20 wk resistance training (RT) in 70 y olds improves glucose handling and leg blood flow (LBF) responsiveness to feeding and exercise‐plus‐feeding without reversing age‐related declines in protein kinase B (PKB) responses or increasing endothelial markers

Ageing blunts glucose tolerance and the LBF responses to exercise and feeding. We hypothesized that 20 wk RT would improve these and tested this in studies of healthy, normal weight (BMI 23–28 kg·m −2 ) young (Y) (n=12, 25±3 y, means±SE), middle‐aged (M) (n=12, 50±3 y,) and old (O) (n=8, 70±4 y) men and women (≈50:50). LBF was measured (Doppler) and muscle biopsies taken in post‐absorptive (PA) conditions and 150 min after beginning intermittent feeding (Fortisip: 16% protein, 49% carbohydrate, 35% fat; ≈6.5 kJ −1 ·kg −1 ·30 min −1 ), with one leg rested and the other recovering from exercise (6×8 reps, 75% 1RM). In O, plasma [glucose] before RT was greater ( P ≤0.05) than in Y in both PA (5.86±0.15 vs. 5.02±0.19 mM) and peak fed (8.82±0.70 vs. 7.94±0.42 mM) conditions and this was associated with blunted PKB kinase responses to feeding in O (+63% vs. +363%; P ≤0.01). However, after RT, post‐feed glucose AUC fell in all (Y, −41±3; M, −34±3; O, −22±1 mM·min) without improvements in PKB responsiveness. After RT, LBF responses to exercise+feeding in M and O were enhanced (M: 147±32% vs. 101±16%; O: 115±47% vs. 59±15%, both P ≤0.01) without changing whole‐muscle abundance of CD31, eNOS or α1/β2‐adrenoceptor proteins. Thus, RT rejuvenates glucose handling and LBF responsiveness in older people without resensitization of PKB or increases in endothelial markers. Support: UK BBSRC, EC EXEGENESIS