Endurance Training Improves Leg Proton Release and Decreases Potassium Release During High-Intensity Exercise in Normoxia and Hypobaric Hypoxia.

AIM: To assess the impact of endurance training on skeletal muscle release of H+ and K+. METHODS: Nine participants performed one-legged knee extension endurance training at moderate and high intensities (70%-85% of Wpeak), three to four sessions·week-1 for 6 weeks. Post-training, the trained and untrained (control) leg performed two-legged knee extension at low, moderate, and high intensities (40%, 62%, and 83% of Wpeak) in normoxia and hypoxia (~4000 m). The legs were exercised simultaneously to ensure identical arterial inflow concentrations of ions and metabolites, and identical power output was controlled by visual feedback. Leg blood flow was measured (ultrasound Doppler), and acid-base variables, lactate- and K+ concentrations were assessed in arterial and femoral venous blood to study K+ and H+ release. Ion transporter abundances were assessed in muscle biopsies. RESULTS: Lactate-dependent H+ release was similar in hypoxia to normoxia (p = 0.168) and was lower in the trained than the control leg at low-moderate intensities (p = 0.060-0.006) but similar during high-intensity exercise. Lactate-independent and total H+ releases were higher in hypoxia (p < 0.05) and increased more with power output in the trained leg (leg-by-power output interactions: p = 0.02). K+ release was similar at low intensity but lower in the trained leg during high-intensity exercise in normoxia (p = 0.024) and hypoxia (p = 0.007). The trained leg had higher abundances of Na+/H+ exchanger 1 (p = 0.047) and Na+/K+ pump subunit α (p = 0.036). CONCLUSION: Moderate- to high-intensity endurance training increases lactate-independent H+ release and reduces K+ release during high-intensity exercise, coinciding with increased Na+/H+ exchanger 1 and Na+/K+ pump subunit α muscle abundances.

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; V˙O2max : 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.