Gas bubbles are the primary agent in producing the pathogenic effects of decompression sickness. Bubble formation during decompression is not simply the consequence of inert gas supersaturation. Numerous experiments indicate that bubbles originate as pre-existing gas nuclei. Radii are on the order of 1 microm or less. Heterogeneous nucleation processes are involved in generating these gas entities. Musculoskeletal activity could be the main promoter of gas nuclei from stress-assisted nucleation. The half-life and faculty for nuclei to initiate bubble formation during decompression depend on many factors. Oxygen window and surface tension are involved in resolving bubbles. Two factors have been proposed to stabilize gas nuclei against dissolution: gas nuclei trapped in hydrophobic crevices and gas nuclei coated with surface-active molecules such as surfactants. Diffusion and surface tension could play an important role in the formation of gas nuclei crevices. However, while the concept of in vivo hydrophobic crevices remains a theoretical possibility, none have yet been identified in tissues and/or in microcapillaries. Moreover, while surfactants seem present in numerous tissues and could play a role in gas nuclei stabilization, they could also be involved in bubble elimination. The understanding of such mechanisms is of primary importance to neutralize nuclei and for modeling bubble growth. Here we present in a single document a summary of the original findings and views from authors in this field.