In vivo supraspinatus muscle contractility and architecture in rabbit

Abstract

The rotator cuff (RC) muscles are crucial in moving and stabilizing the glenohumeral joint, and tears can be functionally devastating. Chronic fatty and fibrotic muscle changes, which are non-responsive to surgical tendon repair, are a focus of contemporary research. The rabbit model recapitulates key biological features of human RC tears, but function and physiology are poorly characterized-limited force and stress data are inconsistent with literature norms in other mammalian species. Here, we present an improved method to assess the physiology of the rabbit SSP, and report values for healthy SSP architecture and physiology. Using female New Zealand White Rabbits (n=6) under 2% isofluorane anesthesia, the SSP was surgically isolated and maximum isometric force measured at 4-6 muscle lengths. Architectural analysis was performed, and maximum isometric stress was computed. Whole muscle length-tension curves were generated using architectural measurements to compare experimental physiology to theoretical predictions. Maximum isometric force (80.87± 5.58N) was dramatically greater than previous reports (11.06 and 16.1N, p<0.05). Architectural measurement of fiber length (34.25 ± 7.18mm), muscle mass (9.9 ± 0.93g), pennation angle (23.67 ± 8.32°), and PCSA (2.57 ± 0.20cm2) were consistent with prior literature. Isometric stress (30.5 ± 3.07N/cm2) was greater than previous reports of rabbit SSP (3.10 and 4.51 N/cm2), but similar to mammalian skeletal muscles (15.7-30.13 N/cm2). Previous studies underestimated peak force by ~90%, having profound implications for interpreting physiological changes as a function of disease state. Data presented here enable understanding the physiological implications of disease and repair in the RC of the rabbit.

Transcriptional Time Course After Rotator Cuff Tear

“…The rabbit model is an advantageous system to use to study this question due to similar morphological changes such as increased fat, fibrosis, and degeneration (Rubino et al, 2007;Farshad et al, 2012;Valencia et al, 2018;Hyman et al, 2020Hyman et al, , 2021Vargas-Vila et al, 2021) to what is observed in the supraspinatus (SSP) in humans (Gibbons et al, 2017(Gibbons et al, , 2018b without the need of a neurectomy as in smaller animal models (Rowshan et al, 2010). The major physiological changes noted in this model include significant decrease in muscle fiber crosssectional area (CSA) at 4 and 16 weeks, degeneration of muscle fibers with a ∼25% muscle mass reduction after 16 weeks, and an increase in collagen and fat between 4 to 16 weeks (Rubino et al, 2007;Farshad et al, 2012;Valencia et al, 2018;Hyman et al, 2020Hyman et al, , 2021Vargas-Vila et al, 2021). Understanding the progression of RC disease before repair may help determine the potential effectiveness of a surgical intervention with or without adjuvant therapeutics.…”