Differences in Abdominal Muscle Thickness, Strength, and Endurance in Persons Who Are Runners, Active, and Inactive.

BACKGROUND: Core musculature is important for efficiency during activities including running. Both abdominal muscle strength and endurance contribute to this efficiency. The purpose of this study is to determine what differences and relationships exist in abdominal muscle thickness, strength, and endurance among persons who are runners, active, and inactive. HYPOTHESIS: Persons in the running group would show significantly greater abdominal muscle thickness, muscle strength, and muscle endurance compared with those in the nonrunning groups. STUDY DESIGN: Quantitative cohort design. LEVEL OF EVIDENCE: Level 2b. METHODS: A total of 78 subjects aged 18 to 27 years were divided into 3 groups: runners, active, and inactive. Assessment included abdominal muscle thickness via diagnostic ultrasound (Mindray North America), strength using a static Isotrack dynamometer (JTech Medical), and abdominal muscle endurance using a side plank. Statistical analysis using analysis of variance, t tests, and Pearson's correlation coefficients and partial correlations was performed using SPSS Version 26 with a significance level of P < 0.05. RESULTS: Significantly greater muscle thickness of internal obliques (IOs) at rest and during contraction was found in the running group compared with the active group, the active group compared with the inactive group, and the running group compared with the inactive group. There were no statistically significant differences in overall strength measured by dynamometry among the 3 groups. Plank time was significantly greater for the running group compared with the other 2 groups. Male participants were greater in all areas: strength, plank time as a measure of muscle endurance, and muscle thickness. Body mass index was significantly correlated with resting thickness, muscle endurance, and muscle strength. CONCLUSION: Persons who run, are active, and are inactive use their abdominal muscles differently. Runners have thicker IOs and better abdominal muscle endurance than the other 2 groups. Focusing on endurance training of the obliques may be beneficial for persons who run. CLINICAL RELEVANCE: This research could contribute to developing core training programs to ensure runners target the correct abdominal muscles with the best type of training.

Hyaluronan injection in murine osteoarthritis prevents TGFbeta 1-induced synovial neovascularization and fibrosis and maintains articular cartilage integrity by a CD44-dependent mechanism.

INTRODUCTION: The mechanism by which intra-articular injection of hyaluronan (HA) ameliorates joint pathology is unknown. Animal studies have shown that HA can reduce synovial activation, periarticular fibrosis and cartilage erosion; however, its specific effects on the different cell types involved remain unclear. We have used the TTR (TGFbeta1 injection and Treadmill Running) model of murine osteoarthritis (OA), which exhibits many OA-like changes, including synovial activation, to examine in vivo tissue-specific effects of intra-articular HA. METHODS: The kinetics of clearance of fluorotagged HA from joints was examined with whole-body imaging. Naïve and treated knee joints were examined macroscopically for cartilage erosion, meniscal damage and fibrosis. Quantitative histopathology was done with Safranin O for cartilage and with Hematoxylin & Eosin for synovium. Gene expression in joint tissues for Acan, Col1a1, Col2a1, Col3a1, Col5a1, Col10a1, Adamts5 and Mmp13 was done by quantitative PCR. The abundance and distribution of aggrecan, collagen types I, II, III, V and X, ADAMTS5 and MMP13 were examined by immunohistochemistry. RESULTS: Injected HA showed a half-life of less than 2 h in the murine knee joint. At the tissue level, HA protected against neovascularization and fibrosis of the meniscus/synovium and maintained articular cartilage integrity in wild-type but not in Cd44 knockout mice. HA injection enhanced the expression of chondrogenic genes and proteins and blocked that of fibrogenic/degradative genes and proteins in cartilage/subchondral bone, whereas it blocked activation of both groups in meniscus/synovium. In all locations it reduced the expression/protein for Mmp13 and blocked Adamts5 expression but not its protein abundance in the synovial lining. CONCLUSIONS: The injection of HA, 24 h after TGFbeta1 injection, inhibited the cascade of OA-like joint changes seen after treadmill use in the TTR model of OA. In terms of mechanism, tissue protection by HA injection was abrogated by Cd44 ablation, suggesting that interaction of the injected HA with CD44 is central to its protective effects on joint tissue remodeling and degeneration in OA progression.

Knockout of ADAMTS5 does not eliminate cartilage aggrecanase activity but abrogates joint fibrosis and promotes cartilage aggrecan deposition in murine osteoarthritis models.

To investigate the role of ADAMTS5 in murine osteoarthritis (OA), resulting from destabilization of the medial meniscus (DMM model) or from TGFb1 injection and enforced uphill treadmill running (TTR model). Wild-type (WT) and ADAMTS5-/- mice were subjected to either DMM or TTR and joints were evaluated for meniscal damage, cartilage changes, and fibrotic ingrowths from the joint margins. Cartilage lesions were quantified on an 8-point scoring system. Cartilage chondroitin sulfate (CS) content was evaluated by SafraninO staining and by quantitative electrophoresis (FACE). The abundance of aggrecan, versican, and specific aggrecanase-generated products was determined by Western analysis. Joint changes were similar for WT mice taken through either the DMM or the TTR model. ADAMTS5 ablation essentially eliminated cartilage erosion and fibrous overgrowth in both models. In the TTR model, ADAMTS5 ablation did not eliminate aggrecanase activity from the articular cartilage but blocked fibrosis and resulted in the accumulation of aggrecan in the articular cartilage. The cartilage protection provided by ADAMTS5 ablation in the mouse does not result from prevention of aggrecanase activity per se, but it appears to be due to a blockade of joint tissue fibrosis and a concomitant increase in cartilage aggrecan content.