The effect of blood‐flow‐restricted interval training on lactate and H⁺ dynamics during dynamic exercise in man

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; : 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 [ ] 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.