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  1. Michael R

    CR and Exercise

    I wrote this survey of the literature in the early 200s; there have been a few studies examining the intersection of CR and exercise since then, but none to my knowledge have been lifespan studies, and therefore don't ultimately resolve anything. The findings from existing studies are that: 1. Exercise-induced Caloric deficit (ECD) ALONE does not extend maximum lifespan (LS) (1-10). The majority (1,3-6) of studies find that it increases average LS, but a substantial minority (2,8,9,10) haven't even found this. It improves health, but it does not slow aging. 2. CR alone increases max and average LS (2,5-10). It slows aging, and thus improves health. 2a. CR alone causes a greater increase in average LS than does an equal degree of CD from exercise alone (2,5,6); likewise, albeit less powerfully (because less rigorously), 40% CR ALONE causes a greater increase in average LS than does the large ECD (alone) typical of the AL, voluntary-exercising rat (2). Likewise for alternate-day fasting (EOD] vs voluntary exercise (7,10). The health results of slowing aging (thru' doing CR) are greater than those from exercising. 3. Within the confines of what Steve Austad once called "full-blown, weep-on-your-knees CR" (≥40% CR [the most commonly used in studies on "the effect of CR on parameter X,"]) none of the studies (2,7-10) examining the effect of adding extra CD via ECD at a given absolute caloric intake in CR found further increases max LS. (9), in fact (which was on forced exercise, unlike the voluntary exercise in the other studies), found a decrease in max LS. The above points clearly show that ECD is NOT equivalent to CD from CR. 5. CR + ECD at a given absolute caloric intake yields inconsistent results on average LS relative to that level of CR alone: 2 studies found a benefit ([2,9] — NB this latter still found a shorter max!), another reported a detriment (5), as apparently did (7); (8) found no effect. Now things get tricky! 6. What happens when you put an animal on full-blown CR, and compare it to an animal on LESS CR, but with the difference in CD "topped up" with ECD, such that the total CD is equal to "full-blown, weep-on your knees CR"? This is what (3) tested in comparing groups C and D (both at 44% CD). And, the "responsible" reading is that the two are equivalent. That is, there ARE nominal differences between the two — the CR-only group DID have longer average AND max LS than the combined-CD group — but the differences were statistically insignificant. Likewise with Holloszy's earlier work (5): when a group given full-blown CR (group E, 40% CR) is compared w/a group on mild CR (24%CR) + ECD to bring the total CD down to the same level (as assessed by BW: group D), there there are no statistically significant differences in max or average LS; yet the nominal data favor the CR-only group on both points. The most scientifically respectable conclusion to draw from this (these are AFAIK the only data on this key point) would be that "two nonsignificant differences do not create a significant one." But to see the same patter repeated twice is, to me, "suspicious" -- esp in light of all the other data clearly showing the greater LS results from CR vs ECD. The cohorts having been so small (n=30 (D) & 44 (E) in (5), & 31 © & 65 (D) in (3)), it's easy to see a significant difference being masked by sheer lack of statistical power. This, unfortunately, is the one piece of data MOST relevant to the human CR practitioner. We don't have the answer. But clearly, ECD is not fully equivalent to CR, even when the 2 are combined, under any other circumstances; my guess is that the same holds here. Implications for Human Practice I simply don't believe that anyone is doing the human equivalent of genuine "weep-on-your-knees" CR on a voluntary basis: few of us are doing CR at all, as vs. healthy weight maintenance, so my point (3) above simply falls out of it. The key findings are therefore those discussed in my points (5) and (6) above. There's obviously a bit of a tension between these 2 sets of findings, in terms of how one should govern oneself and extrapolate from current practice, unfortunately, but Holloszy's key study (1) below, and the centerpiece of my point (6) is a better-quality study, and probably should be given more weight. Thus, it does appear that, once you pass a certain minimum threshold (significantly more than healthy weight maintenance), Calories burned thru' exercise probably does add to Calories not consumed in the first place — just not as fully, and with some manner of ceiling or asymptote. At the end of the day, clearly, a person should do as intense a level of CR as s/he finds tolerable, subjectively and on a risk-management basis; any additional benefits to Calories burned to exercise (as opposed to the direct benefits of cardiovascular fitness, bone health, strength, etc) are gravy — but should not be assumed to be fully equivalent to Calories not consumed in making tradeoff decisions. Also, Holloszy's studies in particular are consistent on every point except one: does combining exercose with a given level of CR increase early mortality? (5) found yes; (3) found no. The data on the same point published by other labs are likewise inconsistent. We ought to suspend judgement on this point, IMHO. Another interesting point: (7) reports that CR animals overall ran less for the first ~3.5 mo of CR than ALers, & cites previous work (8,9) as reporting the same thing. 3.5 mo ~11.6 human years. Not too damned many of us fall into that length of CR! Semi-Digression on Mitochondria Another interesting tie-in is with de Grey's hypothesis on why CR reduces mtDNA damage and, thus, ultimately, aging.((15), and see (14) for background) It involves shuttling more NADH away from the mt to a surface membrane electron acceptor — the PMRS. de Grey's theory predicted this phenomenon, and subsequent experiments (16,17) confirmed it. Fewer electrons into the electron transport chain, fewer fumbled, less mitochondrial inner membrane damage, less passed along to mtDNA. But ALSO, less energy being produced per electron run thru' the system at peak output. Perhaps the subjective feeling of a paradoxical inability to run harder, despite the fact that one is not really breathing hard yet, is the subjective correlate of this experience? One last point. There may be another reason exercise might help slow aging, under the right circumstances — again, tying in with MiFRA. One intuitively expects that MiFRA ought to mean that exercising should speed aging due to more ROS being produced. Yet it doesn't. The reason, as de Grey points out, is that exercise doesn't actually increase the number of e- being rushed thru' each mt, because the number of mt are increased. Thus, the danger of ROS damage to mtDNA remains the SAME for each mt. And yet, this isn't quite the whole story, because an equal chance of an accident happening per car still leads to more accidents total when there are more cars on the road. De Grey agrees that this thus predicts some pro-aging effects of exercise, but that they would be minor. I've never found this to be fully convincing. Well, exercise has a mitigating effect. Apparently, "physical exercise .. modifie the fatty acid profile of the mitochondrial membranes. Total monounsaturated fatty acids decrease [and] Total polyunsaturated fatty acids in mitochondrial membranes of LIVER increase (P < 0.005) after exercise but [PUFA] in mitochondrial membranes of skeletal muscle decrease (P < 0.05)." (13) As those familiar with MiFRA will know, the former "don't count," but the latter are central, to the hypothesis. A decrease in mt membrane PUFA (which, NB, by the structure of phospholipids entails of necessity a concomitant increase in MUFA) would decrease the desaturation index of individual mt, increase their resistance to oxidation, & thus actually reduce the odds of each mt going evil on us. References 1: Holloszy JO. Longevity of exercising male rats: effect of an antioxidant supplemented diet. Mech Ageing Dev. 1998 Feb 16;100(3):211-9. PMID: 9578110 [PubMed - indexed for MEDLINE] 2: McCarter RJ, Shimokawa I, Ikeno Y, Higami Y, Hubbard GB, Yu BP, McMahan CA. Physical activity as a factor in the action of dietary restriction on aging: effects in Fischer 344 rats. Aging (Milano). 1997 Feb-Apr;9(1-2):73-9. PMID: 9177588 [PubMed - indexed for MEDLINE] 3: Holloszy JO. Mortality rate and longevity of food-restricted exercising male rats: a reevaluation. J Appl Physiol. 1997 Feb;82(2):399-403. PMID: 9049716 [PubMed - indexed for MEDLINE] 4: Holloszy JO. Exercise increases average longevity of female rats despite increased food intake and no growth retardation. J Gerontol. 1993 May;48(3):B97-100. PMID: 8482812 [PubMed - indexed for MEDLINE] 5: Holloszy JO, Schechtman KB. Interaction between exercise and food restriction: effects on longevity of male rats. J Appl Physiol. 1991 Apr;70(4):1529-35. PMID: 2055832 [PubMed - indexed for MEDLINE] 6: Holloszy JO, Smith EK, Vining M, Adams S. Effect of voluntary exercise on longevity of rats. J Appl Physiol. 1985 Sep;59(3):826-31. PMID: 4055572 [PubMed - indexed for MEDLINE] 7. Goodrick CL, Ingram DK, Reynolds MA, Freeman JR, Cider NL. Effects of intermittent feeding upon growth, activity, and lifespan in rats allowed voluntary exercise. Exp Aging Res. 1983 Fall;9(3):203-9. PMID: 6641783; UI: 84057947 "There is also an indication that [EOD CR] was somewhat less effective in enhancing [LS] in the exercised rats, when compared to the survival of groups fed EOD in conventional cages. The mean [ls] of 124 weeks in the exercised EOD group is nearly 14 weeks shorter than that of a caged EOD group prevously observed in our laboratory. Of course, [comparing data from seperate studies is problematic]." 8. Goodrick CL, Ingram DK, Reynolds MA, Freeman JR, Cider NL. Differential effects of intermittent feeding and voluntary exercise on body weight and lifespan in adult rats. J Gerontol. 1983 Jan;38(1):36-45. PMID: 6848584 [PubMed - indexed for MEDLINE] Max LS data cribbed from (11): 158 vs. 145 weeks, sedentary vs. exercising CRONies. Max LS in ALers: 88 vs. 115 weeks -- ie neither AL group broke SPECIES max LS. 9. McCay CM, Maynard LA, Sperling G, and Osgood H. Nutritional requirement during the latter half of life. J Nutr. 1941;21:45-60. (Yes, THAT McCay!) result cribbed from (11). 10. Beauchenne RE, , DellwoM, Darabian P, Haley-Ziltin V, Wright DL. Biological aging and longevity in diet-restricted and exercised rats. Abstracts of Biological Effects of Dietary Restriction, an international Conference. Washington, DC:1990. Results cribbed from (11). 11. McCarter RJ. Effects of exercise and dietary restriction on energy metabolism and longevity. In Yu BP (ed). Modulation of aging processes by dietary restriction. Boca Raton, FL: CRC Press, 1994. 12. Austad, Steven. Why We Age: What Science Is Discovering About The Body's Journey Through Life. Paperback, 256 pages . April 1999: John Wiley & Sons, Inc. ISBN: 0471296465 13. Quiles JL, Huertas JR, Manas M, Battino M, Mataix J. Physical exercise affects the lipid profile of mitochondrial membranes in rats fed with virgin olive oil or sunflower oil. Br J Nutr 1999 Jan 81:1 21-4 14. The Mitochondrial Free Radical Theory of Aging Aubrey D.N.J. de Grey Landes Bioscience, 810 South Church Street Georgetown, TX, USA tel: +1 512 863 7762, fax: +1 512 863 0081 ISBN: 1-57059-564-X 15: de Grey AD. A proposed mechanism for the lowering of mitochondrial electron leak by caloric restriction. Mitochondrion. 2001 Aug;1(2):129-39. PubMed PMID: 16120273. 16: Hyun DH, Emerson SS, Jo DG, Mattson MP, de Cabo R. Calorie restriction up-regulates the plasma membrane redox system in brain cells and suppresses oxidative stress during aging. Proc Natl Acad Sci U S A. 2006 Dec 26;103(52):19908-12. Epub 2006 Dec 13. PubMed PMID: 17167053; PubMed Central PMCID: PMC1750890. 17: López-Lluch G, Rios M, Lane MA, Navas P, de Cabo R. Mouse liver plasma membrane redox system activity is altered by aging and modulated by calorie restriction. Age (Dordr). 2005 Jun;27(2):153-60. doi: 10.1007/s11357-005-2726-3. Epub 2005 Dec 10. PubMed PMID: 23598622; PubMed Central PMCID: PMC3458500.
  2. People starting CR would very much like to have definitive, hard-and-fast answers to these questions, and unfortunately, there just isn't any way to give one in free-living humans! No one can tell you the exact point at which you're "on CR" or what "%CR" you are. These are guidelines and principles for entering the "CR continuum." Under laboratory conditions, it's easy to put a mouse or rat "on CR" and prescribe a "%CR" to it, because scientists have full, lifelong control of its genetics, diet, and environment. To establish a healthy ad libitum (AL) intake for the control group, researchers begin with a few hundred mice from a genetically-homogeneous strain, and watch what they eat when given unlimited access to lab chow under their laboratory conditions. In the best studies, researchers then cut back about 10-15% from that to keep them from getting overweight: it's this slightly "restricted" diet that actually constitutes the "AL" baseline Calorie intake for the controls. The CR group then has Calories cut from this baseline, and that's the "%CR" of the CR animals. For humans, however, we don't have anything like this level of precision, unless you've got a colony of a hundred or so identical twins that you can lock up and force to eat the same AL diet and get the same amount of exercise for the first two decades of life. It's therefore quite impossible to judge the exact point at which a person transitions to CR — let alone determining exactly what a given person's "% CR" is as a translation of the rodent phenomenon — in free-living, genetically unique humans based on some arbitrary BMI, %body fat, or Caloric intake standard. If you are lucky enough to have had a clear, healthy 'setpoint' in your youth — a weight to which you tended to gravitate when you were in your early twenties, and that was within the healthy BMI range — take that as your baseline, and restrict Calories down to a level that keeps you at least 15% below that. Unfortunately, of course, since the 1980s, fewer and fewer people at that point in their lives have been in the healthy range, or had a stable weight rather than a slow upward creep during that period — and once a higher weight is established, the body resets its setpoint to the new, abnormal fat mass. If that's you, you're stuck with a somewhat more arbitrary starting point, somewhere around the middle of the 'healthy' 18-25 BMI range, but taking some account of your build, % body fat, waist-to-hip ratio, and (ideally) visceral adiposity. if you're extremely lean and muscular at BMI 25 and only moderately active, that should work fine; if you can still "pinch an inch" and can't count your ribs at BMI 22, you probably need to start from a lower baseline. But CR is not about your weight or body fat: the effect comes from Calories, Calories, Calories. That's probably a big part of the reason why the epidemiology fails to find a longevity benefit to low BMI: the vast, vast majority of people with low BMI aren't on CR. Just having a small body frame can give a low BMI, and people of South Asian descent carry substantially more visceral adipose tissue than Caucasians, resulting in metabolic syndrome linked to excess metabolically-active fat in people who look slim to all the world. Some skinnier people are eating tons but getting lots of exercise, or have pre-existing illnesses or malabsorption issues (Crohn's disease), hyperthyroidism (associated with high cardiovascular and other risks), high Non-Exercise Activity Thermogenesis (NEAT), use amphetamines, smoke, have tapeworms, or what have you. These people are merely slim — they're not on CR. Wherever you start from, you need to cut Calories. Ultimately, the goal is to keep Calories lower than your physiology 'thinks' it needs, and a level of Calorie intake that only normalizes an overweight body will simply return you to the historical norm for our species, not induce the anti-aging metabolic shift that characterizes CR. You should also look for the endocrinological (TSH, T4, and T3; IGF-1 and IGF-BP3 if possible) and risk factor (blood glucose, fasting insulin, cholesterol profile, etc) signs discussed in The Longevity Diet by CR Society President Brian M. Delaney and Emeritus Board member Lisa Walford, p. 36.