Loss of muscle mass and insulin sensitivity are common phenotypic traits of immobilisation and increased inflammatory burden. The suppression of muscle protein synthesis is the primary driver of muscle mass loss in human immobilisation, and includes blunting of post-prandial increases in muscle protein synthesis. However, the mechanistic drivers of this suppression are unresolved. Immobilisation also induces limb insulin resistance in humans, which appears to be attributable to the reduction in muscle contraction per se. Again mechanistic insight is missing such that we do not know how muscle senses its "inactivity status" or whether the proposed drivers of muscle insulin resistance are simply arising as a consequence of immobilisation. A heightened inflammatory state is associated with major and rapid changes in muscle protein turnover and mass, and dampened insulin-stimulated glucose disposal and oxidation in both rodents and humans. A limited amount of research has attempted to elucidate molecular regulators of muscle mass loss and insulin resistance during increased inflammatory burden, but rarely concurrently. Nevertheless, there is evidence that Akt (protein kinase B) signalling and FOXO transcription factors form part of a common signalling pathway in this scenario, such that molecular cross-talk between atrophy and insulin signalling during heightened inflammation is believed to be possible. To conclude, whilst muscle mass loss and insulin resistance are common end-points of immobilisation and increased inflammatory burden, a lack of understanding of the mechanisms responsible for these traits exists such that a substantial gap in understanding of the pathophysiology in humans endures.

Although virtually unknown in Europe since the widespread adoption of artificial insemination (AI), infection by the sexually transmitted protozoan parasite Tritrichomonas foetus (Fig. 1) results in substantial economic losses throughout the major cattle-rearing areas of the world where natural breeding is relied upon. Infection by T. foetus is increasingly recognized as a significant cause of bovine infertility. In this review, Alex Yule, Susan Skirrow and Robert BonDurant summarize the current knowledge of bovine trichomoniasis and the problems of diagnosis and control of this economically important disease.

Highlights Ageing is associated with declines in muscle mass, quality and insulin sensitivity. These features of ageing quickly manifest in young exposed to physical inactivity. The cellular mechanisms of inactivity-driven muscle dysregulation are unclear. The precise contribution of inactivity to muscle decline with age is unknown. Muscle ageing caused by lifestyle factors may be at least partly reversible.