The capacity for human exercise performance can be enhanced with prolonged exercise training, whether it is endurance- or strength-based. The ability to adapt through exercise training allows individuals to perform at the height of their sporting event and/or maintain peak physical condition throughout the life span. Our continued drive to understand how to prescribe exercise to maximize health and/or performance outcomes means that our knowledge of the adaptations that occur as a result of exercise continues to evolve. This review will focus on current and new insights into endurance and strength-training adaptations and will highlight important questions that remain as far as how we adapt to training.

Analysis 2.5. Comparison 2 Combined spinal-epidural versus low-dose epidural, Outcome 5 Number of women who mobilise....

Advancing age is associated with a progressive loss of skeletal muscle (SkM) mass and function. Given the worldwide aging demographics, this is a major contributor to morbidity, escalating socio-economic costs and ultimately mortality. Previously, it has been established that a decrease in regenerative capacity in addition to SkM loss with age coincides with suppression of insulin/insulin-like growth factor signalling pathways. However, genetic or pharmacological modulations of these highly conserved pathways have been observed to significantly enhance life and healthspan in various species, including mammals. This therefore provides a controversial paradigm in which reduced regenerative capacity of skeletal muscle tissue with age potentially promotes longevity of the organism. This paradox will be assessed and considered in the light of the following: (i) the genetic knockout, overexpression and pharmacological models that induce lifespan extension (e.g. IRS-1/s6K KO, mTOR inhibition) versus the important role of these signalling pathways in SkM growth and adaptation; (ii) the role of the sirtuins (SIRTs) in longevity versus their emerging role in SkM regeneration and survival under catabolic stress; (iii) the role of dietary restriction and its impact on longevity versus skeletal muscle mass regulation; (iv) the crosstalk between cellular energy metabolism (AMPK/TSC2/SIRT1) and survival (FOXO) versus growth and repair of SkM (e.g. AMPK vs. mTOR); and (v) the impact of protein feeding in combination with dietary restriction will be discussed as a potential intervention to maintain SkM mass while increasing longevity and enabling healthy aging.

Thirty-eight healthy women undergoing elective Caesarean section under spinal anaesthesia at term were allocated randomly to receive boluses of either phenylephrine 100 micrograms or ephedrine 5 mg for maintenance of maternal arterial pressure. The indication for administration of vasopressor was a reduction in systolic pressure to < or = 90% of baseline values. Maternal arterial pressure (BP) and heart rate (HR) were measured every minute by automated oscillometry. Cardiac output (CO) was measured by cross-sectional and Doppler echocardiography before and after preloading with 1500 ml Ringer lactate solution and then every 2 min after administration of bupivacaine. Umbilical artery pulsatility index (PI) was measured using Doppler before and after spinal anaesthesia. The median (range) number of boluses of phenylephrine and ephedrine was similar; 6 (1-10) vs 4 (1-8) respectively. Maternal systolic BP and CO changes were similar in both groups, but the mean [95% CI] maximum percentage change in maternal HR was larger in the phenylephrine group (-28.5 [-24.2, -32.9]%) than in the ephedrine group (-14.4 [-10.6, -18.2]%). As a consequence atropine was required in 11/19 women in the phenylephrine group compared with 2/19 in the ephedrine group (P < 0.01). Mean umbilical artery pH [95% CI] was higher in the phenylephrine group (7.29 [7.28-7.30]) than in the ephedrine group (7.27 [7.25-7.28]). The results of the present study support the use of phenylephrine for maintenance of maternal arterial pressure during spinal anaesthesia for elective Caesarean section.