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Since October 1996, Statoil and its Sleipner partners have injected CO 2 into a saline aquifer, the Utsira Sand, at a depth of approximately 1000 m. The aquifer has a thickness of more than 200 m near the injection site and is sealed by thick shales. A multi-institutional research project SACS (Saline Aquifer CO 2 Storage) was formed to predict and monitor the migration of the injected CO 2 . To this end two time-lapse seismic surveys over the injection area have been acquired, one in October 1999 after 2.3 million tonnes of CO 2 had been injected and the second in October 2001 after approximately 4.4 million tonnes of CO 2 had been injected. Comparison with the base seismic survey of 1994 prior to injection provides insights into the development of the CO 2 plume. In this paper some selected results of the seismic interpretation of the CO 2 plume at the two different time-steps will be shown.

CO2produced at the Sleipner natural gas field is being injected into the Utsira Sand, a major saline aquifer. Time-lapse seismic data were acquired in 1999 and 2001, with 2.35 and 4.26 million tonnes of CO2in the reservoir respectively. The CO2plume is imaged as a number of bright sub-horizontal reflections within the reservoir unit, growing with time, and underlain by a prominent velocity pushdown. No leakage has been detected from the repository reservoir. The reflections are interpreted as tuned responses from thin (<8 m thick) layers of CO2trapped beneath thin intra-reservoir mudstones and the reservoir caprock. However, these alone are unable to account for the amount of observed pushdown. A two-component 3D saturation model is therefore developed for the 1999 dataset, with high-saturation CO2forming the layers and a lesser component of low-saturation CO2between the layers. Saturations are calculated from the observed reflectivity and velocity pushdown and the resulting model contains 85% of the known injected mass of CO2. A 2D synthetic seismic section through the saturation model matches the observed seismic response well and the model is considered to provide an acceptable description of the CO2distribution. Signal attenuation is more pronounced within the 2001 plume and its effects are likely to become more significant with time, perhaps reducing the efficacy of seismic verification techniques as the plume grows further. Other geophysical methods, such as microgravimetry, may become increasingly useful at this stage.

Exposure to simulated altitude of ~4,000 m does not seem to worsen the whole body mass and fat-free mass reductions or alter resting energy expenditure and appetite during a 21-day simulated microgravity.

We explored the assembly of intestinal microbiota in healthy male participants during the run-in (5 day) and experimental phases [21-day normoxic bed rest (NBR), hypoxic bedrest (HBR)], and hypoxic ambulation (HAmb) in a strictly controlled laboratory environment, balanced fluid, and dietary intakes, controlled circadian rhythm, microbial ambiental burden, and 24/7 medical surveillance. The fraction of inspired O2 (FiO2) and partial pressure of inspired O2 (PiO2) were 0.209 and 133.1 ± 0.3 mmHg for NBR and 0.141 ± 0.004 and 90.0 ± 0.4 mmHg for both hypoxic variants (HBR and HAmb; ~4,000 m simulated altitude), respectively. A number of parameters linked to intestinal transit spanning Bristol Stool Scale, defecation rates, zonulin, α1-antitrypsin, eosinophil derived neurotoxin, bile acids, reducing sugars, short chain fatty acids, total soluble organic carbon, water content, diet composition, and food intake were measured (167 variables). The abundance, structure, and diversity of butyrate producing microbial community were assessed using the two primary bacterial butyrate synthesis pathways, butyryl-CoA: acetate CoA-transferase (but) and butyrate kinase (buk) genes. Inactivity negatively affected fecal consistency and in combination with hypoxia aggravated the state of gut inflammation (p < 0.05). In contrast, gut permeability, various metabolic markers, the structure, diversity, and abundance of butyrate producing microbial community were not significantly affected. Rearrangements in the butyrate producing microbial community structure were explained by experimental setup (13.4%), experimentally structured metabolites (12.8%), and gut metabolite-immunological markers (11.9%), with 61.9% remaining unexplained. Many of the measured parameters were found to be correlated and were hence omitted from further analyses. The observed progressive increase in two immunological intestinal markers suggested that the transition from healthy physiological state toward the developed symptoms of low magnitude obesity-related syndromes was primarily driven by the onset of inactivity (lack of exercise in NBR) that were exacerbated by systemic hypoxia (HBR) and significantly alleviated by exercise, despite hypoxia (HAmb). Butyrate producing community in colon exhibited apparent resilience toward short-term modifications in host exercise or hypoxia. Progressive constipation (decreased intestinal motility) and increased local inflammation marker suggest that changes in microbial colonization and metabolism were taking place at the location of small intestine.

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The effects of reduced muscle perfusion pressure on dynamic exercise performance and cardiovascular and respiratory functions were investigated. Eight subjects were studied during supine cycle ergometry at stepwise increasing workloads until exhaustion with and without the legs exposed to a supra-atmospheric pressure of 50 mmHg (Leg Positive Pressure, LPP), a novel and convenient means of reducing the perfusion pressure in the working muscles. In the LPP condition exercise performance was reduced by 40% which, judging from assessments of perceived exertion, was due to premature muscle fatigue, indicating local or overall underperfusion of the working muscles. At any given work load, the arterial pressure response was considerably stronger during LPP than in the control condition. LPP also caused greater increases in blood lactate concentration and pulmonary ventilation, the differences from control increasing with the work load. Furthermore, the ventilatory equivalent for O2 at a given work load was markedly higher in the LPP than in the control condition, while exercise-induced decreases in end-tidal PCO2 were considerably exaggerated by LPP. The augmented pressor response during flow-restricted exercise, together with the strong ventilatory response which was out of proportion to overall O2 uptake, suggests increased activation of muscle chemoreflexes by accumulation of metabolic end products, the increased pressor response tending to reduce the local flow error in the working muscles.