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The present study examined and compared the impact of exercise training on redox and molecular properties of human microvascular endothelial cells derived from skeletal muscle biopsies from sedentary recent (RPF, ≤ 5 years as postmenopausal) and late (LPF, ≥ 10 years as postmenopausal) postmenopausal females. Resting skeletal muscle biopsies were obtained before and after 8 weeks of intense aerobic exercise training for isolation of microvascular endothelial cells and determination of skeletal muscle angiogenic proteins and capillarisation. The microvascular endothelial cells were analysed for mitochondrial respiration and production of reactive oxygen species (ROS), glycolysis and proteins related to vascular function, redox balance and oestrogen receptors. Exercise training led to a reduced endothelial cell ROS formation (∼50%; P = 0.009 and P = 0.020 for intact and permeabilized cells (state 3), respectively) in RPF only, with no effect on endothelial mitochondrial capacity in either group. Basal endothelial cell lactate formation was higher (7%; P = 0.028), indicating increased glycolysis, after compared to before the exercise training period in RPF only. Baseline endothelial G protein‐coupled oestrogen receptor (P = 0.028) and muscle capillarisation (P = 0.028) was lower in LPF than in RPF. Muscle vascular endothelial growth factor protein was higher (32%; P = 0.002) following exercise training in LPF only. Exercise training did not influence endothelial cell proliferation or skeletal muscle capillarisation in either group, but the CD31 level in the muscle tissue, indicating endothelial cell content, was higher (>50%; P < 0.05) in both groups. In conclusion, 8 weeks of intense aerobic exercise training reduces ROS formation and enhances glycolysis in microvascular endothelial cells from RPF but does not induce skeletal muscle angiogenesis. Key points: Late postmenopausal females have been reported to achieve limited vascular adaptations to exercise training.There is a paucity of data on the effect of exercise training on isolated skeletal muscle microvascular endothelial cells (MMECs).In this study the formation of reactive oxygen species in MMECs was reduced and glycolysis increased after 8 weeks of aerobic exercise training in recent but not late postmenopausal females.Late postmenopausal females had lower levels of G protein‐coupled oestrogen receptor in MMECs and lower skeletal muscle capillary density at baseline.Eight weeks of intense exercise training altered MMEC properties but did not induce skeletal muscle angiogenesis in postmenopausal females. [ABSTRACT FROM AUTHOR]

The effect of oral ribose supplementation on the resynthesis of adenine nucleotides and performance after 1 wk of intense intermittent exercise was examined. Eight subjects performed a random double-blind crossover design. The subjects performed cycle training consisting of 15 x 10 s of all-out sprinting twice per day for 7 days. After training the subjects received either ribose (200 mg/kg body wt; Rib) or placebo (Pla) three times per day for 3 days. An exercise test was performed at 72 h after the last training session. Immediately after the last training session, muscle ATP was lowered (P < 0.05) by 25 [+ or -] 2 and 22 [+ or -] 3% in Pla and Rib, respectively. In both Pla and Rib, muscle ATP levels at 5 and 24 h after the exercise were still lower (P < 0.05) than pretraining. After 72 h, muscle ATP was similar (P > 0.05) to pretraining in Rib (24.6 [+ or -] 0.6 vs. 26.2 [+ or -] 0.2 mmol/kg dry wt) but still lower (P < 0.05) in Pla (21.1 [+ or -] 0.5 vs. 26.0 [+ or -] 0.2 mmol/kg dry wt) and higher (P < 0.05) in Rib than in Pla. Plasma hypoxanthine levels after the test performed at 72 h were higher (P < 0.05) in Rib compared with Pla. Mean and peak power outputs during the test performed at 72 h were similar (P > 0.05) in Pla and Rib. The results support the hypothesis that the availability of ribose in the muscle is a limiting factor for the rate of resynthesis of ATP. Furthermore, the reduction in muscle ATP observed after intense training does not appear to be limiting for high-intensity exercise performance. adenosine 5'-triphosphate; purines, skeletal muscle

Potassium fluxes in red blood cells and muscle during muscle contractions were investigated. Seven subjects were asked to perform two-legged submaximal knee-extensor exercise for 30 min. Intense arm exercise was also performed for 10 min after 10 min of leg exercise. Findings showed that contracting muscle can take up K+ through a combination of K+ and hormone activation of the Na+-K+ pump. Also, changes in red blood cell K+ concentrations during muscle contraction may be caused by water movements and not transmembrane fluxes of K+.

Seven subjects were employed in the investigation of purine exchange in exercised and rested muscles and its relation to ATP levels in muscles after intense physical activity. Results reveal that significant levels of purines are released into the blood stream after one session of sustained physical activity thereby depleting the muscle ATP stores. Further, muscles undergoing heavy exercise were also observed to extract urate from the blood.

Resting muscles take up NH3 during intermittent exercise and are involved in the removal of NH3 during exercise and immediately after it. Intermittent arm exercises and exercises involving one leg were performed, with NH3 measured in the resting leg muscle. NH3 seems to be metabolized in the resting muscles. Comparison with data from other studies suggests that extraction of NH3 by resting muscles is probably less during one-legged than during whole body exercises. The arterial NH3 concentrations are greater in whole body exercises. Uptake of NH3 by the muscles decreases to resting values 5 min after exercise stops.