The effect of a dietary nitrate supplementation in the form of a single shot of beetroot juice on static and dynamic apnoea performance

Introduction: The purpose of the present study was to assess the effects of acute nitrate (NO3-)-rich beetroot juice supplementation on peripheral oxygen saturation (SpO2), heart rate (HR), and pulmonary gas exchange during submaximal static and dynamic apnoea. Methods: Nine (six male, three female) trained apneists (age: 39.6 ± 8.2 years, stature: 170.4 ± 11.5cm, body mass: 72.0 ± 11.5 kg) performed three submaximal static apnoeas at 60%, 70% and 80% of the participant’s current reported personal best time, followed by three submaximal (~ 75% or personal best distance) dynamic apnoeas following the consumption of either a 140 ml concentrated NO3--rich beetroot juice (BRJ; 7.7 mmol NO3-) or a NO3--depleted placebo (PLA; 0.1 mmol NO3-) in double-blind randomised manner. HR and SpO2 were measured via fingertip pulse oximetry at the nadir, and online gas analysis was used to assess pulmonary oxygen uptake (V̇O2) during recovery following breath-holds. Results: There were no differences (P <0.05) between conditions for HR (PLA = 59 ± 11 bpm and BRJ = 61 ± 12 bpm), SpO2 (PLA = 83 ± 14% and BRJ = 84 ± 9%) or V̇O2 (PLA = 1.00 ± 0.22 L.min-1 and BRJ = 0.97 ± 0.27 L.min-1). Conclusion: The consumption of 7.7mmol of beetroot juice supplementation prior to a series of submaximal static and dynamic apnoeas did not induce a significant change in SpO2, HR and V̇O2, when compared to placebo. Therefore there is no apparent physiological response that may benefit free-divers as a result of the supplementation

Cell biology of stress: Cytoplasmic rearrangements and signaling events

Recent reports show that formation of COPII coated vesicles and ER exit are regulated by kinases and that more generally, many components of the secretory pathway have been found phosphorylated. However the conditions under which these events occur are so far poorly understood. As the main aim of this thesis, we asked how the function and organization of the early secretory pathway respond to nutrient stress. In particular, we examine the behavior the components of the early secretory pathway under nutrient restriction, their contribution to other processes that are also regulated by the same stress (such as protein translation arrest and stress granule formation), and the nature of the signaling events regulating these responses. We follow up on the results of a kinase screen designed to identify regulators of the early secretory pathway and find that the extracellularly regulated kinase 7 (Erk7, also known as MAPK15) mediates the response of the ERES to serum starvation. These findings establish that the early secretory pathway is sensitive to nutrient signals, that pathways sensing nutrient abundance regulate its functional organization and that the key ERES component, Sec16 is the platform that integrates these signals. These results fuelled the further experiments to examine the behavior of the ERES components upon amino-acid starvation. We find that this response is even more dramatic than the one observed with serum deprivation. Indeed the ERES are remodeled into the Sec bodies, a novel, non-membrane bound, reversible structure that does not support protein transport and acts as a reservoir for ERES components. We find that the formation of Sec bodies is critical to cell survival and re-adaptation to normal growth conditions after the stress is relieved. Our quest to understand the nature of this novel structure reveals that it behaves like a liquid droplet, linking it to the cytoplasmic reorganization that occurs during stress, a well-documented manifestation of which is the assembly of stress granules. The similarities we observed between the Sec bodies and the stress granules prompted us to investigate the hypothesis that the formation of two structures is somehow linked. Indeed, we find that even though Sec bodies and stress granules are distinct both morphologically and functionally the specific ERES components that are required for Sec body assembly are also necessary for stress granule formation. These observations reveal a so far unexplored link between ER exit and mRNA sorting and turnover. Furthermore we study the stress granule assembly under a different type of stress, heat exposure, which does not affect the early secretory pathway. We find that TORC2 signaling is required for their formation. Having characterized the heat sensitivity phenotype of Rictor mutant flies we set out to understand the molecular mechanisms of this phenotype. Using S2 cells initially and then confirming our observations in Drosophila tissues we show that during heat stress TORC2 mediates the assembly of stress granules, possibly via its effector, Akt

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A stress assembly that confers cell viability by preserving ERES components during amino-acid starvation

Nutritional restriction leads to protein translation attenuation that results in the storage and degradation of free mRNAs in cytoplasmic assemblies. In this study, we show in Drosophila S2 cells that amino-acid starvation also leads to the inhibition of another major anabolic pathway, the protein transport through the secretory pathway, and to the formation of a novel reversible non-membrane bound stress assembly, the Sec body that incorporates components of the ER exit sites. Sec body formation does not depend on membrane traffic in the early secretory pathway, yet requires both Sec23 and Sec24AB. Sec bodies have liquid droplet-like properties, and they act as a protective reservoir for ERES components to rebuild a functional secretory pathway after re-addition of amino-acids acting as a part of a survival mechanism. Taken together, we propose that the formation of these structures is a novel stress response mechanism to provide cell viability during and after nutrient stress