CC BY
50
Section 7. Physical Education
12. MacDougall, J. D., Sale, D. G., Moroz, J. R., Elder, G. C. B., Sutton, J. R., and Howald, H. (1979). Mitochondrial volume density in human skeletal muscle following heavy resistance training. Med Sci Sports Exerc 11: 164-166.
13. Noakes, T. D. (2003). Lore of running. 4th ed. Champaign: Human kinetics. P. 19-21.
14. Paavolainen, L., Nummela, A., Rusko, H. (2000). Muscle power factors and VO2max as determinants of horizontal and uphill running performance. Scand J Med Sci Sports.; 10: 286-91.
15. Paavolainen, L., Hakkinen, K., Hamalainen, I., et al. (1999). Explosive strength training improves 5-km running time by improving running economy and muscle power. J Appl Physiol.; 86: 1527-33.
16. Paavolainen, L., Hakkinen, K., Hamalainen, I., et al. (1999). Explosive strength training improves 5-km running time by improving running economy and muscle power. J Appl Physiol.;86: 1527-33.
17. Paavolainen, L. M., Nummela, A. T., Rusk, H. K. (1999). Neuromuscular characteristics and muscle power as determinants of 5 km running performance. Med Sci Sports Exerc.; 31:124-30.
18. Saunders, P. U., Pyne, D. B., Telford, R. D., et al. (2004). Factors affecting running economy in trained distance runners. Sports Med.; 34 (7): 465-85.
19. Storen, O., Helgerud, J., Stoa, E. M., and Hoff, J. (2008). Maximal strength training improves running economy in distance runners. Med Sci Sports Exerc 40: 1087-1092.
20. Wilson, G. J., Newton, R. U., Murphy, A.J., and Humphries, B. J. (1993). The optimal training load for the development of dynamic athletic performance. Med Sci Sports Exerc 25: 1279-1286.
Spahiu Elton, Erindi Altin, QeleshiAnesti, Sports University of Tirana PhD student at Sport Sciences E-mail: eltonsph@yahoo.it
Relationship between diet and body fitness, with adjustment for resting energy expenditure and physical activity
Abstract:
Introduction: Research efforts for effective treatment strategies still focus on diet and exercise programs, the individual components of which have been investigated in intervention trials in order to determine the most effective recommendations for sustained changes in bodyweight. Obesity, particularly central adiposity, has been increasingly cited as a major health issue in recent decades. Indeed, some of the leading causes of preventable death and disability, including heart disease, stroke, type 2 diabetes, degenerative joint disease, low back pain, and specific types of cancer are obesity-related [1, 104-108]. Annual obesity-related medical costs in the United States were estimated to be as high as $147 billion in 2009 [3, 822-831].
Experimental design: A total of 70 recreationally active males and females between the ages of 15 and 18 years were recruited to participate in the study. In this study, recreationally active was defined as participating in less than or equal to two exercise sessions per week over the previous 30days. Subjects were required to have a body mass index (BMI) greater than 27kg/m 2 and body fat greater than 20% (for males) or greater than 25% (for females). This study utilized a randomized, placebocontrolled, parallel-group, double-blind design. Subjects were matched according to sex and BMI prior to being randomized into different groups based on the physical activity patterns.
Conclusions: Basal metabolism is lower in people that have a lower physical activity based on the fact that they have a lower muscle mass. Basal metabolism is higher in the moderate physical activ-
56
Relationship between diet and body fitness, with adjustment for resting energy expenditure and physical activity
ity. The total energy expenditure is higher in relation with the time in high and moderate physical activity; this shows that the muscles are better adapted in high intensity training in using the energy. The moderated physical activity intensity doesn’t make the subjects to have a higher energy intake necessities so it can be considered the best way for lowering body fat without he necessity to have a higher food intake. There is a better relationship between the intensity of the physical activity and food intake, so this shows that there is a better understanding of the body from those that make physical activity than those that don’t.
Keywords: Basal metabolism, Diet, Physical activity.
Introduction
Research efforts for effective treatment strategies still focus on diet and exercise programs, the individual components of which have been investigated in intervention trials in order to determine the most effective recommendations for sustained changes in bodyweight. Obesity, particularly central adiposity, has been increasingly cited as a major health issue in recent decades. Indeed, some of the leading causes of preventable death and disability, including heart disease, stroke, type 2 diabetes, degenerative joint disease, low back pain, and specific types of cancer are obesity-related [1, 104-108]. In the United States, more than one-third of adults (35.7%) are obese [2, 1-2]. Annual obesity-related medical costs in the United States were estimated to be as high as $147 billion in 2009 [3, 822-831]. Excess body weight is also a major risk factor for the development of Metabolic Syndrome. Metabolic Syndrome is a constellation of medical disorders including hypertension, central adiposity, hyperglycemia and dyslipidemia [4, 1-2; 5, 148-153] that increase the risk of premature cardiovascular disease. Dysregulation of certain adipocytokines can contribute to insulin resistance, amplified systemic inflammation and lead to the development of Metabolic Syndrome and hypertension [6, 1787 -1801]. For example, plasma levels of adiponectin have been reported to be significantly reduced in obese humans [7, 79-83] and in patients with type-2 diabetes mellitus, hypertension and metabolic syndrome [8,1595-1619; 9, 85-89; 10, 231-234; 11, 167-175].
Objectives
• Evaluation of BMI based on the training effort.
• Evaluation of the changes on the metabolism due to physical activity.
• The evaluation in energy expenditure due to specific training values.
Methods
Subjects
A total of 70 recreationally active males and females between the ages of 15 and 18 years were recruited to participate in the study. In this study, recreationally active was defined more participating in less than or equal to two exercise sessions (aerobic or anaerobic activity) per week over the previous 30 days. Subjects were required to have a body mass index (BMI) greater than 27 kg/m 2and body fat greater than 20% (for males) or greater than 25% (for females). Subjects were excluded if they had used weight-loss supplements within the 30 days prior to the start of the study, had gained or lost more than 4.5 kg over the previous 30 days, were currently taking medications that alter insulin sensitivity, or were using lipid lowering or antihypertensive drugs. Subjects were also excluded if they had metabolic disorders, heart disease, and hypertension, a known allergy to any ingredients in the supplement or placebo or had smoked cigarettes in the last six months. Prior to being enrolled in the study, all subjects underwent a physical examination by a licensed physician, 12-lead electrocardiogram, health history screen and provided written informed consent.
Experimental design
This study utilized a randomized, placebo-controlled, parallel-group, double-blind design. Subjects were matched according to sex and BMI prior to being randomized into different groups based on the physical activity patterns.
Discussion
Weight gain is known to occur with aging in healthy subjects. Weight gain is the result of energy intake exceeding energy expenditure. Food intake has never been shown to increase with age; on the contrary, it seems to decrease in older people [12, 894-931]. Whether energy expenditure is normal
57
Section 7. Physical Education
or lower in older subjects has not yet been clearly established. Physical activity most certainly decreases with increasing age and represents possibly one of the major factors in the process of weight gain with age [13, 1-8]. The thermo effect of glucose was also reported to decrease in older subjects [14, 144-148] and this may be true for other macronutrients as well. However, there are some contradictory reports concerning the effect of age on the basal metabolic rate. The age-related decrease in basal metabolic rate was described in normal men aged > 50 y in crosssectional studies involving a large number of sub-
jects [15,468-484; 16, 303-311; 17,447-51; 18, 31-40]. However in 1973, Keys et al [19, 579-87], in longitudinal studies over 20 y, found that these cross-sectional studies had greatly overestimated the true age effect. They concluded that the reduction in basal metabolism attributable to aging per se is no more than 1-2% per decade over the range of 20-75 y. They also showed for the first time that most of the age effect on energy metabolism is accounted for by a change in body composition. Keys’ results were later confirmed by Webb’s observations [20, 1816-26].
Rasa I Metabo [ism (jti C cal)
1900.00
1850.00
1800.00
1750.00
1700.00 1650 00
1600.00 1550.00
■ Low
■ Moderate
■ Medium
■ HiRh
58
Relationship between diet and body fitness, with adjustment for resting energy expenditure and physical activity
Effect ofphysical fitness on energy expenditure
Whether physical training and therefore physical fitness increases energy expenditure beyond that generated by the exercise period itself remains an open question [21, 146]. One of the major reasons for this confusion relates to the effect of the last bout of exercise vs the prolonged effect of training. In some studies, elevated oxygen consumption has been reported to last up to 48 h after exercise [22, 532-5; 23, 452-6; 24, 689-7; 25, 314-21; 26, 69-82]. In his review, however, Steinhaus [27, ЮЗ-47] concluded that no subsequent change in basal metabolic rate can be demonstrated in response to exercise and this was confirmed by Freedman et al [28, 545-9]. The differences in intensity and duration of the bout of exercise as well as the physical fitness of the subject in these studies can partly explain the discrepancy in the results and conclusions. Whether the bevel of physical training has an effect on the thermo effect of food is also not clearly established [29, 334-7; 30, 743-9]. Very little is known as to whether fitter individuals have higher metabolic rates in the resting state. To avoid any confounding effect of the last bout of exercise, the resting metabolic rate was measured after the subjects had lived on the metabolic ward without performing any kind of vigorous exercise for at least 7 days. In these subjects the maximal 02 uptake varied from 34 to 55 ml
02 — kg FFM’ — min. There was no significant relationship between resting metabolic rate adjusted for fat-free body mass, fat mass, age, and sex and any muscle characteristics. People with large fat-free body mass have a lower capillary density (r = -0.49, p < 0.0001) and artificially reduced metabolic rate. This represents another example of erroneous normalization of energy expenditure data, which can lead to the wrong conclusions.
Conclusions
Basal metabolism is lower in people that have a lower physical activity based on the fact that they have a lower muscle mass. Basal metabolism is higher in the moderate physical activity. The total energy expenditure is higher in relation with the time in high and moderate physical activity; this shows that the muscles are better adapted in high intensity training in using the energy.
The moderated physical activity intensity doesn’t make the subjects to have a higher energy intake necessities so it can be considered the best way for lowering body fat without he necessity to have a higher food intake.
There is a better relationship between the intensity of the physical activity and food intake, so this shows that there is a better understanding of the body from those that make physical activity than those that don’t.
References:
1. Dixon J.B.: The effect of obesity on health outcomes. Mol Cell Endocrinol 2009, 316: 104-108.
2. Cynthia L. Ogden, Ph. D.; Molly M. Lamb, Ph. D.; Margaret D. Carroll, M. S.P. H.; and Katherine M. Fle-gal, Ph. D. Obesity and Socioeconomic Status in Adults: United States, 2005-2008: NCHS Data Brief, No. 50, December 2010: 1-2.
3. Finkelstein E.A., Trogdon J.G., Cohen JW, Dietz W: Annual medical spending attributable to obesity; payer-and service-specific estimates. Health Aff 2009, 28: w822-w831.
4. Kaur J. A. Comprehensive Review on Metabolic Syndrome. Hindawi Publishing Corporation Cardiology Research and Practice Volume 2014, Article ID 943162; 1-2.
5. Scarpellini E., Tack J.: Obesity and metabolic syndrome: an inflammatory condition. Dig Dis 2012, 30:148-153.
6. Smith M.M., Minson C.T.: Obesity and adipokines: effects on sympathetic over activity. J Physiol 2012, 590 (Pt 8):1787 -1801.
7. Arita Y., Kihara S., Ouchi N., Takahashi M., Maeda K., Miyagawa J., Hotta K., Shimomura I., Nakamura T., Miyaoka K., Kuriyama H., Nishida M., Yamashita S., Okubo K., Matsubara K., Mura-guchi M., Ohmoto Y., Funahashi T., Matsuzawa Y.: Paradoxical decrease of an adipose-specific protein, adiponectin, in obesity.
8. BiochemBiophys Res Commun 1999, 257:79-83.
59
Section 7. Physical Education
9. Hotta K., Funahashi T., Arita Y., Takahashi M., Matsuda M., Okamoto Y., Iwahashi H., Kuriyama H., Ou-chi N., Maeda K., Nishida M., Kihara S., Sakai N., Nakajima T., Hasegawa K., Muraguchi M., Ohmoto Y., Nakamura T., Yamashita S., Hanafusa T., Matsuzawa Y: Plasma concentrations of a novel, adipose-specific protein, adiponectin, in type 2 diabetic patients. ArteriosclerThrombVascBiol 2000, 20:1595-1619.
10. Kumada M., Kihara S., Sumitsuji S., Kawamoto T., Matsumoto S., Ouchi N., Arita Y., Okamoto Y., Shi-momura I., Hiraoka H., Nakamura T., Funahashi T., Matsuzawa Y., Osaka CAD, Study Group: Association of hypoadiponectinemia with coronary artery disease in men. ArteriosclerThrombVascBiol 2003, 23:85-89.
11. Ouchi N., Ohishi M., Kihara S., Funahashi T., Nakamura T., Nagaretani H: Association of hypoadiponectinemia with impaired vasoreactivity. Hypertension 2003, 42:231-234.
12. Trujillo M.E., Scherer P.E.: Adiponectin: Journey from an adipocyte secretory protein to biomarker of the metabolic syndrome. J Intern Med 2005, 257:167-175.
13. Buskirk E.R. Health maintenance and longevity: exercise. In: Finch CE, Schneider EL. eds. The handbook ofthe biology ofaging. New York: Van Nostrand Reinhold Company. I 985:894-931.
14. Newman A., (January 31, 2009) “Obesity in Older Adults” OJIN: The Online Journal of Issues in Nursing Vol. 14, No. 1, Manuscript 3; 1-8
15. Golay, A., Schutz, Y., Broquet, C., Moeri, R., Felber, J. P., Jequier, E. Decreased thermogenic response to an oral glucose load in older subjects. J Am Geriatr Soc. 1983;31:144-148
16. Boothby W.M., Berkson J. & Dunn H.L. (1936) Studies of the energy of metabolism of normal individuals: a standard for basal metabolism with a nomogram for chemical application. Am. J. Physiol. 116: 468-484.
17. Du Bois D. and Du Bois E.F. A formula to estimate the approximate surface area if height and weight be known. 1916. Nutrition 5: 303-311, 1989.
18. Binet L., Bochet M., Bourliere R. Le metabolisme de base et la dispense de fond des personnes ages, leurs variations. Bull AcadNatIMed (Paris) 1945: 129:447-51.
19. Shock N.W., Yiengst MJ. Age changes in basal respiratory measurements and metabolism in males. JGerontol 1955; 10:31-40.
20. Keys A., Taylor H.L., Grande F. Basal metabolism and age of adult man. Metabolism 1973;22:579-87.
21. Webb P. Energy expenditure and fat-free mass in men and women. Am J ClinNutr 198 1;34:1816-26.
22. Kolata G. Metabolic catch-22 of exercise regimens. Science I 987;236: 146.
23. Edwards H.T., Thorndike A., Dill DB. The energy requirement in strenuous muscular exercise. N Engl J Med l935;2 13:532-5.
24. Passmore R, Johnson RE. Some metabolic changes following prolonged moderate exercise. Metabolism l960;9:452-6.
25. Margaria R., Edwards HT, Dill DB. The possible mechanism of contracting and paying 02 debt and the role oflactic acid in muscle contraction. Am J Physiol 1973: 106:689-7 15.
26. deVries H.A., Gray De. After effects ofexercise upon resting meta- bolicrate. ResQ1983;34:314-21.
27. Bielinski R, Schutz Y., Energy metabolism during postexercise recovery in man. Am J ClinNutr 1985:42:69-82.
28. Steinhaus A.H. Chronic effects of exercise. Physiol Rev 1983: 13: 103-47.
29. Freedman-Akabas 5, Colt E., Kissileff H.R. Pi-Sunyer F.X. Lack of sustained increase in VO2 following exercise in fit and unfit subjects. Am J ClinNutr 1985:41:545-9.
30. LeBlanc J., Mercier P. Samson P. Diet induced thermogenesis with relation to training state in female subjects. Can J PhysiolPharmacob I984; 62: 334-7.
31. Hill J.O., Heymsfield S.B., McMannus C. DiGirolamo M. Meal size and thermic response to food in male subjects as a function of maximum aerobic capacity. Metabolism 1984; 33:743-9.
60
