Effect of a myocardial volume overload on lactate transport in skeletal muscle sarcolemmal vesicles

William G. Aschenbach, Gregory L. Brower, Robert J. Talmadge, John L. Dobson, L. Bruce Gladden

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5 Scopus citations

Abstract

This study sought to determine the effect of a myocardial volume overload (MVO) on sarcolemmal (SL) lactate (La-) transport and the aerobic profile of skeletal muscle. SL vesicles were obtained from female rats 10 wk after either a MVO was induced by creation of an infrarenal fistula (n = 10), or sham surgeries were performed (n = 11). Influx of 14C-labeled L(+)-La- was measured at various unlabeled La- concentrations under zero-trans conditions. La- transport kinetics were determined using a Michaelis-Menten equation with an added linear component to discriminate between carrier-mediated and diffusional transport. Although heart and lung weights were significantly increased (P < 0.0001) in the MVO group, left ventricular function was only modestly altered (P < 0.05). A significant reduction in type I myosin heavy chain (MHC) in the soleus and a strong trend (P = 0.06) for a reduced type IIx MHC in the plantaris were observed in MVO rats, but no differences in citrate synthase activity or monocarboxylate transporter proteins (MCT)-1 expression were noted in any muscle. Carrier-mediated La- influx into SL vesicles was similar between sham and MVO (Km = 12 ∓ 1 and 18 ∓ 3 mM; apparent Vmax = 772 ∓ 99 and 827 ∓ 80 nmol·mg-1·min-1, respectively). Total influx at 100 mM was lower in MVO, and this was due to a 30% reduction in membrane diffusion. In conclusion, a 10-wk MVO did not alter MCT-mediated La- transport or protein expression but was associated with modest changes in myofibrillar proteins and impaired SL diffusive properties.

Original languageEnglish
Pages (from-to)R176-R186
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume281
Issue number1 50-1
DOIs
StatePublished - 2001

Scopus Subject Areas

  • General Medicine

Keywords

  • Congestive heart failure
  • Membrane diffusion
  • Monocarboxylate
  • Monocarboxylate transporter proteins

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