Key pointsr Training with blood flow restriction (BFR) is a well-recognized strategy for promoting muscle hypertrophy and strength. However, its potential to enhance muscle function during sustained, intense exercise remains largely unexplored.r In the present study, we report that interval training with BFR augments improvements in performance and reduces net K + release from contracting muscles during high-intensity exercise in active men.r A better K + regulation after BFR-training is associated with an elevated blood flow to exercising muscles and altered muscle anti-oxidant function, as indicated by a higher reduced to oxidized glutathione (GSH:GSSG) ratio, compared to control, as well as an increased thigh net K + release during intense exercise with concomitant anti-oxidant infusion.r Training with BFR also invoked fibre type-specific adaptations in the abundance of Na + ,K + -ATPase isoforms (α 1 , β 1 , phospholemman/FXYD1).r Thus, BFR-training enhances performance and K + regulation during intense exercise, which may be a result of adaptations in anti-oxidant function, blood flow and Na + ,K + -ATPase-isoform abundance at the fibre-type level.Abstract We examined whether blood flow restriction (BFR) augments training-induced improvements in K + regulation and performance during intense exercise in men, and also whether these adaptations are associated with an altered muscle anti-oxidant function, blood flow and/or with fibre type-dependent changes in Na + ,K + -ATPase-isoform abundance. Ten recreationally-active men (25 ± 4 years, 49.7 ± 5.3 mL kg −1 min −1 ) performed 6 weeks of Danny Christiansen is a researcher based in the Section of Integrative Physiology at the Department of Nutrition, Exercise and Sports in Copenhagen. His research focuses on optimizing strategies that aim to enhance human physical performance and health by understanding the molecular factors that drive skeletal muscle adaptation. His work has involved the use of cold-water immersion, simulated altitude, anti-oxidant infusion and blood flow restriction in combination with exercise to study the regulation of muscle ion transport, blood flow, oxygenation and glucose metabolism in man.This article was first published as a preprint. Christiansen D, Eibye KH, Rasmussen V, Voldbye HM, Thomassen M, Nyberg M, Gunnarsson TGP, Skovgaard C, Lindskrog MS, Bishop DJ, Hostrup M, Bangsbo J. 2018. Cycling with blood flow restriction improves performance and muscle K + regulation and blunts the effect of antioxidant infusion in humans. bioRxiv. https://doi. J Physiol 597.9 interval cycling, where one leg trained without BFR (control; CON-leg) and the other trained with BFR (BFR-leg, pressure: ß180 mmHg). Before and after training, femoral arterial and venous K + concentrations and artery blood flow were measured during single-leg knee-extensor exercise at 25% (Ex1) and 90% of thigh incremental peak power (Ex2) with I.V. infusion of N-acetylcysteine (NAC) or placebo (saline) and a resting muscle biopsy was collected. After training, performance...

Key points Endurance‐type training with blood flow restriction (BFR) increases maximum oxygen uptake (V̇O2max) and exercise endurance of humans. However, the physiological mechanisms behind this phenomenon remain uncertain. In the present study, we show that BFR‐interval training reduces the peripheral resistance to oxygen transport during dynamic, submaximal exercise in recreationally‐trained men, mainly by increasing convective oxygen delivery to contracting muscles. Accordingly, BFR‐training increased oxygen uptake by, and concomitantly reduced net lactate release from, the contracting muscles during relative‐intensity‐matched exercise, at the same time as invoking a similar increase in diffusional oxygen conductance compared to the training control. Only BFR‐training increased resting femoral artery diameter, whereas increases in oxygen transport and uptake were dissociated from changes in the skeletal muscle content of mitochondrial electron‐transport proteins. Thus, physically trained men benefit from BFR‐interval training by increasing leg convective oxygen transport and reducing lactate release, thereby improving the potential for increasing the percentage of V̇O2max that can be sustained throughout exercise. Abstract In the present study, we investigated the effect of training with blood flow restriction (BFR) on thigh oxygen transport and uptake, and lactate release, during exercise. Ten recreationally‐trained men (50 ± 5 mL kg−1 min−1) completed 6 weeks of interval cycling with one leg under BFR (BFR‐leg; pressure: ∼180 mmHg) and the other leg without BFR (CON‐leg). Before and after the training intervention (INT), thigh oxygen delivery, extraction, uptake, diffusion capacity and lactate release were determined during knee‐extensor exercise at 25% incremental peak power output (iPPO) (Ex1), followed by exercise to exhaustion at 90% pre‐training iPPO (Ex2), by measurement of femoral‐artery blood flow and femoral‐arterial and ‐venous blood sampling. A muscle biopsy was obtained from legs before and after INT to determine mitochondrial electron‐transport protein content. Femoral‐artery diameter was also measured. In the BFR‐leg, after INT, oxygen delivery and uptake were higher, and net lactate release was lower, during Ex1 (vs. CON‐leg; P < 0.05), with an 11% larger increase in workload (vs. CON‐leg; P < 0.05). During Ex2, after INT, oxygen delivery was higher, and oxygen extraction was lower, in the BFR‐leg compared to the CON‐leg (P < 0.05), resulting in an unaltered oxygen uptake (vs. CON‐leg; P > 0.05). In the CON‐leg, at both intensities, oxygen delivery, extraction, uptake and lactate release remained unchanged (P > 0.05). Resting femoral artery diameter increased with INT only in the BFR‐leg (∼4%; P < 0.05). Oxygen diffusion capacity was similarly raised in legs (P < 0.05). Mitochondrial protein content remained unchanged in legs (P > 0.05). Thus, BFR‐interval training enhances oxygen utilization by, and lowers lactate release from, submaximally‐exercising muscles of recreationally‐trained men m...

The purpose of the present study was to investigate whether exercise training‐induced adaptations in human skeletal muscle mitochondrial bioenergetics are magnified under thermal conditions resembling sustained intense contractile activity and whether training‐induced changes in mitochondrial oxidative phosphorylation (OXPHOS) efficiency influence exercise efficiency. Twenty healthy men performed 6 wk of high‐intensity exercise training [i.e., speed endurance training (SET; n = 10)], or maintained their usual lifestyle (n = 10). Before and after the intervention, mitochondrial respiratory function was determined ex vivo in permeabilized muscle fibers under experimentally‐induced normothermia (35°C) and hyperthermia (40°C) mimicking in vivo muscle temperature at rest and during intense exercise, respectively. In addition, activity and content of muscle mitochondrial enzymes and proteins were quantified. Exercising muscle efficiency was determined in vivo by measurements of leg hemodynamics and blood parameters during one‐legged knee‐extensor exercise. SET enhanced maximal OXPHOS capacity and OXPHOS efficiency at 40°C, but not at 35°C, and attenuated hyperthermia‐induced decline in OXPHOS efficiency. Furthermore, SET increased expression of markers of mitochondrial content and up‐regulated content of MFN2, DRP1, and ANT1. Also, SET improved exercise efficiency and capacity. These findings indicate that muscle mitochondrial bioenergetics adapts to high‐intensity exercise training in a temperature‐dependent manner and that enhancements in mitochondrial OXPHOS efficiency may contribute to improving exercise performance.—Fiorenza, M., Lemminger, A. K., Marker, M., Eibye, K., Iaia, F. M., Bangsbo, J., Hostrup, M. High‐intensity exercise training enhances mitochondrial oxidative phosphorylation efficiency in a temperature‐dependent manner in human skeletal muscle: implications for exercise performance. FASEB J. 33, 8976–8989 (2019). http://www.fasebj.org

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Aim To assess how blood‐flow‐restricted (BFR) interval‐training affects the capacity of the leg muscles for pH regulation during dynamic exercise in physically trained men. Methods Ten men (age: 25 ± 4y; trueV˙normalO2truemax: 50 ± 5 mL∙kg−1∙min−1) completed a 6‐wk interval‐cycling intervention (INT) with one leg under BFR (BFR‐leg; ~180 mmHg) and the other without BFR (CON‐leg). Before and after INT, thigh net H+‐release (lactate‐dependent, lactate‐independent and sum) and blood acid/base variables were measured during knee‐extensor exercise at 25% (Ex25) and 90% (Ex90) of incremental peak power output. A muscle biopsy was collected before and after Ex90 to determine pH, lactate and density of H+‐transport/buffering systems. Results After INT, net H+ release (BFR‐leg: 15 ± 2; CON‐leg: 13 ± 3; mmol·min−1; Mean ± 95% CI), net lactate‐independent H+ release (BFR‐leg: 8 ± 1; CON‐leg: 4 ± 1; mmol·min−1) and net lactate‐dependent H+ release (BFR‐leg: 9 ± 3; CON‐leg: 10 ± 3; mmol·min−1) were similar between legs during Ex90 (P > .05), despite a ~142% lower muscle intracellular‐to‐interstitial lactate gradient in BFR‐leg (−3 ± 4 vs 6 ± 6 mmol·L−1; P < .05). In recovery from Ex90, net lactate‐dependent H+ efflux decreased in BFR‐leg with INT (P < .05 vs CON‐leg) owing to lowered muscle lactate production (~58% vs CON‐leg, P < .05). Net H+ gradient was not different between legs (~19%, P > .05; BFR‐leg: 48 ± 30; CON‐leg: 44 ± 23; mmol·L−1). In BFR‐leg, NHE1 density was higher than in CON‐leg (~45%; P < .05) and correlated with total‐net H+‐release (r = 0.71; P = .031) and lactate‐independent H+ release (r = 0.74; P = .023) after INT, where arterial [HCO3‐] and standard base excess in Ex25 were higher in BFR‐leg than CON‐leg. Conclusion Compared to a training control, BFR‐interval training increases the capacity for pH regulation during dynamic exercise mainly via enhancement of muscle lactate‐dependent H+‐transport function and blood H+‐buffering capacity.