Effects of Consecutive Versus Non-consecutive Days of Resistance Training on Strength, Body Composition, and Red Blood Cells

Health authorities worldwide recommend 2–3 days per week of resistance training (RT) performed ∼48–72 h apart. However, the influence of recovery period between RT sessions on muscle strength, body composition, and red blood cells (RBCs) are unclear.Aim: Examine the effects of three consecutive (C) or non-consecutive (NC) days of RT per week for 12 weeks on strength, body composition, and RBCs.Methods: Thirty young, healthy and recreationally active males were randomly assigned to 3 C (∼24 h between sessions) or NC (∼48–72 h between sessions) days of RT per week for 12 weeks. Both groups performed three sets of 10 repetitions at 10-repetition maximum (RM) of leg press, latissimus pulldown, leg curl, shoulder press, and leg extension for each session. Ten RM and body composition were assessed pre- and post-RT. RBC parameters were measured on the first session before RT, and 0 and 24 h post-3rd session in untrained (week 1) and trained (week 12) states.Results: No training × group interaction was found for all strength and body composition parameters (p = 0.075–0.974). Training increased strength for all exercises, bone mineral density, and total body mass via increased lean and bone mass (p < 0.001). There was no interaction (p = 0.076–0.994) and RT induced temporal changes in all RBC parameters (p < 0.001–0.003) except RBC corrected for plasma volume changes (time × training interaction; p = 0.001). Training increased hematocrit and lowered mean corpuscular hemoglobin and mean corpuscular hemoglobin concentration (p = 0.001–0.041) but did not alter uncorrected RBC, hemoglobin, mean corpuscular volume and RBC distribution width (p = 0.178–0.797).Conclusion: Both C and NC RT induced similar improvements in strength and body composition, and changes in RBC parameters

Mitochondrial targeted catalase suppresses invasive breast cancer in mice

<p>Abstract</p> <p>Background</p> <p>Treatment of invasive breast cancer has an alarmingly high rate of failure because effective targets have not been identified. One potential target is mitochondrial generated reactive oxygen species (ROS) because ROS production has been associated with changes in substrate metabolism and lower concentration of anti-oxidant enzymes in tumor and stromal cells and increased metastatic potential.</p> <p>Methods</p> <p>Transgenic mice expressing a human catalase gene (mCAT) were crossed with MMTV-PyMT transgenic mice that develop metastatic breast cancer. All mice (33 mCAT positive and 23 mCAT negative) were terminated at 110 days of age, when tumors were well advanced. Tumors were histologically assessed for invasiveness, proliferation and metastatic foci in the lungs. ROS levels and activation status of p38 MAPK were determined.</p> <p>Results</p> <p>PyMT mice expressing mCAT had a 12.5 per cent incidence of high histological grade primary tumor invasiveness compared to a 62.5 per cent incidence in PyMT mice without mCAT. The histological grade correlated with incidence of metastasis with 56 per cent of PyMT mice positive for mCAT showing evidence of pulmonary metastasis compared to 85.4 per cent of PyMT mice negative for mCAT with pulmonary metastasis (p ≤ 0.05). PyMT tumor cells expressing mCAT had lower ROS levels and were more resistant to hydrogen peroxide-induced oxidative stress than wild type tumor cells, suggesting that mCAT has the potential of quenching intracellular ROS and subsequent invasive behavior. The metastatic tumor burden in PyMT mice expressing mCAT was 0.1 mm²/cm²of lung tissue compared with 1.3 mm²/cm²of lung tissue in PyMT mice expressing the wild type allele (p ≤ 0.01), indicating that mCAT could play a role in mitigating metastatic tumor progression at a distant organ site. Expression of mCAT in the lungs increased resistance to hydrogen peroxide-induced oxidative stress that was associated with decreased activation of p38MAPK suggesting ROS signaling is dependent on p38MAPK for at least some of its downstream effects.</p> <p>Conclusion</p> <p>Targeting catalase within mitochondria of tumor cells and tumor stromal cells suppresses ROS-driven tumor progression and metastasis. Therefore, increasing the antioxidant capacity of the mitochondrial compartment could be a rational therapeutic approach for invasive breast cancer.</p> <p>Please see related commentary article: <url>http://www.biomedcentral.com/1741-7015/9/62</url></p

Exercise enhances wound healing and prevents cancer progression during aging by targeting macrophage polarity

10.1016/j.mad.2014.06.004MECHANISMS OF AGEING AND DEVELOPMENT139141-4

Exercise alarms the immune system: A HMGB1 perspective

10.1016/j.cyto.2018.06.031CYTOKINE110222-22

Effects of blood flow restriction (BFR) with resistance exercise on musculoskeletal health in older adults: a narrative review

10.1186/s11556-022-00294-0EUROPEAN REVIEW OF AGING AND PHYSICAL ACTIVITY19

Exercise training and immune crosstalk in breast cancer microenvironment: exploring the paradigms of exercise-induced immune modulation and exercise-induced myokines

AMERICAN JOURNAL OF TRANSLATIONAL RESEARCH65422-U21

Pre-tumor exercise decreases breast cancer in old mice in a distance-dependent manner

AMERICAN JOURNAL OF CANCER RESEARCH44378-38

Are Exercise and Mitochondrial Antioxidants Compatible in the Treatment of Invasive Breast Cancer?

10.4172/2167-7662.1000101Bioenergetics: Open access1