Chronic Blood Pressure Reductions and Increments in Plasma Nitric Oxide Bioavailability.

This study analyzed the effects of 12 weeks of resistance training (RT) on resting blood pressure (BP) and plasma levels of nitric oxide metabolites (NOx) in pre- and hypertensive older women, and evaluated the relationship between these 2 parameters. Thirty-five older women (68.2±5.7 years, 70.0±14.4 kg, 157.1±6.4 cm, 28.3±5.0 kg.m-2) were randomly allocated into a training group (TG; n=17), which performed a 12-week RT program, and a control group (CG; n=18), which did not perform any physical exercise. Anthropometry, one repetition maximum (1RM), body composition analysis by dual energy X-ray absorptiometry, blood samples, and resting BP were measured. There was a significant interaction for all variables analyzed, in which reductions of systolic BP (-8.5%), diastolic BP (-8.4%), and mean arterial pressure (-8.5%), and increases of NOx (+35.2%) were observed only for the TG. Moreover, a negative and significant correlation was observed (P<0.05; r=-0.63) between NOx and systolic BP in the TG. Results suggest that a 12-week RT program is sufficient to induce reductions in BP in pre- and hypertensive older women and that the decrease in systolic BP is associated with an increase in plasma NOx concentration.

Resistance Training Attenuates Activation of STAT3 and Muscle Atrophy in Tumor-Bearing Mice.

Purpose: Although the role of signal transducers and activators of transcription (STAT3) in cachexia due to the association of circulating IL-6 and muscle wasting has been extensively demonstrated, the effect of resistance training on STAT3 in mediating muscle atrophy in tumor-bearing mice is unknown. The aim of this study is to investigate the effects of resistance exercise training on inflammatory cytokines and oxidative-mediated STAT3 activation and muscle loss prevention in tumor-bearing mice. Methods: Male Swiss mice were inoculated with Ehrlich tumor cells and exposed or not exposed to resistance exercise protocol of ladder climbing. Skeletal muscle STAT3 protein content was measured, compared between groups, and tested for possible association with plasma interleukins and local oxidative stress markers. Components of the ubiquitin-proteasome and autophagy pathways were assessed by real-time PCR or immunoblotting. Results: Resistance training prevented STAT3 excessive activation in skeletal muscle mediated by the overabundance of plasma IL-6 and muscle oxidative stress. These mechanisms contributed to preventing the increased key genes and proteins of ubiquitin-proteasome and autophagy pathways in tumor-bearing mice, such as Atrogin-1, LC3B-II, and Beclin-1. Beyond preventing muscle atrophy, RT also prevented strength loss and impaired locomotor capacity, hallmarks of sarcopenia. Conclusion: Our results suggest that STAT3 inhibition is central in resistance exercise protective effects against cancer-induced muscle atrophy and strength loss.

Syngeneic B16F10 Melanoma Causes Cachexia and Impaired Skeletal Muscle Strength and Locomotor Activity in Mice.

Muscle wasting has been emerging as one of the principal components of cancer cachexia, leading to progressive impairment of work capacity. Despite early stages melanomas rarely promotes weight loss, the appearance of metastatic and/or solid tumor melanoma can leads to cachexia development. Here, we investigated the B16F10 tumor-induced cachexia and its contribution to muscle strength and locomotor-like activity impairment. C57BL/6 mice were subcutaneously injected with 5 × 104 B16F10 melanoma cells or PBS as a Sham negative control. Tumor growth was monitored during a period of 28 days. Compared to Sham mice, tumor group depicts a loss of skeletal muscle, as well as significantly reduced muscle grip strength and epididymal fat mass. This data are in agreement with mild to severe catabolic host response promoted by elevated serum tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and lactate dehydrogenase (LDH) activity. Tumor implantation has also compromised general locomotor activity and decreased exploratory behavior. Likewise, muscle loss, and elevated inflammatory interleukin were associated to muscle strength loss and locomotor activity impairment. In conclusion, our data demonstrated that subcutaneous B16F10 melanoma tumor-driven catabolic state in response to a pro-inflammatory environment that is associated with impaired skeletal muscle strength and decreased locomotor activity in tumor-bearing mice.

Resistance exercise prevents impaired homocysteine metabolism and hepatic redox capacity in Walker-256 tumor-bearing male Wistar rats.

OBJECTIVE: The aim of this study was to investigate changes in homocysteine (Hcy) metabolism and redox balance in response to exercise treatment in a tumor-bearing rat model. METHODS: Male Wistar rats were exposed, or not, to a resistance exercise program 6 wk before inoculation with Walker-256 tumor cells or vehicle. After application, rats maintained their routine for 12 d and were then sacrificed for plasma and liver analyses. RESULTS: Impaired Hcy metabolism was evident after 12 d of tumor cell inoculation as demonstrated by significantly increased (P < 0.05) plasma total homocysteine (tHcy) concentration (53%) and decreased plasma cysteine, methionine, and vitamin B12 concentrations. Decreased hepatic cystathionine ß-synthase (CBS) and betaine-homocysteine S-methyltransferase mRNA levels were found in tumor-bearing rats but not in controls. Tumor inoculation also decreased levels of liver reduced glutathione (GSH) and increased hepatic oxidative stress compared with non-tumor controls. However, resistance exercise prevented the tumor-impaired transsulfuration pathway as demonstrated by the decreased plasma tHcy, hepatic CBS expression, and increased GSH in tumor-exercised versus tumor-sedentary rats. Remarkably, all measures of liver oxidative stress were suppressed by exercise training. Tumor weight was unchanged between groups. CONCLUSION: Resistance exercise prevented tHcy accumulation and liver oxidative damage caused by Walker-256 tumor cell inoculation; the modulatory effects of resistance exercise on Hcy metabolism appear to be at the level of transsulfuration pathway.

Effect of resistance training and detraining on the oxidative stress in obese older women / Efeito do treinamento com pesos e do destreinamento sobre o estresse oxidativo em mulheres idosas obesas

Abstract The aim of this study was to investigate the effect of resistance training (RT) followed by a similar detraining period on the modulation of oxidative stress (OS) in obese older women. Fourteen obese women (age: 68.7 ± 4.8 years, body mass: 71.3 ± 14.8 kg, height: 156.3 ± 7.2 cm, body fat: 44.3 ± 4.4%) were submitted to 12 weeks of a RT program followed by a similar detraining period. Advanced oxidation protein products (AOPP) and total radical-trapping antioxidant potential (TRAP) were used as oxidative stress indicators. AOPP was not changed by RT or detraining (P = 0.31). Furthermore, TRAP was increased with RT (+ 15.1%; P < 0.001) and remained high even after 12 weeks of detraining (10.5%; P < 0.001). The results suggest that OS can be improved by RT and the 12-week detraining period does not seem to be enough to reverse adaptations induced by RT in obese older women.

Resumo O objetivo deste estudo foi investigar a efetividade do treinamento com pesos (TP), seguido por um período semelhante de destreinamento, sobre a modulação do estresse oxidativo (EO) em mulheres idosas obesas. Quatorze mulheres (idade: 68,7 ± 4,8 anos; massa corporal: 71,3 ± 14,8 kg; estatura: 156,3 ± 7,2 cm; gordura corporal: 44,3 ± 4,4%) obesas (gordura corporal relativa ≥ 30%) foram submetidas a 12 semanas de um programa de TP seguido por igual período de destreinamento. Os produtos de proteínas de oxidação avançada (AOPP) e a capacidade antioxidante total plasmática (TRAP) foram utilizados como indicadores de estresse oxidativo. A AOPP não foi alterada pelo TP ou pelo destreinamento (P = 0,31). Por outro lado, a TRAP foi aumentada com o TP (+15,1%; P < 0,001) e se manteve elevada mesmo após 12 semanas de destreinamento (+10,5%; P < 0,001). Os resultados sugerem que o EO pode ser melhorado pelo TP e o período de 12 semanas de destreinamento não parece ser suficiente para desfazer as adaptações induzidas pelo TP em mulheres idosas obesas.