Irisin is mainly released from skeletal muscle (myocytes) and promotes thermogenesis by browning of the white adipose tissue. Although exercise has been shown to increase irisin concentration in blood and myocytes via up-regulation peroxisome proliferator receptor γ coactivator-1α (PGC-1α) expression, the influence of exercise intensity on irisin secretion remains unclear. Therefore, we determined circulating irisin responses following a single bout of running at different intensities. Six sedentary males underwent treadmill running under two different conditions: a low-intensity (40% of V 4 O 2max ) exercise trial (LIE) or a high-intensity (80% of V 4 O 2max ) exercise trial (HIE). The exercises in LIE and HIE were lasted for 20 and 40 min, respectively. All subjects underwent the two trials on separate days, and a randomized cross-over design was used. Blood samples were collected before (Pre) and immediately after exercise, at 3, 6, and 19 h after exercise. Energy consumption during exercise did not significantly differ between the two trials. HIE significantly increased blood lactate and serum lactate dehydrogenase levels (P < 0.05). Compared with pre-exercise levels, the irisin concentrations were elevated at 6 h (18% increase) and 19 h (23% increase) after HIE, but significantly decreased after LIE. The relative irisin concentrations (compared with pre-exercise levels) were significantly greater in HIE than in LIE immediately after exercise, and at 6 and 19 h after exercise (P < 0.05). These findings suggest that irisin secretion after acute running exercise is affected by exercise intensity, independent of energy consumption.
in Koshu City, Japan, and their mothers. Maternal smoking during early pregnancy was the exposure studied. Main outcome measures: Childhood body mass index (BMI) and BMI z-score trajectories of the children born to the smoking and non-smoking mothers by gender. Multilevel analysis that includes both individual and age as different-level variables was used for statistical analyses. Results: The participating mothers delivered 1619 babies during the study period. Birth weight and anthropometric data were collected from 1603 (at birth, 99.0%), 1358 (at age 3, 83.9%), 1248 (at age 5, 77.1%), 1270 (at age 7-8, 78.4%) and 1274 (at age 9-10, 78.7%) of these children. The mean birth weight of both the male and female children whose mothers had smoked during pregnancy was significantly low compared with those born to non-smoking mothers (Po0.01). However, the childhood BMI at each subsequent checkup age significantly increased only among the male children born to the smoking mothers. Moreover, this increase was continuously observed after 3 years of age. The results of BMI z-score analysis were also similar to these of BMI analysis. Conclusions: Smoking by pregnant women decreases the infant birth weight irrespective of gender but increases childhood weight gain especially by male children. The results might be valuable to explore the mechanism of fetal programming.
BackgroundWe previously reported that a number of factors related to maternal lifestyle during early pregnancy, including smoking, are associated with childhood obesity at 5 years of age. In the present study, we investigated whether the association with maternal smoking persisted to the age of 9–10 years.MethodsThe study population comprised children born between April 1, 1991 and March 31, 1999, and their mothers. The dependent variables—childhood overweight and obesity at 5 and 9–10 years of age—were defined according to internationally acknowledged cut-off values. Maternal smoking during early pregnancy was used as the independent variable.ResultsMothers who completed a specifically designed questionnaire gave birth to a total of 1644 infants during the study period. Anthropometric data were collected from 1302 of these children during medical checkups at 9–10 years of age (follow-up rate: 79.2%). Maternal smoking during early pregnancy was associated with obesity in 9- to 10-year-old children (adjusted odds ratio, 1.91; 95% confidence interval, 1.03–3.53). However, the point estimates at the age of 9–10 years were considerably lower than those at the age of 5 years.ConclusionsOur results suggest that fetal environment, including exposure to maternal smoking, continues to be associated with childhood obesity at the age of 9–10 years.
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