It is well known that GH therapy of GH deficient children leads to a rapid increase in muscle mass. Hulthen et al. show that the reverse happens when GH therapy is stopped after final height is reached 1. Lean body mass decreased by about 10% within two years after the discontinuation of GH treatment, whereas healthy age-matched controls (17 to 21 years old) kept increasing their lean body mass. Despite decreasing lean body mass in the GH deficient subjects, their muscle 'strength' remained stable. However, this compared unfavorably with the increasing muscle strength of healthy individuals. You do not have to search far to find a solution to this problem. A paper by the same group of researchers in the same issue of JCEM2 provides the expected answer: GH. They studied 21 patients with childhood-onset GH deficiency who now were 31 years old on average. GH therapy over five years was associated with an increase in lean body mass, muscle strength and bone mass. GH is a great target for research, because it has a confusing number of effects that wait to be disentangled. A popular approach is to inject GH, measure a handful of things and conclude that GH actions are complex (meaning that it is hard to make sense of the data). Forwood et al. used a more successful strategy 3

. Two GH injections were given to rats at a 12 hour interval. One hour after the second injection, the rats' right tibiae were subjected to a single period of four point bending and the bone response was measured by histomorphometry. GH had no effect on the non-loaded left tibiae and the mechanical stimulus on the right tibiae had no effect on controls that had not received GH. However, high dose GH and high-load mechanical stimulation together led to a significant increase in bone formation. The authors concluded that GH modulates the responsiveness of bone tissue to mechanical stimuli by changing thresholds for bone formation. If this conclusion has a familiar ring to you, maybe it is because you remember a 1998 article from ISMNI's honorary president, where the same idea was put forward as a hypothesis 4

.

Many of GH's actions are mediated by insulin-like growthfactor-1. Overexpression of insulin-like growth factor-1 inthe osteoblasts of mice had similar effects as injecting GH to rats: the response to mechanical stimulation was amplified. Another analogy to the rat studies was that overexpression of insulin-like growth factor-1 alone or mechanical stimulation alone had little effect. DXA applications for ambitious users. Are you tired of predicting other people's future from the printout of your DXA machine? If so, there are some new ideas that might stir your interest. Duan and colleagues show new ways to make use of lumbar spine densitometry6,7. They start out from the idea that the occurrence of non-traumatic vertebral fractures depends not only on bone strength but also on the forces that are applied to the vertebra. This may appear trivial to outsiders, but is nevertheless revolutionary in this particular research

area. Traditional densitometry completely ignores the forces that challenge bone strength. Duan and colleagues estimate the strength of the L3 vertebral body from an anteroposterior and a lateral DXA scan. The forces that are applied to this vertebral body are assumed to depend on body weight, height and the lever arm of the erector spinae muscle. The length of this lever arm is measured on the lateral spine scan.

Forces and bone strength are combined into a number dubbed 'Fracture Risk Index'. This Index thus not only has a biomechanical basis, but also can be determined with widelyavailable technology and has a catchy name. Even better, the Fracture Risk Index comes with a brand-new 'fracturethreshold', which happens to be 1. Thus, there are all the ingredients that should guarantee a successful career of thisindex within the osteoporosis research community.

The authors regard peroxisome pro-liferator-activated as a possible mediator. PGC-1 is known to influence, among other things, uncoupling proteins (see above). Indeed, PGC-1 was increased in CaMKIV* transgenic mice. Cross education It is quite hard to get exercise effects without effort: no pain, no gain. Yet, there are ways to cheat. For example, if you expose your right biceps brachii muscle to resistance exercise, its isometric force will increase, hopefully. However, your left untrained biceps may become stronger at the same time, even though it was not trained. This well known but rarely discussed phenomenon is called cross education. It is probably caused by both peripheral (muscle hypertrophy

20) and central effects. As to the latter, an improvement of intra-muscular co-ordination, recruitment patterns 21, and central nervous excitability have been suggested. Shima at al. investigated cross education effects during training and detraining of the plantar flexor 22. Training increased peak force during maximum voluntary contraction (MVC) by 18.6% on the trained limb and by 7.3 % on the contralateral limb. After 6 weeks of detraining, 11.0% and 2.9% of the MVC gain were preserved, respectively. Concomitant changes were observed in integrated EMG and in the degree of voluntary activation as assessed with the twitch interpolation technique 23. Thus, central nervous effects seem to play the major role in cross education.Shift the paradigm. The JMNI reader may be aware of (and hopefully taking part in) the paradigm shift that is going on in the 'bone field'. In simplistic terms, that new paradigm is: structures adapt to their usage, and they do so by two different processes, i.e. modeling and remodeling. Other fields may have their own paradigm shifts. An illustration of this is given by Taub, Uswatte and Elbert, who review 'new treatments in neurore habilitation founded on basic research' 24. It has long been known that the central nervous system is not 'hard-wired' but exhibits plasticity 25. In their article, the authors summarize

recent evidence that central plasticity may be exploited for

rehabilitation strategies. One such strategy is constraint induced therapy. This is as peculiar as the 'cross education'

mentioned above: artificial impairment of undisrupted functions (e.g., the less damaged arm) improves the disrupted functions (the more damaged arm). The authors suggest a model in which the 'learned non-use' is overcome by breaking the positive feed-back loop of frustrated function overwhelming activity of non-disrupted functions. These principles were first developed in the sensomotor context, and

only recently have they been transferred to the treatment of

aphasia, focal hand dystonia and dyslexia.

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