We propose an integrated kinematic model with mechanical constrains of the Maipo–Tunuyán transect (33°40′S) across the Andes. The model describes the relation between horizontal shortening, uplift, crustal thickening and activity of the magmatic arc, while accounting for the main deep processes that have shaped the Andes since Early Miocene time. We construct a conceptual model of the mechanical interplay between deep and shallow deformational processes, which considers a locked subduction interface cyclically released during megathrust earthquakes. During the coupling phase, long-term deformation is confined to the thermally and mechanically weakened Andean strip, where plastic deformation is achieved by movement along a main décollement located at the base of the upper brittle crust. The model proposes a passive surface uplift in the Coastal Range as the master décollement decreases its slip eastwards, transferring shortening to a broad area above a theoretical point S where the master detachment touches the Moho horizon. When the crustal root achieves its actual thickness of 50 km between 12 and 10 Ma, it resists further thickening and gravity-driven forces and thrusting shifts eastwards into the lowlands achieving a total Miocene–Holocene shortening of 71 km.

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Contractional deformation in Costa Rica is usually attributed to the subduction of the aseismic Cocos Ridge. In this work, we review the evidences for contraction in the middle to late Miocene, prior to the arrival of the Cocos Ridge at the Middle America Trench. We find that the Miocene phase of contractional deformation is found in all of Costa Rica, probably extending to Nicaragua as well. The widespread distribution of this event requires a regional or plate geodynamic trigger. We analyze the possible mechanisms that could produce the onset of contractional deformation, using the better known case of subduction orogeny, the Andes, as an analog. We propose that a change in the direction of the Cocos plate since ∼19 Ma led to a change from oblique to orthogonal convergence, producing contractional deformation of the upper plate.

The influence of sleep on ventilation, metabolic rate, cardiovascular function, and regional distribution of blood flow during hypoxemia (PaO2 of 45-50 mm Hg (1 mm Hg = 133.3 Pa)) was studied in piglets at 6+/-1 and 34+/-5 days (mean+/-SD). Measurement of ventilation and metabolic rate was done in a metabolic chamber, and blood flow was measured using the microsphere technique. A subgroup of animals was instrumented for cardiac output measurement (dye-dilution technique) and continuous monitoring of the hemoglobin saturation in oxygen (SaO2). We found that although sleep did not influence the metabolic and cardiac output response to hypoxemia, it affected the ventilatory response as well as the brain and the respiratory muscle blood flows. During active sleep in the older animals, the ventilatory response to hypoxemia was smaller than in the other two states; marked drops in SaO2 occurred with changes in the breathing pattern; and that state was associated with the highest rate of brain blood flow. As well, age affected the ventilatory and metabolic response, but not the cardiovascular response to hypoxemia. The age-dependent ventilatory changes with hypoxemia (smaller ventilatory response in the young than in the older animals) were related to the different levels of oxygen consumption. In summary, active sleep was responsible for all the sleep-dependent changes in the response to a moderate degree of hypoxemia.