Muscles and tendons are highly adaptive to changes in chronic loading, though little is known about the adaptative time course. We tested the hypothesis that, in response to unilateral lower limb suspension (ULLS), the magnitude of tendon mechanical adaptations would match or exceed those of skeletal muscle. Seventeen men, (1.79±0.05 m, 76.6±10.3 kg, 22.3±3.8 years underwent ULLS for 23 days (n=9) or acted as controls (n=8). Knee extensors (KE) torque, voluntary activation (VA), cross‐sectional area (CSA) (by magnetic resonance imaging), vastus lateralis fascicle length (Lf) and pennation angle (vartheta), patellar tendon stiffness and Young's modulus (by ultrasonography) were measured before, during and at the end of ULLS. After 14 and 23 days, (i) KE torque decreased by 14.8±5.5% and 21.0±7.1%, respectively (P<0.001); (ii) VA did not change; (iii) KE CSA decreased by 5.2±0.7% (P<0.001) and 10.0±2.0% (P<0.001); Lf decreased by 5.9% (NS) and 7.7% (P<0.05) and vartheta by 3.2% (P<0.05) and, (iv) tendon stiffness and modulus decreased by 9.8±8.2% (P<0.05) and 9.2±8.2% (P<0.05) at 14 days, and by 29.3±11.5% (P<0.005) and 30.1±11.9% (P<0.01) at 23 days, with no changes in the controls. Hence, ULLS induces rapid losses of KE muscle size, architecture and function, but not in neural drive. Significant deterioration in tendon mechanical properties also occurs within 2 weeks, exacerbating in the third week of ULLS. Rehabilitation to limit muscle and tendon deterioration should probably start within 2 weeks of unloading.

Rheumatoid cachexia is under-recognized in clinical practice. The loss of lean body tissue, which characterizes cachexia, is often compensated for by gain in body fat-so called 'cachectic obesity'-so that 85% or more RA patients have a normal BMI. Severe cachexia with loss of weight leads to increased morbidity and premature mortality but loss of muscle bulk with a normal BMI also associates with poor clinical outcomes. Increasing BMI, even into the obese range, is associated with less joint damage and reduced mortality. Measurement of body composition using DXA and other techniques is feasible but the results must be interpreted with care. Newer techniques such as whole-body MRI will help define with more confidence the mass and distribution of fat and muscle and help elucidate the relationships between body composition and outcomes. Cachexia shows little response to diet alone but progressive resistance training and anti-TNF therapies show promise in tackling this potentially disabling extra-articular feature of RA.

Leucine catabolism is regulated by either of the first two degradative steps: (reversible) transamination to the keto acid or subsequent decarboxylation. A method is described to measure rates of leucine transamination, reamination, and keto acid oxidation. The method is applied directly to humans by infusing the nonradioactive tracer, L-[15N,1-13C]leucine. Leucine transamination was found to be operating several times faster than the keto acid decarboxylation and to be of equal magnitude in adult human males under two different dietary conditions, postabsorptive and fed. These results indicate that decarboxylation, not transamination, is the rate-limiting step in normal human leucine metabolism.

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Whole body exercise at intensities up top 50% VO2max has no effect on the concentration of blood ammonia but a threefold rise in blood ammonia is observed at workloads up to maximal. There is a linear relationship between blood ammonia and lactate production during exercise which suggests that the two processes may be linked to a common process of short-term energy provision. Blood glutamine and blood alanine both show rises linearly related to power output during exercise, suggesting that if these amino acids are sinks for ammonia then the process of ammonia incorporation is saturated at high workloads.