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...

The purpose of this study was to examine whether speed endurance training (SET, repeated 30-s sprints) and heavy resistance training (HRT, 80-90% of 1 repetition maximum) performed in succession are compatible and lead to performance improvements in moderately trained endurance runners. For an 8-wk intervention period (INT) 23 male runners [maximum oxygen uptake (V̇O(2max)) 59 ± 1 ml·min(-1)·kg(-1); values are means ± SE] either maintained their training (CON, n = 11) or performed high-intensity concurrent training (HICT, n = 12) consisting of two weekly sessions of SET followed by HRT and two weekly sessions of aerobic training with an average reduction in running distance of 42%. After 4 wk of HICT, performance was improved (P < 0.05) in a 10-km run (42:30 ± 1:07 vs. 44:11 ± 1:08 min:s) with no further improvement during the last 4 wk. Performance in a 1,500-m run (5:10 ± 0:05 vs. 5:27 ± 0:08 min:s) and in the Yo-Yo IR2 test (706 ± 97 vs. 491 ± 65 m) improved (P < 0.001) only following 8 wk of INT. In HICT, running economy (189 ± 4 vs. 195 ± 4 ml·kg(-1)·km(-1)), muscle content of NHE1 (35%) and dynamic muscle strength was augmented (P < 0.01) after compared with before INT, whereas V̇O(2max), muscle morphology, capillarization, content of muscle Na(+)/K(+) pump subunits, and MCT4 were unaltered. No changes were observed in CON. The present study demonstrates that SET and HRT, when performed in succession, lead to improvements in both short- and long-term running performance together with improved running economy as well as increased dynamic muscle strength and capacity for muscular H(+) transport in moderately trained endurance runners.

The aim of this study was to investigate the mRNA response related to mitochondrial biogenesis, metabolism, angiogenesis, and myogenesis in trained human skeletal muscle to speed endurance exercise (S), endurance exercise (E), and speed endurance followed by endurance exercise (S + E). Seventeen trained male subjects (maximum oxygen uptake (VO2‐max): 57.2 ± 3.7 (mean ± SD) mL·min−1·kg−1) performed S (6 × 30 sec all‐out), E (60 min ~60% VO2‐max), and S + E on a cycle ergometer on separate occasions. Muscle biopsies were obtained at rest and 1, 2, and 3 h after the speed endurance exercise (S and S + E) and at rest, 0, 1, and 2 h after exercise in E. In S and S + E, muscle peroxisome proliferator‐activated receptor‐γ coactivator‐1 (PGC‐1α) and pyruvate dehydrogenase kinase‐4 (PDK4) mRNA were higher (P < 0.05) 2 and 3 h after speed endurance exercise than at rest. Muscle PGC‐1α and PDK4 mRNA levels were higher (P < 0.05) after exercise in S + E than in S and E, and higher (P < 0.05) in S than in E after exercise. In S and S + E, muscle vascular endothelial growth factor mRNA was higher (P < 0.05) 1 (S only), 2 and 3 h after speed endurance exercise than at rest. In S + E, muscle regulatory factor‐4 and muscle heme oxygenase‐1 mRNA were higher (P < 0.05) 1, 2, and 3 h after speed endurance exercise than at rest. In S, muscle hexokinase II mRNA was higher (P < 0.05) 2 and 3 h after speed endurance exercise than at rest and higher (P < 0.05) than in E after exercise. These findings suggest that in trained subjects, speed endurance exercise provides a stimulus for muscle mitochondrial biogenesis, substrate regulation, and angiogenesis that is not evident with endurance exercise. These responses are reinforced when speed endurance exercise is followed by endurance exercise.

The effect of repeated intense training interventions was investigated in eight trained male runners (maximum oxygen uptake [VO -max]: 59.3±3.2 mL/kg/min, mean±SD) who performed 10 speed endurance training (SET; repeated 30-seconds "all-out" bouts) and 10 aerobic moderate-intensity training sessions during two 40-day periods (P1 and P2) separated by ~80 days of habitual training. Before and after both P1 and P2, subjects completed an incremental test to exhaustion to determine VO -max and a repeated running test at 90% vVO -max to exhaustion (RRT) to determine short-term endurance capacity. In addition, running economy (RE) was measured at 60% vVO -max (11.9±0.5 km/h) and v10-km (14.3±0.9 km/h), a 10-km track-running test was performed, and a biopsy from m. vastus lateralis was collected. 10-km performance and VO -max (mL/min) were the same prior to P1 and P2, whereas RE was better (P<.05) before P2 than before P1. During P1 and P2, 10-km performance (2.9% and 2.3%), VO -max (2.1% and 2.6%), and RE (1.9% and 1.8% at 60% vVO -max; 1.6% and 2.0% at v10-km) improved (P<.05) to the same extent, respectively. Performance in RRT was 20% better (P<.05) after compared to before P2, with no change in P1. No changes in muscle expression of Na ,K -ATPase α1, α2 and β1, NHE1, SERCA1 and SERCA2, actin, and CaMKII were found during neither P1 nor P2. Thus, the present study demonstrates that a second period of intense training leads to improved short-term performance and further improved RE, whereas 10-km performance and VO -max improve to the same extent as during the first period.

The aim of the present study was to examine whether improved running economy with a period of speed endurance training and reduced training volume could be related to adaptations in specific muscle fibers. Twenty trained male (n = 14) and female (n = 6) runners (maximum oxygen consumption (VO2‐max): 56.4 ± 4.6 mL/min/kg) completed a 40‐day intervention with 10 sessions of speed endurance training (5–10 × 30‐sec maximal running) and a reduced (36%) volume of training. Before and after the intervention, a muscle biopsy was obtained at rest, and an incremental running test to exhaustion was performed. In addition, running at 60% vVO 2‐max, and a 10‐km run was performed in a normal and a muscle slow twitch (ST) glycogen‐depleted condition. After compared to before the intervention, expression of mitochondrial uncoupling protein 3 (UCP3) was lower (P < 0.05) and dystrophin was higher (P < 0.05) in ST muscle fibers, and sarcoplasmic reticulum calcium ATPase 1 (SERCA1) was lower (P < 0.05) in fast twitch muscle fibers. Running economy at 60% vVO 2‐max (11.6 ± 0.2 km/h) and at v10‐km (13.7 ± 0.3 km/h) was ~2% better (P < 0.05) after the intervention in the normal condition, but unchanged in the ST glycogen‐depleted condition. Ten kilometer performance was improved (P < 0.01) by 3.2% (43.7 ± 1.0 vs. 45.2 ± 1.2 min) and 3.9% (45.8 ± 1.2 vs. 47.7 ± 1.3 min) in the normal and the ST glycogen‐depleted condition, respectively. VO 2‐max was the same, but vVO 2‐max was 2.0% higher (P < 0.05; 19.3 ± 0.3 vs. 18.9 ± 0.3 km/h) after than before the intervention. Thus, improved running economy with intense training may be related to changes in expression of proteins linked to energy consuming processes in primarily ST muscle fibers.