Accuracy of1H and31P MRS analyses of lactate in skeletal muscle

Hsu, Alex C.; Dawson, M. Joan

doi:10.1002/1522-2594(200009)44:3<418::aid-mrm12>3.0.co;2-g

Cited by 19 publications

(30 citation statements)

References 36 publications

(72 reference statements)

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“…Cytosolic lipids also include diglycerides, acylcarnitines, and nonesterified fatty acids at substantial levels, especially the latter, with distinct functions (4,5). Lactate methyl resonance peak also overlaps with the lipid methylene resonance (6,7). To measure TG, it is sometimes assumed that cellular phospholipids produce broad peaks that are lost in the background (8).…”

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confidence: 97%

Intramyocellular lipids versus intramyocellular triglycerides

Zhou

Guo

2011

Magnetic Resonance in Med

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confidence: 97%

Intramyocellular lipids versus intramyocellular triglycerides

Zhou

Guo

2011

Magnetic Resonance in Med

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“…Muscles were bathed in modified Ringer's solution (105 mM NaCl, 2.5 mM KCl, 2.0 mM CaCl 2 , 10 mM TRIS, pH = 7.0 at 4°C), oxygenated for a minimum of 30 min, and stored overnight in oxygenated Ringer's. The following day, four pairs of muscles were oxygenated for 30 min, placed in Ringer's with 2.0 mM NaCN 1 hr prior to and throughout data acquisition to inhibit oxidative metabolism, and mounted in a previously described experimental chamber (9) for force, 1 H, and 31 P MRS data acquisition. Under these metabolic conditions, similar to sprinting conditions in man, glycogenolysis and PCr hydrolysis are the only sources of ATP.…”

Section: Methodsmentioning

confidence: 99%

“…The methods previously used to monitor CGC suffer from potential errors. Several 31 P MRS methods for calculating Lac − concentration have been shown to be of questionable accuracy (9). Most importantly, in these 31 P MRS methods the dependent variable (Lac − ) and the independent variables (ADP, AMP, P i , PCr, pH, ATP turnover, etc.)…”

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confidence: 99%

“…are derived from the same 31 P data. This results in an inherent correlation between the dependent and independent variables, which undermines any biological conclusions (9). Extracts are destructive and introduce quantitative errors by hydrolysis of labile metabolites and activation of metabolism during the extraction procedure.…”

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confidence: 99%

“…We have therefore used a quantitatively accurate 1 H MRS method (9), together with 31 P MRS, to verify the metabolic stasis following CGC in isolated anaerobic frog skeletal muscles. By using isolated tissues, MRS localization issues are avoided.…”

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confidence: 99%

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Muscle glycogenolysis is not activated by changes in cytosolic P‐metabolites: A ³¹P and ¹H MRS demonstration

Hsu¹,

Dawson²

2003

Magnetic Resonance in Med

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Skeletal muscle contraction and glycogenolysis are closely coupled. The standard explanation for this coupling, as taught in modern biochemistry textbooks, is that the metabolic products of contraction (ADP, AMP, P i ) feed back to activate glycogenolytic enzymes, thus providing for resynthesis of ATP. However, both in vivo 31 P MRS analyses and chemical analyses of muscle extracts have provided results that are contrary to this theory, at least in its simplest form. The MRS studies suffer from ambiguous assumptions. More importantly, in 31 P MRS studies the dependent and independent variables are often confounded because the glycogenolytic rate is calculated from the same data which are used to calculate the other metabolic variables. The analysis of biopsies has been necessarily quite limited, and suffers from a different set of experimental artifacts. Thus, the problem of contraction-glycogenolysis-coupling was reassessed using a quantitatively accurate 1 H MRS method. It is confirmed that glycogenolysis and contractions are closely coupled during repetitive exercise, while glycogenolysis and P-metabolite concentrations are not. A simple metabolic feedback system cannot explain contraction-glycogenolysis-coupling.Magn Despite its fundamental importance in all prokaryotic and eukaryotic life, the in vivo regulation of glycolysis is still not fully understood. In standard textbook descriptions, glycolysis is activated by a feedback mechanism at phosphofructokinase (PFK) by metabolites such as ADP and P i , direct products of the actomyosin-ATPase, and AMP, which is in equilibrium with ADP through adenylate kinase (1). By this simple feedback mechanism, glycolysis is activated whenever the direct and indirect products of ATP hydrolysis are increased. However, during the past 20 years it has been shown that, as calculated from changes in the 31 P MRS spectrum of intact ex vivo and in vivo animal and human muscle, glycolysis is closely coupled to contractions and not to metabolite levels (2-6).Similar results have been obtained using muscle biopsies and extracts (7,8).Close coupling of glycolysis or glycogenolysis to contraction is referred to as contraction-glycolysis-coupling or contraction-glycogenolysis-coupling (CGC). In this article, glycogenolysis refers to the degradation of glycogen to lactate. In the absence of oxygen, CGC is characterized by a partial metabolic recovery from contraction, followed by metabolic stasis during anaerobic rest, i.e., very low glycogenolytic rate with little to no net change in metabolite concentrations. During and closely following contraction the glycogenolytic rate is increased by orders of magnitude over the resting rate and then it falls to near zero without restoring P-metabolites to their precontractile values. In other words, glycogenolysis and contractions are coupled temporally. Glycogenolysis and contractions are also coupled quantitatively, since the amount of lactate (Lac -) produced is proportional to the magnitude of mechanical activity.The methods previously us...

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Intracellular acidification and volume increases explain R₂ decreases in exercising muscle

Damon

Gregory

Hall

et al. 2001

Magnetic Resonance in Med

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Exercise-induced decreases in the 1 H transverse relaxation rate (R 2 ) of muscle have been well documented, but the mechanism remains unclear. In this study, the hypothesis was tested that R 2 decreases could be explained by pH decreases and apparent intracellular volume (V i ) increases. 31 P and 1 H spectroscopy, biexponential R 2 analysis, and imaging were performed prior to and following fatiguing exercise in iodoacetate-treated (IAA, to inhibit glycolysis), NaCN-treated (to inhibit oxidative phosphorylation), and untreated frog gastrocnemii. In all exercised muscles, the apparent intracellular R 2 (R 2i ) and pH decreased, while intracellular osmolytes and V i increased. These effects were larger in NaCN-treated and untreated muscles than in IAAtreated muscles. Multiple regression analysis showed that pH and V i changes explain 70% of the R 2i variance. Separate experiments in unexercised muscles demonstrated causal relationships between pH and R 2i and between V i and R 2i . These data indicate that the R 2 change of exercise is primarily an intracellular phenomenon caused by the accumulation of the end-products of anaerobic metabolism. In the NaCN-treated and untreated muscles, the R 2i change increased as field strength increased, suggesting a role for pH-modulated chemical exchange. Key words: skeletal muscle; exercise; hydrogen-ion concentration; osmolarity; nuclear magnetic resonance Exercise-induced increases in the apparent 1 H transverse relaxation time (T 2 ) of muscle water have been well documented. The amount of T 2 change increases as exercise intensity increases; T 2 plateaus 3-4 min after the onset of exercise (1). Following isometric leg extension to fatigue, T 2 recovery follows an approximately exponential time course and is complete after ϳ35 min. (2). The increase in signal intensity from active muscles in T 2 -weighted images allows muscle activity to be detected reliably and noninvasively, which may aid in the placement of regions of interest or surface coils in spectroscopic studies (2,3). With a full understanding of the mechanism(s) of the T 2 change, this phenomenon may also be useful in functional studies of muscle activation during exercise (e.g., Refs. 4 -6), noninvasive studies of pathologic conditions in which the T 2 response to exercise is altered (e.g., Refs. 7 and 8), and as a means of studying noninvasively those physiological changes that increase T 2 .The most universally offered and best-studied explanation for the T 2 increase during exercise is the concomitant increase in muscle volume. However, the mechanism of the T 2 increase is more complex than total water accumulation. For example, recovery of the muscle's anatomical cross-sectional area is faster than T 2 recovery (2), and enhancement of the extracellular fluid volume increase during exercise is not proportional to the T 2 increase (9). A further complication is that both ex vivo amphibian (10) and in vivo mammalian (11) studies suggest that exchange between the intra-and extracellular spaces in muscle is sl...

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Accuracy of1H and31P MRS analyses of lactate in skeletal muscle

Cited by 19 publications

References 36 publications

Intramyocellular lipids versus intramyocellular triglycerides

Intramyocellular lipids versus intramyocellular triglycerides

Muscle glycogenolysis is not activated by changes in cytosolic P‐metabolites: A ³¹P and ¹H MRS demonstration

Intracellular acidification and volume increases explain R₂ decreases in exercising muscle

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Accuracy of1H and31P MRS analyses of lactate in skeletal muscle

Cited by 19 publications

References 36 publications

Intramyocellular lipids versus intramyocellular triglycerides

Intramyocellular lipids versus intramyocellular triglycerides

Muscle glycogenolysis is not activated by changes in cytosolic P‐metabolites: A 31P and 1H MRS demonstration

Intracellular acidification and volume increases explain R2 decreases in exercising muscle

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Muscle glycogenolysis is not activated by changes in cytosolic P‐metabolites: A ³¹P and ¹H MRS demonstration

Intracellular acidification and volume increases explain R₂ decreases in exercising muscle