Linear dependence of muscle phosphocreatine kinetics on oxidative capacity

Paganini, Anthony T.; Foley, Jeanne M.; Meyer, Ronald A.

doi:10.1152/ajpcell.1997.272.2.c501

Cited by 162 publications

(191 citation statements)

References 14 publications

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“…Both the rate constant for PCr recovery (1/ ) and V O 2 max are indexes of the maximal rate of oxidative ATP synthesis and are traditionally considered to be linearly dependent on muscle oxidative capacity (9,18). Thus, as discussed previously (7), PCr recovery data are clearly indicative of both the maximal rate of oxidative ATP synthesis and muscle oxidative capacity.…”

Section: Discussionmentioning

confidence: 90%

Skeletal muscle oxidative metabolism in sedentary humans: ³¹P-MRS assessment of O₂ supply and demand limitations

Haseler

Lin

Richardson

2004

Journal of Applied Physiology

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[2013][2014][2015][2016][2017][2018] 1999. To further elucidate these population-specific limitations to metabolic rate, we used 31 P-magnetic resonance spectroscopy to study the exercising human gastrocnemius muscle under conditions of varied FI O 2 in sedentary subjects. To test the hypothesis that PCr recovery from submaximal exercise in sedentary subjects is not limited by O 2 availability, but rather by their mitochondrial capacity, six sedentary subjects performed three bouts of 6-min steady-state submaximal plantar flexion exercise followed by 5 min of recovery while breathing three different FI O 2 (0.10, 0.21, and 1.00). PCr recovery time constants were significantly longer in hypoxia (47.0 Ϯ 3.2 s), but there was no difference between hyperoxia (31.8 Ϯ 1.9 s) and normoxia (30.0 Ϯ 2.1 s) (mean Ϯ SE). End-exercise pH was not significantly different across treatments. These results suggest that the maximal muscle oxidative rate of these sedentary subjects, unlike their exercise-trained counterparts, is limited by mitochondrial capacity and not O 2 availability in normoxia. Additionally, the significant elongation of PCr recovery in these subjects in hypoxia illustrates the reliance on O 2 supply at the other end of the O2 availability spectrum in both sedentary and active populations. oxidative capacity; mitochondria; exercise; intracellular oxygenation; 31-phosphorous-magnetic resonance spectroscopy THERE IS A GROWING APPRECIATION of the concept that O 2 supply and demand limitations to maximal metabolic rate are dependent on the population studied (4, 26, 31). However, it should be noted that the preponderance of data have been collected from physically active or endurance-trained subjects who reveal O 2 supply dependence at maximal O 2 uptake (V O 2 max ). The supply of O 2 and its utilization by skeletal muscle is a tightly interwoven process that cannot easily be assessed by a single measurement. Although 31 P-magnetic resonance spectroscopy (MRS) measurements of phosphocreatine (PCr) recovery provide an accurate measure of skeletal muscle oxidative metabolism (2,11,15,17), alone this methodology is unable to discern limitation caused by O 2 supply from that of mitochondrial O 2 demand.However, the combination of PCr recovery measurement under conditions of altered O 2 availability, manipulated by varying the inspired O 2 fraction (FI O 2 ), has been utilized to demonstrate that, in exercise-trained humans, under normoxic conditions, O 2 availability limits maximal oxidative rate (7). The practical implication of these data is that PCr recovery measurements alone should be interpreted with caution because differences in PCr recovery between subjects may not be due to metabolic limitations (1, 5, 19) but rather to limitations in O 2 supply (30). To solidify this unique approach of combining manipulations in O 2 availability with PCr recovery, it is important to demonstrate that this methodology is able to determine the difference between mitochondrial limitation vs. O 2 supply limitation across subje...

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Section: Discussionmentioning

confidence: 90%

Skeletal muscle oxidative metabolism in sedentary humans: ³¹P-MRS assessment of O₂ supply and demand limitations

Haseler

Lin

Richardson

2004

Journal of Applied Physiology

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“…A different situation is observed in rat skeletal muscle, where the NMR detectable Cr/PCr concentration is 27 mM, 45 while 38 mM are found biochemically in tissue extracts. 55 This invisible Cr/ PCr amount is larger than needed to account for the MT effect or be bound to CK. Whether this is due to the role of an energy transport system or a storage process remains unclear.…”

Section: In Vivo Applicationsmentioning

confidence: 98%

Magnetization transfer MRS

Leibfritz¹,

Dreher²

2001

NMR in Biomedicine

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This review deals with magnetization transfer (MT) effects observed in in vivo NMR spectroscopy. The basic experimental methods of MT experiments, the underlying kinetic mechanisms as well as the evaluation of measured data by fits to two-or three-pool models are described. Experimental results of both 31 P and 1 H in vivo MRS are reviewed showing the potential of MT experiments to characterize kinetic equilibrium reactions. This includes reactions where all involved components are MR visible, as well as situations where one indirectly measures pools of bound spins which cannot directly be observed in vivo. In particular, MT effects are described which have been observed in in vivo 1 H NMR spectra measured on the animal or human brain or on skeletal muscle. Possible mechanisms for the strong MT effects observed for the signals of creatine/phosphocreatine, lactate, alcohol and other metabolites are discussed. It is also emphasized that MT effects caused by water suppression techniques may lead to systematic errors in the quantification of in vivo 1 H NMR spectra.

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“…The area under each peak indicates the relative concentration of each compound, which can be monitored continuously, noninvasively, and repeatedly. Following a brief contraction in which intracellular pH is relatively unaltered, the kinetics of PCr recovery follow a mono-exponential curve that is strictly attributable to mitochondrial ATP production Meyer 1988;Paganini et al 1997;Quistorff et al 1993). From this D r a f t 4 curve, the rate constant of PCr recovery (k PCr , s -1 ) can be determined and used as an index of muscle oxidative capacity (Kent-Braun et al 1995); this measure has become the "gold standard" for evaluating muscle oxidative capacity in vivo.…”

Section: Introductionmentioning

confidence: 99%

Heterogeneous effects of old age on human muscle oxidative capacity in vivo: a systematic review and meta-analysis

Fitzgerald

Christie

Kent

2016

Appl. Physiol. Nutr. Metab.

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https://mc06.manuscriptcentral.com/apnm-pubs Applied Physiology, Nutrition, and Metabolism D r a f t 2 ABSTRACTDespite intensive efforts to understand the extent to which skeletal muscle mitochondrial capacity changes in older humans, the answer to this important question remains unclear. To determine what the preponderance of evidence from in vivo studies suggests, we conducted a systematic review and meta-analysis of the effects of age on muscle oxidative capacity as measured noninvasively by magnetic resonance spectroscopy. A secondary aim was to examine potential moderators contributing to differences in results across studies, including: muscle group, physical activity status, and sex. Candidate papers were identified from PubMed searches (n=3,561 papers) and the reference lists of relevant papers. Standardized effects (Hedges' g) were calculated for age and each moderator using data from the 22 studies that met the inclusion criteria (n=28 effects). Effects were coded as positive when older (≥55 years) adults had higher muscle oxidative capacity than younger (20-45 years) adults. The overall effect of age on oxidative capacity was positive (g=0.171, p<0.001), indicating modestly greater oxidative capacity in old. Notably, there was significant heterogeneity in this result (Q=245.8, p<0.001; I 2 ~70-90%). Muscle group, physical activity, and sex were all significant moderators of oxidative capacity (p≤0.029). This analysis indicates that the current body of literature does not support a de facto decrease of in vivo muscle oxidative capacity in old age. The heterogeneity of study results and identification of significant moderators provide clarity regarding apparent discrepancies in the literature, and indicate the importance of accounting for these variables when examining purported age-related differences in muscle oxidative capacity.

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Linear dependence of muscle phosphocreatine kinetics on oxidative capacity

Cited by 162 publications

References 14 publications

Skeletal muscle oxidative metabolism in sedentary humans: ³¹P-MRS assessment of O₂ supply and demand limitations

Skeletal muscle oxidative metabolism in sedentary humans: ³¹P-MRS assessment of O₂ supply and demand limitations

Magnetization transfer MRS

Heterogeneous effects of old age on human muscle oxidative capacity in vivo: a systematic review and meta-analysis

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Linear dependence of muscle phosphocreatine kinetics on oxidative capacity

Cited by 162 publications

References 14 publications

Skeletal muscle oxidative metabolism in sedentary humans: 31P-MRS assessment of O2 supply and demand limitations

Skeletal muscle oxidative metabolism in sedentary humans: 31P-MRS assessment of O2 supply and demand limitations

Magnetization transfer MRS

Heterogeneous effects of old age on human muscle oxidative capacity in vivo: a systematic review and meta-analysis

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Skeletal muscle oxidative metabolism in sedentary humans: ³¹P-MRS assessment of O₂ supply and demand limitations

Skeletal muscle oxidative metabolism in sedentary humans: ³¹P-MRS assessment of O₂ supply and demand limitations