The increase or decrease in isometric force following active muscle lengthening or shortening, relative to a reference isometric contraction at the same muscle length and level of activation, are referred to as residual force enhancement (rFE) and residual force depression (rFD), respectively. The purpose of these experiments was to investigate the trainability of rFE and rFD on the basis of serial sarcomere number (SSN) alterations to history-dependent force properties. Maximal rFE/rFD measures from the soleus and extensor digitorum longus (EDL) of rats were compared after 4 weeks of uphill or downhill running with a no-running control. SSN adapted to the training: soleus SSN was greater with downhill compared with uphill running, while EDL demonstrated a trend towards more SSN for downhill compared with no running. In contrast, rFE and rFD did not differ across training groups for either muscle. As such, it appears that training-induced SSN adaptations do not modify rFE or rFD at the whole-muscle level.

Low back pain disorders affect more than 80% of adults in their lifetime and are the leading cause of global disability. The muscles attaching to the spine (ie, paraspinal muscles) are critical for proper spine health and play a crucial role in the functioning of the spine and whole body; however, reports of muscle dysfunction and insufficiency in chronic LBP (CLBP) patients are common. This article presents a review of the current understanding of the relationship between paraspinal muscle pathophysiology and spine‐related disorders. Human literature demonstrates a clear association between altered muscle structure/function, most notably fatty infiltration and fibrosis, and low back pain disorders; other associations, including muscle cell atrophy and fiber type changes, are less clear. Animal literature then provides some mechanistic insight into the complex relationships, including initiating factors and time courses, between the spine and spine muscles under pathological conditions. It is apparent that spine pathology can directly lead to changes in the paraspinal muscle structure, function, and biology. It also appears that changes to the muscle structure and function can directly lead to changes in the spine (eg, deformity); however, this relationship is less well studied. Future work must focus on providing insight into possible mechanisms that regulate spine and paraspinal muscle health, as well as probing how muscle degeneration/dysfunction might be an initiating factor in the progression of spine pathology.

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50The increase or decrease in isometric force following active muscle lengthening or shortening, 51 relative to a reference isometric contraction at the same muscle length and level of activation, are 52 referred to as residual force enhancement (rFE) and residual force depression (rFD), respectively. 53The purpose of these experiments was to gain further mechanistic insight into the trainability of 54 rFE and rFD, on the basis of serial sarcomere number (SSN) alterations to length-dependent 55properties. Maximal rFE/rFD measures from the soleus and extensor digitorum longus (EDL) of 56 rats were compared after 4 weeks of uphill/downhill running and a no running control. Serial 57 sarcomere numbers adapted to the training: soleus serial sarcomere number was greater with 58 downhill compared to uphill running, while EDL demonstrated a trend towards more serial 59 sarcomeres for downhill compared to no running. In contrast, absolute and normalized rFE/rFD 60 did not differ across training groups for either muscle. As such, it appears that training-induced 61 SSN adaptations do not modify rFE/rFD at the whole-muscle level. 62 63 65

Study Design. Basic science study of the relationship between spine pathology and the contractile ability of the surrounding muscles.Objective. The aim of this study was to investigate single muscle fiber contractile function in a model of progressive spine mineralization (ENT1 À/À mice). Summary of Background Data. Altered muscle structure and function have been associated with various spine pathologies; however, studies to date have provided limited insight into the fundamental ability of spine muscles to actively contract and generate force, and how this may change in response to spine pathology. Methods. Experiments were performed on two groups (ENT1 À/ À [KO] and ENT1 þ/þ [WT]) of mice at 8 months of age (n ¼ 12 mice/group). Single muscle fibers were isolated from lumbar multifidus and erector spinae, as well as tibialis anterior (a non-spine-related control) and tested to determine their active contractile characteristics. Results. The multifidus demonstrated decreases in specific force (type IIax fibers: 36% decrease; type IIb fibers: 29% decrease), active modulus (type IIax: 35% decrease; type IIb: 30% decrease), and unloaded shortening velocity (V o ) (type IIax: 31% decrease) in the ENT1 À/À group when compared to WT controls. The erector spinae specific force was reduced in the ENT1 À/À mice when compared to WT (type IIax: 29% decrease), but active modulus and V o were unchanged. There were no differences in any of the active contractile properties of the lower limb TA muscle, validating that impairments observed in the spine muscles were specific to the underlying spine pathology and not the global loss of ENT1. Conclusion. These results provide the first direct evidence of cellular level impairments in the active contractile force generating properties of spine muscles in response to chronic spine pathology.