The relationship of hip muscle performance to leg, ankle and foot injuries: a systematic review.

OBJECTIVES: Hip control affects movement and muscle firing patterns in the leg, ankle and foot, and may contribute to overuse injuries. Muscle performance can be measured as strength, endurance or muscle activation patterns. Our objective was to systematically review whether hip muscle performance is associated with leg, ankle and foot injuries. DATA SOURCES: A structured and comprehensive search of six medical literature databases was combined with forward and backward citation tracking (AMED, CINAHL, EMBASE, Medline, Scopus and SportDiscus). STUDY SELECTION: Eligible studies measured hip muscle performance in individuals with musculoskeletal injuries below the tibial tuberosity, using dynamometry or electromyography (EMG). All studies compared an injured group with a control group or compared the injured and non-injured limb in the same individual. DATA EXTRACTION: Data was extracted from each study independently by two authors. DATA SYNTHESIS: Twenty case-control and four prospective studies (n = 24) met the inclusion criteria. Injury classifications included chronic ankle instability (n = 18), Achilles tendinopathy (n = 2), medial tibial stress syndrome and tibial stress fracture (n = 1), posterior tibial tendon dysfunction (n = 1), and exertional medial tibial pain (n = 2). Eleven of the studies revealed differences in hip muscle performance indicating less strength, delayed onset activation and decreased duration of activation in the injured groups. Two studies found evidence for differences between groups only in some of their measurements. Three out of the four prospective studies revealed that hip muscle performance was not a risk factor for leg, ankle and foot injuries. CONCLUSIONS: This review provides limited evidence that hip muscle performance variables are related to leg, ankle and foot injuries. Emerging evidence indicates this might be a result of the injury rather than a contributor to the injury.

Evidence of the TNF-α system in the human Achilles tendon: expression of TNF-α and TNF receptor at both protein and mRNA levels in the tenocytes.

UNLABELLED: Understanding adaption to load is essential for prevention and treatment of tendinopathy/tendinosis. Cytokine release in response to load is one mechanism involved in mechanotransduction. The cytokine tumor necrosis factor alpha (TNF-α) is implicated in tendinosis and can induce apoptotic effects via tumor necrosis factor receptor 1 (TNFR1). The complete absence of information concerning the TNF-α system in Achilles tendon is a limitation as mid-portion Achilles tendinosis is very frequent. PURPOSE: To examine expression patterns of TNF-α and its two receptors (TNFR1 and TNFR2) in human Achilles tendinosis and control tissue and to biochemically confirm the presence of TNF-α in tendinosis tissue. METHODS: TNF-α and TNFR1 mRNA were detected via in situ hybridization. TNF-α, TNFR1, and TNFR2 were demonstrated immunohistochemically. Apoptosis markers were utilized. ELISA was used to detect TNF-α. RESULTS: TNF-α and TNFR1 mRNA was detected in tenocytes of both tendinosis and control tendons. Tenocytes from both groups displayed specific immunoreactions for TNF-α, TNFR1, and TNFR2. The widened/rounded tenocytes of tendinosis samples exhibited the most intense immunoreactions. Apoptosis was detected in only a subpopulation of the tenocytes in tendinosis tissue. TNF-α was measurable in tendinosis tissue. Inflammatory cells were not seen. CONCLUSION: This is the first evidence of the existence of the TNF-α system in the human Achilles tendon. Findings are confirmed at mRNA and protein levels as well as biochemically. The TNF-α system was in principle confined to the tenocytes. The connection between tenocyte morphology and the expression pattern of TNF-α, TNFR1, and TNFR2 suggests that the TNF-α system may be involved in tenocyte activation in Achilles tendinosis.

Tenocyte hypercellularity and vascular proliferation in a rabbit model of tendinopathy: contralateral effects suggest the involvement of central neuronal mechanisms.

OBJECTIVE: To determine whether there are objective findings of tendinosis in a rabbit tendinopathy model on exercised and contralateral (non-exercised) Achilles tendons. DESIGN: Four groups of six New Zealand white rabbits per group were used. The animals of one (control) group were not subjected to exercise/stimulation. INTERVENTIONS: Animals were subjected to a protocol of electrical stimulation and passive flexion-extension of the right triceps surae muscle every second day for 1, 3 or 6 weeks. MAIN OUTCOME MEASURES: Tenocyte number and vascular density were calculated. Morphological evaluations were also performed as well as in-situ hybridisation for vascular endothelial growth factor (VEGF) messenger RNA. RESULTS: There was a significant increase in the tenocyte number after 3 and 6 weeks of exercise, but not after 1 week, in comparison with the control group. This was seen in the Achilles tendons of both legs in experimental animals, including the unexercised limb. The pattern of vascularity showed an increase in the number of tendon blood vessels in rabbits that had exercised for 3 weeks or more, compared with those who had exercised for 1 week or not at all. VEGF-mRNA was detected in the investigated tissue, with the reactions being more clearly detected in the tendon tissue with tendinosis-like changes (6-week rabbits) than in the normal tendon tissue (control rabbits). CONCLUSIONS: There were bilateral tendinosis-like changes in the Achilles tendons of rabbits in the current model after 3 weeks of training, suggesting that central neuronal mechanisms may be involved and that the contralateral side is not appropriate as a control.

Dyslipidemia in Achilles tendinopathy is characteristic of insulin resistance.

UNLABELLED: Overuse is considered to be a main causative factor for tendinopathies; however, recent reports indicate that tendinopathy is also common among both overweight and inactive individuals. These factors are associated with abdominal obesity, dyslipidemia, hypertension, and insulin resistance. We hypothesized that these features would be associated with tendinopathy. PURPOSE: To compare lipid profile between participants with Achilles tendinopathy and matched controls. METHODS: Fasting serum lipids were measured among 60 participants with chronic painful midportion Achilles tendinopathy (54% male) and 60 control subjects matched for gender, age (+/-10 yr), and body mass index (+/-2 kg x m(-2)). RESULTS: The participants with Achilles tendinopathy showed evidence of underlying dyslipidemia. They had higher triglyceride (TG) levels (P = 0.039), lower %HDL-C (P = 0.016), higher TG/HDL-C ratio (P = 0.036), and elevated apolipoprotein B concentration (P = 0.017) in comparison to the well-matched control group. CONCLUSIONS: This pattern of dyslipidemia is characteristic of the dyslipidemia displayed by individuals with insulin resistance and is common in the metabolic syndrome. Two additional aspects of tendinopathy research support a connection with the metabolic syndrome. First, tendinopathy has been associated with greater waist circumference, as has the metabolic syndrome. Second, insulin resistance has been associated with fat deposition in muscle (primarily intracellular), whereas fat deposition in tendon has been found among those with tendon pain.If tendinopathy is confirmed to be associated with dyslipidemia and the metabolic syndrome in larger studies, it may be appropriate to redefine our concept of tendinopathy to that of a cardiovascular disease (CVD). In this case, we may be able to draw considerably on CVD research to improve our understanding of tendinopathy, and perhaps treating CVD risk factors will improve the treatment of tendinopathy.