The impact of a single bout of high intensity circuit training on myokines' concentrations and cognitive functions in women of different age.

The study aimed to assess effect of a single bout of high-intensity circuit training (HICT) on myokines concentration: interleukin-6 and irisin, inteleukin-10, brain-derived neurotrophic factor (BDNF), heat shock proteins (HSP27, HSP70) and cognitive functions among women participated in HICT. It also attempted evaluating whether vitamin D could have modified the effect of HICT. Fourteen healthy, non-active women participating in the experiment were assigned to a young or middle-aged group. They performed a single session HICT using body weight as a resistance, based on the ACSM recommendations. Blood samples were taken before, one and 24h after training. Cognitive functions were assessed before and 1h after the HICT session. Simple statistics and effects of changes for dependent variables were determined using mixed linear modeling, and evaluated by means of magnitude-based inference (MBI). Following a single session of HICT the young group exhibited improved concentration and spatial memory, whereas in middle-aged women these functions were attenuated. A varied tendency was also observed in the levels of myokine IL-6 and cytokine IL-10. Vitamin D was covariate for changes in cognitive functions and myokines' levels after exercise. Its concentration modified the anti-inflammatory effect of HICT, expressed in decreasing HSP70.

Prolonged swimming promotes cellular oxidative stress and p66Shc phosphorylation, but does not induce oxidative stress in mitochondria in the rat heart.

Exercise-induced changes in p66Shc-dependent signaling pathway are still not fully understood. The p66Shc protein is one of the key players in cell signaling, particularly in response to oxidative stress. Therefore, the aim of this study was to investigate the effect of prolonged swimming on the phosphorylation of p66Shc as well as the induction of mitochondrial and cellular oxidative stress in rat hearts. Male Wistar rats were divided into a sedentary control group and an exercise group. The exercised rats swam for 3 hours and were burdened with an additional 3% of their body weight. After the cessation of exercise, their hearts were removed immediately for experiments. The exercise protocol caused increased levels of the following oxidative stress parameters in cardiac cells: DNA damage, protein carbonyls, and lipid dienes. There was also increased phosphorylation of p66Shc without any alterations in Akt and extracellular signal-regulated kinases. Changes in the ferritin L levels and the L to H subunit ratio were also observed in the exercised hearts compared with the control hearts. Despite increased phosphorylation of p66Shc, no significant increase was observed in either mitochondrial H2O2 release or mitochondrial oxidative stress markers. Regardless of the changes in phosphorylation of p66Shc, the antioxidant enzyme activities (superoxide dismutase and catalase) and anti-apoptotic (Bcl2), and pro-apoptotic (Bax) protein levels were not affected by prolonged swimming. Further studies are required to investigate whether p66Shc phosphorylation is beneficial or detrimental to cardiac cells after exercise cessation.

Changes in skeletal muscle iron metabolism outpace amyotrophic lateral sclerosis onset in transgenic rats bearing the G93A hmSOD1 gene mutation.

OBJECTIVE: Recently, iron and the adaptor protein "p66Shc" have been shown to play an important role in the development of amyotrophic lateral sclerosis (ALS) in rats. We hypothesized that changes in muscle p66Shc activity and iron metabolism would appear before visible symptoms of the disease occurred. METHODS: In the present study, we used transgenic rats bearing the G93A hmSOD1 gene mutation and their non-transgenic littermates to test this hypothesis. We examined muscle p66Shc phosphorylation and iron metabolism in relation to oxidative stress in animals at three disease stages: asymptomatic (ALS I), disease onset (ALS II), and end-stage disease (ALS III). RESULTS: Significant changes in iron metabolism and markers of lipid and protein oxidation were detected in ALS I animals, which manifested as decreased levels of ferritin H and ferroportin 1 (Fpn1) and increased levels of ferritin L levels. Muscles of ALS I rats possessed increased levels of p66Shc phosphorylated at Ser(36) compared with muscles of control rats. During disease progression, level of ferritin H significantly increased and was accompanied by iron accumulation. CONCLUSIONS: This study showed that multiple mechanisms may underlie iron accumulation in muscles of ALS transgenic rats, which include changes in blood hepcidin and muscle Fpn1 and increased level of muscle ferritin H. These data suggest that impaired iron metabolism is not a result of changes in motor activity.