Metformin improves performance in high-intensity exercise, but not anaerobic capacity in healthy male subjects.

The aim of this study was to determine the ergogenic effects of metformin in high-intensity exercise, as well as its effects on anaerobic capacity, in healthy and physically active men. Ten subjects (mean (± standard deviation) maximal oxygen uptake (V˙O2max ) 38.6 ± 4.5 mL/kg per min) performed the following tests in a cycle ergometer: (i) an incremental test; (ii) six submaximal constant workload tests at 40%-90% (V˙O2max ); and (iii) two supramaximal tests (110% (V˙O2max ). Metformin (500 mg) or placebo was ingested 60 min before the supramaximal test. There were no significant differences between the placebo and metformin groups in terms of maximum accumulated oxygen deficit (2.8 ± 0.6 vs 3.0 ± 0.8 L, respectively; P = 0.08), lactate concentrations (7.8 ± 2.6 vs 7.5 ± 3.0 mmol/L, respectively; P = 0.75) or O2 consumed in either the last 30 s of exercise (40.4 ± 4.4 vs 39.9 ± 4.0 mL/kg per min, respectively; P = 0.35) or the first 110 s of exercise (29.0 ± 2.5 vs 29.5 ± 3.0 mL/kg per min, respectively; P = 0.42). Time to exhaustion was significantly higher after metformin than placebo ingestion (191 ± 33 vs 167 ± 32 s, respectively; P = 0.001). The fast component of V˙O2 recovery was higher in the metformin than placebo group (12.71 vs 12.18 mL/kg per min, respectively; P = 0.025). Metformin improved performance and anaerobic alactic contribution during high-intensity exercise, but had no effect on overall anaerobic capacity in healthy subjects.

MCT1 and MCT4 kinetic of mRNA expression in different tissues after aerobic exercise at maximal lactate steady state workload.

We evaluate the mRNA expression of monocarboxylate transporters 1 and 4 (MCT1 and MCT4) in skeletal muscle (soleus, red and white gastrocnemius), heart and liver tissues in mice submitted to a single bout of swimming exercise at the maximal lactate steady state workload (MLSSw). After 72 h of MLSS test, the animals were submitted to a swimming exercise session for 25 min at individual MLSSw. Tissues and muscle samples were obtained at rest (control, n=5), immediately (n=5), 5 h (n=5) and 10 h (n=5) after exercise for determination of the MCT1 and MCT4 mRNA expression (RT-PCR). The MCT1 mRNA expression in liver increased after 10 h in relation to the control, immediate and 5 h groups, but the MCT4 remained unchanged. The MCT1 mRNA expression in heart increased by 31 % after 10 h when compared to immediate, but no differences were observed in relation to the control group. No significant differences were observed for red gastrocnemius in MCT1 and MCT4 mRNA expression. However, white gastrocnemius increased MCT1 mRNA expression immediately when compared to rest, 5 and 10 h test groups. In soleus muscle, the MCT1 mRNA expression increased immediately, 5 and 10 h after exercise when compared to the control. In relation to MCT4 mRNA expression, the soleus increased immediately and 10 h after acute exercise when compared to the control group. The soleus, liver and heart were the main tissues that showed improved the MCT1 mRNA expression, indicating its important role in controlling MLSS concentration in mice.

Interval versus continuous training with identical workload: physiological and aerobic capacity adaptations.

The interval model training has been more recommended to promote aerobic adaptations due to recovery period that enables the execution of elevated intensity and as consequence, higher workload in relation to continuous training. However, the physiological and aerobic capacity adaptations in interval training with identical workload to continuous are still uncertain. The purpose was to characterize the effects of chronic and acute biomarkers adaptations and aerobic capacity in interval and continuous protocols with equivalent load. Fifty Wistar rats were divided in three groups: Continuous training (GTC), interval training (GTI) and control (CG). The running training lasted 8 weeks (wk) and was based at Anaerobic Threshold (AT) velocity. GTI showed glycogen super-compensation (mg/100 mg) 48 h after training session in relation to CG and GTC (GTI red gastrocnemius (RG)=1.41+/-0.16; GTI white gastrocnemius (WG)=1.78+/-0.20; GTI soleus (S)=0.26+/-0.01; GTI liver (L)=2.72+/-0.36; GTC RG=0.42+/-0.17; GTC WG=0.54+/-0.22; GTC S=0.100+/-0.01; GTC L=1.12+/-0.24; CG RG=0.32+/-0.05; CG WG=0.65+/-0.17; CG S=0.14+/-0.01; CG L=2.28+/-0.33). The volume performed by GTI was higher than GTC. The aerobic capacity reduced 11 % after experimental period in GTC when compared to GTI, but this change was insignificant (19.6+/-5.4 m/min; 17.7+/-2.5 m/min, effect size = 0.59). Free fatty acids and glucose concentration did not show statistical differences among the groups. Corticosterone concentration increased in acute condition for GTI and GTC. Testosterone concentration reduced 71 % in GTC immediately after the exercise in comparison to CG. The GTI allowed positive adaptations when compared to GTC in relation to: glycogen super-compensation, training volume performed and anabolic condition. However, the GTI not improved the aerobic performance.

Time to exhaustion at anaerobic threshold in swimming rats: metabolic investigation.

The purpose of this study was to determine the time to exhaustion (tlim) for swimming exercise at anaerobic threshold (AT) intensity in rats and to analyze metabolic consequences on serum and tissues levels. Eighteen rats were divided in control (CG) and exercised (EG) groups, being the former submitted to tlim. We analyzed the glycogen content of liver and ten skeletal muscles, as well as serum parameters. Parametric statistic was used with significance level at p < 0.05. The tlim, which was correspondent to 114.37 ± 36.23 min, promoted significant decrease in blood glucose (42.99 %; p < 0.01) and an increase in free fatty acids (167.12 %; p < 0.01) when EG was compared to CG. We did not find differences in albumin, total protein uric acid and creatinine between groups. The proposed exercise at individualized AT intensity promoted severe glycogen depletion for all tissues (mean of 78.05 % for all muscles and 89 % for liver). With substantial control of exercise intensity, our study establishes a useful rodent model that can be further explored, contributing to the advancement on knowledge and better understanding of exhaustion mechanisms.