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1 Department of Health and Human Performance, Auburn University and 2 Department of Anatomy, Physiology, and Pharmacology, Auburn University College of Veterinary Medicine, Auburn, Alabama 36849; and 3 Department of Human Nutrition, Foods, and Exercise Science, Virginia Tech, Blacksburg, Virginia 24061
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.
congestive heart failure; monocarboxylate transporter proteins; monocarboxylate; membrane diffusion
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