It variables using a force platform. Sixty-two subjects performed ten gait trials each, stepping on the force platform five times with each leg. From these gait trials a symmetry index was calculated for 34 gait variables. The upper and lower limits of normal gait were calculated such that 95% of all symmetry indices obtained from this subject population fell within these limits. Upper and lower limits were found to vary from ±4% to over ±13,000%. Extremely high percentages were found for variables which had absolute magnitudes close to zero and/or variables which occurred at distinctly different instants during the gait cycle. The results of these variables need to be interpreted with caution. ©1989The American College of Sports Medicine...

The sliding filament and cross-bridge theories of muscle contraction provide discrete predictions of the tetanic force-length relationship of skeletal muscle that have been tested experimentally. The active force generated by a maximally activated single fiber (with sarcomere length control) is maximal when the filament overlap is optimized and is proportionally decreased when overlap is diminished. The force-length relationship is a static property of skeletal muscle and, therefore, it does not predict the consequences of dynamic contractions. Changes in sarcomere length during muscle contraction result in modulation of the active force that is not necessarily predicted by the cross-bridge theory. The results of in vivo studies of the force-length relationship suggest that muscles that operate on the ascending limb of the force-length relationship typically function in stretch-shortening cycle contractions, and muscles that operate on the descending limb typically function in shorten-stretch cycle contractions. The joint moments produced by a muscle depend on the moment arm and the sarcomere length of the muscle. Moment arm magnitude also affects the excursion (length change) of a muscle for a given change in joint angle, and the number of sarcomeres arranged in series within a muscle fiber determines the sarcomere length change associated with a given excursion.

Inflammation can arise in response to a variety of stimuli, including infectious agents, tissue injury, autoimmune diseases, and obesity. Some of these responses are acute and resolve, while others become chronic and exert a sustained impact on the host, systemically, or locally. Obesity is now recognized as a chronic low-grade, systemic inflammatory state that predisposes to other chronic conditions including metabolic syndrome (MetS). Although obesity has received considerable attention regarding its pathophysiological link to chronic cardiovascular conditions and type 2 diabetes, the musculoskeletal (MSK) complications (i.e., muscle, bone, tendon, and joints) that result from obesity-associated metabolic disturbances are less frequently interrogated. As musculoskeletal diseases can lead to the worsening of MetS, this underscores the imminent need to understand the cause and effect relations between the two, and the convergence between inflammatory pathways that contribute to MSK damage. Muscle mass is a key predictor of longevity in older adults, and obesity-induced sarcopenia is a significant risk factor for adverse health outcomes. Muscle is highly plastic, undergoes regular remodeling, and is responsible for the majority of total body glucose utilization, which when impaired leads to insulin resistance. Furthermore, impaired muscle integrity, defined as persistent muscle loss, intramuscular lipid accumulation, or connective tissue deposition, is a hallmark of metabolic dysfunction. In fact, many common inflammatory pathways have been implicated in the pathogenesis of the interrelated tissues of the musculoskeletal system (e.g., tendinopathy, osteoporosis, and osteoarthritis). Despite these similarities, these diseases are rarely evaluated in a comprehensive manner. The aim of this review is to summarize the common pathways that lead to musculoskeletal damage and disease that result from and contribute to MetS. We propose the overarching hypothesis that there is a central role for muscle damage with chronic exposure to an obesity-inducing diet. The inflammatory consequence of diet and muscle dysregulation can result in dysregulated tissue repair and an imbalance toward negative adaptation, resulting in regulatory failure and other musculoskeletal tissue damage. The commonalities support the conclusion that musculoskeletal pathology with MetS should be evaluated in a comprehensive and integrated manner to understand risk for other MSK-related conditions. Implications for conservative management strategies to regulate MetS are discussed, as are future research opportunities.

We investigated force enhancement following stretching in the in situ cat soleus muscle on the ascending and descending limb of the force-length relationship by varying the amount and speed of stretching and the frequency of activation (5 Hz, 30 Hz). There was a small but consistent(P<0.05) amount of force enhancement following muscle stretching on the ascending limb of the force—length relationship for both stimulation frequencies. The steady-state active isometric forces following stretches of 9 mm on the descending limb of the force—length relationship were always equal to or greater than the corresponding forces from the purely isometric contractions at the length at which the stretch was started. Therefore, force production for these trials showed positive stiffness and was associated with stable behavior. Following active stretching of cat soleus on the descending limb of the force—length relationship,the passive forces at the end of the test were significantly greater than the corresponding passive forces for purely isometric contractions, or the passive forces following stretching of the passive muscle. This passive force enhancement following active stretching increased with increasing magnitude of stretch, was not associated with structural damage, and only disappeared once the muscle was shortened. For stretches of 6 mm and 9 mm, the passive force enhancement accounted for more than 50 % of the total force enhancement,reaching a peak contribution of 83.7 % for the stretches of 9 mm at a speed of 3 mm s^-1. The results of this study suggest that a passive structural element provides a great part of the force enhancement on the descending limb of the force—length relationship of the cat soleus. Furthermore, the results indicate that mechanisms other than sarcomere length non-uniformity alone are operative.