|Title||Southern Ocean heat uptake, redistribution, and storage in a warming climate: The role of meridional overturning circulation|
|Publication Type||Journal Article|
|Year of Publication||2018|
|Authors||Liu W, Lu J., Xie SP, Fedorov A.|
|Journal||Journal of Climate|
|Type of Article||Article|
|Keywords||atmosphere model; carbon; co2; dependence; mechanisms; Mesoscale eddies; Meteorology & Atmospheric Sciences; sea-ice; sensitivity; transient-response; winds|
Climate models show that most of the anthropogenic heat resulting from increased atmospheric CO2 enters the Southern Ocean near 60 degrees S and is stored around 45 degrees S. This heat is transported to the ocean interior by the meridional overturning circulation (MOC) with wind changes playing an important role in the process. To isolate and quantify the latter effect, we apply an overriding technique to a climate model and decompose the total ocean response to CO2 increase into two major components: one due to wind changes and the other due to direct CO2 effect. We find that the poleward-intensified zonal surface winds tend to shift and strengthen the ocean Deacon cell and hence the residual MOC, leading to anomalous divergence of ocean meridional heat transport around 60 degrees S coupled to a surface heat flux increase. In contrast, at 45 degrees S we see anomalous convergence of ocean heat transport and heat loss at the surface. As a result, the wind-induced ocean heat storage (OHS) peaks at 46 degrees S at a rate of 0.07 ZJ yr(-1) (degrees lat)(-1) (1 ZJ = 10(21) J), contributing 20% to the total OHS maximum. The direct CO2 effect, on the other hand, very slightly alters the residual MOC but primarily warms the ocean. It induces a small but nonnegligible change in eddy heat transport and causes OHS to peak at 42 degrees S at a rate of 0.30 ZJ yr(-1) (degrees lat)(-1), accounting for 80% of the OHS maximum. We also find that the eddy-induced MOC weakens, primarily caused by a buoyancy flux change as a result of the direct CO2 effect, and does not compensate the intensified Deacon cell.