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Division of Cardiology, Internal Medicine, University of Texas-Houston Medical School, Houston, Texas 77030
We postulate that metabolic conditions that develop
systemically during exercise (high blood lactate and high nonesterified fatty acids) are favorable for energy homeostasis of the heart during
contractile stimulation. We used working rat hearts perfused at
physiological workload and levels of the major energy substrates and
compared the metabolic and contractile responses to an acute low-to-high work transition under resting versus exercising systemic metabolic conditions (low vs. high lactate and nonesterified fatty acids in the perfusate). Glycogen preservation, resulting from better
maintenance of high-energy phosphates, was a consequence of improved
energy homeostasis with high fat and lactate. We explained the result
by tighter coupling between workload and total 
-oxidation. Total
fatty acid oxidation with high fat and lactate reflected increased
availability of exogenous and endogenous fats for respiration, as
evidenced by increased long-chain fatty acyl-CoA esters (LCFA-CoAs) and
by an increased contribution of triglycerides to total -oxidation. Triglyceride turnover (synthesis and degradation) also appeared to
increase. Elevated LCFA-CoAs caused high total -oxidation despite
increased malonyl-CoA. The resulting bottleneck at mitochondrial uptake
of LCFA-CoAs stimulated triglyceride synthesis. Our results suggest the
following. First, both malonyl-CoA and LCFA-CoAs determine total fatty
acid oxidation in heart. Second, concomitant stimulation of peripheral
glycolysis and lipolysis should improve cardiac energy homeostasis
during exercise. We speculate that high lactate contributes to the
salutary effect by bypassing the glycolytic block imposed by fatty
acids, acting as an anaplerotic substrate necessary for high
tricarbocylic acid cycle flux from fatty acid-derived acetyl-CoA.
fatty acids; carnitine palmitoyltransferase I; malonyl-coenzyme A; long-chain fatty acyl-coenzyme A esters
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