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EDITORIAL FOCUS
Department of Biology, University of Western Ontario, London, Ontario N6A 5B7, Canada
ABOUT 45 YEARS AGO, Edgar Black and coworkers (1-7) began examining the consequences of exhaustive exercise to fish muscle. These early pioneering studies laid the groundwork for the building of a fairly comprehensive model explaining how muscle fuels these bouts of high-intensity, exhaustive-type exercise (12). The early stage of exhaustive exercise (first 15-20 s) is fueled by hydrolysis of high-energy phosphates (e.g., ATP, PCr). There is a shift away from the initial phosphagen hydrolysis to activation of "anaerobic" glycogenolysis and glycolysis, as the rate of ATP demand exceeds that which can be provided via oxidative metabolism (8, 9). Consequently, at exhaustion, there is a decline in muscle ATP, PCr, muscle glycogen, and accumulation of lactate (12). Regeneration of muscle ATP, PCr, and glycogen and clearance of the lactate load are necessary if fish are to regain their ability to sprint or burst perform. It is generally accepted that the accumulated lactate is not used as an oxidative substrate to fuel the recovery process; rather it is retained within the muscle as the main substrate for glycogenesis (12). So, the question emerges: what is fueling the recovery processes? The obvious candidates are carbohydrate, protein, or lipid. The first two are unlikely given that fish (at least salmonid) muscle does not readily take up or use exogenous carbohydrate (e.g., glucose, lactate, pyruvate; Refs. 10, 11) and protein makes a negligible contribution to oxidative metabolism. That leaves lipid as the prime substrate to fuel recovery from exhaustive exercise. Because the white muscle of trout and other salmonids have considerable lipid reserves, they are considered "fatty fish." However, relatively little is known about the contribution this fuel makes to muscle metabolism and how muscle lipid metabolism is regulated.
Recently, Richards and coworkers (15) examined the role of lipid as a fuel for trout white muscle and found that during recovery from exhaustive exercise, both intra- and extramuscular lipid is oxidized by the white muscle to fuel the regeneration of ATP, PCr, and glycogen (15). In a current study in this issue of the American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (14), the question of how lipid traverses the muscle cell and the plasticity of the process is investigated. Richards et al. (14) test the hypotheses that 1) fatty acids traverse the muscle membrane via facilitated transport and 2) the rate of transport may be limiting to lipid use. Using sarcolemmal vesicles isolated from both red and white muscle fibers and palmitate as a representative long-chain fatty acid (LCFA), Richards et al. were able to demonstrate that LCFA uptake is via a saturable process, specific to LCFA and partially inhibited by compounds known to modify membrane proteins (e.g., phloretin, HgCl2). Although the maximal uptake rate of vesicles from red fibers was about twice that of white fibers, the affinities of the two for palmitate were similar. This difference in Vmax is consistent with the greater capacity of red fibers to oxidize lipid compared with white fibers (13). Sulfo-N-succinimidyoleate (SSO), a specific inhibitor of LCFA uptake in rat muscle, only weakly (15-20%) inhibited palmitate uptake by trout vesicles. Thus it can be said that LCFA uptake by both trout red and white muscle is via a protein-mediated carrier, which may share some similarities with the mammalian counterpart (e.g., SSO sensitivity). One of the major LCFA transport proteins in mammalian muscle membranes is a fatty acid translocase (FAT/CD36), which is specifically inhibited by SSO. Western blot analysis failed to demonstrate the presence of this protein in trout red or white muscle membranes but did identify a mammalian-like plasma membrane fatty acid binding protein. Thus there are some similarities between the trout and mammalian muscle LCFA transport systems. Whether an FAT/CD36-like protein mediates the transport process partially sensitive to SSO in trout remains to be seen.
To assess the plasticity of the lipid transport process and whether it may be limiting to lipid oxidation, muscle lipid use was manipulated in two ways: fish were subjected to either 5 days of continuous "aerobic" swimming or 9 days of chronic cortisol elevation. Both chronic elevations in plasma cortisol and continuous aerobic swimming have been reported to stimulate lipid oxidation in trout. The hypothesis Richards et al. tested is that increased lipid use by muscle would be reflected in an increase in fatty acid uptake by the muscle. However, this hypothesis was not supported by the data, as palmitate uptake by vesicles from both red and white muscle was not altered by either treatment. This contrasts with what is seen in mammals where chronic muscle stimulation (akin to sustained swimming) results in an increase in both fatty acid uptake and oxidation, suggesting a link between rates of uptake and use. This was not the case in trout. It could be that either the treatment did not alter lipid oxidation as predicted or that processes unrelated to transmembrane transport regulate the rate of lipid oxidation.
In summary, this paper presents a novel and integrative approach to the study of fat transport and metabolism in fish, an important and poorly understood metabolic process in fish. Evidence is presented suggesting the existence of novel fatty acid transport proteins in red and white muscle of rainbow trout that likely represent another member of a family of fatty acid transport proteins.
FOOTNOTES
Address for reprint requests and other correspondence: C. L. Milligan, Dept. of Biology, Univ. of Western Ontario, London, ON N6A 5B7, Canada (E-mail: milligan{at}uwo.ca).
REFERENCES
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