In order to answer this questions appropriately, it is necessary to look at both the quantitative and qualitative aspects of dieting, and the physiological and psychological responses they each elicit.

Dieting – what are we really talking about?

The dictionary definition of “diet” and “dieting” is “to eat and drink sparingly or according to prescribed rules” or “a controlled intake of foods, as for medical reasons or cosmetic weight loss”.

However, these definitions do not tell us anything about the two different aspects of dieting; the quantitative and qualitative parts, and their respective consequences.  In everyday parlance, dieting usually implies both eating less calories (quantitative aspect) than usual and eating “specific” foods (qualitative aspect).

Nevertheless, when considering the consequences of “cheating” (more formally known as dieting consistency / inconsistency) and trying to answer the question whether it is a good or bad practice, it is important to distinguish these aspects of dieting. Let’s take a quick look at each:

Calorie restriction

Calorie restriction (also known as dietary restriction). When reducing calories our bodies respond by lowering basal metabolic rate, and there also is reduction is spontaneous physical activity. If the calorie restriction is severe enough, our bodies go into starvation mode, which will counteract any fat loss efforts ^1,2.

Specific food restriction

A diet usually has an explicit (or implicit) list of foods that it recommends. Eating specific foods has a more psychological impact than calorie restriction per see, especially if you don’t like the foods that are part of your diet plan.

The different types of “cheating”

Now back to the issue of cheating. Looking at calorie restriction and specific food restriction separately, you see that that you can cheat in three different ways:

- eating more calories from the same “dieting foods” = quantitative cheating

- eating non-dieting “forbidden” foods, but still within your daily calorie allotment  = quantitative cheating

- eating non-dieting “forbidden” foods, and exceeding your daily calorie allotment  = double whammy cheating!!

Dieting consistency/inconsistency is not yo-yo dieting!

Before we continue I want to make clear that this discussion on diet cheating (dieting consistency) should not be confused with yo-yo dieting (also called weight cycling; when one is repeatedly losing and regaining weight). Yo-yo dieting definitely has detrimental effects, especially psychologically ^3,4.

Dieting consistency in this context is about maintaining the same diet regimen on weekends as on weekdays. For many people, diet and activity patterns differ substantially on weekends as compared to weekdays, with potential consequences on long term body fat weight that could promote the development or maintenance of excess fat storage and obesity if the pattern is repeated throughout the year.

Possible benefits and risk with cheating on a diet?

Allowing some diet flexibility on weekends, holidays, and vacations might reduce boredom, which is a known contributor to dieting lapses ⁵, and be more realistic from a long-term perspective. However, flexibility might also increase exposure to high-risk situations, a the chance for loss of control. This is especially true among people with addictive personalities ⁶.

What does the research say?

While it is well documented that holidays are associated with fat gain ^7-9 it wasn’t until recently that studies started to investigate the influence of weekend eating patterns on short- and long-term body fat weight. The first study on weekend eating patterns was done on National Weight Control Registry subjects, who had successfully maintained a weight loss of at least 13.6 kg for 8 years ¹⁰. The purpose of the study was to examine whether maintaining the same diet regimen across the week and year promotes weight control or if dieting more strictly on weekdays and/or non-holidays is more conducive to long-term maintenance. Participants who reported greater dieting consistency were more likely to maintain their weight within 2.3 kg during the subsequent year, whereas participants with lower dieting consistency scores were more likely to regain weight during the subsequent year ¹⁰. A more recent study, where subjects consumed on average 236 calories more on weekend days, confirmed that weekend dietary indulgences contribute to weight gain or cessation of weight loss ¹¹.

It has also been documented that as the duration of a diet increases, a shift in the balance between the effort and pleasure of weight maintenance may occur, which makes it easier to stick to the diet and thereby increases the likelihood of continued maintenance ¹². This is supported by findings showing that repeated exposure trains flavor preference ¹³. In other words, a strong correlation exists between a person’s customary intake of a flavor and his preference for that flavor.

Bottom Line

Whether cheating on a diet (that is, a low diet consistency) will cause you any harm or good depends on your personal inclinations, and the reasons for the cheating.

From a biological perspective, I believe quantitative cheating, when you eat more calories from the same “dieting foods”, can be a good thing, since it can prevent lowering your resting metabolic rate and drops in spontaneous physical activity.

When it comes to the other types of  cheating, the consequences are more of a psychological origin. If you have an addictive personality, do not even think about cheating. Remember, the best cure for any addiction is complete abstinence.

If you don’t have an addictive personality, but have a lot of fat to loose, it is ok for you to engage in quantitative or qualitative cheating on weekends, when you eat non-dieting “forbidden” foods, but still within your daily calorie allotment. But only do this if you feel that it helps you stay on track with your diet during the week days.

If you don’t have much fat to loose, and are just dieting to get in a little better shape, you can indulge  in double whammy cheating, when you eat non-dieting “forbidden” foods AND exceed your daily calorie allotment. Just don’t go too much overboard; your body and mind will still take note of what you’re doing.

In any case, the reason for you to cheat on a diet should be that it helps you to stick to in the long run. Not because other people coerce you into it or are trying to make you believe that you “have to” cheat on your diet to get results. That’s nonsense you often hear from folks who don’t have the willpower and discipline themselves. It has actually been shown that friends have an even larger impact on a person’s risk of obesity than genes do ¹⁴. So don’t fall for the peer-pressure and never engage in risky behaviors because your friends do!

My advice to you is to be your own scientist and lab rat; try and see how you feel. If you lose control you know cheating on a diet is not for you, and you better put your foot down and stick to your guns. However, a slip doesn’t have to mean failure; turn the experience you gain from it into good data to guide your for future dietary decisions and long-term success!

About Monica Mollica > www.trainergize.com

Monica Mollica has a Bachelor’s and Master’s degree in Nutrition from the University of Stockholm, Sweden, and is an ISSA Certified Personal Trainer. She works a dietary consultant, health journalist and writer for www.BrinkZone.com, and is also a web designer and videographer.

Monica has admired and been fascinated by muscular and sculptured strong athletic bodies since childhood, and discovered bodybuilding as an young teenager. Realizing the importance of nutrition for maximal results in the gym, she went for a BSc and MSc with a major in Nutrition at the University.

During her years at the University she was a regular contributor to the Swedish bodybuilding magazine BODY, and she has published the book (in Swedish) “Functional Foods for Health and Energy Balance”, and authored several book chapters in Swedish publications.

It was her insatiable thirst for knowledge and scientific research in the area of bodybuilding and health that brought her to the US. She has completed one semester at the PhD-program “Exercise, Nutrition and Preventive Health” at Baylor University Texas, at the department of Health Human Performance and Recreation, and worked as an ISSA certified personal trainer. Today, Monica is sharing her solid experience by doing dietary consultations and writing about topics related to health, fitness, bodybuilding, anti-aging and longevity.

References:

1. Maclean PS, Bergouignan A, Cornier MA, Jackman MR. Biology’s response to dieting: the impetus for weight regain. American journal of physiology. Regulatory, integrative and comparative physiology. Sep 2011;301(3):R581-600.

2. Goran MI, Calles-Escandon J, Poehlman ET, O’Connell M, Danforth E, Jr. Effects of increased energy intake and/or physical activity on energy expenditure in young healthy men. J Appl Physiol. Jul 1994;77(1):366-372.

3. Osborn RL, Forys KL, Psota TL, Sbrocco T. Yo-yo dieting in African American women: weight cycling and health. Ethnicity & disease. Summer 2011;21(3):274-280.

4. Amigo I, Fernandez C. Effects of diets and their role in weight control. Psychology, health & medicine. May 2007;12(3):321-327.

5. Smith CF, Burke LE, Wing RR. Vegetarian and weight-loss diets among young adults. Obesity research. Mar 2000;8(2):123-129.

6. Avena NM, Rada P, Hoebel BG. Sugar and fat bingeing have notable differences in addictive-like behavior. The Journal of nutrition. Mar 2009;139(3):623-628.

7. Hull HR, Radley D, Dinger MK, Fields DA. The effect of the Thanksgiving holiday on weight gain. Nutrition journal. 2006;5:29.

8. Klesges RC, Klem ML, Bene CR. Effects of dietary restraint, obesity, and gender on holiday eating behavior and weight gain. Journal of abnormal psychology. Nov 1989;98(4):499-503.

9. Yanovski JA, Yanovski SZ, Sovik KN, Nguyen TT, O’Neil PM, Sebring NG. A prospective study of holiday weight gain. The New England journal of medicine. Mar 23 2000;342(12):861-867.

10. Gorin AA, Phelan S, Wing RR, Hill JO. Promoting long-term weight control: does dieting consistency matter? International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity. Feb 2004;28(2):278-281.

11. Racette SB, Weiss EP, Schechtman KB, et al. Influence of weekend lifestyle patterns on body weight. Obesity (Silver Spring). Aug 2008;16(8):1826-1830.

12. Klem ML, Wing RR, Lang W, McGuire MT, Hill JO. Does weight loss maintenance become easier over time? Obesity research. Sep 2000;8(6):438-444.

13. Liem DG, de Graaf C. Sweet and sour preferences in young children and adults: role of repeated exposure. Physiology & behavior. Dec 15 2004;83(3):421-429.

14. Christakis NA & Fowler JH (2007). The spread of obesity in a large social network over 32 years. N Engl J Med 357, 370–379.

Cheating on a diet – good or bad? is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

This is a long article, so here are some jump-to links:

Exercise Mimetics

PQQ

Quercetin

Resveratrol

Nootkatone

Naringin

Downsides…

Conclusion

To navigate back up, just hit ctrl+home. Oki, roll up your sleeves and off we go….

Age related mitochondrial changes and implications

Brain, heart, and skeletal muscle mitochondria are especially susceptible to age-induced declines in the capacity to produce energy (ATP), and ability to respond to increased energy demands ^2-6. It is well documented that mitochondrial number, mass and function declines with aging ^2-5, and that this decline plays an important role in the etiology of many disorders, including cardiovascular diseases, obesity, diabetes, neurodegenerative diseases, and cancer ^7-15. Physical inactivity and poor exercise capacity is a risk factor not only for the development of these diseases ^{8 16-18}, but also causes frailty, age-related physiologic functional declines ^19-22, and accelerates secondary aging (i.e., aging caused by diseases and environmental factors) ¹⁵.

The importance of exercise for mitochondrial function and prevention of age-related declines

We all know that exercise training increases muscle mitochondria number, mass and function ^23-26. Regular exercise counteracts the age-related decline in muscle mitochondrial expression and function ^27-32 and protects against development of age-related metabolic diseases like the metabolic syndrome, obesity, and diabetes ^{9 28 29 33-36}. Thus, regular exercise increases healthy life expectancy and prolongs life span through beneficial effects, in large part, at the level of the mitochondria ²⁸.

Muscle is the tissue with the largest capacity to increase caloric expenditure and energy production, and possesses the unique ability to increase metabolic rate nearly 100-fold during the transition from a basal resting state to maximal contractile activity ³⁷. Being such a metabolic prowess, the importance of mitochondria in muscle tissue is obvious. However, exercise training also has beneficial effects on mitochondria in other tissues, especially the heart ^{38 39}, and brain ⁴⁰. In the resting state, these tissues actually consume more calories on a per gram basis than does muscle tissue ^{41 42}. Several of the beneficial cardioprotective effects of exercise training can be traced to improved cardiac mitochondrial function ³⁸, and regular exercise also increases brain mitochondrial biogenesis ⁴⁰. This may have important implications, not only with regard to fatigue, but also with respect to various central nervous system diseases and age-related dementia that are often characterized by mitochondrial dysfunction ⁴⁰.

Recent advances in molecular biology have shed light on the mechanisms that regulate mitochondrial biogenesis (production of new mitochondria), and how exercise stimulates mitochondrial biogenesis. This is interesting not only from a physiological standpoint, but also from practical standpoint since it has allowed discovery of dietary substances (and potentially drugs) that could help us combat the age related mitochondrial decline. More on this in a bit. First, let’s take a quick look at what happens to our mitochondria when we exercise.

Mitochondria at the molecular level – exercise induced signaling targets

Energy stress from exercise triggers a host of signaling pathways in muscle cells ^43-47. One of the identified exercise-induced signals is AMPK (AMP-activated protein kinase) ^48-50. AMPK functions as a metabolic “fuel sensor” in muscle cells because it becomes activated in response to decreased energy levels (like for ex. during muscle contractions), and in turn activates catabolic processes that generate and restore ATP levels ^{48 51 52}.

Another energy sensor is SIRT1 (Sirtuin-1) ^{51 53 54}. There are actually seven sirtuins ⁵⁵;  they have generated a lot of scientific interest after the discovery that sitruins partly mediate the increase in longevity with calorie restriction that has been seen in lower organism and animals ^56-60. But sirtuins regulate a wide range of important biological processes ⁶¹. One of them is muscle precursor cell (MPC) proliferation. The finding that SIRT1 increases muscle precursor cell proliferation is very interesting since MPC proliferation has important implications in regulating muscle growth, maintenance, repair, and the aging-related loss of skeletal muscle mass ⁶².

Adult muscle stem cells, also called satellite cells or muscle precursor cells (MPCs), play an important role in the remarkable ability of muscle fibers to grow in size, repair and regenerate ^{63 64}. A hallmark of aging is diminished regenerative ability of muscle tissues, which is in large part due to age-related changes in tissue-specific stem cells ⁶⁵. Muscle precursor cells are important not only for regeneration after tissue damage, but also for maintenance. Age-related muscle loss (sarcopenia) is caused in large part by atrophy of type II muscle fibers ⁶⁶, which is associated with a fiber type-specific decline in muscle precursor cell content ⁶⁶. Thus, SIRT1 is an attractive target for dietary/exercise interventions to prevent the loss of muscle mass and function with aging ⁶⁶.

SIRT1 also works jointly with AMPK in regulating cellular fuel metabolism, inflammation, and mitochondrial function ⁵¹. In addition, SIRT1 activates and increases the activity of PGC-1 (peroxisome proliferator-activated receptor-γ coactivator,  a transcriptional coactivator), which finally activates transcription factors that turn on genes in our DNA that produce new mitochondria ^{23-25 54 67}. One such transcription factor is PPAR-gamma, which also contributes to mitochondrial biogenesis ⁶⁸.

Of the mentioned “control points” (AMPK, SIRT1, PPAR-gamma and PGC-1), PGC-1 is considered the “master regulator” of mitochondrial biogenesis ^69-71. It also increases oxidative phosphorylation and ATP (energy) production ⁷¹. As a result, increased expression of PGC-1 has been shown to increase peak oxygen uptake and delay fatigue during prolonged exercise ⁶⁹. In addition to its stimulatory effect on mitochondrial biogenesis and function, PGC-1 also regulates muscle fueling stores by increasing muscle glucose uptake, augmenting muscle glycogen storage, and preventing muscle glycogen depletion during exercise ⁷².

Ok, now you know enough molecular biology to understand the rationale behind exercise mimetics, which we will focus on next.

Exercise Mimetics

Elucidation of the molecular mechanisms behind mitochondrial biogenesis and function, coupled with the identification of dietary substances that seem to increase the expression of PGC-1, SIRT1, AMPK etc. and/or their regulators, has led to great interest in developing drugs and dietary supplements to target the SIRT1-PGC-1 complex and related signaling pathways ^{47 50 73-75}.

Because these supplements and drugs activate some of the signaling pathways that are activated by exercise, they have been labeled as “exercise mimetics” ^{47 74}. Here’s a rundown of some dietary bioactive substances that are currently in the scientific spotlight for their potential exercise mimetic effects.

PQQ

PQQ (short for Pyrroloquinoline Quinone, and also called methoxatin) is a less well known dietary compound that was discovered 1979 ^76-78. PQQ is present in tissues and body fluids, including human milk ^79-81 and in foods. The richest dietary sources are ⁸²:

Natto (fermented soybeans)         61 ng PQQ/g

Parsley                                               34 ng PQQ/g

Green tea                                          30 ng PQQ/g

Green pepper                                   28 ng PQQ/g

Kiwi                                                     27 ng PQQ/g

Papaya                                               27 ng PQQ/g

Tofu (soybean curd)                        24 ng PQQ/g

Spinach                                              22 ng PQQ/g

Carrot                                                17 ng PQQ/g

When you read supplement labels, remember that 1 milligram (mg) = 1,000,000 nanogram (ng)

PQQ acts as an antioxidant ⁸³, enzyme cofactor ^84-91, nero-protectant ^92-95, cardio-protectant ^96-98, and may have an important role in cell signaling ^{92 99-101}. In this context, the most interesting function of PQQ is that it affects the expression of genes involved in mithochondrial functions and biogenesis (most notably, PGC-1) ^{99 102}.

The nutritional importance of PQQ has been demonstrated by feeding rats and mice a diet that is devoid of PQQ; the animals show growth retardation, reproductive failure, compromised immune responses, skeletal deformities aortic aneurysms, and fragile skin ^{91 103 104}. This strongly suggests that PQQ is necessary for normal body functions and health. It is actually being debated whether PQQ might become the “next vitamin” ^{78 88}.

What’s more interesting is that varying the amount of PQQ in diets causes modulation in mitochondrial content, alters lipid metabolism, and reverses inhibition elicited by classical mitochondrial function inhibitors ^{97 104-106}. PQQ deficiency decreases both mitochondrial function and number ¹⁰⁶. The most recent study on PQQ fed rats a nutritionally complete diet either with or without PQQ ¹⁰⁵. The rats that got the PQQ diet not only exhibited lower blood triglycerides but also showed increased energy expenditure, hepatic (liver) mitochondrial content. In contrast, the rats that were fed the PQQ deficient diet instead exhibited deterioration in mitochondrial function, a lowered energy expenditure and reduced capacity to oxidize fat for energy (that is, reduced fat burning) ¹⁰⁵. However, at the time of this writing, no human study has investigated the effect(s) of PQQ on metabolic, muscular and mitochondrial parameters. PQQ can already be found on the supplement market, but for now we will have to be our own lab rats.

Quercetin

A natural polyphenolic flavonoid, quercetin is present in a wide variety of food plants, including red onions, apples, and berries ^{107 108}. Known for its multiple health benefits ^109-118, it has recently been shown that quercetin also beneficially affects mitochondrial energetics ^{119 120} and stimulates mitochondrial biogenesis (by increasing expression of PGC-1alpha and SIRT1) ¹²¹. The quercetin-induced increase in mitochondrial biogenesis was accompanied ¹²¹ with both maximal endurance capacity and voluntary wheel-running activity in mice ¹²¹.

However, findings from the few research studies on the ergogenic (i.e. performance enhancing) effects of quercetin supplementation in humans are equivocal ^122-127. A small preliminary study showed that when given in combination with other antioxidants for 6 weeks, quercetin improved endurance time-trial performance on a bicycle ergometer in humans ¹²⁶. Another study, conducted by the same research team that showed performance enhancing effects in mice, gave healthy but untrained participants 500 mg of quercetin twice daily. After 7 days it was shown that the quercetin supplementation resulted in a modest increase in VO2max along with a substantial (13.2%) increase in ride time to fatigue ¹²⁵. It was concluded that quercetin supplementation can increase endurance without previous exercise training in untrained participants ¹²⁵. In contrast, another controlled study conducted by another research team, which gave young healthy recreationally active men 1 g/day of quercetin in a sports hydration for 16 days failed to show any benefits over placebo; the quercetin supplementation did not improve neither muscle oxidative capacity or performance in a 10 min maximal-effort cycling test ¹²⁴. Also, supplementing with 1 g/day of quercetin for 3 weeks in trained cyclists failed to show a performance benefits ¹²⁷.

A recently published meta-analysis of human studies on quercetin and performance concluded that quercetin supplementation significantly endurance performance, but that the effect is very small ¹²⁸. The computed effect size for the performance enhancement was 3-5% over placebo ¹²⁸. This can be compared to the effect size for the performance enhancement with caffeine, which is in the range of 12% over placebo ¹²⁹. If at all, people with low fitness levels will probably most likely experience a performance benefit of quercetin supplementation, since highly fit individuals already have an elevated mitochondrial density and function.

There is a possibility that a longer supplementation duration is necessary for quercetin to exert a performance enhancing effect, and/or that it could be ergogenic in elderly. Hopefully, future studies will address that. Thus, while quercetin is a prudent supplement to take for its beneficial health effect, if you’re looking for a boost in mitochondrial function and/or performance, don’t expect too much.

Resveratrol

Resveratrol is the most well known SIRT1 activator ^130-132. A  natural compound present in grapes (especially grape skin) ^{133 134}, resveratrol has been in the spotlight since it was found to be one major factor explaining the French paradox and conferring the cardioprotective effect of red wine ^135-140. Fresh grape skin contains about 0.05-0.1 mg resveratrol per gram, while red wine is a concentrated source of resveratrol providing up to 14 mg per liter. Resveratrol also protects against cancer ¹³⁵, and induces several signaling pathways that are also seen with calorie restriction (I will cover this more in an upcoming article on calorie restriction mimetics).

More recently, it has been shown that resveratrol also might improve mitochondrial function and stimulate mothochondrial biogenesis ^{131 141}. In mice, intake of resveratrol together with habitual exercise, suppresses the aging-related decline in physical performance ¹⁴¹. This effect was attributable, at least in part, to improved muscle mitochondrial function ¹⁴¹. Another mice study showed that resveratrol increases aerobic capacity, as evidenced by an increased running time to exhaustion ¹³¹. On a molecular level, this effect was paralleled by an induction of genes for oxidative phosphorylation, increase in PGC-1alpha activity and enhanced mitochondrial biogenesis ¹³¹. Resveratrol also seems to be able to counteract muscle atrophy during periods of physical inactivity (mechanical unloading) in rats ¹⁴².

However, while there is ample of human data on the health promoting effects of resveratrol, at the time of this writing there are no human studies on its potential mitochondrial, metabolic and/or performance enhancing effects.

Nootkatone

A new kid on the block, nootkatone is another bioactive naturally occurring dietary compound that is found primarily in grapefruit (a whole grapefruit contains about 100 mg of nootkatone, mainly in the rind)¹⁴³.

It was recently shown in mice that nootkatone potently activates the AMPK signaling pathway in both muscle and liver, increases energy expenditure, endurance performance, and also suppresses diet-induced development of obesity, abdominal fat accumulation, and insulin resistance ¹⁴³. Body weight in nootkatone-fed mice was significantly decreased despite no significant decrease in energy intake ¹⁴³. It was concluded that activation of AMPK and subsequent induction of PGC-1α, with a possibly enhanced oxidative energy metabolism and stimulation of energy expenditure, is an underlying mechanism of the antiobesity effects of nootkatone ¹⁴³. This study supports the idea that AMPK activators could be useful as exercise mimetics or exercise-supporting supplements in preventing/treating obesity and/or metabolic syndrome, and for improving physical performance.

Nootkatone has a pleasant, citrusy grapefruit aroma, and is GRAS approved ¹⁴⁴ for use as a food flavoring agent, and as a fragrance in perfumes and essential oils ¹⁴⁵. You can even use it as a non-toxic effective repellent/insecticide against mosquitos and other insects ¹⁴⁶. Being this multi-functional, we will most likely hear more about nootkatone, in one way or the other, it in the near future. It is interesting to speculate whether the nootkatone-induced AMPK activation is part of the mechanism underlying the weight loss and increased insulin sensitivity that has been reported after grapefruit supplementation ¹⁴⁷. Even though nootkatone is currently not available as a dietary supplement in isolated form, you can always add some grapefruit to your regimen (remember that whole fruits are better than juice). However, if you are taking any medications, talk to your doctor first because grapefruit interferes with the enzymes that metabolize medications, and can cause a lethal buildup of medication in the body ^148-151.

Naringin

Another potential mitochondrial booster is naringin, which like nootkatone, is a flavonoid present in grapefruit, and also in other citrus fruits ¹⁷⁰ 171. Upon ingestion, the colonic microflora converts naringin to naringenin, which is the active form in the body ¹⁷².  In contrast the other bioactive compounds mentioned in this article, naringin primarily targets the liver, where it activates both PPAR-gamma and PPAR-alpha with a concomitant increase in hepatic fat oxidation (fat burning) and inhibition of fat and cholesterol synthesis ¹⁷³. An interesting recent finding is that naringin also seems to induce PGC-1 transcription, and thereby possibly could stimulate mitochondrial biogenesis in the liver as well. Since the liver is the metabolic hub in the body, this could have beneficial systemic (whole-body) effects. Naringin has already been shown in humans to have several beneficial health effects by preventing cardiovascular disease, protecting against cancer and being anti-inflammatory ^{171 174-177}, so if you try this supplement it won’t hurt you even though the evidence for its potential effect on mitochondrial biogenesis is still in its infancy.

Downsides…

The potential of exercise mimetics certainly appeals to the huge mass of lazy folks who cannot get their butts off the couch, and the pharmaceutical and supplement industry that sees the tremendous market potential. So we’ll most certainly be hearing a lot about these “exercise pills” in the near future. However, I want to emphasize that an “exercise pill” will never ever be a substitute for actual exercise training. Why? For several reasons:

Firstly, mimicking activation of exercise signaling pathways could result in a chronic catabolic state. For example, activation of AMPK could inhibit protein synthesis ¹⁵² and stimulate autophagy (cell cannibalism, that is, degradation of a cell’s own components through the lysosomal machinery) ¹⁵³. Also, while augmenting oxidative capacity in mice, overproduction of PGC-1α in muscle has been shown to result in severe muscle atrophy as mice aged ¹⁵⁴. These effects would clearly be detrimental, especially for aging people. This underscores the importance of striking an optimum balance between continuous compared with transient activation of exercise signaling pathways.

Secondly, intense exercise bouts induce significant temporary stress on various organ systems. With an over 15-fold increase in whole body oxygen consumption when transitioning from complete rest to intense exercise, it is no surprise that a complex myriad of signaling pathways are activated in multiple tissues, of which we only know a few. Even though science is making progress in elucidating the exercise response on a molecular level, we are still barely just scraping the tip of the iceberg.

Thirdly, exercise training has multiple health benefits that do not, at least directly or entirely, relate to the muscle-specific adaptations. For example, cardiovascular adaptations like blood pressure reduction and improved blood lipid profile are not completely (albeit partly) due to muscle-specific adaptations ^{155 156}. This is further underscored by the finding that beneficial effects of regular exercise are even seen in arteries of non-exercise-trained limbs ^157-160. Additionally, regular exercise results in a host of other health benefits; it prevents or reduces the severity of dementia and other neurological disorders, osteoarthritis, osteoporosis, fall-related injuries, depression, certain cancers and cardiovascular diseases ^{16 18 161-165}. Exercise also improves cardiac function and enhances stroke volume, increases VO2max (the maximal oxygen uptake, or aerobic capacity, which is the maximum capacity of the body to transport and use oxygen during exercise), increases nitric oxide levels in vascular endothelial cells, increases bone mass and strength, enhances the immune system, lowers TNF-α and other inflammatory markers, improves insulin sensitivity and blood lipid profiles, and increases muscle capillarization, muscle size and muscle strength ^{161 166}. Obviously, no single pharmaceutical or dietary agent could mimic this multifaceted response.

Fourthly, in order for an “exercise mimetic” to mimic the effect of exercise on obesity, it would have to result in an increase in energy expenditure to the same degree as exercise. Even though PQQ increases energy expenditure in rats (see above), this increase is nowhere near the increase that is seen with exercise. An increase in muscle mitochondria enhances exercise capacity and endurance, making it possible to expend more total energy, or the same amount of energy in a shorter time. So, an increase in mitochondria enhances the capacity to expend calories by means of exercise, and thereby could make exercise more effective in preventing and/or treating obesity. However, an increase in mitochondria per se has no major independent effect (in the absence of exercise) on energy expenditure.

Finally, regular exercise has psychological effects on constructs like self-mastery ¹⁶⁷, self-esteem ¹⁶⁷, self-perception ¹⁶⁷, self-efficacy ¹⁶⁸ self-regulation ¹⁶⁸ and also social engagement ¹⁶⁷, which no “magic” mimetic pill ever will be able to reproduce. The psychological effects of exercise might actually be at least as important as the physiological effects in the achievement of fat loss ¹⁵⁴.  This is an areas that I think deserves more attention.

A poly-pill containing a number of agents aimed at selected targets could theoretically address the second and third objection. However, as indicated in objection one, it is likely to be associated with multiple unwanted effects, and to be of questionable long-term efficacy. Thus, with the discovery and development of tissue-specific targets, only limited aspects of the exercise response can be mimicked. The term ‘exercise mimetic’ is therefore misleading, and could lull a false sense of security and give lazy folk another excuse not to exercise “I took this exercise pill so I don’t have to go to the gym”…. These days, unfortunately the general tendency is to look for a pill to solve our problems anytime we face obstacles. This fact is aptly highlighted by a comment from one of the most prominent researchers on the health benefits of regular physical activity “When will we treat physical activity as a legitimate medical therapy…even though it does not come in a pill?” ¹⁶⁹.

Conclusion

Exercise mimetics work by stimulating some of the molecular pathways that are also activated by actual exercise. Pharmacological stimulation of AMPK and PGC-1 in sedentary mice has been shown to induce metabolic genes and enhanced running endurance even without exercise ⁵⁰. Similarly, SIRT1 activation could protect against metabolic disorders by stimulating fat burning (oxidation). Also, the question remains as to what extent data from cell culture and rodent studies can be extrapolated to humans.

However, the terms “exercise mimetic”, and its synonym “exercise pill”, are very misleading. I prefer the term “mitochondrial booster”, since it doesn’t erroneously imply that these types of pills can substitute for the real thing. A mitochondrial booster (or exercise mimetic, if you wish) supplement could be a great adjunct to exercise, but never ever a substitute.

Bearing all the caveats in mind, since actual exercise and exercise mimetics at least partly target the same molecular pathways at potentially complementary control points, it is extremely interesting to speculate on the possible synergistic effects between exercise and exercise mimetics on muscle, mitochondrial function, performance, and in preventing the age-related declines in muscular function…indeed, there are preliminary data pointing towards promising synergistic effects ⁵⁰. Rest assured I will be keeping you posted here on BrinkZone.com.

However, exercise is and always will be necessary. Sorry folks, there are no magic bullets. There’s simply no way around it. Amen!!!

So here’s the take-home message:

If you are a regular exerciser; an exercise mimetic/mitochondrial booster could give you a little extra “push” and possibly enhance your long-term training response.

If you are a couch potato; no pill in the word will ever make up for your lazy ass!

References:

1. McBride HM, Neuspiel M, Wasiak S. Mitochondria: more than just a powerhouse. Current biology : CB 2006;16(14):R551-60.

2. Kwong LK, Sohal RS. Age-related changes in activities of mitochondrial electron transport complexes in various tissues of the mouse. Archives of biochemistry and biophysics 2000;373(1):16-22.

3. Navarro A, Boveris A. The mitochondrial energy transduction system and the aging process. American journal of physiology. Cell physiology 2007;292(2):C670-86.

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155. Jennings G, Nelson L, Nestel P, Esler M, Korner P, Burton D, et al. The effects of changes in physical activity on major cardiovascular risk factors, hemodynamics, sympathetic function, and glucose utilization in man: a controlled study of four levels of activity. Circulation 1986;73(1):30-40.

156. Kingwell BA, Jennings GL. Effects of walking and other exercise programs upon blood pressure in normal subjects. The Medical journal of Australia 1993;158(4):234-8.

157. DeSouza CA, Shapiro LF, Clevenger CM, Dinenno FA, Monahan KD, Tanaka H, et al. Regular aerobic exercise prevents and restores age-related declines in endothelium-dependent vasodilation in healthy men. Circulation 2000;102(12):1351-7.

158. Green DJ, Bilsborough W, Naylor LH, Reed C, Wright J, O’Driscoll G, et al. Comparison of forearm blood flow responses to incremental handgrip and cycle ergometer exercise: relative contribution of nitric oxide. The Journal of physiology 2005;562(Pt 2):617-28.

159. Lavrencic A, Salobir BG, Keber I. Physical training improves flow-mediated dilation in patients with the polymetabolic syndrome. Arteriosclerosis, thrombosis, and vascular biology 2000;20(2):551-5.

160. Linke A, Schoene N, Gielen S, Hofer J, Erbs S, Schuler G, et al. Endothelial dysfunction in patients with chronic heart failure: systemic effects of lower-limb exercise training. Journal of the American College of Cardiology 2001;37(2):392-7.

161. Booth FW, Lees SJ. Fundamental questions about genes, inactivity, and chronic diseases. Physiological genomics 2007;28(2):146-57.

162. Lee DC, Sui X, Blair SN. Does physical activity ameliorate the health hazards of obesity? British journal of sports medicine 2009;43(1):49-51.

163. Sui X, Laditka JN, Church TS, Hardin JW, Chase N, Davis K, et al. Prospective study of cardiorespiratory fitness and depressive symptoms in women and men. Journal of psychiatric research 2009;43(5):546-52.

164. Lautenschlager NT, Almeida OP, Flicker L, Janca A. Can physical activity improve the mental health of older adults? Annals of general hospital psychiatry 2004;3(1):12.

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Exercise Mimetics & Mitochondrial Boosters is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

Fish oil is well known for its beneficial cardiovascular and cardiac health effects. In 2004 FDA approved a prescription fish oil preparation for treatment of high blood triglycerides (hypertriglyceridemia) ¹. However, recently several studies have shown that fish oil also has other beneficial effects, which might appeal more to the younger population, and especially to fitness and bodybuilding enthusiasts. One of these effects is fat loss.

Fish Oil Induced Fat Loss

In the 80s early 90s, several animal studies showed that fish oil reduces body fat ^2-5 and weight gain ^6-9, and limits adipose tissue expansion ^10-12. These effects have been seen during both a decreased ^{3 7}, constant ⁵ or even increased energy intakes ⁶. This indicates that the fatty acids in fish oil, notably EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid), have an effect on the partitioning of fat between oxidation (fat burning) and storage in the body.

Mechanism – how does it work?

In search for the mechanisms behind fish oil induced fat loss, it has been found that fish oil exerts favorable metabolic effects by modulating gene expression (which is the process by which the information encoded in a gene is converted into protein)^{2 13-26}. While we inherit our genes (or blueprints) from our parents, what determines the way in which our blueprints are interpreted is largely dictated by a collection of environmental factors. The nutrients we consume are among the most influential of these environmental factors ^{27 28}. One dietary constituent that has a strong influence on our genetic makeup is dietary fat ^{2 13 14 16-19 21-23 25 29}. Fatty acids of dietary fat not only influences hormonal signaling events, but also have a very strong direct influence on the molecular events that govern gene expression. More specifically, it has been shown that the fatty acids EPA and DHA from fish oil (by affecting gene expression) inhibit the activities of fat synthesizing (lipogenic) enzymes ^30-37, while at the same time stimulating the activities of key enzymes that govern fat oxidation (fat burning) ^{2 38-46}.

Fish oil also has been shown to increase levels of adiponectin and decrease levels of cortisol ^{47 48}. Adiponectin is a novel adipose tissue-specific protein that circulates in human plasma at high levels ⁴⁹. It is one of the physiologically active polypeptides secreted by adipose tissue, whose multiple functions have started to be understood in the last few years. Some of its beneficial effects are enhanced insulin sensitivity, and lowered plasma glucose (blood sugar) and triglyceride levels ^{49 50}. A reduction in adiponectin expression is associated with insulin resistance ⁴⁹, and adiponectin levels are inversely related to the degree of adiposity ⁵⁰. The activity of adiponectin has also been associated with steroid and thyroid hormones, glucocorticoids, and nitric oxide, and has anti-atherogenic and anti-inflammatory properties ⁵⁰. Thus, it is plausible that fish oil induces some of its effect by affecting adiponectin levels. While the functions of adiponectin are just starting to emerge, it is likely to become a target for therapeutic applications in the future.

It is also interesting that fish oil lowers cortisol. While the exact role of cortisol in obesity isn’t fully elucidated ^{51 52}, it is known that excessive cortisol levels result in substantial fat mass gain ^{53 54}. Thus, the reduction in cortisol levels after fish oil supplementation could contribute to the fat loss effect of fish oil.

What’s in it for me?

At this point you might be thinking “ok, that all sounds nice, but I’m not a rat. Does it work in humans”?

Yes! Read on…

In a landmark study, healthy male participants were given a diet where 6 g of fat from butter, olive oil, sunflower oil and peanut oil was replaced with 6 g fish oil (corresponding to 1.1 g EPA and 0.7 g DHA) per day ⁵⁵. After 3 weeks the researchers noted a significant increase in resting fat oxidation (fat burning) and a 1.94 lb (0.88 kg) decrease in body fat (measured by DEXA), in the face of a constant energy intake. Since there was no change in body weight, this implies that the fish oil supplement increased lean body mass (more on that in an upcoming article). This effect was seen despite the fact that the subjects were told not to change their usual exercise and diet habits.

Another study confirmed the ability of fish oil supplementation to increase fat oxidation (fat burning) during exercise ⁵⁶. In this study, recreationally active men were given a daily fish oil supplement corresponding to 2400 mg EPA and 1600 mg DHA for 3 weeks. At the end of the study subjects performed a 60 min jogging exercise bout at 60% of VO2max, during which fat metabolism was measured. It was shown that the fish oil supplementation significantly increased the oxidation of fat for energy (e.g. fat burning) during the exercise session ⁵⁶. It has also been shown that supplementing with fish oil for 3 weeks (1.1 g EPA and 0.7 g DHA daily) significantly decreases insulin levels and increases fat oxidation (fat burning) by 35% (!) after consumption of carbohydrate rich meals ⁵⁷.

Recently, more studies have been published on the topic. In overweight men and women, the effects of the addition of 6 g of fish oil daily (corresponding to 360 mg EPA and 1560 mg DHA) in combination with regular aerobic activity (walking 45 min three times per week at an intensity of 75% of age-predicted maximal heart rate) for 12 weeks, was investigated ⁵⁸.

The results showed that the combination of fish oil and regular aerobic activity not only improved several risk factors for cardiovascular disease, but also significantly reduced the amount of body fat ⁵⁸. It is interesting that these effects were noted even though the subjects did not change their usual food habits other than adding the fish oil supplement. This indicates the great potential benefits of fish oil combined with regular physical activity for improving body composition and cardiovascular health. In this study, no fat loss was seen in fish oil only group (that didn’t exercise). This could be due to the older age of the subjects (47-51 yrs) in this study compared to the previous studies, and the relatively low dose of EPA. Fish oil supplementation has also been shown to result in a 2.22 lb (1 kg) greater weight loss after 4 weeks of dieting (reduced caloric intake) ⁵⁹.

Perspective on fish oil and fat loss

In contrast to the positive studies, there are a few that didn’t show any fat loss with fish oil supplementation ^60-63. This could be due to differences in subject characteristics (age, initial body fat mass, baseline physical activity), methodological differences, and differences in fish oil preparations (see below). However, several high quality studies have shown that fish oil supplementation has a significant fat loss effect in addition to all its other health promoting effects. Overall, fish oil seems to have the ability to shift fat metabolism away from storage toward burning of body fat.

It’s getting better – fat loss combined with lean mass (muscle) gain

In one of the most recent studies on fish oil’s fat loss effect, men and women (mean age 33 yrs) where given 4 g of fish oil corresponding to 1600 mg EPA and 800 mg DHA ⁴⁸. After for 6 weeks, the placebo group, which was given 4 g of safflower oil, showed a tendency towards fat gain.

The fish oil group instead had lost 0.5 kg of fat mass and gained 0.5 kg of lean mass, with no change in body weight. This is a very beneficial body composition effect and underscores the importance of investigating fat mass and lean mass separately, since just measuring body weight will not tell anything about potential compositional changes, which after all is what is interesting from both a health, esthetic and physical performance viewpoint. I will cover the anti-catabolic and potential lean mass gaining effects of fish oil in more detail in an upcoming article.

Wrap up

Whether you are on a diet or not, adding a fish oil supplement to your regimen can effectively help you get in shape. The additional calories from the fish oil will not get stored ⁶⁴; quite to the contrary, fish oil will help you get rid of calories you already have stored in your body fat. What’s interesting is that fish oil supplementation seems to reduce body fat and waist circumference despite unchanged exercise and/or other dietary practices.

Aim for a daily fish oil intake that provides you with at least 1600 mg EPA and 800 mg DHA, but a higher dose, 2400 mg EPA and 1600 mg DHA (a total of 4 g EPA and DHA total), might result in a larger fat loss. To achieve this high intake of EPA and DHA it is advisable to take a fish oil concentrate. In an upcoming article I will go into more detail about fish oil concentrates, different ratios of EPA to DHA in fish oil preparations, their relative effectiveness, safety aspects of high dose fish oil supplementation, and sort through the myriad of fish oil supplements currently available on the market, to help you find a good fish oil supplement that will give you the best bang and effectiveness for your buck.

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About Monica Mollica > www.trainergize.com

Monica Mollica has a Bachelor’s and Master’s degree in Nutrition from the University of Stockholm, Sweden, and is an ISSA Certified Personal Trainer. She works a dietary consultant, health journalist and writer for www.BrinkZone.com, and is also a web designer and videographer.

Monica has admired and been fascinated by muscular and sculptured strong athletic bodies since childhood, and discovered bodybuilding as an early teenager. Realizing the importance of nutrition for maximal results in the gym, she went for a major in Nutrition at the University.

During her years at the University she was a regular contributor to the Swedish bodybuilding magazine BODY, and she has published the book (in Swedish) “Functional Foods for Health and Energy Balance”, and authored several book chapters in Swedish publications.

It was her insatiable thirst for knowledge and scientific research in the area of bodybuilding and health that brought her to the US. She has completed one semester at the PhD-program “Exercise, Nutrition and Preventive Health” at Baylor University Texas, at the department of Health Human Performance and Recreation, and worked as an ISSA certified personal trainer. Today, Monica is sharing her solid experience by doing dietary consultations and writing about topics related to bodybuilding, fitness, health and anti-aging.

Fish Oil for Fat Loss is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

Alison shows what hard training looks like in the “No Pink Dumbbell Training Zone”

Leg Day With Alison Maldonis! is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

As a full time trainer, I’m keenly aware of the variety of products marketed for weight loss.  My background in science also makes it simple for me to understand product claims and understand their worth, if any.  These days, lots of people in and outside of the gym ask me, “hey what do you think of this weight loss product?” and most of the time, it’s something that I know won’t work for them.

Here are some of the worst questions I’ve encountered:

What do you think of those booty toning slippers? You can see the results of an independent study here or take a look at the funny review Will  covers on that subject here.  If you want a nice booty, learn how to squat, deadlift, lunge, and otherwise build your glutes.

What do you think of (insert whatever brand) fat burner? If you’ve amassed a nice layer of coating over your abs over the winter season and think that popping a pill is going to miraculously correct months of inactivity and poor diet, think again. Certain supplements DO work, those that are properly dosed, from reputable companies, and used in conjunction with exercise programs and a sensible diet.  You can see a list of such products here.

No matter HOW you slice and dice this one, no pill will be of any use to you unless you’ve first addressed the two biggies: diet and exercise.

What do you think of the latest cleansing/detox product? Ack! Explosive bowel movements don’t sound like any fun to me. I can think of a million other better things to do with my day than being chained to the potty holding on to toilet paper for dear life.  A good session in the squat rack and eating clean is all the detox I need.

What do you think of the latest (insert fad weight loss) diet? The cookie diet, the twinkie diet, the Special K challenge, etc etc.  I’ve covered my issues with fad diets here. ANY diet will work in the short term, but success happens when you LEARN what works and figure out how to make it part of your lifestyle.  My gripe with some of the above diets is that they actually ADD more sugar into your diet (how is THAT a healthy strategy?) and they’re making money off of YOU doing so.

What Not To Do To Get Lean This Summer is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

Chest & Back Day With Deb D is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

Below is some -but not all – of the info and data I was looking at to help with my comments in this vid for the more science minded:

Effect of administration of oral contraceptives on the synthesis and breakdown of myofibrillar proteins in young women.

Scand J Med Sci Sports. 2009 Oct 22.

Hansen M, Langberg H, Holm L, Miller BF, Petersen SG, Doessing S, Skovgaard D, Trappe T, Kjaer M.

Institute of Sports Medicine, Bispebjerg Hospital, Copenhagen, Denmark.
Abstract

Oral contraceptive (OC) treatment has an inhibiting effect on protein synthesis in tendon and muscle connective tissue. We aimed to investigate whether OC influence myofibrillar protein turnover in young women. OC-users (24+/-2 years; Lindynette((R))n=7, Cilest((R))n=4) and non-OC-users (controls, 24+/-4 years n=12) performed one-legged kicking exercise.

The next day, the myofibrillar protein fractional synthesis rate (FSR) was measured using stable isotopic tracers ((13)C-proline) while the subjects were fed standardized nutrient drinks. Simultaneously, a marker for myofibrillar protein breakdown, 3-methyl-histidine (3-MH), was measured in the interstitial fluid of the vastus lateralis. Measurements were performed in both legs.

In general, myofibrillar protein FSR was lower in OC-users (two-way analysis of variance, P<0.05), although the difference seemed to depend on the OC type. Interstitial 3-MH in the skeletal muscle was not different between groups and did not vary by OC type. Exercise did not change myofibrillar protein FSR or 3-MH concentrations.

Serum androstenedione and bioavailability of testosterone were lower in OC-users. In conclusion, the results indicate that the use of OC has an inhibiting effect on myofibrillar protein synthesis and the magnitude of the effect may depend on the type of OC. In contrast, there was no effect of OC on myofibrillar protein breakdown in the fed state.
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More damaging, but also a write up from a poster session at conference then fully published data from a journal:

Birth control pills can limit muscle-training gains

Science News

By Janet Raloff

Some female athletes may pay a price for using oral contraception: lower strength gains from resistance exercise. These muscle-building exercises depend on lifting weights (like barbells and those in the big machines at your local gym) or working against tension bands and bars (like those in Bowflex devices).

Personal trainers have long noted that all women don’t garner the same benefits from such exercise and there has been a suspicion that genetics might underlie differences. But exercise physiologist Chang Woock Lee and his colleagues at Texas A&M University wondered if other lifestyle factors might also play a role. And at the Experimental Biology meeting in New Orleans, this week, Lee identified birth control pills as a major suspect.

In an earlier study, Lee’s group noted that many young female athletes reported using oral contraception. These pills have been specifically formulated to alter a woman’s steroid-hormone levels. Since certain steroids can affect how efficiently the body bulks up and gains muscle, Lee wondered whether these pills might also limit strength gains.

So, three times a week for 10 weeks, the researchers had 73 young women (18 to 34 years old) complete 13 different exercises. The regimen was intense, working muscles throughout the body. None of the recruits had been regularly working out beforehand. But they sure were now. Each had to complete her resistance training against weights that were individually tailored to work her muscles at 75 percent of their maximum strength.

Thirty-four of the recruits were taking some type of oral contraceptive. And as a group, they gained 2.1 percent muscle mass over the trial — or 40 percent less than the group not on the pill. So I asked Lee: What do you think is going on?

One clue: Both before and after the trial, he found, women using oral contraception had dramatically lower blood levels of natural anabolic — as in muscle-building — hormones than did recruits not on the pill. The anabolic hormones included DHEA and its more abundant sulfated form, DHEAS. Compared to non-pill-users, women taking oral contraceptives also had substantially higher concentrations of cortisol, a hormone associated with the breakdown of muscle.

So resistance training “did not rescue” this adverse hormone profile in the pill users, Lee points outs. And, he suspects “those hormone differences might be the underlying factor” accounting for why women on the pill gained less muscle.

But that’s not the end of the story. Further analysis showed that not all pill users had an equally hard time gaining muscle through exercise. So Lee analyzed the formula for each woman’s contraceptive and found that many types contained progestins — a synthetic form of progesterone, a natural female sex hormone. In tests, he showed that these synthetic hormones bind to the androgen receptor in cells — the same receptor that binds male sex steroids, such as DHEA and DHEAS.

Lee worries that if progestins dock with a receptor that DHEA would normally have turned on, they could essentially block the true androgen’s ability to trigger muscle growth.

Not all progestins were equally effective at this binding, however. So Lee grouped the contraceptives on the basis of whether their progestins exhibited low, medium or high androgenicity (i.e. androgen-receptor binding). And then a really striking difference emerged.

Women who took pills containing low-androgenicity progestins acquired muscle through exercise as effectively as did women not on the pill. But women whose oral contraceptives contained medium- or highly androgenic progestins attained less than a 0.5 percent gain in muscle mass over 10 weeks — a far cry from what the others achieved. (By the way, Lee didn’t divulge which brands of contraceptives performed which way, so please don’t write me asking.)

What all this means, he says, is that for women taking certain brands of the pill, the difference in strength-building from exercise could “make a difference in the color of her medal.” For the rest of us, he says, getting stronger would just require that we work “much harder.”
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Abstract from the above study:

Oral Contraceptive Use Impairs Muscle Gains in Young Women
Chang Woock Lee1, Mark A. Newman2 and Steven E. Riechman1,3

1 Health and Kinesiology, Texas A&M University, College Station, TX
2 Human Energy Research Laboratory, University of Pittsburgh, Pittsburgh, PA
3 Nutrition, Texas A&M University, College Station, TX

ABSTRACT

Background: Many active young women use oral contraceptive (OC) yet its effect on their body composition and exercise performance has not been thoroughly studied. We examined the effects of oral contraceptive on muscle responses to resistance exercise training (RET).

Methods: 2 groups of 18-31 year old subjects (OC: n=34, no OC: n= 39) underwent 10 week whole-body RET (3x/week, 3 sets, 6-10 reps, at 75% of max strength). Body composition was determined using hydrostatic weighing. Blood samples were taken before/after the training and assayed for DHEA, DHEAS, cortisol, and IGF1.

Results: There were significant differences in lean mass gains (OC: 2.1±2.1%, no OC: 3.5±3.2% / OC: 1.0±1.0kg, no OC: 1.6±1.4kg, p<0.05). Plasma concentrations of DHEA, DHEAS, and IGF1 were significantly lower and cortisol was elevated in OC (DHEA: OC 9.5±4.4, no OC 13.6±4.6 / DHEAS: OC 1451±685, no OC 2196±1008 / IGF1: OC 163±42, no OC 239±126 / cortisol: OC 33.4±10.8, no OC 24.3±9.4, ng/ml, p<0.05). There also were significant differences in lean mass gains depending on androgenicity of the progestin in OC (low=2.5%, medium/high=0.3%, P<0.05).

Conclusion: Oral contraceptive use impaired muscle gains in young women which was associated with lower DHEA, DHEAS and IGF1 and higher cortisol. The diminished lean mass gain may be related to the androgenicity of progestin which may bind to androgen receptor and inhibit its function.

Sources:

http://www.fasebj.org/cgi/content/meeting_abstract/23/1_MeetingAbstracts/955.25

-OR-

http://www.the-aps.org/press/releases/09/16.htm

Does Birth Control Prevent Women From Making Progress In The Gym? is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

Having to deal with a mommymonster. No fun!

I’ve said it once and I’ll say it again, it’s much more fun to eat big and be strong. On 1400 calories a day my energy levels were very low, and I was a grouchy monster on low carbs.  My soon to be 3-year old had enough sense to say, “Mommy, you’re being mean!” But when all was said and done, by the mid-September I was at 112 lbs-and had lost 6 lbs in a about  4 weeks. Certainly not earth shattering results, but I was not after dramatic weight loss, as this could also signify loss in strength and LBM.

Another thing that I lost while cutting was my menstrual cycle.  At 112 lbs, I estimate that I dropped to about 12-13% body fat based on the caliper readings, and the not-so-glamorous part about that is the possible interruption of your cycle.  Clearly, I’m messing with my hormones here! You’ll also want to mentally prepare yourself for reduced energy levels, your workouts feeling waaayyyyy harder to get through, possible losses in strength, and perhaps waking up earlier than normal to get in the cardio.

The worst part of all, bar none, was the dehydration leading up to the photo shoot.  I normally drink a minimum of 1 gallon of water in a day, and it was my decision to use a herbal diuretic, sodium elimination (except whatever was naturally occurring),  and taper down water (from ½ gallon, to 32 oz, to 24 oz, and finally 16 oz the day of the shoot) to lose any puffiness.  It literally felt like a cat was sleeping in me mouth. YUCK! I also had a hard time sleeping well and the sight of anyone drinking water made me want to race to the nearest fountain and drink like a fish.   I didn’t of course, and the process worked for me. I’ll confess that I was totally freaked out when I stepped on the scale the morning of the shoot and clocked in at 109 lbs. I lost another 3 lbs of fluid on the process of dehydrating, but I could see that my abs were tight and hard. Mission accomplished.

Other tools that I used to get picture perfect were the application of a self tanner and baby oil during the shoot.  I actually didn’t have time to get a spray tan, and I have a natural “tan” from being of Indian descent, so I used a mild and gradual tanner which worked perfectly for me.  5 days out from the shoot, I also modified the diet by doing a carb up to load my glycogen-starved muscles with the carbs they needed to “fill out.”  I kept protein and fat at the same levels, but started to eat more starchy carbs (e.g., white rice instead of brown) and larger amounts (1/2 cup to ¾ cup instead of ¼).  I was carb happy again, although I was thirsty as anything!

Throughout my cutting journey, one of the things I faithfully tracked and recorded were my strength logs.  Earlier in this article, I charted my week 1 stats.  After 5 weeks, here’s how I made out.  You can see I really did not lose much strength, and in fact made some gains, a good indication that I was able to maintain some of that hard-earned LBM, though trust me, every rep felt harder towards the end!

The cutting journey really was a learning experience for me, and the next time I do it, the same exact method may not work. Everyone is different and our bodies all react differently.  If you plan to do it, give yourself ample time to experiment with the calories and activity level, and don’t ever give up strength training! It’s what got you the muscles in the first place.  Enlist the help of experts in the field and stay focused on whatever your goal look may be.  Be prepared for the not so fun stuff: to diet hard, to bust through your discomfort zone, to possibly have to pick up lighter weights (like I did!), lose some sleep, be cranky, lose your period, and to possibly have to migrate into an anti-social bubble because 1) you can’t eat or drink like most people and 2) you’re so cranky no one wants to play with you.  Realize that there is a decidedly unhealthy aspect to achieving this look, and for some people, such a look is not maintainable, nor should it be.

Despite all the hard work and effort, and the fact that everyone thought I was insane, it really isn’t impossible.  I wanted to do this, I set my mind to do it, and because part of me loves data and experiments.  I would hope that there’s plenty of room on the planet for a variety of beautiful, fit bodies of all sizes, colors, and ages.  I’m a mom, I work two jobs (one full time, one part-time), am no superwoman, nor do I have any special gift of genetics or superhuman discipline.  I do have the right mindset and attitude to get it done. Anyone can do it.  And if I can, you can too! As Will would say, good luck and see you in the magazines!

So You Want to Look Like a Fitness Model? Part 3 of 3 is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

Welcome to Part 2 of the journey to getting lean and mean!

As the second and third weeks progress and I as I cut calories, I would note some dips in strength for some lifts but not for all.  I could usually attribute a bad day to poor sleep, straying from my usual workout time, or another calorie adjustment.  The fact that I wasn’t seeing dramatic losses in strength was a really good sign that I wasn’t losing much in the way of LBM.  Still, I really, really missed picking up heavy weights, so made a pact that we were just on a “time out.”  I’d be back for more heavy metal in no time! Some people might be able to continue with heavy (i.e., 85% of their 1 RM) while cutting but not me.  It just felt far too taxing.  Cutting made me realize how very much I am in tune with my body, how making minor adjustments always translate into something else, and it reassured me that my instincts would really help me proceed through this journey.  Everyone is different, and what works for me might not work for everyone.

In addition to the new program that I begin in early August, I also slowly and gradually being to add small amounts of easy cardio to the equation.  While bulking on Hybrid, I did very little cardio; there was the Hybrid HIIT day and otherwise I mainly walked briskly with my dog as a form of exercise.  While cutting, I started with 3 sessions of 30 minutes (brisk walking, uphill walks on treadmills, or light jogging). Each week I added one session until I was up to 6 sessions a week.  Nothing intense, and I generally added or subtracted this form of activity depending on what the scale, calipers, mirrors, strength logs, outside observers, and my own level of energy told me. It was really nice to have the input of BBR members and my close gym buddies because at times I felt like I was watching grass grow! Every week I was asking, “where is my six pack?” An extra set of objective eyes always helps.

Speaking of supplements, I did not change much about what I was taking in while bulking. I maintained using creatine monohydrate, and stopped this 3 days out from the shoot, and continued taking beta-alanine, glutamine, and branched chain amino acids.  I did have to start using caffeine to give me the energy and focus I needed to get through the low-carb energy nadirs.  I did try using a couple of thermogenics and some “pre-workout” energy/concentration focus formulas, but not one of them appealed to me in the taste department. The simpler the better!

Stay tuned for part 3 of this series…the fine tuning and “dialing in” of the physique as shoot date approaches. Please feel free to leave comments!

So you want to look like a fitness model? Part 2 of 3 of my Cutting Journey is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

I’ve always wondered just how it is those fitness models and figure competitors get so darn lean for photos and competitions.

I recognize there’s a lot of photo editing that does go on to get models looking so perfect for covers (see here: but for those gals that do decide to compete in a teensy weensy bikini, there’s not much “editing” they can do, other than to look their best, after all that diet, preparation, training, posing, tanning, etc etc.

In preparation for an upcoming photo shoot, I put myself through a temporary “cut” to drop some body fat and look leaner for the pics (more shredded, ripped, etc).

Bodybuilders always talk about “bulking” and “cutting,” so in the spirit of one of my passions, I decided I was ready to do it, and share my experience.  Welcome to part 1 of 3 of my cutting journey to ripped, lean, and sexy!

The journey was truly a learning experience for me (I love data and experiments!), and I learned how rigorous the process of “leaning out” really is.  After all, I’m coming off of lean bulking program, and I worked HARD to gain lean body mass (LBM) and ended up, happily, with 6 lbs of LBM gained over the course of 12 weeks, with minimal body fat.   My weight post bulk was approximately 118 lbs and around 15-16% bodyfat.  I initially told myself I didn’t want to drop below 113 lbs and 12% bodyfat, but I wasn’t sure exactly what numbers I would look “ready” at, so I gave myself ample time- almost 3 months!

Importantly, I was lucky enough to have found some really supportive members in both the body building and figure community, and they truly helped me dial in the physique adjustments as I got closer to my shoot date with valuable input on cardio, diet, program design, and water and sodium manipulation.  It’s an art form! The goal was to maintain as much of that LBM and strength while dropping body fat.  Boy, did I have my work cut out for me. And if you decide that you want to get this look, enlist a great support network.  It’s among one of the many tools you may need to use, and that are discussed in further detail below.

I started dropping cals gradually in early July, making minor modifications every week.  While on my lean bulk, I ate close to 3000 cals every day, and dropped cals by 150-200 each week when I started “cutting.”  One month later, in early August, the scale hadn’t budged downwards one bit and I was determined to get lean and mean by mid-late September!  I told myself not to get frustrated here as the scale might not be the best tool for me (i.e., the goal was not weight loss but fat loss), and it took me lots of practice (and I still am working on it!) to understand how to self-administer the calipers.  Come mid-August, I get to the point where I am operating at 1000 calories less than I was consuming while on the bulking program.  Aside from this, another important tool needed to be implemented, and that was…program modification.

I’ve always been a big fan of the program design described in Fat Loss Revealed’s (FLR) four day split , but had never actually tried it myself since bulking had been my main goal.  But, as one awesome moderator on FLR pointed out, in order to maintain strength and LBM while cutting, a serious level of intensity had to be included in the weightlifting routine.  For me, that meant shorter rest periods (hard since I was spoiled by 5X5 and 6X6 rest periods!), and rep ranges that corresponded with an intensity of 65-75% of my 1 rep max.  I seriously missed operating at 80-85% of my 1RM as I did on the Hybrid program, but as I cut calories, the heavier weights and efforts get harder and too stressful on my body.

My first week on the Phase 3, FLR 4-day split begins on 08/16/2010 and is a far cry from my performance on the Hybrid. The short rest periods are kicking my tail, and the energy level from the reduced calories starts to kick in during set 3 for most lifts and especially by the end of the workout.  It is MUCH more FUN to eat lots and be strong.  I tell myself that the end is in sight!  Here’s how the first week went:

Stay tuned for part 2 of this series (diet, cardio, and progress pics), and feel free to leave comments below! Thanks for tuning in!

So You Want to Look Like a Fitness Model? Here’s What it Takes! is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness