New Findings r What is the central question of this study?Does the combination of sprint interval training with postexercise blood-flow restriction enhance maximal aerobic physiology and performance in trained individuals? r What is the main finding and its importance?We demonstrate the potency of combining blood-flow restriction with sprint interval training in increasing maximal oxygen uptake in trained individuals; however, this did not translate to an enhanced exercise performance. We also show that blood-flow restriction combined with sprint interval training enhanced postexercise hypoxia-inducible factor-1α mRNA expression, suggesting the possibility for greater hypoxia-mediated adaptations, such as enhanced capillary growth, with this intervention.This investigation assessed the efficacy of sprint interval training (SIT) combined with postexercise blood-flow restriction as a novel approach to enhance maximal aerobic physiology and performance. In study 1, a between-groups design was used to determine whether 4 weeks (2 days per week) of SIT (repeated 30 s maximal sprint cycling) combined with postexercise blood-flow restriction (BFR) enhanced maximal oxygen uptake (V O 2 max ) and 15 km cycling time-trial performance (15 km TT) compared with SIT alone (CON) in trained individuals. Thė V O 2 max increased after BFR by 4.5% (P = 0.01) but was unchanged after CON. There was no difference in 15 km TT performance after CON or BFR. In study 2, using a repeated-measures design, participants performed an acute bout of either BFR or CON. Muscle biopsies were taken before and after exercise to examine the activation of signalling pathways regulating angiogenesis and mitochondrial biogenesis. Phosphorylation of p38MAPK Thr180/Tyr182 increased by a similar extent after CON and BFR. There was no difference in the magnitude of increase in PGC-1α, VEGF and VEGFR-2 mRNA expression between protocols; however, HIF-1α mRNA expression increased (P = 0.04) at 3 h only after BFR. We have demonstrated the potency of combining BFR with SIT in increasingV O 2 max in trained individuals, but this did not translate to an enhanced exercise performance. Sprint interval training alone did not induce any observable adaptation. Although the mechanisms are not fully understood, we present preliminary evidence that BFR leads to enhanced HIF-1α-mediated cell signalling.

This study investigated protein kinase activation and gene expression of angiogenic factors in response to low-load resistance exercise with or without blood flow restriction (BFR). In a repeated measures cross-over design, six males performed four sets of bilateral knee extension exercise at 20% 1RM (reps per set = 30:15:15:continued to fatigue) with BFR (110 mmHg) and without (CON). Muscle biopsies were obtained from the vastus lateralis before, 2 and 4 h post-exercise. mRNA expression was determined using real-time RT-PCR. Protein phosphorylation/expression was determined using Western blot. p38MAPK phosphorylation was greater (p = 0.05) at 2 h following BFR (1.3 ± 0.8) compared to CON (0.4 ± 0.3). AMPK phosphorylation remained unchanged. PGC-1α mRNA expression increased at 2 h (5.9 ± 1.3 vs. 2.1 ± 0.8; p = 0.03) and 4 h (3.2 ± 0.8 vs. 1.5 ± 0.4; p = 0.03) following BFR exercise with no change in CON. PGC-1α protein expression did not change following either exercise. BFR exercise enhanced mRNA expression of vascular endothelial growth factor (VEGF) at 2 h (5.2 ± 2.8 vs 1.7 ± 1.1; p = .02) and 4 h (6.8 ± 4.9 vs. 2.5 ± 2.7; p = .01) compared to CON. mRNA expression of VEGF-R2 and hypoxia-inducible factor 1α increased following BFR exercise but only eNOS were enhanced relative to CON. Matrix metalloproteinase-9 mRNA expression was not altered in response to either exercise. Acute low-load resistance exercise with BFR provides a targeted angiogenic response potentially mediated through enhanced ischaemic and shear stress stimuli.

Sprint interval training (SIT) combined with postexercise blood flow restriction (BFR) is a novel method to increase maximal oxygen uptake (V̇o2max) in trained individuals and also provides a potent acute stimulus for angiogenesis and mitochondrial biogenesis. The efficacy to enhance endurance performance, however, has yet to be demonstrated. Trained male cyclists ( n = 21) (V̇o2max: 62.8 ± 3.7 ml·min−1·kg−1) undertook 4 wk of SIT (repeated 30-s maximal sprints) either alone (CON; n = 10) or with postexercise BFR ( n = 11). Before and after training V̇o2max, critical power (CP) and curvature constant ( Wʹ) were determined and muscle biopsies obtained for determination of skeletal muscle capillarity and mitochondrial protein content. CP increased ( P = 0.001) by a similar extent following CON (287 ± 39 W to 297 ± 43 W) and BFR (296 ± 40 W to 306 ± 36 W). V̇o2max increased following BFR by 5.9% ( P = 0.02) but was unchanged after CON ( P = 0.56). All markers of skeletal muscle capillarity and mitochondrial protein content were unchanged following either training intervention. In conclusion, 4 wk of SIT increased CP; however, this was not enhanced further with BFR. SIT was not sufficient to elicit changes in skeletal muscle capillarity and mitochondrial protein content with or without BFR. However, we further demonstrate the potency of combining BFR with SIT to enhance V̇o2max in trained individuals. NEW & NOTEWORTHY This investigation has demonstrated that 4 wk of sprint interval training (SIT) increased critical power in trained individuals; however, postexercise blood flow restriction (BFR) did not enhance this further. SIT, with or without BFR, did not induce any changes in skeletal muscle capillarity or mitochondrial protein content in our trained population. We do, however, confirm previous findings that SIT combined with BFR is a potent stimulus to enhance maximal oxygen uptake.

The aim of the present study was to test the hypothesis that consuming protein does not attenuate AMPK signalling when exercise is commenced in a glycogen-depleted state. After performing a glycogen-depleting protocol the evening before, the subsequent morning ten active men performed 45 min steady-state cycling at 50 % of peak power output (PPO) followed by an exercise capacity test (1-min intervals at 80 % PPO interspersed with 1-min periods at 40 % PPO). In a repeated measures design, subjects consumed 20 g of a casein hydrolysate solution (PRO) 45 min before exercise, 10 g during and a further 20 g immediately post-exercise, or an equivalent volume of a non-calorie taste matched placebo (PLA). Resting (PRO = 134 ± 29; PLA = 136 ± 28 mmol kg(-1)) and post-exercise muscle glycogen (PRO = 43 ± 16; PLA = 47 ± 18 mmol kg(-1)) was not different (P > 0.05) between trials nor was exercise capacity (PRO = 26 ± 9; PLA = 25 ± 10 min, P > 0.05). Phosphorylation of AMPK(Thr172) increased threefold immediately post-exercise (P < 0.05) and PGC1-mRNA increased sixfold at 3 h post-exercise (P < 0.05), though there were no differences between conditions (P > 0.05). In contrast, there was a trend (P = 0.08) for a divergent response in eEF2(Thr56) phosphorylation such that 1.5 fold increases post- and 3 h post-exercise in PLA were blunted with PRO, thus indicative of greater eEF2 activation. We conclude that athletes who deliberately incorporate training phases with reduced muscle glycogen into their training programmes may consume protein before, during and after exercise without negating signalling through the AMPK cascade.