TY - JOUR

T1 - Elevated plasma lactate levels via exogenous lactate infusion do not alter resistance exercise-induced signaling or protein synthesis in human skeletal muscle

AU - Liegnell, Rasmus

AU - Apro, William

AU - Danielsson, Sebastian

AU - Ekblom, Bjoern

AU - van Hall, Gerrit

AU - Holmberg, Hans-Christer

AU - Moberg, Marcus

PY - 2020

Y1 - 2020

N2 - Lactate has been implicated as a potential signaling molecule. In myotubes, lactate incubation increases mechanistic target of rapamycin complex 1 (mTORC1)- and ERK-signaling and induces hypertrophy, indicating that lactate could be a mediator of muscle adaptations to resistance exercise. However, the potential signaling properties of lactate, at rest or with exercise, have not been explored in human tissue. In a crossover design study, 8 men and 8 women performed one-legged resistance exercise while receiving venous infusion of saline or sodium lactate. Blood was sampled repeatedly, and muscle biopsies were collected at rest and at 0, 90, and 180 min and 24 h after exercise. The primary outcomes examined were intracellular signaling, fractional protein synthesis rate (FSR), and blood/muscle levels of lactate and pH. Postexercise blood lactate concentrations were 130% higher in the Lactate trial (3.0 vs. 7.0 mmol/L, P <0.001), whereas muscle levels were only marginally higher (27 vs. 32 mmol/kg dry wt, P = 0.003) compared with the Saline trial. Postexercise blood pH was higher in the Lactate trial (7.34 vs. 7.44, P <0.001), with no differences in intramuscular pH. Exercise increased the phosphorylation of mTOR(S)(2448)( )(similar to 40%), S6K1(T389) (similar to 3-fold), p44(T202/T204) and (similar to 80%) during recovery, without any differences between trials. FSR over the 24-h recovery period did not differ between the Saline (0.067%/h) and Lactate (0.062%/h) trials. This study does not support the hypothesis that blood lactate levels can modulate anabolic signaling in contracted human muscle. Further in vivo research investigating the impact of exercised versus rested muscle and the role of intramuscular lactate is needed to elucidate its potential signaling properties.

AB - Lactate has been implicated as a potential signaling molecule. In myotubes, lactate incubation increases mechanistic target of rapamycin complex 1 (mTORC1)- and ERK-signaling and induces hypertrophy, indicating that lactate could be a mediator of muscle adaptations to resistance exercise. However, the potential signaling properties of lactate, at rest or with exercise, have not been explored in human tissue. In a crossover design study, 8 men and 8 women performed one-legged resistance exercise while receiving venous infusion of saline or sodium lactate. Blood was sampled repeatedly, and muscle biopsies were collected at rest and at 0, 90, and 180 min and 24 h after exercise. The primary outcomes examined were intracellular signaling, fractional protein synthesis rate (FSR), and blood/muscle levels of lactate and pH. Postexercise blood lactate concentrations were 130% higher in the Lactate trial (3.0 vs. 7.0 mmol/L, P <0.001), whereas muscle levels were only marginally higher (27 vs. 32 mmol/kg dry wt, P = 0.003) compared with the Saline trial. Postexercise blood pH was higher in the Lactate trial (7.34 vs. 7.44, P <0.001), with no differences in intramuscular pH. Exercise increased the phosphorylation of mTOR(S)(2448)( )(similar to 40%), S6K1(T389) (similar to 3-fold), p44(T202/T204) and (similar to 80%) during recovery, without any differences between trials. FSR over the 24-h recovery period did not differ between the Saline (0.067%/h) and Lactate (0.062%/h) trials. This study does not support the hypothesis that blood lactate levels can modulate anabolic signaling in contracted human muscle. Further in vivo research investigating the impact of exercised versus rested muscle and the role of intramuscular lactate is needed to elucidate its potential signaling properties.

KW - deuterium oxide

KW - metabolites

KW - mTORC1

KW - p44/ERK

KW - sodium lactate

KW - BLOOD-FLOW RESTRICTION

KW - THIGH MUSCLE

KW - ACTIVATION

KW - STRENGTH

KW - KINETICS

KW - PHOSPHORYLATION

KW - HYPERTROPHY

KW - PERFORMANCE

KW - METABOLISM

KW - SAMPLES

U2 - 10.1152/ajpendo.00291.2020

DO - 10.1152/ajpendo.00291.2020

M3 - Journal article

C2 - 32830552

VL - 319

SP - E792-E804

JO - American Journal of Physiology - Endocrinology and Metabolism

JF - American Journal of Physiology - Endocrinology and Metabolism

SN - 0193-1849

IS - 4

ER -