Effects of strength training and raloxifene on femoral neck metabolism and microarchitecture of aging female Wistar rats.

The aim of this study was to prevent female osteoporosis using strength training (ST), raloxifene (Ral) or a combination of ST plus Ral during the natural female aging process, specifically in the periestropause period. For a total of 120 days, aging female Wistar rats at 18-21 months of age performed ST on a ladder three times per week, and Ral was administered daily by gavage (1 mg/kg/day). Bone microarchitecture, areal bone mineral density, bone strength of the femoral neck, immunohistochemistry, osteoclast and osteoblast surface were assessed. We found that the treatments modulate the bone remodeling cycle in different ways. Both ST and Ral treatment resulted in improved bone microarchitecture in the femoral neck of rats in late periestropause. However, only ST improved cortical microarchitecture and bone strength in the femoral neck. Thus, we suggest that performing ST during the late period of periestropause is a valid intervention to prevent age-associated osteoporosis in females.

Effects of strength training on osteogenic differentiation and bone strength in aging female Wistar rats.

The effects of strength training (ST) on the mechanical bone strength and osteogenic differentiation of bone marrow mesenchymal stromal cells (BMSCs) from adult, aged and exercised aged rats were determined. The exercised aged animals displayed higher values of areal bone mineral density, compression test, alkaline phosphatase activity (ALP) and biological mineralization, while oil red O staining for adipocytes was lower. ST increased gene expression of runt-related transcription factor 2 (Runx2), osterix (Osx) as well as bone matrix protein expression, and reduced expression of peroxisome proliferator-activated receptor gamma (Pparγ). The production of pro-inflammatory cytokine tumor necrosis factor alpha (TNF-α) was lower in BMSCs of the aged exercised group. The ST practice was able to improve the bone mechanical properties in aged female rats, increasing the potential for osteogenic differentiation of BMSCs, reducing the adipogenic differentiation and pro-inflammatory cytokine level. In summary, the data achieved in this study showed that strength training triggers physiological responses that result in changes in the bone microenvironment and bring benefits to biomechanical parameters of bone tissue, which could reduce the risk of fractures during senescent.

Strength training prior to muscle injury potentiates low-level laser therapy (LLLT)-induced muscle regeneration.

We evaluated whether strength training (ST) performed prior to skeletal muscle cryolesion would act as a preconditioning, improving skeletal muscle regeneration and responsiveness to low-level laser therapy (LLLT). Wistar rats were randomly assigned into non-exercised (NE), NE plus muscle lesion (NE + LE), NE + LE plus LLLT (NE + LE + LLLT), strength training (ST), ST + LE, and ST + LE + LLLT. The animals performed 10 weeks of ST (climbing ladder; 3× week; 80% overload). Forty-eight hours after the last ST session, tibialis anterior (TA) cryolesion was induced and LLLT (InGaAlP, 660 nm, 0.035 W, 4.9 J/cm2/point, 3 points, spot light 0.028 cm2, 14 J/cm2) initiated and conducted daily for 14 consecutive days. The difference between intergroups was assessed using Student's t test and intragroups by two-way analysis of variance. Cryolesion induced massive muscle degeneration associated with inflammatory infiltrate. Prior ST improved skeletal regeneration 14-days after cryolesion and potentiated the regenerative response to LLLT. Cryolesion induced increased TNF-α levels in both NE + LE and ST + LE groups. Both isolated ST and LLLT reduced TNF-α to control group levels; however, prior ST potentiated LLLT response. Both isolated ST and LLLT increased IL-10 levels with no additional effect. In contrast, increased TA IL-6 levels were restricted to ST and ST + LE + LLLT groups. TA myogenin mRNA levels were not changed by neither prior ST or ST + LLLT. Both prior ST and LLLT therapies increased MyoD mRNA levels and, interestingly, combined therapies potentiated this response. Myf5 mRNA levels were increased only in ST groups. Taken together, our data provides evidences for prior ST potentiating LLLT efficacy in promoting skeletal muscle regeneration.

Influência da terapêutica hormonal estrogênica e do treinamento de força sobre o tecido muscular esquelético de ratas senis / Influence of hormonal estrogenic therapy and strength training on skeletal muscle of senile rats

A diminuição das concentrações plasmáticas de estrógeno está intimamente relacionada com o aumento do estresse oxidativo e a diminuição da massa muscular em idosos. A terapêutica hormonal estrogênica (THE) e o treinamento de força (TF) apresentam resultados efetivos sobre a manutenção do tecido muscular em idosos. No entanto, os mecanismos responsáveis pelas melhorias induzias por ambas as intervenções são pouco elucidados. Nesse sentido, avaliamos os efeitos da THE, do TF e a associação sobre a manutenção do tecido muscular esquelético de ratas periestropausadas. Ratas Wistar (18 meses) foram distribuídas em: Grupo não treinado (NT-Veh), Grupo NT tratado com a THE (NT-E2), Grupo TF (TF-Veh) e Grupo TF-E2. Os animais receberam a THE (17ß estradiol; 2 x semana; 25 µg/kg/administração) e/ou praticaram TF (3 x semana; 80% sobrecarga) durante 16 semanas. A THE e o TF induzem benefícios ao tecido muscular esquelético de ratas periestropausadas, no entanto, por diferentes maneiras. Enquanto a THE induziu diminuição do estresse oxidativo muscular (Dihidroetidina), o TF resultou em melhoras significativas na função muscular, no sistema antioxidante muscular (Catalase) e na expressão de miRNAs (206, 146b e 133a). Já a interação das intervenções resultou em melhora no estado redox (Sirt1, Sirt3, PGC-1α, COXIV), na responsividade dos receptores estrogênicos (ERα, ERß e GPR30), e atividade de vias de sinalização do tecido muscular (IGF-1/Akt-1/mTOR). Além disso, as intervenções de maneira isolada ou em associação, levaram ao aumento no percentual de fibras glicolíticas e redução das oxidativas. Sugerimos que a aderências das intervenções (associadas ou não) possam minimizar/atenuar a perda da massa muscular observada em fases tardias durante o processo de envelhecimento(AU)

The decrease of estrogen (E2) circulating levels is strongly related to increased oxidative stress and the loss of muscle mass in elderly. The hormone replacement therapy (HRT) and strength training (ST) are the main effective interventions to prevent the loss of muscle mass, however, the mechanisms involved in interventions-induced benefits are not well elucidated. In this sense we evaluate the effect of HRT, ST and association on skeletal muscle maintenance of periestropaused rats. Female Wistar rats (18 months old) were randomly assigned into: non-exercised and non-treated group (NE-Veh), NE treated group (NE-E2), exercised and non-treated group (ST-Veh) and ST-E2 group. The animals received the HRT (17ß estradiol; 2 x week; 50 µg/kg/week) and/or performed ST (3 x week, 80% overload) for 16 weeks. The HRT and ST promoted beneficial effects on skeletal muscle of periestropaused rats, however, by different manners. While HRT treatment leaves the reduction of oxidative stress (Dihidroetidine), the ST resulted in significate improvement on skeletal muscle function, in skeletal muscle antioxidant system (Catalase) and in miRNAs expression (2016, 146b and 133a). Already, the association of interventions resulted in improvement of redox state (Sirt1, Sirt3, PGC-1α, COXIV), in estrogen receptor responsiveness (ERα, ERß and GPR30) and the activity of skeletal muscle signaling pathways (IGF-1/Akt-1/mTOR). In addition, the interventions, isolated or combinated, leaves an increase of the percentage of glycolytic fibers and reduced percentage of oxidative fibers. We suggest that the adherence to interventions (combinated or not) could minimize/attenuate the loss of skeletal muscle mass observed in later phases of aging process(AU)

Effects of neonatal castration and androgenization on sexual dimorphism in bone, leptin and corticosterone secretion.

This study investigated the role of neonatal sex steroids in rats on sexual dimorphism in bone, as well as on leptin and corticosterone concentrations throughout the lifespan. Castration of males and androgenization of females were used as models to investigate the role of sex steroids shortly after birth. Newborn Wistar rats were divided into four groups, two male groups and two female groups. Male pups were cryoanesthetized and submitted to castration or sham-operation procedures within 24 h after birth. Female pups received a subcutaneous dose of testosterone propionate (100 µg) or vehicle. Rats were euthanized at 20, 40, or 120 postnatal days. Body weight was also measured at 20, 40, and 120 days of age, and blood samples and femurs were collected. The length and thickness of the femurs were measured and the areal bone mineral density (areal BMD) was determined by dual-energy X-ray absorptiometry (DEXA). Biomechanical three-point bending testing was used to evaluate bone breaking strength, energy to fracture, and extrinsic stiffness. Blood samples were submitted to a biochemical assay to estimate calcium, phosphorus, alkaline phosphatase, leptin, and corticosterone levels. Weight gain, areal BMD and bone biomechanical properties increased rapidly with respect to age in all groups. In control animals, skeletal sexual dimorphism, leptin concentration, and dimorphic corticosterone concentration patterns were evident after puberty. However, androgen treatment induced changes in growth, areal BMD, and bone mass properties in neonatal animals. In addition, neonatally-castrated males had bone development and mechanical properties similar to those of control females. These results suggest that the exposure to neonatal androgens may represent at least one covariate that mediates dimorphic variation in leptin and corticosterone secretions. The study indicates that manipulation of the androgen environment during the critical period of sexual differentiation of the brain causes long-lasting changes in bone development, as well as serum leptin and corticosterone concentrations. In addition, this study provides useful models for the investigation of bone disorders induced by hypothalamic hypogonadism.

Efeito da suplementação com L-Arginina sobre a produção de mediadores inflamatórios e fatores regenerativos pelo tecido muscular esquelético decorrente de uma sessão de exercício resistido de alta intensidade / Effect of L-Arginine supplementation upon the production of inflammatory mediators and regenerative factors of skeletal muscle tissue arising from a course of oriented pratice of resistance training

Os mecanismos envolvidos na adaptação do tecido muscular à prática de exercícios aeróbios, já está bem elucidada em diversos estudos. Essa adaptação ocorre por meio de um processo de reparo desencadeado por dano muscular (processo inflamatório). O objetivo do presente estudo foi avaliar o efeito da suplementação com L-arginina sobre os mecanismos envolvidos na liberação de mediadores inflamatórios e fatores regenerativos do tecido muscular esquelético após uma simples sessão de exercício resistido (ER) de alta intensidade, e avaliar o possível papel protetor da L-arginina sobre os efeitos desencadeados pelo ER no tecido muscular esquelético. Ratos machos Wistar foram divididos em 5 grupos: (grupo controle (C), pós-exercício(0), 8, 24 e 48 horas pós-exercício), suplementados com L-arginina (1 g/kg) uma hora antes do início do exercício, ou aminoguanidina (50 mg/kg) 30 minutos antes do início do treino, ambos por gavagem. Os animais foram submetidos a prática do TR durante 4 dias por meio de uma escada com 80° de inclinação, e com aparato de sobrepeso, correspondentes à 80% do peso corporal de cada animal, acoplado aos animais somente no quarto dia de treinamento. O sangue periférico e o tecido muscular esquelético (extensor digitorum longus) foram coletados para a análise de Mieloperoxidase (MPO), fator de necrose tumoral (TNF-α), citocina-induzida quimiotática para neutrófilos (CINC-2), fator transformador de crescimento (TGF-β), Colágeno tipo 1, Fator de crescimento endotelial vascular (VEGF), creatina quinase (CK), alanina aminotransferase (ALT), aspartato aminotransferase (AST) e a Proteína C Reativa (CRP) por RT-PCR e ELISA. A suplementação com L-arginina promoveu grande redução na migração de neutrófilos no tecido muscular esquelético, na produção de TNF-α, CINC-2 e CRP, e potencializou a produção e expressão dos fatores regenerativos musculares (TGF-β, Colágeno tipo 1 e VEGF). O pré-tratamento com aminoguanidina reverteu o processo. A suplementação com...

The mechanisms involved of muscular adaptation to aerobic exercise have previously been described in several studies. This adaptation occurred through a repair process following tissue damage (inflammatory process). The aim of this study was to analyze the effect of the L-arginine supplementation upon the mechanisms involved on release of inflammatory mediators and regenerative factors of skeletal muscle tissue post a single bout of high intensity of resistance exercise (RE), and evaluate the possible protective role of L-arginine supplementation in the effects of RE in skeletal muscle tissue. Male Wistar rats were divided into 5 groups: (control group (C), post-exercise (0), 8, 24 and 48 hours post-exercise), with L-arginine (1 g/kg) one hour before training began or aminoguanidine (50 mg/kg), 30 minutes before starting training, both by gavage. The animals were subjected to RE practice for four days, through a staircase with 80° tilt, with the overload apparatus corresponding to 80% relative to the body weight on the fourth day. Peripheral blood plasma samples, skeletal muscle (extensor digitorum longus) were collected for analysis of myeloperoxidase (MPO), tumor necrosis factor (TNF-α), cytokine-induced neutrophil chemoattranct-2 (CINC-2), transforming growth factor β (TGF-β), Collagen type 1, vascular endothelial growth factor (VEGF), creatine kinase (CK), alanine aminotransferase (ALT), aspartate aminotransferase (AST) and C-Reactive protein (CRP) by RT-PCR and ELISA. L-arginine promoted a great reduction in neutrophil migration, TNF-α, CINC-2 and CRP, and up-regulated the regenerative factors of skeletal muscle (TGF-β, collagen type 1 and VEGF). Aminoguanidine pre-treatment reversed the process. L-arginine (nitric oxide precursor) supplementation played a protective role in the skeletal muscle tissue and increased the expression of regenerative factors after a high intensity RE session. We suggest that this protection is related to the nitric oxide (NO)...