Effect of fatigue strength exercise on anterior thigh skin temperature rewarming after cold stress test.

Although dynamic thermography skin temperature assessment has been used in medical field, scientific evidence in sports is scarce. The aim of the study was to assess changes in anterior thigh skin temperature in response to a cold stress test after a strength exercise fatiguing protocol. Ten physically active adults performed a familiarization session and two strength exercise sessions, one with dominant and the other with non-dominant lower limb. Participants performed bouts of 10 concentric and eccentric contractions of leg extensions in an isokinetic device until reaching around 30% of force loss. Infrared thermographic images were taken at baseline conditions and after the fatigue level from both thighs after being cooled using a cryotherapy system. ROIs included vastus medialis, rectus femoris, adductor and vastus lateralis. Skin temperature rewarming was assessed during 180s after the cooling process obtaining the coefficients of the following equation: ΔSkin temperature = ß0 + ß1 * ln(T), being ß0 and ß1 the constant and slope coefficients, respectively, T the time elapsed following the cold stress in seconds, and ΔSkin temperature the difference between the skin temperature at T respect and the pre-cooling moment. Lower ß0 and higher ß1 were found for vastus lateralis and rectus femoris in the intervention lower limb compared with baseline conditions (p < 0.05 and ES > 0.6). Adductor only showed differences in ß0 (p = 0.01 and ES = 0.92). The regressions models obtained showed that ß0 and ß1 had a direct relationship with age and muscle mass, but an inverse relationship with the number of series performed until 30% of fatigue (R2 = 0.8). In conclusion, fatigue strength exercise results in a lower skin temperature and a faster thermal increase after a cold stress test.

Neuronal Effects of Sugammadex in combination with Rocuronium or Vecuronium.

Rocuronium (ROC) and Vecuronium (VEC) are the most currently used steroidal non-depolarizing neuromuscular blocking (MNB) agents. Sugammadex (SUG) rapidly reverses steroidal NMB agents after anaesthesia. The present study was conducted in order to evaluate neuronal effects of SUG alone and in combination with both ROC and VEC. Using MTT, CASP-3 activity and Western-blot we determined the toxicity of SUG, ROC or VEC in neurons in primary culture. SUG induces apoptosis/necrosis in neurons in primary culture and increases cytochrome C (CytC), apoptosis-inducing factor (AIF), Smac/Diablo and Caspase 3 (CASP-3) protein expression. Our results also demonstrated that both ROC and VEC prevent these SUG effects. The protective role of both ROC and VEC could be explained by the fact that SUG encapsulates NMB drugs. In BBB impaired conditions it would be desirable to control SUG doses to prevent the excess of free SUG in plasma that may induce neuronal damage. A balance between SUG, ROC or VEC would be necessary to prevent the risk of cell damage.

PPARγ as an indicator of vascular function in an experimental model of metabolic syndrome in rabbits.

BACKGROUND AND AIMS: Underlying mechanisms associated with vascular dysfunction in metabolic syndrome (MetS) remain unclear and can even vary from one vascular bed to another. METHODS: In this study, MetS was induced by a high-fat, high-sucrose diet, and after 28 weeks, aorta and renal arteries were removed and used for isometric recording of tension in organ baths, protein expression by Western blot, and histological analysis to assess the presence of atherosclerosis. RESULTS: MetS induced a mild hypertension, pre-diabetes, central obesity and dyslipidaemia. Our results indicated that MetS did not change the contractile response in either the aorta or renal artery. Conversely, vasodilation was affected in both arteries in a different way. The aorta from MetS showed vascular dysfunction, including lower response to acetylcholine and sodium nitroprusside, while the renal artery from MetS presented a preserved relaxation to acetylcholine and an increased sensitivity to sodium nitroprusside. We did not find vascular oxidative stress in the aorta from MetS, but we found a significant decrease in PPARγ, phospho-Akt (p-Akt) and phospho-eNOS (p-eNOS) protein expression. On the other hand, we found oxidative stress in the renal artery from MetS, and PPARγ, Akt and p-Akt were overexpressed. No evidence of atherosclerosis was found in arteries from MetS. CONCLUSIONS: MetS affects vascular function differently depending on the vessel. In the aorta, it decreases both the vasodilation and the expression of the PPARγ/Akt/eNOS pathway, while in the renal artery, it increases the expression of PPARγ/Akt signalling pathway without decreasing the vasodilation.