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The aim was to investigate the long-term effects of metformin ingestion on high-intensity interval training on performance, glycogen concentration (GC), GLUT-4 content, and metabolomics outcomes in rats. Fifty male Wistar rats were randomly divided into baseline, metformin (500 mg daily), and control groups. Training consisted of 4 sets of 10 jumps with 30 s of passive recovery per day, 5 days/week for 8 weeks. The intensity equivalent was 50% of body mass (BM) in the first four weeks and 70% of BM in the last four weeks. The animals were submitted to a weekly jump test until exhaustion at 50% of BM. Serum and tissues were collected at baseline and after 4 and 8 weeks for biochemical and metabolomics analysis. The number of jumps increased in the Control group without a significant difference between groups at 4 and 8 weeks. GLUT4 was lower in the gastrocnemius muscle in the Metformin at the fourth week compared to Control (P=0.03) and compared to Metformin (P=0.02) and Control (P=0.01) at eight weeks. Hepatic and soleus GC were not altered by metformin. Gastrocnemius GC was lower after 8 weeks in the Metformin group compared to Control (P=0.01). Significantly lower levels of pyruvate and phenylalanine and higher levels of ethanol, formate, betaine, very low-density lipoprotein, low-density lipoprotein, and creatine were found in the Metformin compared to the Control. Although chronic administration of metformin decreased food intake and negatively influenced the synthesis of muscle glycogen, it did not significantly change physical performance compared to the Control.

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The aim was to investigate the long-term effects of metformin ingestion on high-intensity interval training on performance, glycogen concentration (GC), GLUT-4 content, and metabolomics outcomes in rats. Fifty male Wistar rats were randomly divided into baseline, metformin (500 mg daily), and control groups. Training consisted of 4 sets of 10 jumps with 30 s of passive recovery per day, 5 days/week for 8 weeks. The intensity equivalent was 50% of body mass (BM) in the first four weeks and 70% of BM in the last four weeks. The animals were submitted to a weekly jump test until exhaustion at 50% of BM. Serum and tissues were collected at baseline and after 4 and 8 weeks for biochemical and metabolomics analysis. The number of jumps increased in the Control group without a significant difference between groups at 4 and 8 weeks. GLUT4 was lower in the gastrocnemius muscle in the Metformin at the fourth week compared to Control (P=0.03) and compared to Metformin (P=0.02) and Control (P=0.01) at eight weeks. Hepatic and soleus GC were not altered by metformin. Gastrocnemius GC was lower after 8 weeks in the Metformin group compared to Control (P=0.01). Significantly lower levels of pyruvate and phenylalanine and higher levels of ethanol, formate, betaine, very low-density lipoprotein, low-density lipoprotein, and creatine were found in the Metformin compared to the Control. Although chronic administration of metformin decreased food intake and negatively influenced the synthesis of muscle glycogen, it did not significantly change physical performance compared to the Control.

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AIMS: The synthesis of monocarboxylate transporters (MCTs) can be stimulated by aerobic training, but few is known about this effect associated or not with non-voluntary daily activities. We examined the effect of eight weeks of aerobic training in MCTs on the skeletal muscle and hypothalamus of less or more physically active mice, which can be achieved by keeping them in two different housing models, a small cage (SC) and a large cage (LC). MAIN METHODS: Forty male C57BL/6J mice were divided into four groups. In each housing condition, mice were divided into untrained (N) and trained (T). For 8 weeks, the trained animals ran on a treadmill with an intensity equivalent to 80 % of the individual critical velocity (CV), considered aerobic capacity, 40 min/day, 5 times/week. Protein expression of MCTs was determined with fluorescence Western Blot. KEY FINDINGS: T groups had higher hypothalamic MCT2 than N groups (ANOVA, P = 0.032). Significant correlations were detected between hypothalamic MCT2 and CV. There was a difference between the SC and LC groups in relation to MCT4 in the hypothalamus (LC > SC, P = 0.044). Trained mice housed in LC (but not SC-T) exhibited a reduction in MCT4 muscle (P < 0.001). SIGNIFICANCE: Our findings indicate that aerobically trained mice increased the expression of MCT2 protein in the hypothalamus, which has been related to the uptake of lactate in neurons. Changes in energy metabolism in physically active mice (kept in LC) may be related to upregulation of hypothalamic MCT4, probably participating in the regulation of satiety.

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This study tested the ergogenic effects of acute administration of melatonin on exhaustive exercise (tlim) at the anaerobic threshold intensity (iAnT) during periods of lower (L) and higher (H) spontaneous physical activity in swimming rats. Additionally, we evaluated the time of day effect on aerobic exercise tolerance. The periods of L and H were determined gravimetrically. All animals were subjected to an incremental test to determine the iAnT. Melatonin was administered (10 mg.kg(-1), intraperitoneal) and after 30 min, the rats were subjected to tlim during the L (LM) or H (HM) period. Control groups were called LC and HC. The criterion of significance was 5%. Melatonin enhanced tlim by 169% during H (HC=72 min; HM=194 min; P<0.01; ES=1.23) and by 90% during L (LC=31 min vs. LM=59 min; P=0.39; ES=1.18), demonstrating a significant effect on tlim (F=10.35; P<0.01) and a strong effect size (ES). Additionally, tlim was higher during H (F=14.24; P<0.01). Melatonin is a reasonable ergogenic aid, particularly during the wakefulness period, and the exercise tolerance is dependent on the time of day for swimming rats.

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UNLABELLED: We investigated the exercise and different environmental luminosities effects on blood platelets count in order to identify primary and secondary thrombocytosis, respectively. BACKGROUND: Platelets alteration has been associated with important pathological events, such as neurodegenerative diseases, and the count of these cells in bloodstream is influenced by several effects, including physical and chemical. Owing the difficulty to study the aetiology of thrombocytosis in human models, we employed acute and chronic free drug interventions in order to identify these two types of this important disease in laboratory animals. METHODS: Forty rats were exposed to standard (SI) or experimental (EI) illumination from 45 days-old. Both groups were exposed to 12 h daylight (2700 K; 565-590 nm; < 60 lux; from 06:00 h to 18:00 h). During dark period SI animals were kept in total darkness while EI remained under red light (> 600 nm, < 15 lux). At 92 days-old, exercised animals were submitted to an acute bout of swimming at individualized intensity and control animals remained at rest. RESULTS: Blood samples were collected immediately after the exercise for platelets count, which were among 849000 ± 115817 and 1085600 ± 177089/mm³ of blood. Exercise (F = 6.91; p = 0.01) and EI (F = 6.66; p = 0.01) increased platelets count, showing no interaction between effects (F = 0.01; p = 0.89). CONCLUSION: Primary thrombocytosis was detected owing an acute exercise and the secondary thrombocytosis due to the constant red light during dark period, without any pharmacological interventions and strongly respecting the ethical aspects, enabling future studies on aetiology of thrombocytosis through this model (Fig. 2, Ref. 35).

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