Reduced Satellite Cell Numbers and Myogenic Capacity in Aging Can Be Alleviated by Endurance Exercise

Background: Muscle regeneration depends on satellite cells, myogenic stem cells that reside on the myofiber surface. Reduced numbers and/or decreased myogenic aptitude of these cells may impede proper maintenance and contribute to the age-associated decline in muscle mass and repair capacity. Endurance exercise was shown to improve muscle performance; however, the direct impact on satellite cells in aging was not yet thoroughly determined. Here, we focused on characterizing the effect of moderate-intensity endurance exercise on satellite cell, as possible means to attenuate adverse effects of aging. Young and old rats of both genders underwent 13 weeks of treadmill-running or remained sedentary. Methodology: Gastrocnemius muscles were assessed for the effect of age, gender and exercise on satellite-cell numbers and myogenic capacity. Satellite cells were identified in freshly isolated myofibers based on Pax7 immunostaining (i.e., exvivo). The capacity of individual myofiber-associated cells to produce myogenic progeny was determined in clonal assays (in-vitro). We show an age-associated decrease in satellite-cell numbers and in the percent of myogenic clones in old sedentary rats. Upon exercise, there was an increase in myofibers that contain higher numbers of satellite cells in both young and old rats, and an increase in the percent of myogenic clones derived from old rats. Changes at the satellite cell level in old rats were accompanied with positive effects on the lean-to-fat Gast muscle composition and on spontaneous locomotion levels. The significance of these data is that they suggest that the endurance exercise-mediated boost in bot

Reactive oxygen species and male reproductive hormones

Reports of the increasing incidence of male infertility paired with decreasing semen quality have triggered studies on the effects of lifestyle and environmental factors on the male reproductive potential. There are numerous exogenous and endogenous factors that are able to induce excessive production of reactive oxygen species (ROS) beyond that of cellular antioxidant capacity, thus causing oxidative stress. In turn, oxidative stress negatively affects male reproductive functions and may induce infertility either directly or indirectly by affecting the hypothalamus-pituitary-gonadal (HPG) axis and/or disrupting its crosstalk with other hormonal axes. This review discusses the important exogenous and endogenous factors leading to the generation of ROS in different parts of the male reproductive tract. It also highlights the negative impact of oxidative stress on the regulation and cross-talk between the reproductive hormones. It further describes the mechanism of ROS-induced derangement of male reproductive hormonal profiles that could ultimately lead to male infertility. An understanding of the disruptive effects of ROS on male reproductive hormones would encourage further investigations directed towards the prevention of ROS-mediated hormonal imbalances, which in turn could help in the management of male infertility

BODY MASS AND V’O2 AT REST AFFECT GROSS EFFICIENCY DURING MODERATE-INTENSITY CYCLING IN UNTRAINED YOUNG HEALTHY MEN: CORRELATIONS WITH V’O2Max

Seventeen young healthy physically active males (age 23 ±3 years; body mass (BM) 72.5 ±7.9 kg; height 178 ±4 cm, (mean ±SD)), not specifically trained in cycling, participated in this study. The subjects performed two cycling incremental tests at the pedalling rate of 60 rev·min–1. The first test, with the power output (PO) increases of 30 W every 3 min, was to determine the maximal oxygen uptake (V’O2max) and the power output (PO) at V’O2max, while the second test (series of 6 minutes bouts of increasing intensity) was to determine energy expenditure (EE (V’O2)), gross efficiency (GE (V’O2/PO)) and delta efficiency (DE(DV’O2/DPO)) during sub-lactate threshold (LT) PO. V’O2max was 3.79 ±0.40 L·min–1 and the PO at V’O2max was 288 ±27 W. In order to calculate GE and DE the V’O2 was expressed in W, by standard calculations. GE measured at 30 W, 60 W, 90 W and 120 W was 11.6 ±1.4%, 17.0 ±1.4%, 19.6 ±1.2% and 21.4 ±1.1%, respectively. DE was 29.8 ±1.9%. The subjects’ BM (range 59–87 kg) was positively correlated with V’O2 at rest (p<0.01) and with the intercept of the linear V’O2 vs. PO relationship (p<0.01), whereas no correlation was found between BM and the slope of V’O2 vs. PO. No correlation was found between BM and DE, whereas GE was negatively correlated with BM (p<0.01). GE was also negatively correlated with V’O2max and the PO at V’O2max (p<0.01). We conclude that: V’O2 at rest affects GE during moderate-intensity cycling and GE negatively corelates with V’O2max and the PO at V’O2max in young healthy men