In elderly persons, weak tendons contribute to functional limitations, injuries, and disability, but resistance training can attenuate this age-related decline. We evaluated the effects of resistance training on the extracellular matrix (ECM) of the calcaneal tendon (CT) in young and old rats and its effect on tendon remodeling. Wistar rats aged 3 mo (young, = 30) and 20 mo (old, = 30) were divided into 4 groups: young sedentary, young trained, old sedentary (OS), and old trained (OT). The training sessions were conducted over a 12-wk period. Aging in sedentary rats showed down-regulation in key genes that regulated ECM remodeling. Moreover, the OS group showed a calcification focus in the distal region of the CT, with reduced blood vessel volume density. In contrast, resistance training was effective in up-regulating connective tissue growth factor, VEGF, and decorin gene expression in old rats. Resistance training also increased proteoglycan content in young and old rats in special small leucine-rich proteoglycans and blood vessels and prevented calcification in OT rats. These findings confirm that resistance training is a potential mechanism in the prevention of aging-related loss in ECM and that it attenuates the detrimental effects of aging in tendons, such as ruptures and tendinopathies.-Marqueti, R. C., Durigan, J. L. Q., Oliveira, A. J. S., Mekaro, M. S., Guzzoni, V., Aro, A. A., Pimentel, E. R., Selistre-de-Araujo, H. S. Effects of aging and resistance training in rat tendon remodeling.

RESUMOObjetivo: Verificar a associação da posição do atleta com o tipo de lesão dos membros inferiores em profissionais de futebol do Norte do Brasil. Métodos: 44 atletas profissionais de futebol da cidade de Manaus foram submetidos a um questionário com dados sobre a idade, a posição de jogo, o tipo e o local da lesão. Resultados: Encontrouse associação estatisticamente significante entre o tipo de lesão com a posição do jogador (p = 0,035). Os dois tipos de lesão mais recorrentes nos atletas da cidade de Manaus foram as lesões ligamentares (52,27%) e as musculares (29,55%), sendo que o ligamento do tornozelo e a musculatura posterior da coxa foram os locais mais afetados, ambos com 15,91% de incidência. Conclusão: Foram encontradas associações positivas entre a posição e o tipo de lesão em atletas de futebol do Norte do Brasil.

The aim of the present study is to compare the effects of 12 weeks of resistance training with machines and elastic tubes on functional capacity and muscular strength in older women aged 60 years or over. The participants were randomized into two groups: a machine group (n = 23) and an elastic group (n = 20). They performed 12 weeks of progressive resistance training, twice a week, with similar exercises. Outcomes were assessed at three time points: baseline, postintervention, and 8 weeks after the end of the training. A significant intragroup effect was demonstrated for both groups at postintervention on functional tests and muscle strength. For the functional reach test and elbow flexion strength (180°/s), only the machine group demonstrated significant intragroup differences. No differences were observed between groups for any outcome. At the 8-week follow-up, functional capacity outcome values were maintained. The muscle strength outcome values decreased to baseline scores, without differences between groups.

Several side effects of anabolic-androgenic steroid (AAS) administration associated with training are reported in the biomechanical properties of the calcaneal tendon (CT) of rats. Thus, the aim of the present study is to evaluate the effects of the detraining and discontinuation of AAS administration on the CT morphology of rats submitted to exercise in water. Animals were divided into two groups (20/group): (1) Immediately after training (IA), and (2) Six weeks of detraining and AAS discontinuation (6W). The IA group included four subgroups: Sedentary (S), Trained (T), Sedentary with AAS administration (SAAS), and trained with AAS administration (TAAS). The 6W group included four subgroups: Sedentary (6W-S), six weeks of detrained (6W-T), six weeks of sedentary with AAS discontinuation (6W-SAAS), and six weeks of detrained with AAS discontinuation (6W-TAAS). Data show significant reduction in adipose cells volume density (Vv%) in the distal CT in 6W-TAAS group, indicating that training can exert a positive effect on the tendon. The 6W-SAAS group exhibited increased adipose cells Vv% in the distal region, compared with the W6-S and W6-T groups. A decrease in tendon proper cells Vv% and in peritendinous sheath cells Vv% of proximal and distal regions was also observed. In 6W-TAAS group showed increase in adipose cells, blood vessels, peritendinous sheath cells, and tendon proper cells Vv% in the distal region of the CT. The vertical jumps in water were not able to protect CT regions from the negative effects of AAS discontinuation for six weeks. However, after detraining and AAS discontinuation, many protective factors of the mechanical load in the long-term could be observed.(tenocytes) embedded in a unique extracellular matrix (ECM) [2]. The main function of tendons is to transfer the contractile forces generated by the muscles to the bones, generating movement [3].It is well-documented that mechanical loading (e.g., exercise) increases the expression and secretion of several regulatory factors of tenocyte proliferation, ECM remodeling, and collagen synthesis in tendons [4][5][6][7]. It is generally presumed that the increased secretion of these growth factors and enzymes is responsible for the development of exercise-induced adaptations, which include an increased tendon cross-sectional area, tendon stiffness, and collagen crosslinking [2,8,9]. Thus, it is clear that physiological loads influence tendon cells, producing cellular signals that lead to positive adaptations to the tissue.On the other hand, a systematic review investigated the effects of training interruption on tendon mechanobiology, indicating that detraining (four weeks of no exercise in animals) causes rearrangement in the collagen fiber, increasing collagen type III and reducing collagen type I, causing a loss of resistance to tension, increasing rigidity and the risk of rupture in the entheses [10]. In addition, detraining leads to a reduction in collagen type I and III synthesis and tenocyte activity, despite the matrix metalloproteinases (M...