Associations of body composition with physical activity, nutritional intake status, and chronotype among female university students in Japan.

BACKGROUND: Having higher muscle mass in early adulthood is an important factor in preventing sarcopenia. However, university students undergo lifestyle changes compared to their high school years, which may lead to changes in body composition, such as an increase in body fat and a decrease in muscle mass. The study aimed to investigate the association between body composition and lifestyle behaviors, including chronotype, among Japanese female university students, due to the prevalence of underweight among young females in the country. METHODS: The physical activity level (PAL), daily dietary intake status, morningness-eveningness questionnaire (MEQ) score, and body composition of 230 students were assessed in this cross-sectional study. Body composition was measured using a multifrequency bioelectrical impedance analyzer, and body mass index (BMI), body fat percentage (%BF), and skeletal muscle mass index (SMI) were determined. RESULTS: Individuals who were evening type (ET) had a higher %BF and lower SMI than those who were non-ET, but no differences in body weight or BMI were found. Although ET individuals had lower total energy intake, protein intake, and PALs than non-ETs, the differences were small. However, multiple regression analyses showed that SMI was significantly positively associated with MEQ and PAL, and %BF was significantly negatively associated with MEQ and PAL. CONCLUSION: These results suggest that female university students with lateness of chronotype and low physical activity have a body composition imbalance resulting in higher body fat and lower muscle mass. Therefore, young females may need to take chronotype-specific measures (especially ET individuals) to help them maintain an appropriate body composition.

Effects of Nutrient Intake Timing on Post-Exercise Glycogen Accumulation and its Related Signaling Pathways in Mouse Skeletal Muscle.

We investigated the effects of nutrient intake timing on glycogen accumulation and its related signals in skeletal muscle after an exercise that did not induce large glycogen depletion. Male ICR mice ran on a treadmill at 25 m/min for 60 min under a fed condition. Mice were orally administered a solution containing 1.2 mg/g carbohydrate and 0.4 mg/g protein or water either immediately (early nutrient, EN) or 180 min (late nutrient, LN) after the exercise. Tissues were harvested at 30 min after the oral administration. No significant difference in blood glucose or plasma insulin concentrations was found between the EN and LN groups. The plantaris muscle glycogen concentration was significantly (p < 0.05) higher in the EN group-but not in the LN group-compared to the respective time-matched control group. Akt Ser473 phosphorylation was significantly higher in the EN group than in the time-matched control group (p < 0.01), while LN had no effect. Positive main effects of time were found for the phosphorylations in Akt substrate of 160 kDa (AS160) Thr642 (p < 0.05), 5'-AMP-activated protein kinase (AMPK) Thr172 (p < 0.01), and acetyl-CoA carboxylase Ser79 (p < 0.01); however, no effect of nutrient intake was found for these. We showed that delayed nutrient intake could not increase muscle glycogen after endurance exercise which did not induce large glycogen depletion. The results also suggest that post-exercise muscle glycogen accumulation after nutrient intake might be partly influenced by Akt activation. Meanwhile, increased AS160 and AMPK activation by post-exercise fasting might not lead to glycogen accumulation.

Effects of ß-hydroxybutyrate treatment on glycogen repletion and its related signaling cascades in epitrochlearis muscle during 120 min of postexercise recovery.

We investigated the effects of ß-hydroxybutyrate (ß-HB), the most abundant type of ketone body in mammals, on postexercise glycogen recovery in skeletal muscle by using an in vitro experimental model. Male ICR mice swam for 60 min and then their epitrochlearis muscles were removed and incubated with either physiological levels of glucose (8 mmol/L) and insulin (60 µU/mL) or glucose and insulin plus 1, 2, or 4 mmol/L of sodium ß-HB. Four millimoles per liter ß-HB had a significant positive effect on glycogen repletion in epitrochlearis muscle at 120 min after exercise (p < 0.01), while 2 mmol/L of ß-HB showed a tendency to increase the glycogen level (p < 0.09), and 1 mmol/L of ß-HB had no significant effect. We further investigated the effect of 4 mmol/L ß-HB treatment on the signaling cascade related to glycogen repletion in the epitrochlearis muscles throughout a 120-min recovery period. After incubating the muscles in 4 mmol/L of ß-HB for 15 min postexercise, the Akt substrate of 160 kDa Thr642 (p < 0.05) and Akt Thr308 (p < 0.05) phosphorylations were significantly increased compared with the control treatment. At the same time point, 5'-AMP-activated protein kinase and acetyl-coenzyme A carboxylase phosphorylations were significantly lower (p < 0.05) in the epitrochlearis muscle incubated with 4 mmol/L of ß-HB than in the control muscle. Our results demonstrate that postexercise 4 mmol/L ß-HB administration enhanced glycogen repletion in epitrochlearis muscle. Four millimoles per liter ß-HB treatment was associated with alternation of the phosphorylated status of several proteins involved in glucose uptake and metabolic/energy homeostasis at the early stage of postexercise.

Effects of Royal Jelly Administration on Endurance Training-Induced Mitochondrial Adaptations in Skeletal Muscle.

We investigated the effect of royal jelly (RJ), a natural secretion from worker bees, on the endurance training-induced mitochondrial adaptations in skeletal muscles of ICR mice. Mice received either RJ (1.0 mg/g body weight) or distilled water for three weeks. The mice in the training group were subjected to endurance training (20 m/min; 60 min; 5 times/week). There was a main effect of endurance training on the maximal activities of the mitochondrial enzymes, citrate synthase (CS), and ß-hydroxyacyl coenzyme Adehydrogenase (ß-HAD), in the plantaris and tibialis anterior (TA) muscles, while no effect of RJ treatment was observed. In the soleus muscle, CS and ß-HAD maximal activities were significantly increased by endurance training in the RJ-treated group, while there was no effect of training in the control group. Furthermore, we investigated the effects of acute RJ treatment on the signaling cascade involved in mitochondrial biogenesis. In the soleus, phosphorylation of 5'-AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) were additively increased by a single RJ treatment and endurance exercise, while only an exercise effect was found in the plantaris and TA muscles. These results indicate that the RJ treatment induced mitochondrial adaptation with endurance training by AMPK activation in the soleus muscles of ICR mice.