Effects of Disability-Associated Low Energy Expenditure Deconditioning Syndrome, Rimmer 2012
The theme of this paper might sound familiar: how sedentary behaviour can lead to deconditioning, making activity harder and so a vicious cycle is set off leading to more disability.
Actually, there are some interesting ideas in this piece, and I particularly the fact that it is clear this is a hypothesis and not a complete explanation for disability. It also proposes some novel ideas for very low-level activity using virtual reality games.
Abstract
People with neuromuscular disabilities have high rates of sedentary behavior predisposing them to severe deconditioning and significant health risk. We describe this as disability-associated low energy expenditure deconditioning syndrome and propose new approaches for promoting light-to-moderate intensity physical activity in people with disabilities.
The easiest way to explain the basic idea, and it's similarity with some models of CFS, is this diagram summarising a model presented in an earlier paper by the same author:
reproduced with permission. The full original article with diagram (fig 1) can be found here.
So essentially this is the same loop that some people (including the PACE authors) believe is responsible for perpetuating CFS - at least that was the explicit rationale for the GET programme. It looks very plausible and no doubt is true to some extent, but there is virtually no evidence out there that has demonstrated deconditioning has an important clinical effect.
Some key quotes from the 2012 Rimmer paper (note the caveats throughout):
The theme of this paper might sound familiar: how sedentary behaviour can lead to deconditioning, making activity harder and so a vicious cycle is set off leading to more disability.
Actually, there are some interesting ideas in this piece, and I particularly the fact that it is clear this is a hypothesis and not a complete explanation for disability. It also proposes some novel ideas for very low-level activity using virtual reality games.
Abstract
People with neuromuscular disabilities have high rates of sedentary behavior predisposing them to severe deconditioning and significant health risk. We describe this as disability-associated low energy expenditure deconditioning syndrome and propose new approaches for promoting light-to-moderate intensity physical activity in people with disabilities.
The easiest way to explain the basic idea, and it's similarity with some models of CFS, is this diagram summarising a model presented in an earlier paper by the same author:
reproduced with permission. The full original article with diagram (fig 1) can be found here.
So essentially this is the same loop that some people (including the PACE authors) believe is responsible for perpetuating CFS - at least that was the explicit rationale for the GET programme. It looks very plausible and no doubt is true to some extent, but there is virtually no evidence out there that has demonstrated deconditioning has an important clinical effect.
Some key quotes from the 2012 Rimmer paper (note the caveats throughout):
we provide a conceptual framework for understanding how disability-associated conditions lead to high rates of physical inactivity, which in turn result in an accelerated physical decline in people with disabilities...
We propose that a certain percentage (and in some cases, a significant percentage) of the decline in physiological and musculoskeletal functioning observed in people with neuromuscular disabilities is related to a substantial reduction in energy expenditure leading to the clinical presentation of disability-associated low-energy expenditure deconditioning syndrome (DALEEDS)...
Building on clinical consensus that skeletal muscle-related declines in strength and exercise tolerance, accommodated by increases in fat mass, lead to dysregulated energetics, we hypothesize that these physiological changes can be ordered into one of two pathways: Pathway 1, fitness decline; and Pathway 2, increase in cardiometabolic risk factors...
We also hypothesize that either of these two pathways could become self-sustaining and act as independent contributors to the adverse health outcomes listed at the bottom of the figure and, in some cases, may even dominate the clinical presentation independent of its initial cause
the end result is reduced total energy expenditure, which creates a continuous cycle of health risk leading to metabolic/physiological changes that cause further advancements in physical decline across time