Dietary Intake and Energy Expenditure During Two Different Phases of Athletic Training in Female Collegiate Lacrosse Players.

Kumahara, H, Ohta, C, Nabeshima, E, Nakayama, A, Mine, S, and Yamato, T. Dietary intake and energy expenditure during two different phases of athletic training in female collegiate lacrosse players. J Strength Cond Res 34(6): 1547-1554, 2020-This study aims to investigate the state of nutrient intake and energy expenditure (EE) among various phases of periodization in female collegiate lacrosse players. A total of 17 Japanese female collegiate lacrosse players (age: 20.0 ± 0.9 years) were enrolled in this study. Physical activity (PA) and dietary intake were assessed over each 1-week period during the training preparatory phase (P-phase) and transition phase (T-phase). The exercise training-related EE (EEE) and EE associated with other daily living activities (i.e., nonexercise activity thermogenesis [NEAT]), were measured using accelerometers and heart rate (HR) monitoring using the flex-HR method. The total daily EE during the P-phase was significantly higher than that of the T-phase (2,168 ± 248 vs. 1744 ± 138 kcal·d; p < 0.01); however, no significant differences were observed in the total energy intake. Moreover, EEE during the P-phase was significantly higher than that of the T-phase, whereas no significant difference was found in NEAT. Furthermore, no significant differences were noted in any macronutrient intake variable observed between the 2 phases (protein:fat:carbohydrate ratio: 12.6 ± 1.5:32.9 ± 3.9:54.1 ± 5.1% in the P-phase vs. 12.1 ± 1.7:30.7 ± 3.9:55.7 ± 5.2% in the T-phase). The carbohydrate and protein intake were below recommended levels during the P-phase. Conversely, the saturated fatty acid ratio was higher than the dietary goals for disease prevention. Based on the changes in the PA volume observed during different training phases, female collegiate lacrosse players did not attain optimal nutrient intake required for optimal athletic performance and health.

High saturated fatty acid intake induces insulin secretion by elevating gastric inhibitory polypeptide levels in healthy individuals.

Insulin resistance is central to the etiology of the metabolic syndrome cluster of diseases. Evidence suggests that a high-fat diet is associated with insulin resistance, which may be modulated by dietary fatty acid composition. We hypothesized that high saturated fatty acid intake increases insulin and gastric inhibitory polypeptide (GIP) secretion. To clarify the effect of ingested fatty acid composition on glucose levels, we conducted an intervention study to investigate the insulin and plasma GIP responses in 11 healthy women, including a dietary control. Subjects were provided daily control meals (F-20; saturated fatty acids/monounsaturated fatty acids/polyunsaturated fatty acids [S/M/P] ratio, 3:4:3) with 20 energy (E) % fat, followed by 2 isoenergetic experimental meals for 7 days each. These meals comprised 60 E% carbohydrate, 15 E% protein, and 30 E% fat (FB-30; high saturated fatty acid meal; S/M/P, 5:4:1; F-30: reduced saturated fatty acid meal; S/M/P, 3:4:3). On the second day of the F-20 and the last day of F-30 and FB-30, blood samples were taken before and 30, 60, and 120 minutes after a meal tolerance test. The plasma glucose responses did not differ between F-20 and FB-30 or F-30. However, insulin levels were higher after the FB-30 than after the F-20 (P < .01). The GIP response after the FB-30 was higher than that after the F-30 (P < .05). In addition, the difference in the incremental GIP between FB-30 and F-30 correlated significantly and positively with that of the insulin. These results suggest that a high saturated fatty acid content stimulates postprandial insulin release via increased GIP secretion.

Diabetes modulates ethanol-induced increase in serotonin release from rat hippocampus: an in vivo microdialysis study.

We examined whether diabetes mellitus (DM) affects the acute ethanol (EtOH)-induced increase in serotonin (5-HT) release from the rat hippocampus, and compared the findings with those obtained from non-DM rats. Hippocampal 5-HT was measured by using in vivo microdialysis. Rats were rendered diabetic by an injection of streptozotocin (STZ). EtOH (0.5, 1.0, or 2.0 g/kg) was intraperitoneally administered or EtOH (25, 50, 100, or 200 mM) was given by intracerebral infusion. EtOH enhanced the extracellular 5-HT levels in both non-DM and DM rats in a dose-dependent manner, especially in non-DM rats, irrespective of administration route. Among three kinds of alcohols tested at same concentration (100 mM), methanol was the most effective in increasing extracellular 5-HT levels of non-DM rats; then, in descending order, EtOH and isopropanol. However, no such tendency was observed in DM rats. Experiments using various antagonists and agonists of 5-HT receptors showed that the functions of 5-HT(1B), 5-HT(2), 5-HT(3), and/or 5-HT(4) receptors in the hippocampus of DM rats differ from those in non-DM rats, suggesting that DM induces dysfunction of central neurotransmitter systems including 5-HT receptors. Acetaldehyde (100 mM), a major metabolite of EtOH, also significantly increased 5-HT release in both non-DM and DM rats. Based on the results that EtOH could increase the 5-HT in non-DM rats than in DM rats while acetaldehyde worked on both rats, it is more likely that alcohol dehydrogenase 1B activity was decreased in DM rats. The present study is the first, to our knowledge, to show that DM modulated the EtOH-induced 5-HT release from the hippocampus in type-1 diabetic rats.

Effects of ion channel blockers on basal hippocampal monoamine levels in freely moving diabetic and non-diabetic rats.

This study characterized the ion channel activities in the hippocampus of diabetic rats by monitoring the levels of monoamines. Extracellular levels of serotonin and dopamine were measured in the hippocampus of awake, freely moving streptozotocin-induced diabetic rats, spontaneously diabetic rats, and non-diabetic rats, using in vivo microdialysis. Sodium, calcium, and potassium ion channel blockers were used to assess the ion channel activities. The results suggest that there are no abnormalities in the ion channels of diabetic brain, but the reduced levels of monoamines could be due to any problems of reuptake, release, and rate of breakdown of these molecules.

Simultaneous measurement of nitric oxide, blood glucose, and monoamines in the hippocampus of diabetic rat: an in vivo microdialysis study.

The present study was undertaken to examine the relationships among the levels of nitric oxide (NO), monoamines, and blood glucose in the diabetic hippocampus. The levels of NO and monoamines (serotonin, 5-hydroxytryptamine [5-HT] and dopamine [DA]) were simultaneously measured in several experiments, using in vivo microdialysis techniques. We used both experimentally and spontaneously diabetic rats as the diabetic animal model, and compared the findings with those obtained from non-diabetic rats. The effects of the changed level of blood glucose due to insulin administration on the levels of NO, 5-HT, and DA were assessed. Total NO metabolite levels (NOx) were calculated as the sum of nitrite (NO2-) and nitrate (NO3-) levels. The results in the present study showed that: (1) the plasma levels of NOx in both diabetic rats were low compared to those in control rats, (2) the hippocampal NOx levels in both diabetic rats were almost the same as those in control rats, while the levels of 5-HT and DA were low in the diabetics, and (3) a sudden decrease in the plasma glucose level due to insulin administration reduced the NOx level as well as enhanced the 5-HT level in the diabetic hippocampus, a finding consistent with the results of 7 days administration of insulin. Taken together, these findings suggest that changes in the plasma glucose level cause, at least in part, the changes in the levels of NOx and monoamines in the diabetic brain.

Modulation of the stress response by coffee: an in vivo microdialysis study of hippocampal serotonin and dopamine levels in rat.

We studied whether coffee and its components (caffeine and chlorogenic acid) have stress-relaxing effects. In vivo brain microdialysis was used to characterize the effects of coffee, stress, and their interaction on the serotonergic and dopaminergic systems in the rat hippocampus. Restraint stress for 100 min caused a marked increase in dopamine and serotonin (5-HT) levels in the hippocampus, and then, 100 min resting (freely-moving) time reduced them to basal levels. Pretreatment with 33 mg/kg coffee or 1.7 mg/kg caffeine reduced the second restraint-induced increase in the neurotransmitters, especially 5-HT, but neither saline nor 1.7 mg/kg chlorogenic acid did. These results suggest that coffee contributes to the reduction of restraint-induced stress and that these effects could be due to caffeine. Possible mechanisms of the effects are considered.