An excellent question.
I would say that the effect is most likely very relevant for higher-level skills, for the following reasons:
The effect has been shown for motor planning, for estimation of timing, and for several other plastic features. Thus, it isn’t limited to sensory processing alone.
If we assume a “worst case scenario” in which the higher-level networks are themselves exempt from this effect, we still have to expect an indirect improvement. The reason for this is relatively simple: higher-level mental behaviors are based on metanetworks that interconnect subnetworks which certainly are subject to attentional modulation.
I would say that transferability of the effect would depend on how transferable the trained skill is itself. If you train yourself to be really good at the go/no-go task where a red dot appears on the screen, you’ll get good at it, and it won’t make a difference anywhere else in your life—no matter how much attention you paid while training. If you train yourself to enunciate words better (which is predominantly motor training, and the attention effect has been shown to make a huge difference), this could transfer into many other higher-level behaviors which can be improved by speaking clearly.
Similar indirect improvements would also apply in case of music (tone discernment training is attention-dependent) and chess (spatial combinatorial thinking is dependent on attention-trainable circuitry).
So, in the worst case, this is still highly applicable, by choosing your training targets wisely.
Finally, there is no reason to assume the above worst case scenario. I don’t know of any studies that examined the effects of attention on higher-level skills—most likely because studies would be incredibly difficult to do (there is no possible control group, since you can’t have someone learn chess while not paying attention to it). But the molecular systems involved here seem to be pretty universal. Specifically, the effect has been shown to be dependent on acetylcholine release, and on the detection of this neurotransmitter by muscarinic receptors—which are present in many neurons within the higher-order associative and planning areas of the brain.
For a molecular pathway overview, see, for instance, Conner et al. in Neuron, Vol. 38, 819–829, 2003.
Therefore, the null hypothesis based on the data we currently have is that we should see this effect in higher-level skills directly, as well as indirectly.
Ok, now we are squeezing a comment way too far. Let me give you a fuller view: I am a neuroscientist, and I specialize in the biochemistry/biophysics of the synapse (and interactions with ER and mitochondria there). I also work on membranes and the effect on lipid composition in the opposing leaflets for all the organelles involved.
Looking at what happens during cryonics, I do not see any physically possible way this damage could ever be repaired. Reading the structure and “downloading it” is impossible, since many aspects of synaptic strength and connectivity are irretrievably lost as soon as the synaptic membrane gets distorted. You can’t simply replace unfolded proteins, since their relative position and concentration (and modification, and current status in several different signalling pathways) determines what happens to the signals that go through that synapse; you would have to replace them manually, which is a) impossible to do without destroying surrounding membrane, and b) would take thousands of years at best, even if you assume maximally efficient robots doing it (during which period molecular drift would undo the previous work).
Etc, etc. I can’t even begin to cover complications I see as soon as I look at what’s happening here. I’m all for life extension, I just don’t think cryonics is a viable way to accomplish it.
Instead of writing a series of posts in which I explain this in detail, I asked a quick side question, wondering whether there is some research into this I’m unaware of.
Does this clarify things a bit?