Superfast contractions without superfast energetics: ATP usage by SR-Ca2+ pumps and crossbridges in toadfish swimbladder muscle

The rate at which an isometrically contracting muscle uses energy is thought to be proportional to its twitch speed. In both slow and fast muscles, however, a constant proportion (25-40 %) of the total energy has been found to be used by SR-Ca2+ pumps and the remainder by crossbridges. We examined whether SR-Ca2+ pumps account for a larger proportion of the energy in the fastest vertebrate muscle known (the toadfish swimbladder), and whether the swimbladder muscle utilizes energy at the superfast rate one would predict from its mechanics.The ATP utilization rates of the SR-Ca2+ pumps and crossbridges were measured using a coupled assay system on fibres skinned with saponin. Surprisingly, despite its superfast twitch speed, the ATP utilization rate of swimbladder was no higher than that of much slower fast-twitch amphibian muscles.The swimbladder achieves tremendous twitch speeds with a modest steady-state ATP utilization rate by employing two mechanisms: having a small number of attached crossbridges and probably utilizing intracellular Ca2+ buffers (parvalbumin) to spread out the time over which Ca2+ pumping can occur.Finally, although the total ATP utilization rate was not as rapid as expected, the relative proportions used by SR-Ca2+ pumps and the crossbridges were similar to other muscles

Tipping the inflammatory balance: inflammasome activation distinguishes metabolically unhealthy from healthy obesity

Item does not contain fulltextExpansion of adipose tissue mass, predominantly in the visceral depot, strongly associates with the development of metabolic complications that are often observed in obesity. In addition, in obesity, an increased prevalence of nonalcoholic fatty liver disease and reduced cardiorespiratory fitness are observed. However, not all obese individuals develop metabolic abnormalities. To better understand the molecular mechanisms that predispose obese humans to the development of metabolic diseases, comparing the metabolically healthy obese (MHO) vs an unhealthy obese phenotype (MUO) may be of great value. A new study by Esser et al (DOI: 10.1007/s00125-013-3023-9 ) now provides important evidence that the MHO phenotype is associated with a lower activation of the NOD-like receptor family pyrin domain containing-3 (NLPR3) inflammasome in macrophages of visceral adipose tissue and a more favourable inflammatory profile as compared with the MUO phenotype. This finding could promote novel studies in humans to decipher stimuli and mechanisms leading to increased inflammasome activity, not only in adipose tissue, but also in other organs that are involved in the regulation of metabolism