We discuss two competing models for explaining the ground deformation associated with normal faulting earthquake in the brittle elastic upper crust. The classic elastic rebound theory is usually applied for all tectonic settings. In normal fault earthquakes, this model would predict a horizontal stretching eventually responsible for the elastic rebound at the earthquake. However, volumes mostly subside vertically during an extensional earthquake and the collapsed ground in the hanging wall is about one order of magnitude larger than the uplifted volumes of the surrounding hanging wall and footwall. The elastic rebound model would explain this asymmetry with a high horizontal elastic compressibility of the hanging wall and footwall absorbing the coseismic push. We rather suggest that the force activating normal fault earthquakes is mostly dictated by the sliding of the hanging wall, owing gravitational potential. The much larger coseismic subsidence with respect to the uplift can be explained by the closure at depth of a diffuse network of microfractures developed during the interseismic period. Since the horizontal stretching does not exist below ~1 km of depth, with the minimum horizontal stress tensor becoming positive below that depth, the development of a normal fault can be activated only by the vertical maximum stress tensor, i.e., the lithostatic load. The common fluids expulsion at the coseismic stage requires diffuse secondary permeability in the upper crust, in agreement with the presence of a diffuse network of microfractures.
Are normal fault earthquakes due to elastic rebound or gravitational collapse?
Valerio Emanuela;Tizzani Pietro;Lanari Riccardo
2020
Abstract
We discuss two competing models for explaining the ground deformation associated with normal faulting earthquake in the brittle elastic upper crust. The classic elastic rebound theory is usually applied for all tectonic settings. In normal fault earthquakes, this model would predict a horizontal stretching eventually responsible for the elastic rebound at the earthquake. However, volumes mostly subside vertically during an extensional earthquake and the collapsed ground in the hanging wall is about one order of magnitude larger than the uplifted volumes of the surrounding hanging wall and footwall. The elastic rebound model would explain this asymmetry with a high horizontal elastic compressibility of the hanging wall and footwall absorbing the coseismic push. We rather suggest that the force activating normal fault earthquakes is mostly dictated by the sliding of the hanging wall, owing gravitational potential. The much larger coseismic subsidence with respect to the uplift can be explained by the closure at depth of a diffuse network of microfractures developed during the interseismic period. Since the horizontal stretching does not exist below ~1 km of depth, with the minimum horizontal stress tensor becoming positive below that depth, the development of a normal fault can be activated only by the vertical maximum stress tensor, i.e., the lithostatic load. The common fluids expulsion at the coseismic stage requires diffuse secondary permeability in the upper crust, in agreement with the presence of a diffuse network of microfractures.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.