Endurance training, expression, and physiology of LDH, MCT1, and MCT4 in human skeletal muscle.
Level 4 - case-series / case-control
Uncontrolled pre-post physiological intervention study in human volunteers.
PubMed 10751188 · doi:10.1152/ajpendo.2000.278.4.E571
What was done
Human vastus lateralis muscle biopsies were taken before and after 9 weeks of leg cycle endurance training at 75% peak oxygen consumption (VO2 peak). Researchers measured monocarboxylate transporters (MCT1 and MCT4) in total muscle preparations (MU), sarcolemma-enriched (SL), and mitochondria-enriched (MI) fractions using Western blotting. Changes in transporter expression were correlated with in vivo net leg lactate kinetics at rest and during exercise at 65% VO2 peak.
What was found
Training significantly increased muscle citrate synthase activity (+75%, P < 0.05) and type I myosin heavy chain percentage (+50%, P < 0.05), while reducing the lactate dehydrogenase-5 isozyme (-12%, P < 0.05). MCT1 was detected in both SL and MI fractions, whereas MCT4 was confined to the SL fraction. After training, MCT1 significantly increased in MU (+90%), SL (+60%), and MI (+78%). SL MCT4 increased by +47% (P < 0.05), but total MU MCT4 did not change significantly. Mitochondrial MCT1 content negatively correlated with net leg lactate release at rest (r = -0.85, P < 0.02). Sarcolemmal MCT1 and MCT4 contents positively correlated with net leg lactate release during exercise at 65% VO2 peak (r = 0.76, P < 0.03 and r = 0.86, P < 0.01, respectively).
Why it matters
This study provides direct human evidence that endurance training upregulates MCT1 in both mitochondrial and sarcolemmal membranes and MCT4 in sarcolemma, demonstrating cellular mechanisms supporting intracellular and cell-to-cell lactate shuttling.
Limits
The abstract does not disclose the sample size, sex, or baseline training status of the participants. There was no non-training control group to account for potential time-dependent confounders.
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