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Chronic stimulation of β2-receptors with β2-agonists causes desensitisation, which in skeletal muscle is accompanied by myosin heavy chain (MHC) remodelling, similar to that observed in heart failure patients. However, the mechanisms for this skeletal muscle remodelling are not well established. G protein-coupled receptor kinases (GRKs) specifically phosphorylate and desensitise G protein-coupled receptors during periods of agonist activation. However, desensitisation associated with prolonged agonist activation alters β-adrenergic signalling, and downstream affects gene expression. We hypothesised that skeletal muscle remodelling induced by β2-agonist administration could be regulated by GRK expression. Therefore the aim of this study was firstly to characterise which, if any, of the six known isoforms of GRK were expressed in skeletal muscle and then secondly to determine whether remodelled skeletal muscle induced by chronic β2-agonist administration was accompanied by altered expression of GRK isoforms. Male Wistar rats were administered a β2-agonist daily for 8 weeks, and the expression of MHC and GRKs examined in gastrocnemius and soleus muscles. Treatment with β2-agonist caused a change in MHC in soleus from types I to IIA, and in gastrocnemius from MHC types IIA/IIX to IIB. Western blotting revealed that GRK2 and GRK5 were expressed in skeletal muscle. Furthermore, despite changes in MHC and differential muscle-specific expression of GRK isoforms, there was no significant change in expression of GRK2 and GRK5 in soleus or gastrocnemius following β2-agonist administration. In conclusion the level of GRK expression is unlikely to be responsible for MHC switching following chronic β2-receptor stimulation. Experimental Physiology (2003) 88.2, 277-284.
Increasing blood bicarbonate content has long been cited as a potential mechanism to improve contractile function. We investigated whether sodium bicarbonate-induced metabolic alkalosis could positively affect force development during the rest-to-work transition in ischaemic skeletal muscle. Secondly, assuming it could, we investigated whether bicarbonate could augment acetyl group availability through the same equilibrium reaction as sodium acetate pre-treatment and whether this underpins, at least in part, its ergogenic effect. Multiple biopsy samples were obtained from the canine gracilis muscle during 5 min of electrically evoked ischaemic contraction, which enabled the determination of the time course of acetyl group accumulation, substrate utilisation, pyruvate dehydrogenase complex activation and tension development in animals treated with saline (control; n = 6) or sodium bicarbonate (n = 5). Treatment with bicarbonate elevated acetylcarnitine content above the control level at rest (P<0.05), but at no time point during subsequent contraction. The pyruvate dehydrogenase complex was activated following 40 s of contraction in both groups, with no differences existing between treatments at any time point. The requirement for ATP resynthesis from non-oxygen-dependent routes was no different between groups at any time point during contraction. No difference in peak twitch force production existed between groups. However, at 3 min of stimulation, tension development was better maintained in the bicarbonate group (P<0.05), being ∼20% greater than control following 5 min of contraction (P<0.05). The results demonstrate, for the first time, that bicarbonate can augment acetyl group availability prior to contraction, independent of pyruvate dehydrogenase complex activation, but cannot influence the requirement for non-oxidative ATP re-synthesis during subsequent contraction. It would appear, therefore, that the bicarbonate-induced improvement in muscle tension development was probably mediated through the metabolic alkalosis and not via the increased availability of acetyl groups within the cell.
A study was undertaken in man to investigate whether during moderate cold stress, the proportion of carbohydrate (CHO) oxidized is increased, and whether prior prolonged exhaustive exercise compromises thermoregulation. Eight euglycaemic men were cooled by a liquid-conditioned suit (1) after an overnight fast (Con) and (2) [similar]2 h after an exercise protocol in which CHO availability was substantially lowered (Post-Ex). The cooling stimulus lasted 90 min (Cooling) and was preceded by a 30 min thermo-neutral baseline phase (Base). In Con, aural temperature (Taural) and the rate of CHO oxidized (CHOox) were not altered from the values at Base during Cooling, whereas the following were increased: the rate of heat production (Hprod, [similar]1·9-fold), thigh electromyographical activity (EMG, [similar]2·5-fold), and the rate of fat oxidized (FATox, [similar]1·7-fold). In Post-Ex, Taural did not decrease from the value at Base during Cooling, and compared with Con, EMG, CHOox and the rate of heat loss were not different, whereas Hprod (P [less than or equal to] 0·01), FATox (P [less than or equal to] 0·01) and mean skin temperature (P [less than or equal to] 0·01) were higher, and Taural was lower (P [less than or equal to] 0·05). It is concluded that during moderate cold stress, shivering thermogenesis is supported by an increase in the oxidation of fat, and despite an alteration in the initial thermoregulatory responses to Cooling [similar]2 h after exhaustive exercise, thermoregulation was not impaired.
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