Part 2 of this series focuses on current research into the effects of exercise on body fat.
Losing Weight Des Not Mean Too Much: Location Again
The good news is that only a 5-10% decrease in body fat is usually associated with very positive and significant changes in risk factors such as glucose tolerance and insulin sensitivity. Even better news is Phospholipid Transfer Protein Lactate Prostaglandins Prostacyclin Free Fatty Acids Leptin Adiponectin Adipsin and (ASP) Lipoprotein Lipase Free Fatty Acids TNF-ß IL-6 ADIPOCYTE that even a single bout of exercise can reduce triglyceride levels, increase HDL levels, reduce resting blood pressure, increase glucose tolerance, and reduce insulin resistance.16 It is important to take waist and hip measures from the get go because research shows that even without weight loss, exercise is an effective way to reduce VAT. Irwin et al did a large study with postmenopausal, previously sedentary women who were randomly assigned to control (no exercise) or exercise conditions. Even though the weight loss after 12 months was modest, the amount of intra-abdominal fat lost was considerable (8.5g/cm2) and it was dose-dependent. Women performing 200 minutes of exercise/ wk lost 4.2% body fat, and 6.9% VAT without changing their energy intake. However, weight loss be it from either caloric restriction or exercise is an effective way to reduce obesity in moderately obese men.17
Exercise: Getting at the Belly Fat
Here is even more good news for exercisers who tend not to lose much weight from their efforts: People who have a higher cardiorespiratory fitness (CRF) level will tend to have a lower VAT. However, individuals with a moderate to high CRF have lower waist circumferences than men with low CRFs independent of the BMI. In other words, just being in shape usually means a smaller waist (thus less risk) even at the same weight. The large decrease in risk factors with small weight loses is likely due to a preferential loss of VAT. The reduction in VAT is often associated with glucose tolerance and insulin sensitivity. Adding resistance training may further improve insulin sensitivity and an increase in muscle density.17, 18
Can Someone Be Fit and Fat?
Yes! This can be the case. The amount of VAT and fitness in someone is inversely associated. The frustration that some people have with not losing weight, especially elderly women, may be compensated for by the fact they are lowering their risk factors for many diseases and actually losing fat from the areas that really matter — those deep inside. Research shows an overweight or “fat” person who has a high CRF as measured by a treadmill test, will likely have less risk for developing type 2 diabetes than a “leaner” individual who is unfit. High levels of CRF reduce C-Reactive Protein and the cardiovascular mortality, independent of obesity. Moderately fit individuals had a lower VAT and SCAT and lower WC than individuals with a low CRF for a given BMI and WC. So, low CRF is associated with elevated CRP, and reduced fasting glucose control in women with Type 2 diabetes.19 A study by Riechman et al. (2002) found correlations of physical activity (PA) with visceral adipose tissue (VAT) and physical difficulties (PD).
Past research has shown that risk for cardiovascular disease, certain cancers, and diabetes to be associated with abdominal fat, particularly VAT. The level of physical activity from someone was inversely related with those same diseases (20). As people age, the amount of PA decreases, and the incidence of those mentioned diseases increases as does the VAT. They used computed tomography to scan for precise measures of abdominal fat in 65 women and 106 men. They found men had higher VAT and visceral percent adipose than women, but the women had higher subcutaneous and total abdominal adipose compared to the men. In women, the VAT and total adipose was significantly associated to leisure activity, while in the men the amount of occupational activity was significantly (inversely) associated with VAT.
The researchers also found the mean visceral, subcutaneous, and total adipose and VAT were all higher in those reporting PDs in both men and women. Age and gender contributed to the variance in abdominal adipose tissue but did not eliminate the associations of PAs and PDs. Finally, they found there was a threshold beyond which increased physical activity did not result in further abdominal adipose and VAT decreases. This finding supports the critical VAT threshold (CVATT) which Freedland (2004) has proposed.21
The Potential Role of Diet: Low Carb-Low Glycemic Index — the Winner Again
It seems that most of the modern day diets are pointing to multiple meals and either a low carb or low glycemic index diet. Well, it is no accident those diets seem to be working. There are scientific data and multiple physiologic mechanisms which show this to be the way to go. It all seems to boil down to the fact that carbohydrates (CHO) are the preferred source of fuel oxidization- resulting in increased fat deposition.22 The way to increase insulin sensitivity is to “push” the body into oxidizing fat in nonadipose tissue such as liver, pancreas, and skeletal muscle. Several studies have found low carbohydrate, high fat diets which are consumed more than 7 days actually induce adaptations to increase fat oxidation, reduce muscle glycogen content, and carbohydrate oxidation, even in well trained athletes, who are already at increased fat oxidation capacities.23,24 Another study by Sharman et al (2004) found that a ketogenic diet did not cause weight loss but raised the lean body mass.25 A good deal of research also supports controlling the glycemic index (GI) and glycemic load (GL). In a 12 month study on teenagers, those on a low GI diet lost more weight and had greater fat loss without regain for 6 to 12 months, compared to those on the conventional diet. In addition, insulin resistance increased in the conventional diet group and did not change with the low-GI diet group.26
Figure 2-1 (above) shows that both Physical Exercise and a low glycemic or low carb-high fat (ketogenic) diet seem to have similar effects in improving factors related to visceral adipose tissue and metabolic syndrome. Because VAT has a two-fold greater glucose uptake compared to SCAT, if you reduce glucose levels with a low GL you would lower the accumulation of glucose in VAT. Data shows glucose raises insulin which Physical Exercise- Cardiorespiratory Fitness Waist Circumference, BMI, and Body Fat% Hypertension, Diabetes, CHD, Insulin Resistance Amount of VAT, CRP, glucose levels Low Carb-Low GI/ GL Skinny on Fatness 7 stimulates 11-B-HSD1, increases active cortisol in VAT and enhances VAT accumulation. (26). In studies with rats, feeding them a diet high in sucrose compared to lab chow caused a significantly higher fat cell volume in VAT depots even though the total adipose tissue did not change, and higher insulin resistance.
Lower Glycemic Load→Lower Blood Glucose→Lower Insulin→Less 11ß-HSD1→Less Cortisol
Other studies have further shown the links between GL and C-reactive protein (CRP) a strong predictor of diabetes and coronary heart disease, and it is positively associated with insulin resistance and metabolic syndrome. Thus, diets which minimize the glucose levels in the blood seem to better in reducing VAT and factors related to metabolic syndrome and its accompanying effects.
References
1) Kim SK, Kim HJ, Hur KY, Choi SH, Ahn CW, Lim SK, Kim KR, Lee HC, Huh KB, Cha BS: Visceral fat thickness measured by ultrasonography can estimate not only visceral obesity but the also risks of cardiovascular and metabolic diseases. Am J Clin Nutr 2004, 79: 593-599.
2) Lamarch B: Abdominal obesity and its metabolic complications: implications for the risk of ischaemic heart disease. Coron Artery Dis 1998, 9:473-481.
3) Blair D, HabrichtJP, Sims EA, Slyvester D, Abraham S: Evidence for an increased risk for hypertension with centrally located body fat and the effect of race and sex on this risk. Am. J. Epidemiol 1984, 119: 526-540.
4) Carr DB, Utzschneider KM, Hull RL, Kodama K, Retzlaff BM, Brunzell JD, Shoefer JB, Fish BE, Knopp RH, Kahn SE: Intra-abdominal fat is a major determinate of the National Cholesterol Education Program-Adult Treatment Panel III Criteria for metabolic syndrome. Diabetes 2004, 53:1195-1200.
5) Cameron AJ, Shaw JE, Zimmet PZ: The metabolic syndrome: prevalence in worldwide populations. Endocrinol Metab Clin North Am 2006; 28: 629-636
6) Ford ES, Giles WH, Mokdad AH: Increasing prevalence of the metabolic syndrome amount U.S. adults. Diabetes Care 2004; 27: 2444-2449.
7) McLaughlin T, Abbasi F, Cheal K, Chu J, Lamendola C, Reaven G: Use of metabolic markers to identify overweight individuals who are insulin resistant. Ann Intern Med, 2003, 139: 802-809.
8) Reaven GM: Insulin resistance, cardiovascular disease, and the metabolic syndrome: how well do the emperor’s clothes fit? Diabetes Care, 2004, 27: 1011-1012.
9) Ford ES, Giles WH, Dietz WH: Prevalence of the metabolic syndrome among US adults- Findings from the Third National Health and Nutrition Examination Survey. J Am Med Assoc 2002,287: 356-359.
10) Katsuki A, Sumida Y, Urakawa H, Gabazza EC, Murashima S, Maruyama N, Morioka K, Nakatani K, Yano Y, Adachi Y: Increased visceral fat and serum levels of triglycerides are associated with insulin resistance in Japenese metabolically obese, normal weight subjects with normal glucose tolerance. Diabetes Care, 2003, 26: 2341-2344.
11) Ruderman N, Chisholm D,Pi-Sunyer X, Schneider S: The metabolically obese, normal weight individual revisited. Diabetes 1998, 47: 699-713.
12) Fain JN, Madan AK, Hiler ML, Cheema P, Balhouth SW: Comparison of the release of adipokines by adipose tissue, adipose tissue matrix, and adipocytes from visceral and subcutaneous abdominal adipose tissue of obese humans. Endocrinology 2004, 145: 2273-2282.
13) Pantanetti P, Garrapa GG, Mantero F, Boscaro M, Faloia E, Venarucci D: Adipose tissue as an endocrine organ? A review of the recent data related to cardiovascular complications of endocrine dysfuctions. Clin Exp Hypertens 2004, 26: 387-398.
14) Minnoci A, Savia G, Lucantoni R, Berselli ME, Tagliaferri M, Calo G, Petroni ML, de Medici C, Viberti GC, Liuzzi A: Leptin plasma concentrations are dependent on body fat distribution in obese patients. Int J Obese Relat Metab Disord 2000, 24: 1139-1144.
15) Fain JN, Balhouth SW, Madan AK: TNF alpha release by the nonfat cells of the human adipose tissue. . Int J Obese Relat Metab Disord 2004, 28: 615-622.
16) Thompson PD, Crouse SF, Goodpaster B, Kelley D, Moyna N, Pescatello L: The acute versus the chronic response to exercise. Med Sci Sports Exerc 2001, 33: S438-45, discussion S452-3.
17) Paffenbarger, RS, Hyde RT, Wing AL, Le IM, Jung DL, Kampert JB: The association of changes in physical-activity level and other lifestyle characteristics with mortality among men. N Eng J Med 1993, 328:538-545.
18) Cuff DJ, Meneilly GS, Martin A, Ignaszewski A, Tildesley HD, Frohlich JJ: Effective exercise modality to reduce insulin resistance in women with Type 2 diabetes. Diabetes Care 2003, 26:2977-2983.
19) McGavock JM, Mandie S, Vonder I, Mulhill I, Lewanczuk RZ, Quinney HA, Taylor DA, Welsh RC, Haykowsky M: Low cardiorespiratory fitness is associated with elevated C-reactive protein levels in women with Type 2 diabetes. Diabetes Care 2004, 27:320-325.
20) Riechman SE, Schoen RE, Weissfeld JL, Thaete FL, & Kriska AM (2002). Association of physical activity and visceral adipose tissue in older women and men. Obesity Research 10(10): 1065-1073.
21) Freedland ES: Role of a critical visceral adipose tissue threshold (CVATT) in metabolic syndrome: implications for controlling dietary carbohydrates: a review. Nutrition & Metabolism 2004, 1:12doi:10.1186/1743-7075: 1-12.
22) Frisancho AR: Reduced rate of fat oxidation: A metabolic pathway to obesity in the developing nations. Am J Human Biol 2003, 15:522-532.
23) Westman EC, Mavropoulos J, Yancy WS, Volek JS: A review of low-carbohydrate ketogenic diets. Curr Atheroscler Rep 2003, 5: 476-483. Skinny on Fatness 11
24) Phinney SD, Bistrian BR, Wolfe RR, Blackburn GL: The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation. Metabolism 1983, 32: 757-768.
25) Sharman MJ, Kraemer WJ, Love DM, Avery NG, Gomez AL, Asheett TP, Volek JS: A ketogenic diet favorably affects serum biomarkers for cardiovascular disease in normal-weight men. J Nutr 2002, 132: 1879-1885.
26) Ebbling CB, Ludwig DS: Treating obesity in youth: should dietary glycemic load be a consideration? Adv Pediatr 2001, 48:179-212.
27) Bujalska IJ, Kumar S, Stewart PM: Does central obesity reflect “Cushing’s disease of the omentum”? Lancet 1997, 349:1210-1213.
28) Bjorntorp P: Endocrine abnormalities in obesity. Diabetes Reviews 1997, 5:
29) Marin P, Arver S: Androgens and abdominal obesity Baillieres Clin Endocrinol Metab 1998, 12:441-451.
30) Jezova D, Vigas M, Tatar P, Kvetnansky R, Nazar K, Kaciuba-Uscilko H, Kozlowski S: Plasma testosterone and catecholamine responses to physical exercise of different intensities in men. Eur J Appl Physiol 1985, 54:62-66.
31) Volek JS,Kraemer WJ, Bush JA, Incledon T, Boetes M: Testosterone and cortisol in relationship to dietary nutrients and resistance exercise. J. Appl. Physiol. 1997, 82(1): 49-54.
32) Walker BR: 11beta-hydroxysteroid dehydrogenase type 1 in obesity. Obes Res 2004, 12:1-3.
33) Kelley DE, Williams KV, Price JE, McKolanis TM, Goodpaster BM, Thaete FL: Plasma fatty acids adiposity, and variance of skeletal muscle insulin resistance in type 2 diabetes mellitus. J Clin Endocrinol Metab, 2001, 86:5412-5419.
34) Colberg SR, Simoneau JA, Thaete FL, Kelley DE: Skeletal muscle utilization of free fatty acids in women with visceral obesity. J Clin. Invest. 1995, 95:1846-1853.
___________________________________________________________________
Mark P. Kelly has a doctorate in Exercise Physiology and Education Administration, he has specialties in kinesiology, exercise and nutritional biochemistry, weight management, and endurance athletic physiology. He was a nationally ranked duathlete, body building contest winner, trainer of professional athletes, and personal trainer for 20 years. He is a primary writer for the NFPT certification programs, a teacher in universities, and runs Principle Centered Health Human Performance Services, which specializes in assessments and corporate wellness. He can be reached at [email protected].