The metabolic syndrome has become a major public health challenge world-wide and, at least in the industrialized world, the prevalence of the metabolic syndrome is increasing. There is evidence to show that biological and lifestyle risk factors for metabolic syndrome are present in adolescence, which suggests that the antecedents of the disease may lie in early life. The period of adolescence is characterized by a decline in physical activity (PA; lack of PA is a lifestyle risk factor for metabolic syndrome) and an increase in fat mass deposition (a biological risk factor for metabolic syndrome). Therefore, investigating how the development of these two variables relates to adult cardiometabolic risk is important to fuel early intervention. A factor which has the potential to influence these two risk factors, and thus ultimately the metabolic syndrome, is the timing of biological maturity (i.e. whether an individual is early, average or late maturing when compared to peers of the same age). The influence of biological maturity has largely been overlooked in previous research; therefore, the general objective of this thesis was to investigate the associations between biological maturity, adolescent PA and fat mass development, and young adult cardiometabolic risk. Three studies were necessary to realize this objective, and together help to elucidate the role of biological maturity in the adolescent decline in physical activity, fat development, and the development of adult metabolic syndrome. Ultimately, this information will aid in the development and implementation of interventions to decrease prevalence of metabolic syndrome.<p>
Study 1: The purpose of study 1 was to investigate whether observed gender differences in objectively measured PA in children (8 to 13 years) are confounded by biological maturity differences. Methods: Four hundred and one children (194 boys and 207 girls) volunteered for this study. An Actigraph accelerometer was used to obtain 7 consecutive days of minute-by-minute PA data on each participant. Minutes of moderate to vigorous PA per day (MVPA), continuous minutes of MVPA per day (CMVPA), and minutes of vigorous PA per day (VPA) were derived from the accelerometer data. Age at peak height velocity (APHV), an indicator of somatic maturity, was predicted and individuals aligned by this biological age (years from APHV). Gender differences in the PA variables were analyzed using a two-way (gender X age) ANOVA. Results: Levels of PA decreased with increasing chronological ages in both genders (p<0.05). When aligned on chronological age, boys had a higher MVPA at 10 through 13 years, a higher CMVPA at 9 through 12 years, and a higher VPA at 9 though 13 years (p<0.05). When aligned on biological age, PA declined with increasing maturity (p<0.05); however gender differences between biological age groups disappeared. Conclusion: The observed age-related decline in adolescent boys and girls PA is antithetical to public health goals and as such is an important area of research. In order to fully understand gender disparities in PA, consideration must be given to the confounding effects of biological maturity.<p>
Study 2: Understanding the influence of biological age (BA) on the decline in PA would better inform researchers about the effective timing of intervention. The purpose of study 2 was to describe the PA levels and perceived barriers to PA of adolescent girls grouped by school grade and biological maturity status (i.e., early or late maturing) within grades. Methods: 221 girls (aged 8-16 years; grades 4-10) wore an Actical accelerometer for 7 days and then completed a semi-structured, open ended questionnaire on perceived barriers to PA over the 7 day period. Predicted APHV and recalled age at menarche were used to assess maturity among the elementary and high school girls, respectively. Maturity and grade group differences in PA were assessed using MANCOVA and independent sample t-test, and barriers to PA using chi squared statistics. Results: Daily minutes spent in MVPA decreased by 40% between grades 4 to 10. Within grade groupings, no differences in PA were found between early and late maturing girls (p>0.05). Grades 4-6 participants cited more interpersonal (i.e., social) barriers. Grades 9-10 participants cited more institutional barriers to PA, primarily revolving around the institution of school. No differences were found in types of barriers reported between early and late maturing girls. Conclusion: Since PA and types of perceived barriers to PA were dependent on grade, future research should work to identify the most salient (i.e., frequent and limiting) barriers to PA by chronological age in youth.<p>
Study 3: Although the metabolic syndrome is thought to be mainly a consequence of obesity, the mechanisms underpinning its development are not that well understood. The purpose of study 3 was to examine total body fat mass (FM), trunk FM and PA developmental trajectories (aligned to BA; years from APHV) of individuals categorized as low and high for cardiometabolic risk at 26 years, while investigating biological and lifestyle risk factors. Methods: The sample were 55 males and 76 females from the Saskatchewan Pediatric Bone Mineral Accrual Study (1991-2007) who were assessed from childhood to young adulthood and had a measure of cardiometabolic risk at young adulthood (26.0 + 2.3 yrs). Height was measured biannually. Total body FM and trunk FM was assessed annually by dual energy-X-ray absorptiometry. PA and dietary intake was evaluated two to three times annually using surveys. Individuals were grouped into maturity status groups (early, average or late) depending on their APHV. Two composite cardiometabolic risk scores were calculated for males and females separately. The first was derived for a sub-sample (N=48) by summing the standardized residuals of inverted high-density lipoprotein cholesterol, homeostasis model assessment for insulin resistance, mean arterial pressure (MAP) and fasting triglyceride levels. A second score was derived for the whole sample by summing the standardized residuals for MAP. Scores for both samples were regressed on to age and adult smoking status. High and low cardiometabolic risk groups were determined based on a sex- specific median split of risk scores. Data were analyzed using random effects models. Models were built in a stepwise procedure with predictor variables added one at a time, using the log likelihood ratio statistic to determine if one model was a significant improvement over the previous one. Results: The final model indicated that once the independent effects of maturity (years from APHV) and height were controlled, the high risk group males and females had significantly (p<0.05) greater total body FM and trunk FM development at all ages. No association was found between young adult cardiometabolic risk and development of PA. Furthermore, in general, timing of biological maturity was not associated with development of PA or FM. Conclusion: Young adults at higher cardiometabolic risk have greater body fat as early as 8 years of age, which lends support to early intervention.<p>
General Conclusions: Adolescence has been highlighted as a critical period for the development of adult disease, such as the metabolic syndrome. Results from this thesis support this contention by showing a decrease in PA (by both chronological and biological age) in males and females across adolescence. It further showed that an increase in total and central fatness during adolescence may be critical for the development of the metabolic syndrome in adulthood. Timing of biological maturity, in general, was not shown to have an independent impact on adolescent or young adult PA, adolescent perceived barriers to PA, fat mass development, or young adult cardiometabolic risk. However, further research is required before definitive conclusions can be made about the short and long term impacts of timing of biological maturity on health.
| Identifer | oai:union.ndltd.org:USASK/oai:usask.ca:etd-12052008-101132 |
| Date | 26 January 2009 |
| Creators | Sherar, Lauren B |
| Contributors | Muhajarine, Nazeem, Martin, Susanna, Faulkner, Robert A., Chilibeck, Philip D., Baxter-Jones, Adam D. G., Timmons, Brian |
| Publisher | University of Saskatchewan |
| Source Sets | University of Saskatchewan Library |
| Language | English |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | http://library.usask.ca/theses/available/etd-12052008-101132/ |
| Rights | restricted, I hereby certify that, if appropriate, I have obtained and attached hereto a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to University of Saskatchewan or its agents the non-exclusive license to archive and make accessible, under the conditions specified below, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report. |
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