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Unfamiliar, predominantly eccentric exercise, frequently results in muscle damage. A repeated bout of similar eccentric exercise results in less damage and is referred to as the 'repeated bout effect'. Despite numerous studies that have clearly demonstrated the repeated bout effect, there is little consensus as to the actual mechanism. In general, the adaptation has been attributed to neural, connective tissue or cellular adaptations. Other possible mechanisms include, adaptation in excitation-contraction coupling or adaptation in the inflammatory response. The 'neural theory' predicts that the initial damage is a result of high stress on a relatively small number of active fast-twitch fibres. For the repeated bout, an increase in motor unit activation and/or a shift to slow-twitch fibre activation distributes the contractile stress over a larger number of active fibres. Although eccentric training results in marked increases in motor unit activation, specific adaptations to a single bout of eccentric exercise have not been examined. The 'connective tissue theory' predicts that muscle damage occurs when the noncontractile connective tissue elements are disrupted and myofibrillar integrity is lost. Indirect evidence suggests that remodelling of the intermediate filaments and/or increased intramuscular connective tissue are responsible for the repeated bout effect. The 'cellular theory' predicts that muscle damage is the result of irreversible sarcomere strain during eccentric contractions. Sarcomere lengths are thought to be highly non-uniform during eccentric contractions, with some sarcomeres stretched beyond myofilament overlap. Loss of contractile integrity results in sarcomere strain and is seen as the initial stage of damage. Some data suggest that an increase in the number of sarcomeres connected in series, following an initial bout, reduces sarcomere strain during a repeated bout and limits the subsequent damage. It is unlikely that one theory can explain all of the various observations of the repeated bout effect found in the literature. That the phenomenon occurs in electrically stimulated contractions in an animal model precludes an exclusive neural adaptation. Connective tissue and cellular adaptations are unlikely explanations when the repeated bout effect is demonstrated prior to full recovery, and when the fact that the initial bout does not have to cause appreciable damage in order to provide a protective effect is considered. It is possible that the repeated bout effect occurs through the interaction of various neural, connective tissue and cellular factors that are dependent on the particulars of the eccentric exercise bout and the specific muscle groups involved.

Albuminuria reduction could be renoprotective in hypertensive patients with diabetic nephropathy. However, the current use of renin-angiotensin-system intervention is targeted to BP only. Therefore, this study investigated the adequacy of this approach in 1428 patients with hypertension and diabetic nephropathy from the placebo-controlled Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) study. Investigated were the extent of discordance in treatment effects on systolic BP (SBP) and albuminuria and its association with renal outcome in a multivariate Cox model. Among patients with a reduced SBP during treatment, a lack of albuminuria reduction was observed in 37, 26, and 51% (total, losartan, and placebo, respectively) at month 6. SBP or albuminuria reduction was associated with a lower risk for ESRD, whereas combined SBP and albuminuria reduction was associated with the lowest risk for events. Across all categories of SBP change, a progressively lower ESRD hazard ratio was observed with a larger albuminuria reduction. A lower residual level of albuminuria was also associated with lower ESRD risk. In conclusion, changes in albuminuria are not concordant in a substantial proportion of patients when titrated for BP. Meanwhile, the ESRD risk showed a clear dependence on albuminuria reduction. The ESRD risk also showed dependence on the residual level of albuminuria, even in patients who reached the current SBP target. Antihypertensive treatment that is aimed at improving renal outcomes in patients with diabetic nephropathy may therefore require a dual strategy, targeting both SBP and albuminuria reduction.

The relationship between posterior capsule tightness and dysfunction has long been recognized clinically but has not been biometrically quantified. The purpose of this study was to quantify changes in range of motion and posterior capsule tightness in patients with dominant or nondominant shoulder impingement. Measurements of posterior capsule tightness and external and internal rotation range of motion were made in 31 patients with shoulder impingement and in 33 controls without shoulder abnormality. Patients with impingement in the nondominant arm had increased posterior capsule tightness and decreased internal and external rotation range of motion compared with controls. Patients with impingement in their dominant arm had increased posterior capsule tightness and reduced internal rotation range of motion but no significant loss of external rotation range of motion compared with controls. Posterior capsule tightness in impingement patients showed a significant correlation with loss of internal rotation range of motion. Patients with shoulder impingement in their nondominant arm had a more global loss of range of motion compared with patients having impingement in their dominant arm. We believe we have described a valid clinical measurement for identifying posterior capsule tightness in patients with shoulder impingement.

Flexibility measures can be static [end of ROM (range of motion)], dynamic-passive (stiffness/compliance) or dynamic-active (muscle contracted, stiffness/compliance). Dynamic measures of flexibility are less dependent on patient discomfort and are more objective. Acute and chronic changes in flexibility are likely to occur with stretching exercises, but it is difficult to distinguish between changes in stretch tolerance as opposed to changes in muscle stiffness. How flexibility is measured impacts these findings. There is no scientifically based prescription for flexibility training and no conclusive statements can be made about the relationship of flexibility to athletic injury. The literature reports opposing findings from different samples, frequently does not distinguish between strain, sprain and overuse injury, and rarely uses the proper denominator of exposure. There is basic scientific evidence to suggest that active warm-up may be protective against muscle strain injury but clinical research is equivocal on this point. Typically, specific flexibility patterns are associated with specific sports and even positions within sports. The relationship of flexibility to athletic performance is likely to be sport-dependent. Decreased flexibility has been associated with increased in-line running and walking economy. Increased stiffness may be associated with increased isometric and concentric force generation, and muscle energy storage may be best manifested by closely matching muscle stiffness to the frequency of movement in stretch-shorten type contractions.