A study was conducted to determine non-invasively the effects of endurance training on the size of the inferior vena cava in humans. Twelve healthy male subjects were assigned to either an exercise-trained group (ET, n=7) or a sedentary control group (S, n=5) . The ET group underwent cycle-endurance training for 8 weeks (80%Vo₂max, 40 min/day, 4 days/week) . The S group led normal lives during the 8-week period. Before and after the training period, cross-sectional areas (CSA) of the inferior vena cava and the ascending and abdominal aorta were measured by echography. The CSA of the inferior vena cava after training was significantly larger than that before training in the ET group. There was no significant difference in the S group. These results indicate that the inferior versa cava can be morphologically altered as an adaptive response to endurance training. We consider that this adaptation partly contributes to the improvement in the efficiency of venous return from exercising muscles to the heart. Although the present training also increased the CSA of the aorta, the degree of change was smaller than that seen in the inferior vena cava, implying that the factors of adaptation and adaptability to endurance training in the inferior vena cava differ from those in the aorta.

This study examined cytokine responses to cold exposure together with the effects of exercise and thermal adaptation. Ten male short-track skaters who had adapted to a cold environment, and ten male inline skaters who had not, were each assigned to two experimental conditions. For the cold condition, subjects sat for 60 min at 5–8°C, then exercised on a cycle ergometer for 60 min at 65% maximal oxygen uptake (at 5–8°C), and finally sat again for 120 min at room temperature (20–25°C). In the control condition, subjects participated in the same protocol as the above but at room temperature (20–25°C). Blood samples were collected at pre-cold exposure, post-cold exposure (pre-exercise), post-exercise, post-30 min, post-60 min, and post-120 min, and analyzed for plasma concentrations of interleukin (IL)-1 receptor antagonist (IL-1ra), IL-8, IL-10, IL-12p40, soluble tumor necrosis factor receptor I (sTNFR-I), cortisol, and myoglobin by using enzyme-linked immunosorbent assay (ELISA). 60-min cycle ergometer exercise induced significant increases in plasma IL-1ra, IL-10 and IL-12p40 at room temperature in short-track skaters adapted to the cold, but significant decreases in these cytokines were observed with exposure to cold. These results indicate that acute cold exposure has a suppressive effect on cytokine response during exercise, suggesting the possibility of preventive effects on immunosuppression, heat stroke and allergy induced by exercise.

Objective: This study assessed the effectiveness and safety of resistance training in prostate cancer patients receiving androgen deprivation therapy (ADT).
Methods: Ten patients in the absence of metastasis undertook a 20-week progressive resistance training (2 times/week) consisting of 12 different upper and lower body exercises using training machines. Body composition, muscle function, physical performance, bone mineral density, serum biochemical data, plasma insulin and blood markers of prostate cancer were assessed at baseline and after training at weeks 10 and 20.
Results: Training significantly increased muscle strength and muscle endurance capacity (p<0.001) and decreased plasma insulin levels without affecting blood markers of prostate cancer.
Conclusion: Results suggest that resistance training is beneficial for prostate cancer patients with ADT to reduce the side effects of ADT and improve the activity of daily living and quality of life.

Cancer, congestive heart failure, chronic obstructive pulmonary disease, type 2 diabetes and aging induce skeletal muscle atrophy. These diseases and aging promote the formation of reactive oxygen species (ROS), which in turn regulate catabolic pathways involved in muscle atrophy. The first line of antioxidant defense system from ROS is comprised of superoxide dismutase (SOD), which scavenges superoxide (O2•−) to produce the less reactive hydrogen peroxide (H2O2). Mammalian skeletal muscle expresses cytosolic copper/zinc-containing SOD (CuZnSOD or SOD1), manganese SOD (MnSOD or SOD2), and extracellular SOD (EcSOD or SOD3). In this review, we provide an overview of 1) oxidative stress and antioxidants, 2) EcSOD ameliorates skeletal muscle abnormalities, cachexia, and exercise intolerance, 3) muscle-derived EcSOD protects against organ dysfunction, and 4) role of the Keap1-Nrf2 signaling pathway in the regulation of antioxidant defense system.