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Myths Under The Microscope Part 2: False Hopes for Fasted Cardio

Myths Under The Microscope Part 2: False Hopes for Fasted Cardio

By Alan Aragon  ©

False Hopes

The bandwagon is lead by blind horses

Many trainees pigeonhole weight training as an activity exclusively for building muscle, and cardio exclusively for burning fat. On the contrary, weight training can yield very similar results to cardio of similar intensity when 24-hr energy expenditure and macronutrient oxidation is measured [1]. The obvious advantage of weight training is the higher potential for lean mass and strength gains. In the bodybuilding context, cardio should be viewed as merely an adjunctive training mode to further energy expenditure and cross-complement the adaptations specific to weight training. As far as cardio being absolutely necessary for cardiovascular health, well, that depends upon the overall volume and magnitude of your weight training – another topic for another time.

Chaos theory strikes again

On the surface, it seems logical to separate carbs from cardio if you want a maximal degree of fat oxidation to occur during training. But, there’s the underlying mistake – focusing on stored fuel usage during training instead of focusing on optimally partitioning exogenous fuel for maximal lipolytic effect around the clock. Put another way, it’s a better objective to coincide your carb intake with your day’s thermic peaks, where insulin sensitivity & lean tissue reception to carbs is highest. For some reason, this logic is not easily accepted, nor understood. As we know, human physiology doesn’t always cooperate with logic or popular opinion, so let’s scrutinize the science behind the claims.

Let The Research Speak

Carbohydrate ingestion during low-intensity exercise reduces fat oxidation

As far as 3 decades back, Ahlborg’s team observed that carb ingestion during low-intensity exercise (25-45% VO2 max) reduced fat oxidation compared to fasted levels [2]. More recently, De Glisezinski’s team observed similar results in trained men at 50% VO2 max [3]. Efforts to determine the mechanism behind this phenomenon have been made. Coyle’s team observed that at 50% VO2 max, carbohydrate availability can directly regulate fat oxidation by coordinating hyperinsulinemia to inhibit long-chain fatty acid transport into mitochondria [4].

Carbohydrate’s effect on fat oxidation during moderate-intensity exercise depends on conditioning level
Civitarese’s team found glucose ingestion during exercise to blunt lipolysis via decreasing the gene expression involved in fat oxidation in untrained men [5]. Wallis’ team saw suppressed fat oxidation in moderately trained men & women when glucose was ingested during exercise [6].

In contrast to the above trials on beginning and intermediate trainees, Coyle’s team repeatedly showed that carb ingestion during moderate-intensity (65-75% VO2 max) does not reduce fat oxidation during the first 120 min of exercise in trained men [7,8]. Interestingly, the intensity margin proximal to where fat oxidation is highest was unaffected by carb ingestion, and remained so for the first 2 hours of exercise.

Horowitz’ team examined the effect of a during-training solution of high-glycemic carbs on moderately trained men undergoing either low intensity exercise (25% VO2 max) or high-moderate intensity (68% VO2 max) [9]. Similar results to Coyle’s work were seen. Subjects completed a 2-hr cycling bout, and ingested the carb solution at 30, 60, and 90 minutes in. In the low-intensity treatment, fat oxidation was not reduced below fasted-state control group’s levels until 80-90 min of exercise. In the 68% group, no difference in fat oxidation was seen whether subjects were fasted or fed throughout the trial.

Further supporting the evidence in favor of fed cardio in trained men, Febbraio’s team investigated the effects of carb ingestion pre & during training in easily one of the best-designed trials on this topic [10]. Subjects exercised for 2 hrs at an intensity level of 63% VO2 max, which is now known as the point of maximal fat oxidation during exercise. Result? Pre & during-training carbs increased performance – and there was no difference in total fat oxidation between the fasted and fed subjects. Despite the elevated insulin levels in the carb-fueled groups, there was no difference in fat availability or fat utilization.

Summing Up the Research Findings

• At low intensities (25-50% VO2 max), carbs during exercise reduce fat oxidation compared to fasted trainees.

• At moderate intensities (63-68% VO2 max) carbs during exercise may reduce fat oxidation in untrained subjects, but do not reduce fat oxidation in trained subjects for at least the first 80-120 minutes of exercise.
• Carbohydrate during exercise spares liver glycogen, which is among the most critical factors for anticatabolism during hypocaloric & other conditions of metabolic stress. This protective hepatic effect is absent in fasted cardio.
• At the established intensity level of peak fat oxidation (~63% VO2 max), carbohydrate increases performance without any suppression of fat oxidation in trained subjects.

References

1. Melanson EL, et al. Resistance and aerobic exercise have similar effects on 24-h nutrient oxidation.. Med Sci Sports Exerc. 2002 Nov;34(11):1793-800.
2. Ahlborg, G., and P. Felig. Influence of glucose ingestion on fuel-hormone response during prolonged exercise. J. Appl. Physiol. 1976;41:683-688.
3. De Glisezinski I, et al. Effect of carbohydrate ingestion on adipose tissue lipolysis during long-lasting exercise in trained men. J Appl Physiol. 1998 May;84(5):1627-32.
4. Coyle EF, et al. Fatty acid oxidation is directly regulated by carbohydrate metabolism during exercise. Am J Physiol. 1997 Aug;273(2 Pt 1):E268-75.
5. Civitarese AE, et al. Glucose ingestion during exercise blunts exercise-induced gene expression of skeletal muscle fat oxidative genes. Am J Physiol Endocrinol Metab. 2005 Dec;289(6):E1023-9.
6. Wallis GA, et al. Metabolic response to carbohydrate ingestion during exercise in males and females. Am J Physiol Endocrinol Metab. 2006 Apr;290(4):E708-15.
7. Coyle, et al. Muscle glycogen utilization during prolonged strenuous exercise when fed carbohydrate. J. Appl. Physiol. 1986;6:165-172.
8. Coyle, et al.. Carbohydrates during prolonged strenuous exercise can delay fatigue. J. Appl. Physiol. 59: 429-433, 1983.
9. Horowitz JF, et al. Substrate metabolism when subjects are fed carbohydrate during exercise. Am J Physiol. 1999 May;276(5 Pt 1):E828-35.
10. Febbraio MA, et al. Effects of carbohydrate ingestion before and during exercise on glucose kinetics and exercise performance. J Appl Physiol. 2000 Dec;89(6):2220-6.

Visit alanaragon.com for more informative articles

Fraud in the supplement industry

Interesting video about fraud in the supplement industry.  A clip from the movie Bigger Faster Stronger available at  www.biggerstrongerfastermovie.com A good reason to stick to the large brand names

Check out this interesting article from Sports Illustrated.
http://vault.sportsillustrated.cnn.com/vault/article/magazine/MAG1155395/1/index.htm

Let us know what you think!

Fish Oil: Just The Facts

Fish Oil: Just The Facts • By Alan Aragon •

The Dawn of Fat Phobia

If you have a few years under your belt, then you can still remember what I call the “Fat-Free 80’s.” Think back to a time when dietary fat was the enemy. Ah, yes… A time when fat-free products lined the outer shelves of the supermarket. A time when it was not a bad thing to get a box of Entemann’s cinnamon rolls, as long as they were the FAT-FREE cinnamon rolls. Health Valley made some positively disgusting fat-free cookies, along with a host of other fat-free products that tasted like sugary cardboard. And we can’t forget the 75% sugar weight gainer products, those were priceless. 1,000, 2000, 4,000 calories per serving, and all you had to do was mix about a cup of powder into your favourite drink. No worries though, these gainers were virtually fat-free! What we were led to believe was that fat-free products equated to fat-free physiques. Unfortunately, that was far from the truth.

During the 1980’s, a disturbing climb in national obesity rates occurred, and steadily kept its course. Large behavioral trend studies such as the National Health and Nutrition Examination Study (NHANES II & III), the Behavioral Risk Factor Surveillance System (BRFSS), and the Calorie Control Council Report (CCCR) collectively showed a 31% increase in overweight prevalence from 1976-1991. The punch line? This increase in weight was accompanied by an 11% decrease in percentage of calories from fat (from 41.0% to 36.6%). The most recent report by the BRFSS shows a further decrease in fat intake to 33%, accompanied by an increase in obesity from 11.6% to 22.1%. This is a 90.5% increase in US obesity from 1990-2002[1]. It’s obvious that dietary fat is not the evil culprit in the expansion of the population’s waistline.

A Brief Evolution of Our Knowledge of Fats

As indicated by the fat-free product boom a couple of decades back, there indeed was the widespread belief that ALL fats were a substance to be minimized, or avoided altogether. But with the forward march of research, we came to understand that different fats had different effects on health. Since it’s human nature to think in black and white terms, the great divide initially fell between saturated (SFA) and mono- or polyunsaturated fatty acids (MUFA & PUFA). SFA were thought to be the root of all evil, conjuring images of arterial plaque and eventual heart failure, while unsaturated fat was regarded as a universally angelic substance. This turned out to be a gross oversimplification of reality.

The intricacies and widely varying sources and subtypes of SFA is another article altogether, but suffice it to say that it’s not that simple to pigeonhole them as unhealthy. SFA are not created equal. They have markedly variable physiological effects from the detrimental all the way to the beneficial. Given this, it depends on which ones you want throw onto the theoretical chopping block. Stearic acid, an SFA abundant in meat & milk fat, has been consistently observed to actually reduce blood platelet aggregation [2]. This is a good thing. In contrast, trans fats (found in high concentrations in commercially baked goods as well as processed & fried foods)  have been observed to negatively impact blood lipids by not only lowering HDL, but increasing LDL as well [3].
Ironically, experimental research exists on healthy humans showing the least fat was oxidized on the MUFA fat dietary treatment, and the most fat oxidized on a trans fat diet [4]. This result echoes what’s been seen in rats as well. It appears that the tighter the control of the study, the less “superior” unsaturated fats turn out to be for any presumed effect on body composition compared to SFA. Throw in the fact that a reducing SFA intake and increasing the degree of unsaturation of fatty acids in the diet reduces testosterone levels [5], and then you have yet another wrinkle in the mix to concern yourself with

Then you have medium-chain triacylglycerols (MCT), which are SFAs that exhibit physiological behavior that’s closer to carbohydrate than fat. MCT has been hyped to death by those who sell it. But the point is that they are a type of SFA that may potentially have minor benefits on body composition. I personally wouldn’t spend a dime on them, but they nevertheless illustrate the fact that SFAs are a complex and highly varied group of compounds in terms of physiological effect. As always, the effects of each type of fat undoubtedly vary with the population in question, as well as individual response.

Finally, with the black and white fallacy of saturated versus unsaturated fats out of the way, we can now shift the focus on fish oils, which happen to be a rich source of a particular class of fatty acids under intense study, the omega 3’s.

Enter The Omega-3 Fatty Acids

Omega-3 fatty acids are essential for normal growth and development, but are noted specifically for their powerful influence over multiple physiological processes. Alpha-linolenic acid (ALA), one of the two essential fatty acids (EFA) that the body cannot biosynthesize and must get from the diet, is an omega-3. EFA are precursors to a class of biologically significant compounds called eicosanoids, which include prostaglandins, leukotrienes, and thromboxanes. Eicosapentanoic acid (EPA) and docosahexanoic acid (DHA) can be derived from fish oil, and to a lesser degree, flaxseed oil. Consumption of EPA and DHA has an appreciable number of positive health effects, including decreases in blood platelet aggregation, lowered blood pressure, enhancement of smooth muscle function, decreased inflammation, alleviation of dyslipidema, and treatment of mood disorders [6-9]. There’s even emerging evidence pointing to the benefits of omega-3 fatty acids on bone health [10].

Archaeological research postulates that humans were  biologically designed to thrive on a diet whose ratio of omega-6 to omega-3 fatty acids was approximately 1:1, and unlikely greater than 4:1. Today, consumption of n-6 to n-3 fatty acids is estimated at roughly 25:1 [11]. This is due in part to a predominance of omega-6 oils available commercially in our food supply (corn oil, sunflower oil, safflower oil, refined packaged grain products & pastries) and a relative minority of omega-3 sources (fatty marine fish such as salmon, mackerel, herring, and flaxseed oil, walnuts, & small amounts in canola oil). Industrial production of omega-6-rich animal feeds has also resulted in animal tissues (livestock, eggs, and cultured fish) rich in omega-6 and poor in omega-3 fatty acids. This disproportionately high intake of omega 6’s biases our physiology towards thrombosis, hyperlipidemia, and vasoconstriction. The reverse of those effects occurs simply by increasing the proportion of omega-3’s.

Fish Oil as a Fat Loss Supplement?

So far, the resume of fish oil’s health effects is very extensive. But can it add fat loss to the list as well? The buzz in the supplement industry would certainly want consumers to believe so. But as always, the answer can only begin to reveal itself in the research. Human studies examining the effect of fish oil supplementation on body composition are scarce, but that makes it easy to pick them apart.

A decade ago, Couet and colleagues investigated the effect of replacing 6g of visible dietary fat with 6g of fish oil in healthy adults over a 3-week period, done 12 weeks after a 3-week control diet period [12]. Bodyfat mass and respiratory quotient decreased in the fish oil phase. It’s important to note that the flaws in this study’s design are grave enough to almost completely invalidate it. Extremely small sample size (6 subjects total), short trial period (3 weeks), and a complete absence of randomization or treatment balance (opening the distinct possibility for seasonal variation, among other errors) are the main fatal knocks that render this data nearly useless.

In contrast, 2 more recent studies conducted within the past 3 years looking at weight-loss diets supplemented with omega-3’s have not observed any significant effects on body composition beyond what was caused by dietary restriction alone [13,14]. But it’s never that simple, since things may differ according to the population and protocol. In contrast to the previous two trials, Kunesova’s team examined the effects of omega-3 supplementation on severely obese female inpatients undergoing a 3-week very low calorie (525 kcal) in-patient weight reduction treatment [15]. Calories were controlled to accommodate the supplemental omega-3, which was 2.8g/day. Result? The omega-3 supplemented group lost 1.5 kg bodyweight, and 2.2 cm more off the waist than the control group.

How about more relevant populations? As of this writing, there are only three trials in existence examining the effect of omega-3 supplementation combined with a structured aerobic exercise program on body composition. Let’s dig in. In 1989, Warner and colleagues looked at the effect of walking or jogging 3 days/week for 45-50 minutes at 75-80% maximal heart rate in hyperlipidemic subjects randomly assigned to 1 of 4 groups: fish oil + exercise, fish oil alone, corn oil, or control [16]. Body fat was reduced only in the fish oil + exercise group. These data are severely limited by the absence of an exercise-only control group, leaving a huge question mark open regarding the relative contribution of exercise to the bottom line result. A year later, Brilla and Landerholm conducted a well-designed study on healthy, previously sedentary men [17]. This trial did contain an exercise-only control group, and no effect of fish oil on body fat was observed.

In the most recent fish oil + exercise study to date, Hill’s team examined the effect of fish oil supplementation (6g) on overweight hypertensive/hyperlipidemic subjects (24 men and 41 women) over a 12 week period [18]. Exercise was 3 days/week walking at 75% predicted maximal heart rate for 45 minutes. Body composition was assessed by dual energy X-ray absorptiometry (DEXA). Predictably, fish oil supplementation improved blood lipids and arterial vasodilation. As for body composition, fish oil by itself didn’t cause any bodyfat reduction from baseline levels, whereas the sunflower oil control gained bodyfat , but to an insignificant degree. However, fish oil + exercise caused a 1.1% greater bodyfat reduction compared to the sunflower oil + exercise control (1.2% reduction versus a 0.1% reduction in the sunflower oil group). If you re-read those body composition results, they’re nothing to get too excited over, especially considering the small amount of fat lost in the 12 week duration.

The Dark Side of Over-doing Fish Oil Supplementation

Yes, Luke, there is always a dark side. In the world of unchecked marketing hype, fish oil has definitely gotten the “more is better” stamp. The problem is, EPA and DHA have a well-documented ability to suppress the body’s immune response. Although not as consistent as the immune effects, data also exist on the ability of EPA and DHA to increase bleeding time and oxidation. Let’s take a look at a couple of the published peer-reviewed research that no one in the fitness industry talks about.

Thies and colleagues examined the 12-week effect of various fatty acid supplement mixes on healthy subjects [19]. Various blends of placebo oil and oils rich in ALA, GLA, AA, DHA, or EPA (720mg) + DHA (280mg) were compared. Total fat intake from the 9-capsule dose was 4 g/d. The EPA/DHA treatment was the only one that had a negative effect on immunity, significantly decreasing natural killer cell activity by 48%. This effect was reversed after 4 weeks of ceasing intake of the supplement.

Rees and colleagues investigated the effects of various amounts of EPA on immune markers in young and older men [20]. In a 12-week study, EPA was incorporated into plasma and mononuclear cell phospholipids. Supplemental EPA in amounts of 1.35, 2.7, and 4.05g/day caused a dose-dependent decrease in neutrophil respiratory burst, indicating the suppression of a cellular defense against immunity threats. This effect was seen in the older, but not the younger men. Based on these and the previous data, if you’re not a spring chicken, and immunity is an issue, you might not want to go hog-wild on the fish oil dosing.

Suggested Use & Take-Home Tips

The cardio-protective benefits of increasing the dietary proportion of omega-3 fatty acids is seen consistently in trials involving various populations and protocols. Fish oil is one of the few supplements that actually have a substantial body of scientific evidence backing it up. However, it’s easy to think in terms of pills instead of food. Those who love fish (and have the time or resources to prepare or order it) can simply increase or maintain their intake of fatty fish such as salmon, mackerel, lake trout, herring, albacore tuna, and sardines.

The American Heart Association (AHA) recommends at least two servings of fish per week for the general population. Think of a palm-sized piece as a serving. For those with high triacylglycerol levels, a supplemental 2-4g of combined EPA/DHA is their suggested therapeutic dose. However, note that the AHA cautions against supplementing more than 3g outside of a physician’s care [21]. I recommend maxing out your whole food options first before going the supplemental route. There’s always more complete and synergistic nutrition contained within whole foods. For those who can’t or won’t eat fish, there’s always fish oil capsules, which thankfully are inexpensive, and more convenient than getting your omega-3’s through fish.

The amount of EPA/DHA per capsule may vary with the brand. Capsules can contain anywhere from 250-500mg. Most healthy folks don’t need more than 3-6 capsules per day to meet or exceed the amounts that show benefits. There are no definitive conclusions about optimal proportion of EPA:DHA, so to error on the side of safety, I recommend finding roughly an even mix. It’s common and perfectly acceptable for products to contain slightly more EPA than DHA. If at all possible, make sure your supplement is verified by the USP (United States Pharmacopoeia) for the peace of mind that you’re getting what the label is claiming. I would also error on the side of safety and keep them refrigerated. As a side note, there’s a widespread belief that ALA from flaxseed is worthless for increasing EPA/DHA since the conversion is inefficient. However, Harper’s team recently saw 3g ALA/day (from 5.2g flaxseed oil) raise plasma EPA levels by 60% at the end of a 12-week trial [22].

Looking at the body of evidence as a whole, fish oil (or increased fish consumption) has great potential for improving cardiovascular health. But for reducing body fat, the effects are minor to nonexistent. Let’s not forget that fish oil isn’t some magical negative-calorie food. It still contains 9 calories per gram, and no matter how much of those calories are used in its processing within the body, it’s still a net gain in calories after consumption. To sum everything up, fish oil has health benefits, as well as potential risks. It’s certainly not a matter of more-is-better. It might have minor fat loss effects in the obese and overweight population, but their fat loss effect in general is far from conclusively established. Get a variety of fats in your diet, and get them from whole foods whenever possible. Fish oil is merely one of many agents that can contribute to optimal health within the context of well-balanced nutrition. Keep it in perspective, and keep your eye on the facts.

References

1. Centers for Disease Control: Behavioral Risk Factor Surveillance System. 1990-2002 trends data, nationwide. http://apps.nccd.cdc.gov/brfss/Trends/trendchart.asp?qkey=10010&state=US.
2. Thijssen MA, et al. Stearic, oleic, and linoleic acids have comparable effects on markers of thrombotic tendency in healthy human subjects. J Nutr. 2005 Dec;135(12):2805-11.
3. Mozaffarian, et al. Trans fatty acids and cardiovascular disease. N. Engl. J. Med. 2006;354: 1601-1613.
4. Lovejoy JC, et al. Effects of diets enriched in saturated (palmitic), monounsaturated (oleic), or trans (elaidic) fatty acids on insulin sensitivity and substrate oxidation in healthy adults. Diabetes Care. 2002 Aug;25(8):1283-8.
5. Haalaininen E, et al. Diet and serum sex hormones in healthy men.
   J Steroid Biochem. 1984 Jan;20(1):459-64.
6. Schwalfenberg G. Omega-3 fatty acids: their beneficial role in cardiovascular health.
   Can Fam Physician. 2006 Jun;52:734-40.
7. Psota TL, et al. Dietary omega-3 fatty acid intake and cardiovascular risk.
   Am J Cardiol. 2006 Aug 21;98(4A):3i-18i.
8. Ismail HM. The role of omega-3 fatty acids in cardiac protection: an overview.
   Front Biosci. 2005 May 1;10:1079-88.
9. Parker G, et al. Omega-3 fatty acids and mood disorders.
   Am J Psychiatry. 2006 Jun;163(6):969-78. Review. Erratum in: Am J Psychiatry. 2006 Oct;163(10):1842.
10. Griel AE, et al. An increase in dietary n-3 fatty acids decreases a marker of bone resorption in humans. Nutr J. 2007 Jan 16;6:2.
11. Simopolous AP. Omega-3 fatty acids in inflammation and autoimmune diseases. J Am Coll Nutr. 2002 Dec;21(6):495-505.
12. Couet C, et al. Effect of dietary fish oil on body fat mass and basal fat oxidation in healthy adults. Int J Obes Relat Metab Disord. 1997 Aug;21(8):637-43.
13. Fontani G, Corradeschi F, Felici A, et al. Blood profiles, body fat and mood state in healthy subjects on different diets supplemented with omega-3 polyunsaturated fatty acids. Eur J Clin Invest 2005;35:499-507.
14. Krebs JD, et al. Additive benefits of long-chain n-3 polyunsaturated fatty acids and weight-loss in the management of cardiovascular disease risk in overweight hyperinsulinaemic women. Int J Obes (Lond). 2006 Oct;30(10):1535-44.
15. Kunesova , et al. The influence of n-3 polyunsaturated fatty acids and very low calorie diet during a short-term weight reducing regimen on weight loss and serum fatty acid composition in severely obese women. Physiol Res. 2006;55(1):63-72
16. Warner JG, et al. Combined effects of aerobic exercise and omega-3 fatty acids in hyperlipidemic persons. Med Sci Sports Exerc 1989;21:498-505.
17. Brilla LR, Landerholm TE. Effect of fish oil supplementation and exercise on serum lipids and aerobic fitness. J Sports Med Phys Fitness 1990;30:173-80.
18. Hill AM, et al. Combining fish-oil supplements with regular aerobic exercise improves body composition and cardiovascular disease risk factors.
    Am J Clin Nutr. 2007 May;85(5):1267-74.
19. Thies F, et al. Dietary supplementation with eicosapentaenoic acid, but not with other longchain n-3 or n-6 polyunsaturated fatty acids, decreases natural killer cell activity in healthy subjects aged >55 y. Am J Clin Nutr. 2001 Mar;73(3):539-48.
20. Rees D, et al. Dose-related effects of eicosapentaenoic acid on innate immune function in healthy humans: a comparison of young and older men. Am J Clin Nutr. 2006 Feb;83(2):187-8.
21. American Heart Association. New guidelines focus on fish, fish oil, omega-3 fatty acids. 2002. http://www.americanheart.org/presenter.jhtml?identifier=3006624.
22. Harper CR, et al. Flaxseed oil increases the plasma concentrations of cardioprotective (n-3) fatty acids in humans. J Nutr. 2006 Jan;136(1):83-7.Thanks to Alan Aragon www.alanaragon.com  worth checking out!

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How to count calories

If you insist on counting calories at least do it wisely. While I do not advocate “Rule-of-Thumb”
applications there is an interesting little exercise that can serve to guide you in your basic meal planning.
This one is provided by Nancy Clarke from her book; Sports Nutrition Guidebook (2003). This
particular text carries within its pages an incredible amount of information that would be of tremendous
value to any sports professional.

Most of my clients are afraid to eat real meals. They believe that eating, let’s say, a cheese sandwich
makes people fat. Eating diet foods, like rice cakes and carrots, feels safer. The problem is that
the self-created diets commonly allow too few calories and too limited a selection of (boring) foods.
The dieter ends up becoming too hungry. As a result he or she blows the diet and regains any lost
weight, plus more.

I calculate for my clients an appropriate calorie budget, so that they know how much is OK to
eat to maintain or lose weight. Just as you know how much money you can spend when you shop,
you might find it helpful to know how many calories you can spend when you eat. A calorie, or more
correctly, a kilocalorie, is a measure of energy. It is the amount of heat needed to raise one liter of
water by one degree Celsius. To get an accurate (ballpark) assessment of your caloric needs you can
apply the following formula;

• To estimate your resting metabolic rate—the amount of calories you need simply to breathe,
pump blood, and be alive—multiply your healthy weight by 10 calories per pound (or 22 calories
per kilogram). If you are significantly overweight, use an adjusted weight, a weight about halfway
between your desired weight and your current weight. That is, if you weigh 160 pounds but at
one time normally weighed 120 pounds, use 140 as your adjusted weight.
Example: Roberta weighed about 130 pounds but could healthfully weigh about 120 pounds.
Hence, she needed approximately 1,200 calories (120 x 10) simply to do nothing all day except
exist.

Table 5 — Resting Metabolic Rate
Here’s how a 150-pound man burns calories while resting in bed all day.

ORGAN                 CALORIES                    % OF RESTING MR
Brain                         365                                        21
Heart                         180                                        10
Kidney                       120                                         7
Liver                           560                                        32
Lungs                       160                                         9
Other Tissue           370                                         21

• Add more calories for daily activity apart from your purposeful exercise. If you are moderately
active throughout the day, add about 50 percent of your resting metabolic rate (RMR) If you are
sedentary, add 20 to 40 percent; if very active, add 64) to 80 percent of your RMR.
Example: Roberta was moderately active throughout the day with her two kids and her job. She
burned about 600 calories (50 percent x 1,200 calories) for activities of daily living. Her totals
were the following:
1,200 RMR + 600 cal daily activity
= 1,800 cal per day (without purposeful exercise)

• Add more calories for purposeful exercise. For example, when Roberta went to the health club,
she exercised aerobically for about 45 minutes and burned about 400 calories on the treadmill.
Hence, this was her total calorie need:
1,200 cal RMR + 600 cal daily activity + 400 cal purposeful exercise
= 2,200 total cal per day

• To lose weight, subtract 20 percent of your total calorie needs. Roberta deserved to eat about
2,200 calories per day to maintain her weight. Subtracting 20 percent of 2,200 calories (20 percent
x 2,200 = about 400 calories) left her with about 1,800 calories for her reducing diet.
In the past Roberta had tried to reduce on 1,000 to 1,200 calories per day. She was skeptical
about my proposed reducing plan of 1,800 calories. “If I can’t lose weight on 1,000 calories, why
would I lose weight on 1,800?” she questioned. I reminded her that when she cut back too much,
she’d get too hungry and blow her diet. She also lost muscle, slowed her metabolism, and consumed
too few of the nutrients she needed to protect her health and invest in top performance. I reminded
her that slow and steady weight loss stays off; quick weight loss rapidly reappears. A reasonable
weight-loss target is 0.5 to 1 pound (0.23 to 0.45 kilograms) a week for a person who weighs less than
150 pounds (68 kilograms); 1 to 2 pounds a week for heavier bodies.
The theory of “the less you eat, the more fat you will lose” contains little practical truth. Generally,
the less you eat, the more you blow your diet and overeat because of extreme hunger. For example,
if you knock off only 100 calories at the end of the day (the equivalent of two Oreos or a spoonful
of ice cream), you’ll theoretically lose 10 pounds (4.5 kilograms) of fat a year because 1 pound of
fat equals 3,500 calories. If you eat 500 fewer calories per day than you normally do, you should lose
1 pound per week. Now think of the number of times you’ve tried to knock off 1,000 calories per
day and have ended up gaining weight.
Remember, though, that weight loss is not always mathematical. Nature makes weight loss harder
for people who try to get below their set-point weight. If you have no excess fat to lose, nature will
cause your body to conserve energy. I’ve had thin clients who eat far less than they deserve yet maintain
weight.
Once you’ve established your total daily calories, divide them evenly throughout the day. Some
people like having six small meals: breakfast, snack, lunch, snack, dinner, snack. Others, like Roberta,
find that four meals per day work well for them.
I adhere to the philosophy that people should eat at least every four hours. That is, if you have
breakfast at 7:00, you’ll be hungry for lunch at 11:00. Yes, you could hold off until noon to eat, but
your body will be happier if you honor your hunger. Hunger, after all, is simply a request for fuel. By
eating lunch at 11:00, you’ll be hankering for a second lunch at 3:00. I call this afternoon meal a
second lunch, because if I were to call it a snack it would likely become cookies or chips. As a second
lunch, it becomes an apple with peanut butter, or soup and crackers, or cereal and a banana.
Roberta was initially skeptical of this four-meal plan; meals, after all, are “fattening.” She complained,
“I’m afraid I’ll get fat from eating so much at breakfast and two lunches.” I reminded her
that the purpose of the daytime meals is to ruin her appetite for dinner. By eating more during the
day, she would then be less hungry that evening, have more energy to exercise from 5:00 to 6:00
P.M., and be able to eat less (diet) at night.

If you hold the fear that meals are fattening, think again and remember these ideas:

• You won’t gain weight from eating a substantial breakfast or lunch. You’ll have more energy to
exercise and burn calories. Even if you were to eat too much at those meals, you could compensate
by eating less at night.

• If you skimp on daytime meals and develop a deep hunger, you’ll be likely to overeat at night
because of the strong physiological drive to eat.

• You’ll end up eating fewer calories, even though the breakfast and lunch and second lunch may
be larger than before. You’ll simply trade in the evening blown-diet calories for wholesome foods
earlier in the day.

• If you are not hungry at night, you can skimp at dinner and simply eat soup or salad. But don’t
have just soup or salad for lunch. It’s not enough.
Become familiar with the calorie content of the foods you commonly eat and then spend your
calories wisely. That is, include at least three of the five food groups at each meal and two kinds of
foods per snack. Too many dieters repetitively eat a single food, such as cottage cheese, for a meal.
This practice limits their intake of the variety of vitamins, minerals, and other nutrients offered by a
range of foods. Calorie counting can be a helpful bridge to get you in touch with the ability of your
body to tell you how much is OK to eat so that you feel satisfied. You can (and should) quickly replace
calorie counting with listening to your body’s signals for hunger and satiety. Calorie counting
should not become an obsession.

Nutrition and diet section being updated

We are working on our diet and nutrition section. We will include recipies and tips.. Please subscribe now to stay in the loop.

Welcome to BodyGenesis

We are here to help you achieve your goals of building muscle through strength training. Whether you are a Man, Woman, fat or thin.. Our goal is to provide you with the information needed to achieve your goals. With our advisor in chief Franco Licasto trainer to the stars, former IFBB bodybuilder and all around nice guy we’ll provide you with the tools and support.

Are you ready to change your life?
Loose Fat?
Gain weight?
Get fit?

Then it’s time to incorporate strength training into your program. It doesn’t matter is your a man or woman, 16 or 86 it will change your life. Looking to get a 6 pack but have tried everything in the muscle mags only to fail over and over? We’ll give you a free 6 week program to get you started on the road to success. I’ve trained elite level bodybuilders and movie stars and made them ready for competition. Just google Franco Licasto and you’ll see the movie star in particular that inspired me to launch this website.

• It’s not about hours and hours of boring cardio.

• It’s not about using machines to get it done.

• It’s not about training for 3 hours a day.

• It’s not about using useless supplements.

Bodygenesis Philosophy. Intensity. That’s the key. Hit the gym and hit it hard. That is the key to results.. Work hard and the results will come follow the program and diet for the next 60 days and you will see results.