Investigation of possible changes to biochemical indices regarding specific forms of exercise (soccer, swimming etc) in childhood
Bekris E.1, Giovanis V1, Anagnostakos K.2, Dafopoulou G.1, Souglis A1., Sotiropoulos A.1
1National and Kapodistrian University of Athens - Department of Physical Education and Sport Science General Hospital of Karpenissi - Resident Physician Orthopedics
Annotation:
The aim of this study was to investigate possible cardiovascular changes to chosen biochemical indices regarding specific forms of exercise (soccer, swimming etc) in boys 9 - 14 years old. The concentration levels of the following biochemical parameters were measured: reactionary protein (CRP), total antioxidant capacity (T.A.C), and Fibrinogen. Moreover, body fat percentage and body mass index were measured and maximum oxygen intake (VO2 max) was estimated. The sample comprised 168 boys, aged 10.33+0.88, 10.62+0.21, 11.68+0.11 and 10.71+0.24 years old respectively, who were classified into four Groups (1, 2, 3, 4) according to their level of physical activity. Blood samples were taken from all four Groups in the morning of the same day after a 12 - hour, all
- night fasting. The statistical analysis of the results (variance analysis one way anova, post hoc - Bonfer-roni) showed statistically significant differences (a = 0.1) in the levels of reactionary protein (CRP), fibrinogen (fib) and total antioxidant capacity (TAC). More specifically there were statistically significant differences a) regarding CRP, between Group 4 and all other Groups, b) regarding fibrinogen (fib), between Group 4 and Groups 1 and 2, and c) regarding total antioxidant capacity, between Group 4 and Group 2 as well as between Group 3 and Group 2. Additionally, statistical analysis (Pearson correlation) showed statistically significant correlations (a = 0.05) a) between body fat percentage and fibrinogen levels (positive correlation), b) between maximum oxygen intake (VO2 max) and fibrinogen levels (negative correlation) and c) between body mass index and fibrinogen levels (positive correlation). From these results, it is obvious that exercise benefits children, probably protecting their organisms against cardiovascular diseases.
Keywords:
biochemistry of exercise, football, swimming, reactionary protein (CRP), fibrinogen (fib), total antioxidant capacity (TAC).
Бекріс Є., Жіованіс В., Анагностакос К., Дафопулу Ж., Сугліс А., Сотіропулос А. Дослідження можливих змін до біохімічних індексів відносно специфічних форм вправ (футбол, плавання і ін.) в дитинстві. Мета дослідження -розслідувати можливі серцево-судинні зміни до вибраних біохімічних індексів відносно специфічних форм вправи (футбол, плавання і ін.) у хлопчиків 9 -14 років. Концентраційні рівні наступних біохімічних параметрів були розглянуті: реакційний протеїн (CRP), повна антіокислітельная місткість (T.A.C), і фібриноген. Крім того, відсоток жиру тіла і індекс маси тіла були зважені, включаючи максимальну місткість кисню (максимум VO2). Зразок охопив 168 хлопчиків, у віці 10.33+0.88, 10.62+0.21, 11.68+0.11 і 10.71+0.24 років, які відповідно були класифіковані у чотири групи (1, 2, 3, 4) згідно з їх рівнем фізичної діяльності. Зразки крові були узяті зі всіх чотирьох груп вранці того ж дня після 12 годин голодування. Статистичний аналіз результатів (anova, post hoc -Bonferroni) показав статистично істотні відмінності (а = 0.1) в рівнях реакційного протеїну (CRP), фібриногену (fib) і повної антиокислювальної місткості (TAC). Особливо були виявлені такі статистично істотні відмінності: а) відносно CRP, між групою 4 і всіма останніми групами, b) відносно фібриногену (fib), між групою 4 і групами 1 і 2, з) відносно повної антиокислювальної місткості, між групою 4 і групою 2, також як було проведено між групою 3 і групою 2. Додатково, статистичний аналіз (Pearson correlation) показав статистично істотні кореляції (а = 0.05) а) між відсотком жиру тіла і рівнями (позитивна кореляція) фібриногену, b) між максимальною місткістю киснем (максимум Vo2) і рівня (негативна кореляція) фібриногену, з) між індексом маси тіла і рівнями фібриногену (позитивна кореляція). Як результат, ці вправи розвивають дітей, захищаючи їх організми від серцево-судинних хвороб.
біохімія вправ, футбол, плавання, реакційний протеїн (CRP), фібріно-ген (fib), повна антиокислювальна місткість (TAC).
Бекрис Е., Жиованис В., Анагностакос К., Дафопулу Ж., Суглис А., Сотиропулос А. Исследование возможных изменений к биохимическим индексам относительно специфических форм упражнений (футбол, плавание и др.) в детстве. Цель исследования - расследовать возможные сердечно-сосудистые изменения к избранным биохимическим индексам относительно специфических форм упражнения (футбол, плавание и др.) у мальчиков 9 - 14 лет. Концентрационные уровни следующих биохимических параметров были рассмотрены: реакционный протеин (CRP), полная антиокислительная вместимость (T.A.C), и фибриноген. Кроме того, процент жира тела и индекс массы тела были взвешены, включая максимальную вместимость кислорода (максимум VO2). Образец охватил 168 мальчиков, в возрасте 10.33+0.88, 10.62+0.21, 11.68+0.11 и 10.71+0.24 лет, которые соответственно были классифицирован в четырех группах (1, 2, 3, 4) согласно их уровню физической деятельности. Образцы крови были взяты из всех четырех групп утром того же дня после 12 часов голодания. Статистический анализ результатов (anova, post hoc
- Bonferroni) показал статистически существенные отличия (а = 0.1) в уровнях реакционного протеина (CRP), фибриногена (fib) и полной антиокислительной вместимости (TAC). Более особо были выявлены такие статистически существенные отличия: а) относительно CRP, между группой 4 и всеми остальными группами, b) относительно фибриногена (fib), между группой 4 и группами 1 и 2, с) относительно полной антиокисли-тельной вместимости, между группой 4 и группой 2, также как было проведено между группой 3 и группой 2. Дополнительно, статистический анализ (Pearson correlation) показал статистически существенные корреляции (a = 0.05) a) между процентом жира тела и уровнями (положительная корреляция) фибриногена, b) между максимальной вместимостью кислородом (максимум VO2) и уровня (негативная корреляция) фибриногена, с) между индексом массы тела и уровнями фибриногена (положительная корреляция). Как результат, эти упражнения развивают детей, заЩищая их организмы от сердечно-сосудистых болезней.
биохимия упражнений, футбол, плавание, реакционный протеин (CRP), фибриноген (fib), полная антиокислительная вместимость (TAC).
Introduction
One of the most important problems plaguing developed societies is cardiovascular diseases, namely coronary disease, strokes and peripheral occlusive heart disease. According to Murray & Lopez [57], coronary disease (CVD) is the first cause of death in developed countries, while according to Kochanek et al. [40], cardiovascular disease is the main cause of death among men in the USA.
The classical danger factors (high blood pressure, diabetes, smoking, hyperlipidemia, obesity) remain the basic causes of cardiovascular disease, but its increased incidence nowadays cannot be totally attributed to them. Over the last
© Bekris E., Giovanis V., Anagnostakos K., Dafopoulou G., Souglis A., Sotiropoulos A., 2011
few years, researches have been investigating “newer” cardiovascular disease factors, such as Fibrinogen, reactionary protein (CRP) and total antioxidant capacity (TAC). Many researches argue that Fibrinogen is instrumental in causing a number of pathophysiological conditions such as clots, atherosclerosis and inflammation [73,30,71]. Reactionary protein has been involved in all stages of atherosclerosis, from the initial intake of inflammatory cells inside the arterial wall to the rupture of the plaque. CRP not only appears to be an important factor in predicting cardiovascular danger (CVD), [69], but also, increased levels of it point to potential cardiovascular incidents [49]. Atherosclerosis is an example of nosological procedure in which there is tell-
ing evidence regarding the participation of oxidative stress. Drastic oxygen radicals affect the vessel function with a series of pathogenic mechanisms [84,87]. Oxidative damage on the vessel wall leads to atherosclerosis when the balance / equilibrium between its pro-oxidant and antioxidant substances is disrupted [83]. According to Giannakopou-lou [25] and Osganian [61], antioxidants protect the cells’ membranes by neutralizing free oxygen roots, maintaining redox balance (homeostasis) and protecting the heart since they increase the resistivity of the vessels and limit inflammatory factors.
Although the factors of the risk of developing cardiovascular disease clinically appear in adulthood, those that affect coronary disease originate in childhood [81] and according to Colin Boeham et al. [14], the benefits stemming from adequate physical activity during childhood, such as a healthier cardiovascular profile, are multifarious and are also enjoyed in adult life.
Many researches have proven the positive influence of exercise on the prevention of cardiovascular complaints [4,5,86,78], on the minimized likelihood of developing metabolic and heart diseases and its contribution to longevity [62,41,67,86]. Physical activity influences the cardiovascular, neuro - hormonical and muscular tracts, the coagulation and fibrinolysis mechanisms, while it helps the atherosclerosis retrogression and it promotes the endothelial function [75,29,31,51,79,45]. In a number of researches studying adults or children, fibrinogen is inversely related to physical fitness [46,18,17,9], while other studies (on children) have not reached the same conclusion [76,77]. In certain bibliography reviews, it is observed that CRP decreases with regular exercise in adults, whereas, equivocal results are confirmed in another review, regarding children [76]. In recent researches, it is observed that regular exercise improves antioxidant capacity in teenage athletes [2], in adult soccer players after a preparatory program [52] or after a routine of practice and games [23] as well as in mice, after a short exercise program [88]. Nevertheless, there is no bibliographical data considering the effect of exercise on antioxidant capacity in children with different physical activity. The aim of the present study is to investigate the possible influence of different forms of physical activity on cardiovascular biochemical indices, such as reactionary protein (CRP), total antioxidant capacity (TAC) and Fibrinogen in boys aged 9 - 14 years old.
Methodology
Sample
The study was based on 168 boys classified into four groups with diverse physical activity - exercise patterns.
The first group (Group 1) comprised 41 boys aged 10.33+0.88 years old with a Low Physical Activity Level (L.P.A.L.) for whom the only form of exercise was P.E (Physical Education) at school, which took place twice a week and lasted 45 minutes each time.
The second group (Group 2) comprised 42 boys aged 10.62 + 0.21 years old with a Moderate Physical Activity Level (M.P. A.L.) who, apart from P.E. classes participated in 90 - minute soccer practice twice a week.
The third group (Group 3) comprised 45 boys aged 11.68+0.11 years old with a High Physical Activity Level (H.P.A.L.) who, apart from P.E. classes participated in 90
- minute soccer practice three times a week.
The fourth group (Group 4) comprised 40 boys aged 10.71+0.24 years old with a Very High Physical Activity Level (VH.P.A.L.) who, apart from P.E. classes participated in 90 - minute swimming training five times a week.
The planning of the survey was such so as to minimize any differentiation among the four Groups regarding environmental factors. The subjects (boys) were Athens residents since birth. The selection was based on random sampling among a number of volunteers after lots were drawn.
Measurement procedure
The individuals of all four Groups underwent a routine clinical examination test (cardiograph, chest x ray, systolic and diastolic pressure) which did not reveal any obvious pathological condition. Moreover, the same individuals did not have any health problems and were not using any medication during blood taking. At the same time, their eating habits medical history was taken. The boys and their parents were informed on the purpose, the procedure and the planning of the survey in detail. All parents signed a written consent form, allowing their children’s participation in the study.
Measurements
a). Anthropometric. The anthropometric parameters that were examined were height, body fat percentage and body mass index. For the estimate of body composition (fat mass and body fat percentage), the Meyhew method was applied [54]. This method is based on measuring the fat between two skin folds, middle femoral and hyper iliac (table 1).
b). Maximum oxygen intake. To measure maximum oxygen intake (VO2max), the retrograde run endurance test (recurrent 20m running) was used (table 2-3). The test is based on a recorded sound which is heard [39].
c). Blood taking. Blood was taken from all subjects in the morning after a 12 hour fasting and a 36 hour abstenance from exercise. During the donation, the subjects were sitting down. The samples were taken from the Royal Bonanza vein. 9 ml of blood were taken with a Cliss syringe without anti-freezing for serum taking. Reactionary protein (CRP) was determined through the method of anosofelometria in special, automatic Dade Behring reagents. Fibrinogen was determined through the method of anosofelometria in special, automatic Dade Behring reagents. Total antioxidant capacity (TAC) was measured with an Olympus Au - 600 automatic biochemical analyzer (table 2 - 3).
Statistical analysis
The SPSS 15 statistical program was used to statistically process the finds, while one way anova variance analysis was used for the comparisons of different forms of exercise among all four Groups.
The post hoc test - Bonferroni was used for the differences of each variable between any two Groups. All statistical significances were controlled in the entire probability level a = 0.1. Parametrical correlations between physiological characteristics and biochemical indices were made through the linear correlation technique and the Pearson (r) coefficient correlation balance on a
Table 1
Means and standard deviations of boys (n = 168) for the age (years old), training age (years old), height (cm), body weight (kg), body fat percentage (%) and body mass index (kg / m2).
GROUPS WITH DIVERSE PHYSICAL ACTIVITY PATTERNS. N=168 AGE TRAINING AGE HEIGHT BODY WEIGHT (KG) BODY FAT PERCENTAGE (%) BODY MASS INDEX (KG / M2)
Group 1 (L.P.A.L.) N=41 10,33±0,88 0 151,33±8,11 44,93±6,86 10,75±2,06 19,32±1,25
Group 2 (M.P.A.L.) N=42 10,62±0,21 2±0,8 144,90±1,95 40,02±1,28 12,79±1,06 19,02± 0,57
Group 3 (H.P.A.L.) N=45 11,68±0,11 3±0,7 154,94±3,15 46,27±2,40 11,89±2,48 19,30±0,98
Group 4 (V.H.P.A.L) N=40 10,71±0,24 4±1,2 148,04±2,94 41,46±3,02 13,65±1,74 18,67±0,82
Table 2
Means and typical errors in the 4 Groups variables of different forms of exercise
Parameters Group 1 Group 2 Group 3 Group 4
Total antioxidant capacity TAC) 1,30±0,09 1,02±0,06 1,38±0,07 1,32±0,11
Fibrinogen (Fib) 340,33±28,061 377,33±30,76 288,66±15,45 267,00±49,64
Reactionary protein (CRP) 4,52±0,92 4,41±0,32 4,57±0,53 1,97±0,20
Maximum oxygen intake (VO2max) 43,58±0,58 48,76±1,28 54,94±1,02 48,94±1,11
Table 3
One way anova variance analysis on the 4 Groups regarding the TAC, Fib, CRP, VO2max variables which presented statistically significant differences.
ANOVA
Sum of Squares df Mean Square F p-value
Maximum oxygen intake (VO2max) Between Groups 176,179 3 58,73 3,890 0,017
Within Groups 498,188 33 15,10
Total 674,367 36
Total antioxidant capacity (TAC) Between Groups 0,770 3 0,26 4,661 0,007
Within Groups 2,202 40 0,06
Total 2,972 43
Fibrinogen (Fib) Between Groups 96.977,841 3 32.325,95 3,568 0,023
Within Groups 344.230,731 38 9.058,70
Total 441.208,571 41
Reactionary protein (CRP) Between Groups 55,768 3 18,589 14,279 0,000
Within Groups 41,661 32 1,302
Total 97,429 35
significance level a = 0.05.
Results
The results of the comparisons among all 4 Groups (Fig.1-4) showed statistically significant differences regarding the levels of total antioxidant capacity, Fibrinogen, reactionary protein (CRP) as well as maximum oxygen intake (VO2max) on a significance level a = 0.1.
Variance analyses (post hoc test - Bonferroni) showed that there are statistically significant differences in total antioxidant capacity levels between Groups 2 and 3 (p -value = 0.009 < 0.1) and between Groups 2 and 4 (p -value = 0.029 < 0.1).
As far as Fibrinogen levels are concerned, there is statistically significant difference between Groups 1 and 4 (p - value = 0.070 < 0.1), and between Groups 2 and 4 (p - value = 0.071 < 0.1).
Regarding CRP, there is statistically significant difference between Groups 1 and 4 (p - value = 0.000 < 0.1), between Groups 2 and 4 (p - value = 0.000 < 0.1), and between Groups 3 and 4 (p - value = 0.000 < 0.1).
Concerning maximum oxygen intake (VO2 max), there is statistically significant difference between Groups 1 and 3(p - value = 0.014 < 0.1).
Linear correlation checks (a = 0.05) showed that body fat percentage is positively correlated to fibrinogen (correlation coefficient = 0.398), (fig.5), body mass index is positively correlated to fibrinogen (correlation coefficient = 0.462), (fig.6) and maximum oxygen intake (VO2 max) is negatively correlated to fibrinogen (correlation coefficient = - 0.415), (fig.7).
Discussion
Regarding total antioxidant capacity ( TAC) results
A number of researches into adults and teenagers have concluded that regular exercise causes an increase in total antioxidant capacity levels [47,7,2].
In agreement with the studies mentioned above, the present survey confirms the influence of children’s regular exercise on the levels of their antioxidant capacity, since the highest levels of total antioxidant capacity appear in the two more frequently exercising groups, namely Group 3 (HPAL) and Group 4 (VHPAL), which are statistically significantly higher than those of Group 2 (MPAL).
According to Jenkins et al. [34], regular exercise can reduce post workout oxidative stress and limit muscular damage, while he observes that the favorable effects of regular exercise are attributable to the higher capacity of the enzymatic and non-enzymatic oxidative defense system. As the same researcher proved, the mechanism that justifies the belief that antioxidative defense appears to be regulated with physical activity is the increase in the action of catalase and dismutase peroxide on human muscles.
According to the results of this survey, Group 1 (LPAL) antioxidant capacity levels are not the lowest of all Groups as would normally be expected. This is probably due to diet, whose role is pivotal in maintaining a high level of antioxidant capacity, as researches have shown [28,82,53,52]. The increased intake of antioxidant rich foods offers increased antioxidative defenses to combat oxidative stress, and it is necessary, especially to athletes during periods of vigorous workout, when oxidative stress is generated.
The differences of antioxidant capacity levels observed among the Groups seem to be affected by a number of various factors, such as the kind and frequency of training stimuli [52], the duration [6], the quantity and vigor [27] of the applied training program when measurements are taken, the subjects’ age, their diet as well as their physical fitness before the application of a specific workout protocol [21].
Regarding reactionary protein (CRP) results
The favorable influence of exercise on the reduction of CRP levels has been proven by many scholars / researchers [26,54,1,41,66]. This survey’s results agree with those of the aforementioned researches, since Group 4 (VHPAL) shows statistically significantly the lowest levels of CRP in relation to the other Groups, thus affirming Kasapis & Thompson’s [36] view that there is an inverse relationship between CRP serum levels and physical activity level. The same view has also been expressed by King et al. [38], who observed that the significant superiority of those exercising
- regardless of form of exercise - in comparison to the control group (sedentary lifestyle) was independent of age. Reinforcing the significance of regular exercise in children’s health [55], realized that children of normal weight with dyslipidemia (low levels of HDL-C and increased cholesterol) who participate in regular exercise do not show - as would be expected - high levels of CRP, thus sustaining their health on non-dangerous / risk - free levels. According to Moldoveanu et.al [54], moderate to high vigor exercise causes a transient increase in pro-inflammatory cytokines as well as in acute phase proteins, like CRP, whereas longterm and systematic physical activity is linked to lower pro-inflammatory cytokines and acute phase proteins readings in these subjects’ blood. Reactionary protein (CRP) is mainly produced by the liver in response to a variety of stimulators and increases the inflammatory response in all those factors that commence acute phase cataract. Acute phase is a common reaction to a variety of dangers that disrupt homeostasis, one of which is extended exercise [19]. Physical activity seems to cause many of these changes in the subject’s organism, which is mainly attributableto the acute response following vigorous and exhausting exercise. This response includes metabolic changes, such as change in the nitrite balance, changes in the metabolism of lipids, changes in the concentration of cations, changes in the metabolism of iron, activation of the complement, leukocytosis and increased liver - originating protein production that participate in and orchestrate acute phase response. Respectively, albumin, a2 glycoprotein, a fetoprotein and transferrin are reduced, thus reflecting the change of the liver’s functional equilibrium [43]. According to Pedersen et al. [63], CRP’s source is liver-induced production with IL-6 as the major stimulator, which seems to be produced in the highest percentage by the exercised muscle. One of the ways in which exercise can reduce the risk of cardiovascular disease is through inflammation reduction. However, the mechanisms responsible for the protective effect of physical activity are not perfectly clear yet. According to Okita et al. [60], the beneficial effects of regular exercise on CRP levels mainly stem from changes in the fat tissue, while, at the same time, Pitsavos et al. [64] observe that regular exercise greatly reduces the levels of inflammatory
Fig. 1. Total antioxidant capacity means in Groups with different forms of exercise.
CRP (mg/l)
Group 4 Group 3 Group 2 Group 1
0,00 1,00 2,00 3,00 4,00 5,00
Fig. 3. CRP means in Groups with different forms of exercise.
Fig. 4. Maximum oxygen intake (VO2 max) means in Groups with different forms of exercise.
Fig. 6. Correlation between body mass index and fibrinogen in the four experimental groups.
indices contributing to atherosclerosis, causing a 33% reduction in CRP levels.
Regarding fibrinogen results
The present study realized statistically significant differences in fibrinogen levels between Groups 1 and 4 (p
- value = 0.070 < 0.10) as well as between Groups 2 and 4 (p - value = 0.071 < 0.10). Moreover, Group 4 (VHPAL) shows the lowest fibrinogen levels, followed by Group 3 (HPAL). The results are consistent with the conviction that regular exercise reduces fibrinogen levels [15,17,9] and is related with a better cardiovascular function since it seems to intervene in the fibrinogen regulation mechanism [11]. The parameters involved in all these procedures are not always clear but it seems that action on endothelial level plays a pivotal role.
Apart from the quantity of exercise (frequency per week), the level of physical fitness (ergo, the intensity of exercise) seems to play a significant role in fibrinogen levels, as estimated from maximum oxygen intake (VO2 max). According to this study’s results, maximum oxygen intake (VO2 max) is negatively correlated to fibrinogen (correlation coefficient = -0.415). These conclusions have also been reached by various researchers [9,35,58,33], who mention that there is a gradually inverse relationship between fibrinogen and physical activity as well as physical fitness level as estimated from maximum oxygen intake, noting that physical activity and cardiopulmonary condition are independent prognostic indices of fibrinogen levels. The present study believes that this inverse relationship between fibrinogen and maximum oxygen intake may also be valid for children (boys). It also agrees with Blair et al. view [5] that cardiovascular benefits can be unexpectedly big even with a small increase in physical fitness level.
An important find in this research is the fact that body fat percentage is positively correlated to fibrinogen (correlation coefficient = 0.398) and that body mass index (BMI) is positively correlated to fibrinogen (correlation coefficient = 0.462). Other surveys also reached the same conclusions [8,10,3,22,74], reinforcing the view that anthropometric characteristics, such as body fat percentage
and body mass index, which are largely dependent on workout patterns, affect fibrinogen levels in children.
It seems that the favorable influence of exercise on a better cardiovascular function may also be mediated by the influence of exercise on thecoagulation system [12]. More specifically, systematic exercise helps in the secretion of NO [13]. According to surveys, NO is the main vasoli-dation factor and is produced by the vessel endothelium [80,32], while its secretion is related to good endothelium function. Endothelium dysfunction is a basic parameter of atherosclerosis, whose major characteristic is inadequate NO secretion, while at the same time, the substances and procedures that are related to increased inflammation and resulting vessel contraction thrive [16,70,72,20]. NO activates t-PA secretion by inhibiting PAI - I, a molecule which gets involved in blood coagulation and blood clot formation, thus increasing the fibrinogen situation [50]. The generated NO reduces the basic fibrinogen levels, which is why there are lower fibrinogen levels in the plasma of athletes and generally, in the plasma of people with higher levels of physical activity. Thus, there is better cardiovascular function [37]. Moreover, regular exercise contributes to low platelet activation, reduced tendency towards their accumulation and fibrinogen sticking to their surface, resulting in lower concentration of this factor in the plasma of regularly exercising individuals [85].
Conclusions
From the results of the present survey, the protective role of regular exercise and physical fitness level against cardiovascular complaints in children is clear. The beneficial advantages of various forms of physical activity seem to differentiate according to their characteristics such as frequency, intensity, duration and kind as well as the physical fitness level of the exercising children. According to the results, Group 4 (VHPAL), working out 5 times a week, swimming for a total of 7.5 hours, presents the most favorable levels of cardiovascular biochemical indices, since it shows the lowest levels of inflammatory indices contributing to atherosclerosis, such as fibrinogen and CRP, in relation to other forms of exercise, and it also shows the highest antioxidant capacity levels after Group 3 (HPAL).
It is therefore concluded that very frequent weekly exercise through swimming is particularly effective in shielding children’s health. An important find of this survey is the realization that the better the physical activity level and especially the improvement of maximum oxygen intake, the lower the fibrinogen levels, so children are less at risk of cardiovascular complaints. This result denotes the importance of the qualitative characteristics of physical activity (intensity) and not just the quantitative ones (duration). Finally, a particularly important conclusion of this survey is the fact that body fat percentage and body mass index are positively correlated to fibrinogen, proving the emphasis that should be laid by all to children’s normal weightand eating habits, which affect their cardiovascular function irrespective of their physical activity level.
To summarize, the present survey concludes that regular exercise in children is beneficial against atherosclerosis and coronary disease. However, to maximize these benefits, exercise should be combined with a high physical activity level and a proper diet.
Bibliography:
1. Albert M. A., Glynn R. J., Ridker P. M., (2004). Effect of physical activity on serum C-reactive protein. Am. J. Cardiol. 93, 221-225, Medline Crossref 1st Citation.
2. Anja Carlsohna, Sascha Rohnd, Frank Bittmannb, Jens Railaa, Frank Mayerc, Florian J. Schweigerta (2008). Exercise Increases the Plasma Antioxidant Capacity of Adolescent Athletes Ann Nutr Metab. vol 53:96-103.
3. Bao W, Srinivasan S.R, Berenson G.S. (1993). Plasma fibrinogen and its correlates in children from a biracial community: the Bogalusa Heart Study. Pediatr Res 33:323 - 6.
4. Berlin J.A., Colditz G.A. (1990). A meta analysis of physical activity in the prevention of coronary heart disease. Am I Epidemiol 1990:132: 612-628.
5. Blair S.N., Kohi K.W., Barlow C.E., Paffenbarger R.S., Gibbons L.W., Macers C.A. (1995). Changes in physical fitness and all-cause mortality. A prospective study of healthy and unhealthy men JAMA 1995; 273:1093-1098.
6. Bloomer R.J., Davis P.G., Consitt L.A., Wideman L. (2007). Plasma protein carbonyl response to increasing exercise duration in aerobically trained men and women. Am J. Hypertens, 20 (8):825-830.
7. Brites F.D., Evelson P.A., Christiansen M.G., Nicol M.F., Basilico M.J., Wikinski R.W., Llesuy S.F. (1999). Soccer players under regular training show oxidative stress but an improved plasma antioxidant status. Clinical Science 96. 381-385.
8. Cacciari E, Balsamo A, Palareti G. (1988). Haemorheologic and fibrinolytic evaluation in obese children and adolescents. Eur J. Pediatr; 147:381-4.
9. Carmen R. Isasi, Thomas J. Starc, Russell P. Tracy, Richard Deckelbaum, Lars Berglund, Steven Shea (2000). Inverse Association of Physical Fitness with Plasma Fibrinogen Level in Children The Columbia University Bio Markers Study. American Journal of Epidemiology Vol. 152, No.3: 212-218.
10. Carnevale Schianca G.P., Dugnani M., De Simone G.D., Mizza M., Pozzoli G., Franzini C. (1989). Behavior of fibrinogen, hematocrit and platelets in relation to variations in body mass index in agroup of female subjects. La Ricerca in clinica in labaratorio 1989; 19 Suppl 1: 125-8.
11. Chen H.I., Chiang I.P. (1996). Chronic exercise decrease adrenergic agonist - induced vasoconstriction in spontaneously hypertensive rats. The American Journal of physiology 1996; 271: H977-83.
12. Chen H.I., Li H.T. (1993). Physical conditioning can modulate endothelium - dependent vasorexation in rabbits. Arterioscler Thromb 1993; 13:852-6.
13. Chen H.I., Li H.T., Chen C.C. (1994). Physical conditioning decreases norepinephrine -induced vasoconstriction in rabbits. Possible roles of norepinephrine - evoked endothelium - derived relaxing factor. Circulation 1994; 90: 970 - 5.
14. Colin Boreham; Chris Riddoch (2001). The physical activity, fitness and health of children. Journal of Sports Sciences, V http://www. informaworld.com/smpp/title~db=all~content=t713721847~tab=iss ueslist~branches=19 - v1919, Issue 12, pp 915 - 929.
15. Connely J.B., Cooper J.A., Meade T.W. (1992). Strenous exercise, plasma fibrinogen and factor VII activity. British heart Journal 1992; 67:351-4.
16. Dusting G.J. (1996). Nitric oxide in coronary artery disease; roles in atherosclerosis, myocardial reperfusion and heart failure. Exs. 1996; 76:33-55.
17. El-sayed M. S., Davies B. (1995). A physical conditioning program does not alter fibrinogen concentration in young healthy subjects. Med. Sci. Sports Exerc., Vol. 27, No. 4, pp. 485-489.
18. Elwood P.C., Yarnell W.G., Pickering J., (1993). Exercise, fibrinogen, and other risk factors for ischaemic heart disease. Caerphilly Prospective Heart Disease Study. Br Heart J.; 69:183-7.
19. Fallon K., Sivyer G., Sivyer K., Dare A. (1999). Changes in haematological parameters and iron metabolism associated with a 1600 kilometre ultramarathon. Br J. Sports Med. 1999; 33:27-31.
20. Fan J., Watanabe T. (2003). Inflammatory reactions in the pathogenesis of Atherosclerosis. Journal of atherosclerosis and thrombosis 2003; 10:63-71.
21. Fatouros I.G., Jamurtas Az., Viliotou V., Pouliopoulou S., Fotinakis P., Taxildaris K., Deliconstantinos G. (2004). Oxidative stress responses in older men during endurance training and detraining. Med. Sci Sports Exerc., 36 (12): 2065-2072.
22. Ferguson M.A., Gutin B., Owens S. (1998). Fat distribution and hemostatic measures in obese children. Am J. Clin Nutr. 67: 1136-40.
23. Fernando D. Brites, Pablo A. Evelson, Marina Garda Christiansen, Maria F. Nicol, Maria Jose Basilico, Regina W. Wikinski, Susana F.L. Lesuy (1999). Soccer players under regular training show oxidative stress but an improved plasma antioxidant status Clinical Science 1999; 96, (381-385).
24. Ford, E. S. (2002). Does exercise reduce inflammation? Physical activity and C-reactive protein among U.S. adults. Epidemiology 13, 561-568.
25. Giannakopoulou E. (2009). Oxidative stress - antioxidant mechanisms- clinical significance. Medical Association Archives 2009, 26 (1):23-35.
26. Geffken D.F., Cushman M., Burke G.L., Polak J.F., Sakkinen P.A., Tracy R.P. (2001). Association between physical activity and markers of inflammation in a healthy elderly population. American Journal of epidemiology 2001; 153: 242-50.
27. Goto C., Higashi Y, Kimura M., Noma K., Hara K., Nakagawa K., Kawamura M., Chayama K., Yoshizumi M., Nara I. (2003). Effect of different intensities of exercise on endothelium -dependent vasodilation in humans: role of endothelium-dependent nitric oxide and oxidative stress. Circulation, 108 (5):530-535.
28. Guilland J.-C., Penaranda T., Gallet C., Boggio V., Fuchs F., Klepping J. (1989). Vitamin status of young athletes including the effects of supplementation. Med. Sci. Sports Exerc., Vol. 21(4), 441-449.
29. Hambrecht R., Niebauer J., Marbuger C., Grunze M., Kaelberer B., Hauer K., Schlierf G., Kuebler W., Schuler G. (1993). Various intensities of leisure time physical activity in patients with coronary artery disease: effects on cardiorespiratory fitness and progression of coronary atherosclerotic lesions. J. Am Coll Cardiol; 22: 468-477.
30. Harley S.L., Sturge J., Powell J.T. (2000). Regulation by fibrinogen and its products of intercellular adhesion molecule-1 expression in human saphenous vein endothelial cells. Arteriosclerosis, thrombosis, and vascular biology 2000; 20:652-8.
31. Hedback B., Perk J., Wodlin P. (1993). Long - term reduction of cardiac mortality after myocardial infarction: 10 - year results of a comprehensive rehabilition programme. Eur. Heart J. 1993; 14:831-835.
32. Huang A.L.,Vita J.A. (2006). Effects of systemic inflammation on endothelium - dependent vasodilation. Treds in cardiovascular medicine 2006; 16:15-20.
33. Iftikhar J. Kullo, Mahyar Khaleghi, Donald D. Hensrud (2007). Markers of inflammation are inversely associated with VO2 max in asymptomatic men. J. Appl. Physiol. 102: 1374-1379.
34. Jenkins R., Friedland J., Howland H., (1994). The relationship of oxygen uptake to superoxide dismutase and catalase activity in human skeletal muscle. Int. Sci. Sports Med. 5, 11-14.
35. Kaprio J., Kujaka M.U., Koskenuvo M., Sarna S. (2000). Physical activity and other risk factors in male twin - pairs discordant for coronary heart disease. Atherosclerosis 2000; 150: 193-200.
36. Kasapis C., Thompson P.D. (2005). The effects of physical activity on serum C-reactive protein and inflammatory markers: a systematic review. J. Am. Coll. Cardiol. 45, 1563-1569.
37. Kawabata A. (1996). Evidence that endogenous nitric oxide modulates plasma fibrinogen levels in the rat. British Journal of pharmacology 1996; 117:236-7.
38. King, D. E., Carek, P., Mainous, III, A. G. and Pearson, W. S. (2003). Inflammatory markers and exercise: differences related to exercise type. Med. Sci. Sports Exercise 35, 575-581.
39. Kleisouras (1991). Ergometry. Symmetria Publications, Athens.
40. Kochanek K.D., Murphy S.L., Anderson R., Scott C., Hyattsville, M.D. (2002). Deaths: Final data for 2002. National Vital Statistics Reports. 5 Vol. 53.
41. Kohut, M. L., McCann, D. A., Russell, D. W. Kai aw. (2006). Aerobic exercise, but not flexibility/resistance exercise, reduces serum IL-18, CRP, and IL-6 independent of D-blockers, BMI, and psychosocial factors in older adults. Brain Behav. Immunol. 20, 201-209.
42. Kushi L.H., Fee R.M., Folsom A.R., Mink P.J., Anderson K.E. Sellers T.A. (1997). Physical activity and mortality in postmenopausal women. JAMA 1997; 277: 1287-1292.
43. Kushner I. (1982). The phenomenon of the acute phase response. Ann NY Acad. Sci 1982; 389; 39-48.
44. Kushner I., Rzewnicki D. (1994). The acute phase response: general aspects. Baillieres Clin Rheumatol 1994; 8:513-530.
45. Laughlin M.H. (2004). Physical activity in prevention and treatment of coronary disease: the battle line is in exercise vascular cell biology. Med. Sci Sports Exerc. 2004; 352-362.
46. Lee A.J., Smith W.C., Lowe G.D., Tunstall - Pedoe H. (1990). Plasma fibrinogen and coronary risk factors: the Scottish Heart Health Study. Journal of clinical epidemiology 1990; 43:913-9.
47. Leeuwenburgh C., Fiebig R., Chandwaney R.J.L.L. (1994). Aging and exercise training in skeletal muscle: responses of glutathione and antioxidant enzyme systems. Am. J. Physiol. 267, R439-R445.
48. Li J.J., Fang C. H. (2004). C-reactive protein is not only an inflammatory marker but also a direct cause of cardiovascular diseases. Med. Hypotheses 62, 499-506.
49. Libby P., Ridker P. M. (2004). Inflammation and atherosclerosis: role of C-reactive protein in risk assessment. Am. J. Med. 116, (Suppl. 6A), 9S-16S.
50. Lidbury P.S., Korbut R., Vane J.R. (1990). Sodium nitroprusside modulates the fibrinolytic system in the rabbit. British Journal of pharmacology 1990; 101:527-30.
51. Linke A., Schoene N., Gielen S. (2001). Endothelial Dysfunnction in Patients With Chronic Heart Failure: Systemic effects of Lower -Limp Exercise Training. J. Am Coll Cardiol. 2001; 37:392-7.
52. Malgorzata Michalczyk, Barbara Klapcinska, Ewa Sadowska-Kr^pa, Slawomir Jagsz, Wieslaw Pilis, Izabela Szoltysek - Boldys, Jan Chmura, Elzbieta Kimsa, Katarzyna Kempa (2008). Evaluation of the Blood Antioxidant Capacity in Two Selected Phases of the Training Cycle in Professional Soccer Players. Journal of Human Kinetics volume 19, 93-108. Editorial Committee of Journal of Human Kinetics.
53. Mastaloudis Angela (2004). «Vitamin E and exercise». The Linus Pauling Institute, Oregon State University.
54. Mayhew J.L., Piper F.C., Holmes J.A. (1981). Prediction of body density, fat weight and lean body mass in male athletes. J. Sports Med. Phys. Fitness. 21(4): p.383-9.
55. Miguel Arturo Salazar Vazquez, Beatriz Yadira Salazar Vazquez, M Intaglietta, Pedro Cabrales (2009). Nonobese, exercising children diagnosed with dyslipidemia have normal C -reactive proteinVasc Health Risk Manag. 2009; 5: 65-72.
56. Moldoveanu A.I., Shephard R.J., Shek P.N. (2001). The cytokine response yo physical activity and training. Sports Med. 2001; 31:115-44.
57. Murray C. J., Lopez, A.D. (1997). Global mortality, disability and the contribution of risk factors: Global Burden of Disease Study. Lancet 349, 1436-1442.
58. Myers J., Prakash M., Froilicher V., Do D., Partington S., Atwood J.E. (2002). Exersice capacity and mortality among men referred for exersice testing. N Engl. J. Med. 2002; 346:793-801.
59. Nicklas B.J., You T., Pahor M. (2005). Behavioural treatments for chronic systemic inflammation : effects of dietary weight loss and exercise training. CMAJ 2005; 172: 1199-209.
60. Okita K., Nishijima H., Murakami T. (2004). Can exercise training with weight loss lower serum C-reactive protein levels? Arteriosclerosis, thrombosis and vascular biology 2004; 24:1868-
73.
61. Osganian Stavroula K., Meir J Stampfer, Eric Rimm, Donna Spiegelman, Frank B. Hu, Jo Ann, E. Manson, Walter C., Willet (2003). Vitamin C and risk of coronary heart disease in woman. Journal of the American College of Cardiology 42(2): 246-252.
62. Paffenbarger R.S., Jr. Blair S., Lee M.I. (2001). A history of physical activity, cardiovascular health and longevity: the scientific contributions of Jeremy N Morris, Dsc, DPH, FRCP. Int. J. Epidemiology 2001; 30:1184-1192.
63. Pedersen B.K., Febbraio M. (2005). Muscle - derived interleukin - 6 - a possible link between skeletal muscle, adipose tissue, liver, and brain. Brain, behavior and immunity 2005; 19; 371-6.
64. Pitsavos Ch., Chrisohoou Ch., Panagiotakos D, Skoumas J., Zeimbekis A., Kokkinos P., Stefanidis Ch., Toutouzas P. (2003). Association of leisure-time physical activity on inflammation markers (c-reactive protein, white cell blood count, serum amyloid A, and fibrinogen) in healthy subjects (from the Attica study). Am J. Cardiol. 2003; 91:368-370.
65. Plaisance E. P., Grandjean P.W. (2006). Physical activity and high-sensitivity C-reactive protein. Sports Med. 36, 443-458.
66. Plaisance E. P., Grandjean P. W. (2006). Physical activity and high-sensitivity C-reactive protein. Sports Med. 36, 443-458.
67. Possengren A., Wilhelmsen L. (1997). Phisical activity levels and risk coronary death an death from all causes in middle - aged men. Evidence from a 20-year follow up of the primary prevention study in Goeteborg. Ann Epidemiol. 1997; 69-75.
68. Rawson E.S., Freedson P.S., Osganian S.K., Mathews C.E., Reed G., Ockene I.S. (2003). Body mass index, but not physical activity, is associated with C-reactive protein. Med Sci Sports Exerc. 2003; 35:1160-6.
69. Ridker P. M. (2001). High-sensitivity C-reactive protein: potential adjunct for global risk assessment in the primary prevention of cardiovascular disease. Circulation 103, 1813-1818.
70. Ross R. (1999). Atherosclerosis is an inflammatory disease. American heart journal 1999; 138: S 419 -20.
71. Rubel C., Fernadez G.C., Dran G., Bompadre M.B., Isturiz M.A., Palermo M.S. (2001). Fibrinogen promotes neutrophil activation and delayw apopotosis. J. Immunol. 2001; 166:2002-10.
72. Schachinger V., Zeiher A.M. (2000). Atherisclerosis - associated endothelial dysfunction. Zeitschrift fur Kardiologie 2000; 89 Suppl. 9: IX/70- 4.
73. Schneider D.J., Taatjes D.J., Howard D.B., Sobel B.E. (1999). Increased reactivity of platelets induced by fibrinogen independent of its binding to the Iib - IIIa surface glycoprotein: a potential contributor to cardiovascular risk. Journal of the American College of Cardiology 1999; 33:261-6.
74. Seki K., Sumino H., Nara M., Ishiyama N., Nishimo M., Muracami M. (2006). Realationships between blood rheology and age, body mass index, blood cell count, fibginogen and lipids in healthy subjects. Clinical hemorheology and microcirculation 2006; 34:401-
10.
75. Suzuki T., Yamauchi K., Yamada Y., Furumichi T., Furni H., Tsuzuki J., Hayashi H., Sotobata I., Saito H. (1992). Blood coaguability and fibrinolytic activity before and after physical training during the recovery phase of acute myocardial infarction. Clin. Cardiol. 1992; 15:358-364.
76. Thomas N.E., Baker J.S., Davies B. (2003). Established and Recently Identified Coronary Heart Disease Risk Factors in Young People: The Influence of Physical Activity and Physical Fitness Sports Medicine, Volume 33, Number 9, 2003, pp. 633-650 (18).
77. Thomas N.E., Williams D.R. (2008). Inflammatory factors, physical activity and physical fitness in young people. Scand J. Med. Sci Sports. 18(5): 543-56.
78. Tokmakidis S., Volaklis K. (2008). Exercise as a therapeutic agent in patients with coronary artery disease. Pashalidis Publications, Athens.
79. Toutouzas P., Volaklis K., Panagiotidou A., Lalos S., Tokmakidis S. (2002). Exercise as a means of treatment in patients with coronary artery disease. Heart and Vessels 2002, 4:313 -327.
80. Trepels T., Zeiher A.M., Fichtlscherer S. (2006). The endothelium and inflammation. Endothelium 2006; 13:423-9.
81. Twisk J, Kemper H.C.G., Van Mechelen W. (2001). Clustering of risk factors for coronary heart disease the longitudinal relationship with life style. Ann Epidemiol 11:157-165.
82. Urso M.L., Clarson P.M. (2003). Oxidative stress, exercise and antioxidant supplementation. Toxicology 189, 41-54.
83. Valko M., Izakovic M., Mazur M., Rhodes C.J., Telser J. (2004). Role of oxygen radicals in DNA damage and cancer incidence. Molecular and Cellular Biochemistry Volume 266, Numbers 1-2, 37-56.
84. Valko M., Leibfritz D., Moncol J., Cronin M., Mazur M., Telser J. (2007). Free radicals and antioxidants in normal physiological functions. The International Journal of Biochemistry & Cell Biology, Volume 39, Issue 1, 2007, Pages 44-84.
85. Wang J.S., Jen C.J., Kung H.C., Lin L.J., Hsiue T.R., Chen H.I. (1994). Different effects of strenuous exercise and moderate exercise on platelet function in men. Circulation 1994; 90: 2877-85.
86. Wannamethee S.G., Shaper A.G., Walker M. (1998). Changes in physical activity, mortality and incidence of coronary heart disease in older men. Lancet 1998; 351:1603-1608.
87. Witztum J.L., Horkko S. (1997). The role of oxidized LDL in
atherogenesis: Immunological response and antiphospholipid
antibodies.
88. Zergeroglu Murat A., Ficicilar Hakan, Erdogan Ali, Ozdemir Semir, Tekin Demet, Ersoz Gulriz (2005). Science in Sports & Exercise: Volume 37 (5), Supplement, May 2005, p. S30.
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