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This study investigated the impact of resistance training with blood flow restriction during rest (BFRrest) on the accuracy of estimated repetitions to failure (ERF). It also explored associations between error in ERF and mean concentric velocity (MCV) along with physiological responses. In a randomised cross-over study, 18 male trainers (23.4 ± 2.7 years) performed three sets of squats at 70% of their one-repetition maximum until failure. One session integrated BFRrest, while another employed traditional passive inter-set rest (TRAD) during the 3 min inter-set rest intervals. Cardiorespiratory and metabolic measures were taken in the inter-set recovery periods. The results revealed no significant differences between BFRrest and TRAD in terms of ERF and error in ERF. A notable set effect for ERF was observed, with a greater ERF during set 1 compared to sets 2 and 3 (p < 0.001). Additionally, a lower error in ERF was observed during sets 2 and 3 compared to set 1 (p < 0.001). Error in ERF were strongly associated with the respiratory exchange ratio, and moderately associated with end-tidal carbon dioxide partial pressure, carbon dioxide output, and MCV variables. Notably, the precision of ERF seems to be predominantly influenced by indicators of physiological stress rather than the incorporation of BFRrest. [ABSTRACT FROM AUTHOR]

The clinical application of doxorubicin (DOX) for cancer treatment is limited due to its cardiotoxicity. However, the basic pathophysiological molecular mechanisms underlying DOX-induced cardiomyopathy have not yet been completely clarified, and the disease-specific therapeutic strategies are lacking. The aim of the present study was to investigate the potential cardioprotective effect of cardamonin (CAR), a flavone found in Alpinia plant, on DOX-induced cardiotoxicity in a mouse model. At first, in DOX-treated mouse cardiomyocytes, CAR showed significantly cytoprotective effects through elevating nuclear factor erythroid-2 related factor 2 (Nrf2) signaling, and reducing the degradation of Nrf2. This process then improved the anti-oxidant system, as evidenced by the up-regulated expression levels of haem oxygenase-1 (HO1), NAD(P)H:quinone oxidoreductase 1 (NQO1), glutamate-cysteine ligase modifier subunit (GCLM), superoxide dismutase (SOD), glutathione (GSH) and catalase (CAT). In contrast, DOX-induced increases in malondialdehyde (MDA) and reactive oxygen species (ROS) were highly inhibited by CAR treatments. Additionally, DOX-induced apoptosis and inflammatory response in cardiomyocytes were diminished by CAR through reducing the Caspase-3 and nuclear factor-κB (NF-κB) signaling pathways, respectively. Then, in the DOX-induced animal model with cardiotoxicity, we confirmed that through improving Nrf2 signaling, CAR markedly suppressed oxidative stress, apoptosis and inflammatory response in hearts of mice, improving cardiac function eventually. Together, our findings demonstrated that CAR activated Nrf2-related cytoprotective system, and protected the heart from oxidative damage, apoptosis and inflammatory injury, suggesting that CAR might be a potential therapeutic strategy in the prevention of DOX-associated myocardiopathy.