We studied the effects of a 38-day endurance exercise training program on leucine turnover and substrate metabolism during a 90-min exercise bout at 60% peak O(2) consumption (VO(2 peak)) in 6 males and 6 females. Subjects were studied at both the same absolute (ABS) and relative (REL) exercise intensities posttraining. Training resulted in a significant increase in whole body VO(2 peak) and skeletal muscle citrate synthase (CS; P < 0.001), complex I-III (P < 0.05), and total branched-chain 2-oxoacid dehydrogenase (BCOAD; P < 0.001) activities. Leucine oxidation increased during exercise for the pretraining trial (PRE, P < 0.001); however, there was no increase for either the ABS or REL posttraining trial. Leucine oxidation was significantly lower for females at all time points during rest and exercise (P < 0.01). The percentage of BCOAD in the activated state was significantly increased after exercise for both the PRE and REL exercise trials, with the increase in PRE being greater (P < 0.001) compared with REL (P < 0.05). Females oxidized proportionately more lipid and less carbohydrate during exercise compared with males. In conclusion, we found that 38 days of endurance exercise training significantly attenuated both leucine oxidation and BCOAD activation during 90 min of endurance exercise at 60% VO(2 peak) for both ABS and REL exercise intensities. Furthermore, females oxidize proportionately more lipid and less carbohydrate compared with males during endurance exercise.

Hasenfuß, G. et al. (2016) A transcatheter intracardiac shunt device for heart failure with preserved ejection fraction (REDUCE LAP-HF): a multicentre, open-label, single-arm, phase 1 trial. Lancet, 387(10025), pp. 1298-1304.There may be differences between this version and the published version. You are advised to consult the publisher's version if you wish to cite from it.http://eprints.gla.ac.uk/123112/

No abstract

The female sex hormone 17beta-estradiol (E(2)) has been shown to increase lipid and decrease carbohydrate utilization in animals. We administrated oral E(2) and placebo (randomized, double blind, crossover) to eight human male subjects for 8 days ( approximately 3 mg/day) and measured respiratory variables, plasma substrates, hormones (E(2), testosterone, leptin, cortisol, insulin, and catecholamines), and substrate utilization during 90 min of endurance exercise. [6,6-(2)H]glucose and [1,1,2,3,3-(2)H]glycerol tracers were used to calculate substrate flux. E(2) administration increased serum E(2) (0.22 to 2.44 nmol/l, P < 0.05) and decreased serum testosterone (19.4 to 11.5 nmol/l, P < 0.05) concentrations, yet there were no treatment effects on any of the other hormones. Glucose rates of appearance (R(a)) and disappearance (R(d)) were lower, and glycerol R(a)-to-R(d) ratio was not affected by E(2) administration. O(2) uptake, CO(2) production, and respiratory exchange ratio were not affected by E(2); however, there was a decrease in heart rate (P < 0.05). Plasma lactate and glycerol were unaffected by E(2); however, glucose was significantly higher (P < 0. 05) during exercise after E(2) administration. We concluded that short-term oral E(2) administration decreased glucose R(a) and R(d), maintained plasma glucose homeostasis, but had no effect on substrate oxidation during exercise in men.

The data presented here demonstrate for the first time the clinical safety of CMV-specific adoptive T-cell therapy and its potential therapeutic benefit for SOT patients with recurrent and/or drug-resistant CMV infection or disease.