An activity deficit hypothesis was posited that children with movement difficulties are less physically active during recess than age- and gender-matched controls without movement difficulties. Criteria used in identifying children with movement difficulties were (a) a score of at least 4 on the Test of Motor Impairment, (b) regular physical education student, and (c) age 80 to 109 months. An observational study was conducted over a 2-month period in recess settings with 52 subjects. Findings revealed that during recess time, children with movement difficulties were vigorously active less often, played less often with large playground equipment, were not observable for significantly more time, and spent less time in positive social interactions with others of their own gender. Accordingly, it was concluded that the data support the activity deficit hypothesis.
Marcel Bouffard, E. Jane Watkinson, Linda P. Thompson, Janice L. Causgrove Dunn and Sandy K.E. Romanow
Joshua Lowndes, Robert F. Zoeller, George A. Kyriazis, Mary P. Miles, Richard L. Seip, Niall M. Moyna, Paul S. Visich, Linda S. Pescatello, Paul M. Gordon, Paul D. Thompson and Theodore J. Angelopoulos
The purpose of this study was to examine whether leptin levels affect the response of leptin to exercise training (ET) and whether this is also affected by C-reactive protein (CRP) or the three common Apolipoprotein E genotypes (APOE). Ninety-seven (male = 45, female = 52) sedentary individuals underwent 6 months of supervised ET. Blood was sampled before the initiation of ET, and again 24 and 72 hr after completion of the final training session. ET resulted in a small reduction in body mass (80.47 ± 18.03 vs 79.42 ± 17.34 kg, p < .01). Leptin was reduced 24 hr after the final exercise session (p < .01), but returned to normal after 72 hr (p > .05)—Pre: 13.51 ± 12.27, 24hr: 12.14 ± 12.34, 72hr: 12.98 ± 11.40 ng/ml. The most hyperleptinemic individuals had a greater initial response, which was sustained through to 72 hr after the final session in the pooled study population (p < .01), and in both males (p < .05) and females (p < .05) separately. CRP was related to leptin independently of body weight and positively related to the reductions in leptin. APOE genotype was not related to leptin levels and did not affect the response to ET. Leptin levels may only be reduced by ET in those with hyperleptinemia. In addition, both the initial extent of hyperleptinemia and the subsequent reduction in leptin may be related to low grade chronic systemic inflammation.