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Introduction: Caffeine is an exercise performance enhancer widely used by individuals engaged in training or competition under heat-stressed conditions. Caffeine ingestion during exercise in the heat is believed to be safe because it does not greatly affect body temperature responses, heart rate, or body fluid status. However, it remains unknown whether caffeine affects hyperthermia-induced hyperventilation or reductions in the cerebral blood flow index. We tested the hypothesis that under conditions inducing severe hyperthermia, caffeine exacerbates hyperthermia-induced hyperventilation and reduces the cerebral blood flow index during exercise. Methods: Using a randomized, single-blind, crossover design, 12 physically active healthy young men (23 ± 2 yr) consumed a moderate dose of caffeine (5 mg·kg−1) or placebo in the heat (37°C). Approximately 60 min after the ingestion, they cycled for ~45 min at a workload equal to ~55% of their predetermined peak oxygen uptake (moderate intensity) until their core temperature increased to 2.0°C above its preexercise baseline level. Results: In both trials, ventilation increased and the cerebral blood flow index assessed by middle cerebral artery mean blood velocity decreased as core temperature rose during exercise (P < 0.05), indicating that hyperthermia-induced hyperventilation and lowering of the cerebral blood flow occurred. When core temperature was elevated by 1.5°C or more (P < 0.05), ventilation was higher and the cerebral blood flow was lower throughout the caffeine trial than the placebo trial (P < 0.05). Conclusions: A moderate dose of caffeine exacerbates hyperthermia-induced hyperventilation and reductions in the cerebral blood flow index during exercise in the heat with severe hyperthermia. [ABSTRACT FROM AUTHOR]

Backgrounds: The pathogenesis of DVT (deep venous thrombosis) is still unclear, largely due to a lack of an appropriate animal model. Although stasis is a major cause of DVT formation, IVC (inferior vena cava) stasis model is not suitable for in vivo imaging because of its deep location. Real-time imaging in other thrombosis models including FeCl3 and laser injury showed the roles of platelets and leukocytes in the initiation of thrombosis, but those models don't reflect pathogenesis of clinical DVT. Method: We established a novel clinically relevant murine DVT model, suitable for real-time in vivo imaging. Thrombus can be induced and observed simultaneously by the excitation light of epi-fluorescence microscopy at ligated femoral vein without photochemical reagent. Results: Formed DVT in this model mimicked human DVT morphologically, histologically, and rheologically. The thrombus extended in a long axis direction of the blood vessel. The histology revealed red-thrombi with fibrin network. The thrombus formation was initiated frequently at venous valves which are common sites of human DVT. Femoral vein is free from motion artifact from heartbeat, and its superficial location is suitable for in vivo imaging with microscopy. In vivo imaging revealed that erythrocytes aggregation and deposition to the endothelial cells preceded the recruitment of platelets and leukocytes to vessel wall, suggesting DVT was formed in a platelet- and leukocyte- independent manner in this model. In addition, we succeeded in the high-resolution 4D imaging of DVT using intravital two-photon microscopy, enabling visualization of DVT at single-leukocyte level. Conclusion: Our novel murine DVT model mimicked human DVT and suitable for in vivo molecular imaging. Therefore, our model would help better understanding of molecular mechanism of DVT formation and organization. [ABSTRACT FROM AUTHOR]