Eight weeks of taurine supplementation associated with nutritional counseling is able to increase adiponectin levels and to decrease markers of inflammation (high-sensitivity C-reactive protein) and lipid peroxidation (TBARS) in obese women.

Cr supplementation inhibited the increase of inflammation markers TNF-α and CRP, but not oxidative stress markers, due to acute exercise.

In summary, the current used OT protocol based on eccentric exercise sessions impaired the insulin signaling pathway with concomitant increases of IKK, SAPK/JNK, and SOCS3 protein levels.

The aims of the this study were a) to verify whether the performance decrease induced by nonfunctional overreaching (NFOR) is linked to high concentrations of cytokines in serum, skeletal muscles and liver; b) to verify muscle myostatin adaptation to NFOR; c) to verify the effects of chronic glucose supplementation on the parameters mentioned above. Mice were divided into control (C), trained (TR), overtrained (OTR) and supplemented overtrained (OTR + S). The incremental load test (ILT) and exhaustive test (ET) were used to measure performances before and after exercise protocols. 24 h after ET, muscles and liver were removed and stored at -80°C for subsequent measurements. Total blood was collected from decapitation for subsequent determination of cytokine concentrations. Generally, OTR and OTR + S presented higher contents of IL-6, TNF-alpha, GLUT-4 and myostatin in muscle samples compared to C and TR. Glucose supplementation attenuated the high contents of IL-6, TNF-alpha and IL-15 in liver, and of IL-6 in serum. In summary, NFOR led to low-grade chronic inflammation and myostatin upregulation.

The aim of the present study was to investigate the effects of acute administration of taurine overload on time to exhaustion (TTE) of high-intensity running performance and alternative maximal accumulated oxygen deficit (MAODALT). The study design was a randomized, placebo-controlled, crossover design. Seventeen healthy male volunteers (age: 25 ± 6 years; maximal oxygen uptake: 50.5 ± 7.6 mL·kg(-1)·min(-1)) performed an incremental treadmill-running test until voluntary exhaustion to determine maximal oxygen uptake and exercise intensity at maximal oxygen uptake. Subsequently, participants completed randomly 2 bouts of supramaximal treadmill-running at 110% exercise intensity at maximal oxygen uptake until exhaustion (placebo (6 g dextrose) or taurine (6 g) supplementation), separated by 1 week. MAODALT was determined using a single supramaximal effort by summating the contribution of the phosphagen and glycolytic pathways. When comparing the results of the supramaximal trials (i.e., placebo and taurine conditions) no differences were observed for high-intensity running TTE (237.70 ± 66.00 and 277.30 ± 40.64 s; p = 0.44) and MAODALT (55.77 ± 8.22 and 55.06 ± 7.89 mL·kg(-1); p = 0.61), which seem to indicate trivial and unclear differences using the magnitude-based inferences approach, respectively. In conclusion, acute 6 g taurine supplementation before exercise did not substantially improve high-intensity running performance and showed an unclear effect on MAODALT.

Taurine can affect the energy system metabolism, specifically the lipid metabolism, since an increase in lipid oxidation may promote carbohydrate savings. We hypothesized that taurine supplementation associated with high-intensity exercise could increase levels of lipolysis, benefiting swimmer performance. Nine male competitive swimmers performed two 400-m front crawl maximal efforts with a 1-week washout, and the athletes received 6 g of taurine (TAU) or placebo (PLA) supplementation 120 min before performing the effort. Oxygen consumption and the contribution of the energy systems were analyzed post effort using a Quark CPET gas analyzer. Blood samples were collected before, and 5 min post the effort for taurine and glycerol analysis. Immediately before and 3, 5, and 7 min post the effort, blood samples from the earlobe were collected to determine lactate levels. An increase of 159% was observed in taurine plasma levels 120 min post ingestion. Glycerol levels were higher in both groups post effort; however, the TAU condition promoted an 8% higher increase than the PLA. No changes were observed in swimmer performance or lactate levels; however, the percentage change in lactate levels (∆[La]) was different (TAU: 9.36 ± 2.78 mmol L; PLA: 11.52 ± 2.19 mmol L, p = 0.04). Acute taurine supplementation 120 min before performing a maximal effort did not improve swimmer performance; however, it increased glycerol plasma levels and reduced both the ∆[La] and lactic anaerobic system contribution.

The above findings suggest that the OTR/down protocol-induced skeletal muscle ER stress may be linked to a pathological condition in EDL and soleus muscles.

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