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This study examined the acute and resting changes of brain-derived neurotrophic factor (BDNF) and inteleukin-6 (IL-6) andif changes in these biomarkers were correlated during resistance training (RT). Fifteen men with ≥2 years of RT experience (age: 23 }3 years, body mass: 84.4 } 12.3 kg) participated. Subjects performed RT 3×/week for 6 weeks in either a high-repetition (HR; n = 8) orlow-repetition (LR; n = 7) group. Protocols during week 1 were HR – Monday: 4 (sets) × 12 (repetitions) at 60% of 1-repetition maximum,Wednesday: 4 × 10 at 65%, Friday: 5 × 8 at 70%; LR – Monday: 8 × 6 at 75%, Wednesday 9 × 4 at 80%, Friday: 10 × 2 at 85%. Total volumewas equated for the 6 weeks but not for individual sessions. Greater volume and intensity were performed in LR versus HR (p < 0.01)on Mondays. Plasma was collected immediately before and after exercise of the Monday session. There were no significant interactionsor main effects for BDNF (p > 0.05). There was a moderate between-group effect size (0.57) in favor of LR in week 6, suggesting apotentially greater acute increase in BDNF in LR versus HR. For IL-6, a statistically significant main effect was observed for training(p < 0.0001), showing an acute increase in IL-6 in both weeks (p < 0.01); however, no other 3-way or 2-way interactions existed (p > 0.05).A minimum volume threshold of RT may be needed to induce acute elevations in BDNF. [ABSTRACT FROM AUTHOR]

Exercise training and antioxidant supplementation may improve unintentional weight loss and programmed cell death associated with cancer cachexia. The aim of this study was to examine the alterations of body weight and apoptotic indices in skeletal muscle of 4T1 breast cancer-bearing mice with cachexia following 4 weeks of high-intensity interval training (HIIT) and saffron aqueous extract (SAE) supplementation. Female BALB/c mice following induction of breast cancer were divided into (i) controls, (ii) HIIT, (iii) SAE, (iv) HIIT+SAE, and (v) sham groups. Mice were euthanized and gastrocnemius muscle was collected after intervention. The control group elicited a significant weight reduction during third and fourth weeks of tumor injection, while other treatments such as HIIT and SAE, but not HIIT+SAE, showed that they counteracted this adverse event. Furthermore, HIIT and SAE treatments (not HIIT+SAE) demonstrated reduced caspase-3 and Bax levels compared with the control group. The level of Bcl-2 was elevated following both HIIT and SAE treatments compared with the control group. Finally, the ratio of Bcl-2 to Bax was significantly higher in both HIIT and SAE groups, but was lower in HIIT+SAE group compared with sham group. It is likely that either HIIT or SAE intervention alone (not HIIT+SAE) represents a readily applicable approach in the regulation of muscle wasting and apoptosis in cancer cachexia. [ABSTRACT FROM AUTHOR]

Copyright of Applied Physiology, Nutrition & Metabolism is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Applied Physiology, Nutrition & Metabolism is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Pentraxin 3 (PTX3) has been recently identified as a biomarker of vascular inflammation in predicting cardiovascular events. The purpose of this study was to examine the effect of cardiorespiratory fitness on plasma PTX3 and cortisol responses to stress, utilizing a dual-stress model. Fourteen male subjects were classified into high-fit (HF) and low-fit (LF) groups and completed 2 counterbalanced experimental conditions. The exercise-alone condition (EAC) consisted of cycling at 60% maximal oxygen uptake for 37 min, while the dual-stress condition (DSC) included 20 min of a mental stress while cycling for 37 min. Plasma PTX3 revealed significant increases over time with a significant elevation at 37 min in both HF and LF groups in response to EAC and DSC. No difference in plasma PTX3 levels was observed between EAC and DSC. In addition, plasma cortisol revealed a significant condition by time interaction with greater levels during DSC at 37 min, whereas cardiorespiratory fitness level did not reveal different plasma cortisol responses in either the EAC or DSC. Aerobic exercise induces plasma PTX3 release, while additional acute mental stress, in a dual-stress condition, does not exacerbate or further modulate the PTX3 response. Furthermore, cardiorespiratory fitness may not affect the stress reactivity of plasma PTX3 to physical and combined physical and psychological stressors. Finally, the exacerbated cortisol responses to combined stress may provide the potential link to biological pathways that explain changes in physiological homeostasis that may be associated with an increase in the risk of cardiovascular disease. [ABSTRACT FROM AUTHOR]

Obesity has been shown to have profound effects on hemodynamics and neurological states in humans. Previous studies have demonstrated that obese individuals are highly susceptible to increases in tension, anxiety, and depression. However, the relationship between mental stressors and vascular fluidity in obese humans is not well understood. Thus, the purpose of this study was to investigate mental-stress-induced microvascular reactivity (excess blood flow (EBF)) in normal-weight and obese individuals. In addition, the relationships between potential vascular response modulators (heart rate (HR) and norepinephrine (NE)) and EBF were examined. Twenty-two male subjects were classified as obese ( n = 12) or normal-weight ( n = 10), and each subject completed a 20 min bout of acute mental stress. Our analyses demonstrate significant elevations in forearm blood flow (FBF) and EBF immediately after mental stress in both normal-weight and obese groups. HR was only correlated with EBF immediately poststress in the normal-weight group. Furthermore, stress-induced plasma NE was not associated with FBF or EBF in either group, although in the obese group, stress-induced plasma NE was associated with body mass index and percent body fat. These results suggest that microvascular reactivity after mental stress is not directly related to plasma NE in normal-weight or obese individuals. The novel results presented in this study provide a foundation for additional examination of the mechanisms involved in the effects of mental stress on microvascular reactivity. [ABSTRACT FROM AUTHOR]