conducted in young obese subjects have shown that short-term exercise and CR are equally effective in improving insulin sensitivity (720).

 

We have found that long-term major reductions in total body fat and abdominal visceral and subcutaneous fat depots similar to those obtained by CR are achievable with regular exercise if food intake is kept constant (18). The similar improvement in CHD risk in response to the EX-induced and CR-induced fat loss obtained in our trial was unexpected and counter to our initial hypothesis.

 

... We carefully measured energy intake and energy expenditure by using both nutrition assessment software and direct analysis through DLW (18). Our study had a high retention rate of enrolled participants and good adherence to the study interventions, as shown by the successful weight reduction over 12 mo in both groups (18). 

 

In conclusion, the results of this randomized, controlled trial provide evidence that CR- and EX-induced negative energy balances result in substantial and similar improvements in the major risk factors for CHD.

 

So Luigi does have something to say, and a study published, on the topic of CR vs. exercise-induced calorie deficits. According to Luigi, the two interventions appear to have similar positive effects on heart disease risk, the #1 killer of Americans. Of course this doesn't say anything about "true" (i.e. max lifespan) life extension benefits of CR (or exercise) in humans, which from talking to Luigi I get the feeling he's not so sure about.

 

Anecdotally, (as you know) Luigi is both very thin and very active (he bikes a lot).

 

--Dean

 

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

[1] Calorie restriction or exercise: effects on coronary heart disease risk factors. A randomized, controlled trial

 
Luigi Fontana , Dennis T. Villareal , Edward P. Weiss , Susan B. Racette , Karen Steger-May , Samuel Klein , John O. Holloszy
American Journal of Physiology - Endocrinology and Metabolism Published 1 July 2007 Vol. 293 no. 1, E197-E202 DOI: 10.1152/ajpendo.00102.2007
 
 
Abstract
 
Coronary heart disease (CHD) risk factors and the risk of CHD increase with increased adiposity. Fat loss induced by negative energy balance improves all metabolic CHD risk factors. To determine whether fat loss induced by long-term calorie restriction (CR) or increased energy expenditure induced by exercise (EX) has different effects on CHD risk factors in nonobese subjects, we conducted a 1-yr controlled trial involving 48 nonobese subjects who were randomly assigned to one of three groups: CR, 20% CR diet (n = 18); EX, 20% increase in energy expenditure through daily exercise with no increase in energy intake (n = 18); or HL, healthy lifestyle guidelines (n = 10). Subjects were 29 women and 17 men aged 57 +/- 3 yr, with BMI 27.3 +/- 2.0 kg/m(2). Assessments included total body fat by DEXA, lipoproteins, blood pressure, HOMA-IR, C-reactive protein (CRP), and estimated 10-yr CHD risk score. Body fat decreased by 6.3 +/- 3.8 kg in CR, 5.6 +/- 4.4 kg in EX, and 0.4 +/- 1.7 kg in HL, which corresponded to reductions of 24.9, 22.3, and 1.2% of baseline body fat mass, respectively. These CR- and EX-induced energy deficits were accompanied by reductions in most of the major CHD risk factors, including plasma LDL-cholesterol, total cholesterol/HDL ratio, HOMA-IR index, and CRP concentrations that were similar in the two intervention groups. Data from the present study provide evidence that CR- and EX-induced negative energy balance result in substantial and similar improvements in the major risk factors for CHD in normal-weight and overweight middle-aged adults.
 
PMID: 17389710
Edited by Dean Pomerleau

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Thanks Dean.

But, in rodents, my recollection is that CR, but not energy-equivalent exercise, extends maximal and average life span. (Of course, humans are too long-lived for such information -- either way -- to be available. We're the guinea pigs.)

:)

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Saul,

 

Thanks Dean.
But, in rodents, my recollection is that CR, but not energy-equivalent exercise, extends maximal and average life span. (Of course, humans are too long-lived for such information -- either way -- to be available. We're the guinea pigs.)  :)

 

Did you actually read my original post? The paper (and my post) talks about just that issue - the effects of CR vs exercise-induced energy restriction in rodents. It cites the Holloszy (1997) paper [2] as the best research on the topic, which found that the two treatments lead to equivalent lifespan extension in rats. 

 

--Dean

 

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

[2] J.O. Holloszy
 
Mortality rate and longevity of food-restricted exercising male rats: a reevaluation
 
J. Appl. Physiol., 82 (1997), pp. 399–403
 
Abstract
 
Food restriction increases the maximal longevity of rats. Male rats do not increase their food intake to compensate for the increase in energy expenditure in response to exercise. However, a decrease in the availability of energy for growth and cell proliferation that induces an increase in maximal longevity in sedentary rats only results in an improvement in average survival, with no extension of maximal life span, when caused by exercise. In a previous study (J. O. Holloszy and K. B. Schechtman. J. Appl. Physiol. 70: 1529-1535, 1991), to test the possibility that exercise prevents the extension of life span by food restriction, wheel running and food restriction were combined. The food-restricted runners showed the same increase in maximal life span as food-restricted sedentary rats but had an increased mortality rate during the first one-half of their mortality curve. The purpose of the present study was to determine the pathological cause of this increased early mortality. However, in contrast to our previous results, the food-restricted wheel-running rats in this study showed no increase in early mortality, and their survival curves were virtually identical to those of sedentary animals that were food restricted so as to keep their body weights the same as those of the runners. Thus it is possible that the rats in the previous study had a health problem that had no effect on longevity except when both food restriction and exercise were superimposed on it. Possibly of interest in this regard, the rats in this study did considerably more voluntary running than those in the previous study. It is concluded that 1) moderate caloric restriction combined with exercise does not normally increase the early mortality rate in male rats, 2) exercise does not interfere with the extension of maximal life span by food restriction, and 3) the beneficial effects of food restriction and exercise on survival are not additive or synergistic.

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Previously in this thread I wrote:

Given that Holloszy's paper [2] is from 1997, I'm sure we hashed all this out on the old CR mailing list many years ago, and perhaps MR will point to that old thread [/size] :).[/size]

 

Since Michael Rae doesn't seem to be chiming in on this thread, I figured I'd channel him  :). Here is a link to his main post on this topic to the old CR mailing list from 14 years ago, in 2001. Ironically, both Saul and I were involved in the thread at the time - some things never change!

 

To summarize, Michael seems to suggest that an exercise-induced calorie deficit alone won't confer the same "max lifespan" benefits as "regular" (lower exercise) CR. But based on Holloszy's rat CR+exercise experiments cited above, exercise on top of modest regular CR might have similar max lifespan benefits as more severe "regular" CR.

 

The sad thing is that there appears to have been little research in the 14 years since this discussion to further elucidate the issue of CR + exercise on lifespan in rodents. 

 

--Dean

Edited by Michael R
Replacing dead link

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You prompted me to do a search on "Fontana Exercise PMID" and came across a very relevant paper [1] by Luigi that I don't remember seeing before. In this paper, Luigi, Holloszy et al tested a 20% energy deficit resulting from eating fewer calories (CR) vs. a 20% energy deficit from increased exercising (EX) in normal and overweight people for one year. 

 

It basically found that the two interventions resulted in similar weight loss (about 6kg in fat mass) and a similar reduction in cardiovascular risk factors.  Here are some quotes from the paper:

 

Two studies conducted in young obese subjects have shown that short-term exercise and CR are equally effective in improving insulin sensitivity (720).

 

We have found that long-term major reductions in total body fat and abdominal visceral and subcutaneous fat depots similar to those obtained by CR are achievable with regular exercise if food intake is kept constant (18). The similar improvement in CHD risk in response to the EX-induced and CR-induced fat loss obtained in our trial was unexpected and counter to our initial hypothesis.

 

... We carefully measured energy intake and energy expenditure by using both nutrition assessment software and direct analysis through DLW (18). Our study had a high retention rate of enrolled participants and good adherence to the study interventions, as shown by the successful weight reduction over 12 mo in both groups (18). 

 

In conclusion, the results of this randomized, controlled trial provide evidence that CR- and EX-induced negative energy balances result in substantial and similar improvements in the major risk factors for CHD.

 

So Luigi does have something to say, and a study published, on the topic of CR vs. exercise-induced calorie deficits. According to Luigi, the two interventions appear to have similar positive effects on heart disease risk, the #1 killer of Americans. Of course this doesn't say anything about "true" (i.e. max lifespan) life extension benefits of CR (or exercise) in humans, which from talking to Luigi I get the feeling he's not so sure about.

 

Anecdotally, (as you know) Luigi is both very thin and very active (he bikes a lot).

 

--Dean

 

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

[1] Calorie restriction or exercise: effects on coronary heart disease risk factors. A randomized, controlled trial

Luigi Fontana , Dennis T. Villareal , Edward P. Weiss , Susan B. Racette , Karen Steger-May , Samuel Klein , John O. Holloszy
American Journal of Physiology - Endocrinology and Metabolism Published 1 July 2007 Vol. 293 no. 1, E197-E202 DOI: 10.1152/ajpendo.00102.2007

 

http://www.runnersworld.com/weight-loss/new-study-examines-health-benefits-of-losing-weight-in-different-ways

 

New Study Examines Health Benefits of Losing Weight in Different Ways

Researchers tested the effects of weight loss from calorie-cutting, exercise, and a combination of both.

By Amby Burfoot Wednesday, August 10, 2016, 11:02 am

exercise or diet for weight loss

Photograph by Thomas MacDonald

 

Anyone who decides to undertake a weight-loss effort faces a number of critical choices. Among them: In terms of the best health outcome, is it smarter to focus on cutting calories, increasing exercise, or a combination of both?

 

A top research team from several universities recently investigated this question in a controlled trial in which each of the three groups lost the same amount of weight. The team expected that the combined approach—cutting calories while increasing exercise—would produce the best health results.

 

It didn’t. In fact, the paper showed that all three approaches yielded roughly the same benefits to cholesterol, blood pressure, glucose control, and other key health markers.

 

But this finding didn’t dissuade the team from its belief in the importance of exercise for healthy weight-loss. “While weight loss lowers the risk for cardiovascular disease, as we showed, substantial evidence indicates that exercise reduces cardiovascular disease through unknown, nontraditional risk factors that we are therefore unable to measure,” first author Edward Weiss, Ph.D., associate professor of nutrition and dietetics at St. Louis University, told Runner's World by email. “Also, in a previous paper, we showed that calorie cutting plus exercise does lower diabetes risk more than just calorie reduction or just exercise increase.”

 

In their new study, Weiss and colleagues asked subjects to lose six to eight percent of their body weight primarily by calorie restriction alone (CR), primarily by exercise (EX), or by a combination of the two (CREX). All subjects were healthy but sedentary individuals, 45 to 65 years old. There were 16 to 19 subjects in each of the three groups.

 

After 12 to 14 weeks, all groups had lost about seven percent of their initial body weight—11.5 pounds on average for the women, and 14 pounds for the men. The CR group decreased calorie consumption by 764 calories a day while remaining inactive; the EX group burned 412 calories a day in exercise, while also dropping 295 food calories a day (for a total energy imbalance of 707 calories); and the CREX group cut 585 food calories a day and burned off 217 through exercise (for a total energy imbalance of 802 calories).

 

Following the study period, all groups had similar health-enhancing changes in blood pressure, total cholesterol, triglycerides, glucose, HDL cholesterol, and C-reactive protein. The researchers estimated that “these changes would be expected to decrease the lifetime risk of cardiovascular disease by 36 to 46 percent.”

 

While there was no added cardiovascular payoff to the CREX routine over the other two approaches, Weiss remains a big exercise fan. “There are enormous benefits from either achieving a healthy weight or from regular exercise,” he says. “And because each provides benefits that the other cannot, even if you reach a healthy weight, you still need to exercise to have an optimally healthy lifestyle."

 

Tags:

 

Newswire

 

Weight Loss

 

Am J Clin Nutr. 2016 Jul 27. pii: ajcn131391. [Epub ahead of print]

Effects of matched weight loss from calorie restriction, exercise, or both on cardiovascular disease risk factors: a randomized intervention trial.

Weiss EP1, Albert SG2, Reeds DN3, Kress KS4, McDaniel JL4, Klein S3, Villareal DT5.

PMID: 27465384

DOI: 10.3945/ajcn.116.131391

 

Abstract

 

BACKGROUND:

 

Weight loss from calorie restriction (CR) and/or endurance exercise training (EX) is cardioprotective. However CR and EX also have weight loss-independent benefits.

 

OBJECTIVE:

 

We tested the hypothesis that weight loss from calorie restriction and exercise combined (CREX) improves cardiovascular disease (CVD) risk factors more so than similar weight loss from CR or EX alone.

 

DESIGN:

 

Overweight, sedentary men and women (n = 52; aged 45-65 y) were randomly assigned to undergo 6-8% weight loss by using CR, EX, or CREX. Outcomes were measured before and after weight loss and included maximal oxygen consumption (VO2max), resting blood pressure, fasting plasma lipids, glucose, C-reactive protein, and arterial stiffness [carotid-femoral pulse wave velocity (PWV) and carotid augmentation index (AI)]. Values are means ± SEs.

 

RESULTS:

 

Reductions in body weight (∼7%) were similar in all groups. VO2max changed in proportion to the amount of exercise performed (CR, -1% ± 3%; EX, +22% ± 3%; and CREX, +11% ± 3%). None of the changes in CVD risk factors differed between groups. For all groups combined, decreases were observed for systolic and diastolic blood pressure (-5 ± 1 and -4 ± 1 mm Hg, respectively; both P < 0.0008), total cholesterol (-17 ± 4 mg/dL; P < 0.0001), non-HDL cholesterol (-16 ± 3 mg/dL; P < 0.0001), triglycerides (-18 ± 8 mg/dL; P = 0.03), and glucose (-3 ± 1 mg/dL; P = 0.0003). No changes were observed for HDL cholesterol (P = 0.30), C-reactive protein (P = 0.10), PWV (P = 0.30), or AI (P = 0.84). These changes would be expected to decrease the lifetime risk of CVD from 46% to 36%.

 

CONCLUSION:

 

Matched weight losses from CR, EX, and CREX have substantial beneficial effects on CVD risk factors. However, the effects are not additive when weight loss is matched.

KEYWORDS:

 

adiposity; aerobic exercise; atherosclerosis; cardiovascular disease; coronary heart disease; diet modification; overweight and obesity; weight management

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Thanks Al,

 

From the new paper you reference (PMID 27465384):

 

Matched weight losses from CR, EX, and CR  [+] EX have substantial beneficial effects on CVD risk factors. However, the effects are not additive when weight loss is matched.
 

So CR, Exercise and CR+Exercise had about the same (quite positive) effect on standard cardiovascular disease risk factors like serum cholesterol, fasting glucose and blood pressure when matched for degree of calorie deficit / weight loss. That is nice to see. But notice what else they found:

 

VO2max changed in proportion to the amount of exercise performed (CR, -1% ± 3%; EX, +22% ± 3%; and CREX, +11% ± 3%).

 

In more detail, from the full text, the 22% improvement in VO2max of the exercise group corresponded to a 5.3 mL/min*kg increase. This compares with no change in VO2max in the CR-only group, and about ½ the VO2max increase in the CR + EX (+2.6 mL/min*kg).

 

So what? Is VO2max (i.e. a measure of cardiorespiratory fitness) important?

 

You bet it is. In fact, this new study [1] found that VO2Max is a very strong predictor of all-cause mortality. Specifically, over 12 years of follow-up among 579 middle-age men (age 42-60 at baseline):

 

[After controlling for a bunch of potential confounders - DP], a 1 mL/min*kg higher ΔVO2max was associated with a 9% relative risk reduction of all-cause mortality (hazard ratio, 0.91; 95% CI, 0.87-0.95).

 

So which group would you rather be in? The CR-only group whose VO2Max didn't change, or the exercise group whose VO2max went up by 5.3 mL/min*kg, which equates to an almost 50% reduction in risk of all cause mortality?

 

The better option looks pretty clear to me.

 

--Dean

 

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

[1] Mayo Clin Proc. 2016 Jul 18. pii: S0025-6196(16)30257-9. doi:

10.1016/j.mayocp.2016.05.014. [Epub ahead of print]
 
Long-term Change in Cardiorespiratory Fitness and All-Cause Mortality: A
Population-Based Follow-up Study.
 
Laukkanen JA(1), Zaccardi F(2), Khan H(3), Kurl S(4), Jae SY(5), Rauramaa R(6).
 
Author information: 
(1)Institute of Public Health and Clinical Nutrition, University of Eastern
Finland, Kuopio, Finland; Central Finland Central Hospital, Jyväskylä, Finland.
Electronic address: jariantero.laukkanen@uef.fi. (2)Diabetes Research Centre,
University of Leicester, Leicester, United Kingdom. (3)Emory University, Atlanta,
GA. (4)Institute of Public Health and Clinical Nutrition, University of Eastern
Finland, Kuopio, Finland. (5)Department of Sports Science, University of Seoul,
Seoul, South Korea. (6)Kuopio Research Institute of Exercise Medicine, Kuopio,
Finland.
 
 
Few studies have investigated long-term changes in cardiorespiratory fitness
(CRF), defined by indirect measures of CRF, and all-cause mortality. We aimed to 
investigate whether long-term change in CRF, as assessed by the gold standard
method of respiratory gas exchange during exercise, is associated with all-cause 
mortality. A population-based sample of 579 men aged 42 to 60 years with no
missing data at baseline examination (V1) and at reexamination at 11 years (V2)
were included. Maximal oxygen uptake (VO2max) was measured at both visits using
respiratory gas exchange during maximal exercise testing, and the difference
(ΔVO2max) was calculated as VO2max (V2) - VO2max (V1). Deaths were ascertained
annually using national death certificates during 15 years of follow-up after V2.
The mean ΔVO2max was -5.2 mL/min*kg. During median follow-up of 13.3 years
(interquartile range, 12.5-14.0 years), 123 deaths (21.2%) were recorded. In a
multivariate analysis adjusted for baseline age, VO2max, systolic blood pressure,
smoking status, low- and high-density lipoprotein cholesterol and triglyceride
levels, C-reactive protein level, body mass index, alcohol consumption, physical 
activity, socioeconomic status, and history of type 2 diabetes mellitus and
ischemic heart disease, a 1 mL/min*kg higher ΔVO2max was associated with a 9%
relative risk reduction of all-cause mortality (hazard ratio, 0.91; 95% CI,
0.87-0.95). This study suggested that in this population, long-term CRF reduction
was associated with an increased risk of mortality, emphasizing the importance of
maintaining good CRF over the decades.
 
Copyright © 2016 Mayo Foundation for Medical Education and Research. Published by
Elsevier Inc. All rights reserved.
 
DOI: 10.1016/j.mayocp.2016.05.014 
PMID: 27444976

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I continue to be surprised by how shallowly/narrowly the mainstream media, and even the authors of the paper themselves, are interpreting the results of the "exercise vs. CR for cardiovascular health" paper (PMID 27465384) that Al shared two posts up. In this coverage of the study in Science Daily, the writer goes from the abstract alone and summarizes the study as:

 

They found the three strategies [diet-only, exercise-only, or diet+exercise] were equally effective in improving cardiovascular health, and were expected to reduce a person's lifetime risk of developing cardiovascular disease 10 percent -- from 46 percent to 36 percent.

 

What they leave out is that the two exercise conditions resulted a large improvement in VO2Max, the ability of the cardiovascular system to carry and utilize oxygen, which as I outlined in the post immediately above, is an important predictor for all-cause mortality. I'm baffled why the authors don't seem to place more (any!) significance on this seemingly important part of their results, either in the abstract or in their interviews with the popular press. At the end of this Science Daily article, the author says:

 

Furthermore, an inactive lifestyle itself is a risk factor for cardiovascular disease, although the physiologic mechanisms for this effect are unknown.

 

I find this all the more puzzling because the authors do indeed address this cardiovascular benefit of exercise vs. CR-alone in the discussion section of the full text of their paper, and point to VO2Max improvements as a likely mediator:

 

A straightforward interpretation of the findings from the present study is that weight loss itself provides the major cardioprotective effect of CREX and that the benefits do not depend on which approach to weight loss is used. However, 3 issues related to this notion warrant consideration. First, although the physiologic mechanisms are not clear, the cardioprotective effects of exercise are not necessarily mediated by changes in CVD risk factors. Accordingly, a sedentary lifestyle and low aerobic capacity increase CVD risk by 50–100%, even after accounting for other risk factors (28, 29). Therefore, despite the fact that the EX and CREX groups did not have greater improvements in BP, lipids, glucose, and body composition, these groups would be at lower risk of CVD because they were no longer sedentary and because of the increases in VO2max.

 

The authors also point out another possible benefit of exercise-induced weight loss (vs. CR alone):

 

ecause adiposity is an independent risk factor for CVD (30), the small nonsignificant tendency for greater fat mass reductions (and preservation of fat free mass), may confer an advantage for exercise-induced weight loss.

 

So once again, it seems to me a case of important, actionable health implications of a study being lost in the translation from published research to the popular press.

 

--Dean

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