A rise in extracellular potassium concentration in human skeletal muscle may play an important role in development of fatigue during intense exercise. The aim of the present study was to examine the effect of intense intermittent training on muscle interstitial potassium kinetics and its relationship to the density of Na + ,K + -ATPase subunits and K ATP channels, as well as exercise performance, in human skeletal muscle. Six male subjects performed intense one-legged knee-extensor training for 7 weeks. On separate days the trained leg (TL) and the control leg (CL) performed a 30 min exercise period of 30 W and an incremental test to exhaustion. At frequent intervals during the exercise periods interstitial potassium ([K + ] I ) was determined by microdialysis, femoral arterial and venous blood samples were drawn and thigh blood flow was measured. Time to fatigue for TL was 28% longer (P < 0.05) than for CL (10.6 ± 0.7 (mean ± S.E.M.) versus 8.2 ± 0.7 min). The amounts of Na + ,K + -ATPase α 1 and α 2 subunits were, respectively, 29.0 ± 8.4 and 15.1 ± 2.7% higher (P < 0.05) in TL than in CL, while the amounts of β 1 subunits and ATP-dependent K + (K ATP ) channels were the same. In CL [K + ] I increased more rapidly and was higher (P < 0.05) throughout the 30 W exercise bout, as well at 60 and 70 W, compared to TL, whereas [K + ] I was similar at the point of fatigue (9.9 ± 0.7 and 9.1 ± 0.5 mmol l −1 , respectively). During the 30 W exercise bouts and at 70 W during the incremental exercise femoral venous potassium concentration ([K + ] v ) was higher (P < 0.05) in CL than in TL, but identical at exhaustion (6.2 ± 0.2 mmol l −1 ). Release of potassium to the blood was not different in the two legs. The present data demonstrated that intense intermittent training reduce accumulation of potassium in human skeletal muscle interstitium during exercise, probably through a larger re-uptake of potassium due to greater activity of the muscle Na + ,K + -ATPase pumps. The lower accumulation of potassium in muscle interstitium in the trained leg was associated with delayed fatigue during intense exercise, supporting the hypothesis that interstitial potassium accumulation is involved in the development of fatigue.

The present review will give an update on temporomandibular joint (TMJ) imaging using CBCT. It will focus on diagnostic accuracy and the value of CBCT compared with other imaging modalities for the evaluation of TMJs in different categories of patients; osteoarthritis (OA), juvenile OA, rheumatoid arthritis and related joint diseases, juvenile idiopathic arthritis and other intra-articular conditions. Finally, sections on other aspects of CBCT research related to the TMJ, clinical decision-making and concluding remarks are added. CBCT has emerged as a cost-and dose-effective imaging modality for the diagnostic assessment of a variety of TMJ conditions. The imaging modality has been found to be superior to conventional radiographical examinations as well as MRI in assessment of the TMJ. However, it should be emphasized that the diagnostic information obtained is limited to the morphology of the osseous joint components, cortical bone integrity and subcortical bone destruction/production. For evaluation of soft-tissue abnormalities, MRI is mandatory. There is an obvious need for research on the impact of CBCT examinations on patient outcome.

We examine the influence of the cytosolic and membrane-bound contents of carbonic anhydrase (CA; CAII, CAIII, CAIV, and CAXIV) and the muscle content of proteins involved in lactate and proton transport [monocarboxylate transporter (MCT) 1, MCT4, and Na(+)/H(+) exchanger 1 (NHE1)] on work capacity during supramaximal exercise. Eight healthy, sedentary subjects performed exercises at 120% of the work rate corresponding to maximal oxygen uptake (W(max)) until exhaustion in placebo (Con) and metabolic alkalosis (Alk) conditions. The total (W(tot)) and supramaximal work performed (W(sup)) was measured. Muscle biopsies were obtained before and immediately after standardized exercises (se) at 120% W(max) in both conditions to determine the content of the targeted proteins, the decrease in muscle pH (DeltapH(m)), and the muscle lactate accumulation ([Lac](m)) per joule of W(sup) (DeltapH(m)/W(sup-se) and Delta[Lac](m)/W(sup-se), respectively) and the dynamic buffer capacity. In Con, W(sup) was positively [corrected] correlated with [corrected] MCT1, and tended to be positively correlated with MCT4 and NHE1. CAII + CAIII were correlated positively with DeltapH(m)/W(sup-se) and negatively with Delta[Lac](m)/W(sup-se), while CAIV was positively related to W(tot). The changes in W(sup) with Alk were correlated positively with those in dynamic buffer capacity and negatively with W(sup) in Con. Performance improvement with Alk was greater in subjects having a low content of proteins involved in pH regulation and lactate/proton transport. These results show the importance of pH regulating mechanisms and lactate/proton transport on work capacity and the role of the CA to delay decrease in pH(m) and accumulation in [Lac](m) during supramaximal exercise in humans.

SUMMARYThe distribution of TNF-a, p55 TNF reeeptor (TNF-R) and p75 TNF-R in normal skin and uninvolved and lesional skin from psoriasis patients has been investigated, using specific mono-and polyclonal antibodies. In normal skin, and uninvolved and lesional skin from psoriasis patients, p55 TNF-R is associated with epidermal keratinocytes and a network of upper dermal dendritic cells. This suggests that the actions oCTNF-a on epidermal ceNs/Hrn-o are mediated by binding to the p55 TNF-R. In Icsionat psoriasis skin, there was staining of the parakeratotic stratum eorneuni and increased expression of p55 TNF-R in association with upper dermal blood vessels. Staining for p75 TNF-R in normal skin was restricted to eccrine sweat ducts and dermal dendritic cells, and was absent from the epidermis. In lesional psoriasis skin, there was slaining for p75 TNF-R in association with upper dermal blood vessels and perivascular infiltrating cells. TNF-a in normal skin was predominantly localized to the basal cell layers ofthe epidermis, and was seen in association with eccrine ducts and sebaceous glands. In lesional psoriasis skin, and to a lesser extent in uninvolved psoriasis skin. TNF-a; was distributed throughout the epidermis, and was also specifically localized to upper dermal blood vessels. Up-regulation of TNF-a. p55 TNF-R and p75 TNF-R on dermal blood vessels in psoriasis may play an important role in the pathogenesis of this condition by promoting cutaneous recruitment of inflatiimatory cells.

Lactic acid accumulation is generally believed to be involved in muscle fatigue. However, one study reported that in rat soleus muscle (in vitro), with force depressed by high external K + concentrations a subsequent incubation with lactic acid restores force and thereby protects against fatigue. However, incubation with 20 mM lactic acid reduces the pH gradient across the sarcolemma, whereas the gradient is increased during muscle activity. Furthermore, unlike active muscle the Na + -K + pump is not activated. We therefore hypothesized that lactic acid does not protect against fatigue in active muscle. Three incubation solutions were used: 20 mM Na-lactate (which acidifies internal pH), 12 mM Na-lactate +8 mM lactic acid (which mimics the pH changes during muscle activity), and 20 mM lactic acid (which acidifies external pH more than internal pH). All three solutions improved force in K + -depressed rat soleus muscle. The pH regulation associated with lactate incubation accelerated the Na + -K + pump. To study whether the protective effect of lactate/lactic acid is a general mechanism, we stimulated muscles to fatigue with and without pre-incubation. None of the incubation solutions improved force development in repetitively stimulated muscle (Na-lactate had a negative effect). It is concluded that although lactate/lactic acid incubation regains force in K + -depressed resting muscle, a similar incubation has no or a negative effect on force development in active muscle. It is suggested that the difference between the two situations is that lactate/lactic acid removes the negative consequences of an unusual large depolarization in the K + -treated passive muscle, whereas the depolarization is less pronounced in active muscle.

Kristensen, Michael, Thomas Hansen, and Carsten Juel. Membrane proteins involved in potassium shifts during muscle activity and fatigue.

. Localization and function of ATP-sensitive potassium channels in human skeletal muscle.

Regional cerebral blood flow (rCBF) was measured with high resolution brain dedicated single photon emission computer tomography (SPECT) and [SS-Tc]-d,lI-hexamethyl-propylene-