scholarly journals Muscle energetics changes throughout maturation: a quantitative 31P-MRS analysis

2010 ◽  
Vol 109 (6) ◽  
pp. 1769-1778 ◽  
Author(s):  
Anne Tonson ◽  
Sébastien Ratel ◽  
Yann Le Fur ◽  
Christophe Vilmen ◽  
Patrick J. Cozzone ◽  
...  
Keyword(s):  
Energy Demand ◽  
Recovery Period ◽  
Exercise Bout ◽  
Oxidative Capacity ◽  
Recovery Phase ◽  
Resonance Spectroscopy ◽  
Compensatory Mechanism ◽  
Muscle Energetics ◽  
Atp Production

We quantified energy production in 7 prepubescent boys (11.7 ± 0.6 yr) and 10 men (35.6 ± 7.8 yr) using 31P-magnetic resonance spectroscopy to investigate whether development affects muscle energetics, given that resistance to fatigue has been reported to be larger before puberty. Each subject performed a finger flexions exercise at 0.7 Hz against a weight adjusted to 15% of their maximal voluntary strength for 3 min, followed by a 15-min recovery period. The total energy cost was similar in both groups throughout the exercise bout, whereas the interplay of the different metabolic pathways was different. At the onset of exercise, children exhibited a higher oxidative contribution (50 ± 15% in boys and 25 ± 8% in men, P < 0.05) to ATP production, whereas the phosphocreatine breakdown contribution was reduced (40 ± 10% in boys and 53 ± 12% in men, P < 0.05), likely as a compensatory mechanism. The anaerobic glycolysis activity was unaffected by maturation. The recovery phase also disclosed differences regarding the rates of proton efflux (6.2 ± 2.5 vs. 3.8 ± 1.9 mM·pH unit−1·min−1, in boys and men, respectively, P < 0.05), and phosphocreatine recovery, which was significantly faster in boys than in men (rate constant of phosphocreatine recovery: 1.3 ± 0.5 vs. 0.7 ± 0.4 min−1; Vmax: 37.5 ± 14.5 vs. 21.1 ± 12.2 mM/min, in boys and men, respectively, P < 0.05). Our results obtained in vivo clearly showed that maturation affects muscle energetics. Children relied more on oxidative metabolism and less on creatine kinase reaction to meet energy demand during exercise. This phenomenon can be explained by a greater oxidative capacity, probably linked to a higher relative content in slow-twitch fibers before puberty.

Comparative analysis of skeletal muscle oxidative capacity in children and adults: a 31P-MRS study

2008 ◽  
Vol 33 (4) ◽  
pp. 720-727 ◽  
Author(s):  
Sébastien Ratel ◽  
Anne Tonson ◽  
Yann Le Fur ◽  
Patrick Cozzone ◽  
David Bendahan
Keyword(s):  
Intermittent Exercise ◽  
Oxidative Capacity ◽  
Voluntary Contraction ◽  
Resonance Spectroscopy ◽  
Muscle Oxidative Capacity ◽  
Atp Production ◽  
Flexor Muscles ◽  
Forearm Flexor Muscles ◽  
Forearm Flexor

The aim of the present study was to compare the oxidative capacity of the forearm flexor muscles in vivo between children and adults using 31-phosphorus magnetic resonance spectroscopy. Seven boys (11.7 ± 0.6 y) and 10 men (35.6 ± 7.8 year) volunteered to perform a 3 min dynamic finger flexions exercise against a standardized weight (15% of the maximal voluntary contraction). Muscle oxidative capacity was quantified on the basis of phosphocreatine (PCr) post-exercise recovery kinetics analysis. End-of-exercise pH was not significantly different between children and adults (6.6 ± 0.2 vs. 6.5 ± 0.2), indicating that indices of PCr recovery kinetics can be reliably compared. The rate constant of PCr recovery (kPCr) and the maximum rate of aerobic ATP production were about 2-fold higher in young boys than in men (kPCr: 1.7 ± 1.2 vs. 0.7 ± 0.2 min–1; Vmax: 49.7 ± 24.6 vs. 29.4 ± 7.9 mmol·L–1·min–1, p < 0.05). Our results clearly illustrate a greater mitochondrial oxidative capacity in the forearm flexor muscles of young children. This larger ATP regeneration capacity through aerobic mechanisms in children could be one of the factors accounting for their greater resistance to fatigue during high-intensity intermittent exercise.

scholarly journals Effects of altered pyruvate dehydrogenase activity on contracting skeletal muscle bioenergetics

2019 ◽  
Vol 316 (1) ◽  
pp. R76-R86 ◽  
Author(s):  
Jonathan D. Kasper ◽  
Ronald A. Meyer ◽  
Daniel A. Beard ◽  
Robert W. Wiseman
Keyword(s):  
Steady State ◽  
Pyruvate Dehydrogenase ◽  
Primary Source ◽  
Atp Synthesis ◽  
Synthesis Rate ◽  
Resonance Spectroscopy ◽  
Phosphate Potential ◽  
Muscle Energetics ◽  
Atp Production

During aerobic exercise (>65% of maximum oxygen consumption), the primary source of acetyl-CoA to fuel oxidative ATP synthesis in muscle is the pyruvate dehydrogenase (PDH) reaction. This study investigated how regulation of PDH activity affects muscle energetics by determining whether activation of PDH with dichloroacetate (DCA) alters the dynamics of the phosphate potential of rat gastrocnemius muscle during contraction. Twitch contractions were induced in vivo over a broad range of intensities to sample submaximal and maximal aerobic workloads. Muscle phosphorus metabolites were measured in vivo before and after DCA treatment by phosphorus nuclear magnetic resonance spectroscopy. At rest, DCA increased PDH activation compared with control (90 ± 12% vs. 23 ± 3%, P < 0.05), with parallel decreases in inorganic phosphate (Pi) of 17% (1.4 ± 0.2 vs. 1.7 ± 0.1 mM, P < 0.05) and an increase in the free energy of ATP hydrolysis (ΔGATP) (−66.2 ± 0.3 vs. −65.6 ± 0.2 kJ/mol, P < 0.05). During stimulation DCA increased steady-state phosphocreatine (PCr) and the magnitude of ΔGATP, with concomitant reduction in Pi and ADP concentrations. These effects were not due to kinetic alterations in PCr hydrolysis, resynthesis, or glycolytic ATP production and altered the flow-force relationship between mitochondrial ATP synthesis rate and ΔGATP. DCA had no significant effect at 1.0- to 2.0-Hz stimulation because physiological mechanisms at these high stimulation levels cause maximal activation of PDH. These data support a role of PDH activation in the regulation of the energetic steady state by altering the phosphate potential (ΔGATP) at rest and during contraction.

scholarly journals High-intensity interval training increases in vivo oxidative capacity with no effect on Pi→ATP rate in resting human muscle

2013 ◽  
Vol 304 (5) ◽  
pp. R333-R342 ◽  
Author(s):  
Ryan G. Larsen ◽  
Douglas E. Befroy ◽  
Jane A. Kent-Braun
Keyword(s):  
High Intensity ◽  
Interval Training ◽  
Oxidative Capacity ◽  
High Energy ◽  
Resonance Spectroscopy ◽  
Vastus Lateralis Muscle ◽  
High Intensity Interval Training ◽  
Atp Production ◽  
High Intensity Interval

Mitochondrial ATP production is vital for meeting cellular energy demand at rest and during periods of high ATP turnover. We hypothesized that high-intensity interval training (HIT) would increase ATP flux in resting muscle ( V Pi→ATP) in response to a single bout of exercise, whereas changes in the capacity for oxidative ATP production ( V max) would require repeated bouts. Eight untrained men (27 ± 4 yr; peak oxygen uptake = 36 ± 4 ml·kg−1·min−1) performed six sessions of HIT (4–6 × 30-s bouts of all-out cycling with 4-min recovery). After standardized meals and a 10-h fast, V Pi→ATP and V max of the vastus lateralis muscle were measured using phosphorus magnetic resonance spectroscopy at 4 Tesla. Measurements were obtained at baseline, 15 h after the first training session, and 15 h after completion of the sixth session. V Pi→ATP was determined from the unidirectional flux between Pi and ATP, using the saturation transfer technique. The rate of phosphocreatine recovery ( k PCr) following a maximal contraction was used to calculate V max. While k PCr and V max were unchanged after a single session of HIT, completion of six training sessions resulted in a ∼14% increase in muscle oxidative capacity ( P ≤ 0.004). In contrast, neither a single nor six training sessions altered V Pi→ATP ( P = 0.74). This novel analysis of resting and maximal high-energy phosphate kinetics in vivo in response to HIT provides evidence that distinct aspects of human skeletal muscle metabolism respond differently to this type of training.

scholarly journals Poor Mitochondrial Health and Systemic Inflammation? Testing of a Classical Hypothesis

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 126-127
Author(s):  
Marta Zampino ◽  
Luigi Ferrucci ◽  
Richard Spencer ◽  
Kenneth Fishbein ◽  
Eleanor Simonsick ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Fat Body ◽  
Reference Group ◽  
Linear Regression Analysis ◽  
Oxidative Capacity ◽  
Conclusive Evidence ◽  
Resonance Spectroscopy ◽  
Low Grade ◽  
Severe Impairment

Abstract Chronic low-grade inflammation often occurs with aging and has been associated with negative health outcomes. Despite extensive research on the origins of “inflammaging”, the causative mechanisms remain unclear. However, a connection between poor mitochondrial health and chronic inflammation has been hypothesized, with decreasing mitochondrial function occurring with age and precipitating an increase in reactive oxygen species and other pro-inflammatory macromolecules such as mitochondrial DNA. We tested this hypothesis on a population of 619 subjects from the Baltimore Longitudinal Study of Aging, measuring muscle mitochondrial oxidative capacity in vivo by phosphorus magnetic resonance spectroscopy (P-MRS), and plasma interleukin (IL)-6, the most widely used biomarker of inflammaging. The P-MRS-derived post-exercise phosphocreatine recovery time constant tau-PCr, a measure of oxidative capacity, was expressed as a categorical variable through assignment to quintiles. Participants in the first quintile of tau-PCr (best mitochondrial function) were taken as reference and compared to the others using linear regression analysis adjusted for sex, age, lean and fat body mass, and physical activity. Those participants with the lowest oxidative capacity had significantly higher log(IL-6) levels as compared to the reference group. However, data from the other quintiles was not significantly different from the reference values. In conclusion, severe impairment of oxidative capacity is associated with increased inflammation. This study design does not provide conclusive evidence of whether increased inflammation and impaired bioenergetic recovery are both caused by underlying poor health status, or whether mitochondrial deficits lead directly to the observed inflammation; we anticipate addressing this important question with longitudinal studies.

scholarly journals CARDIOKIN1: Computational Assessment of Myocardial Metabolic Capability in Healthy Controls and Patients With Valve Diseases

Circulation ◽  
2021 ◽  
Author(s):  
Nikolaus Berndt ◽  
Johannes Eckstein ◽  
Iwona Wallach ◽  
Sarah Nordmeyer ◽  
Marcus Kelm ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Energy Demand ◽  
Heart Diseases ◽  
Cardiac Metabolism ◽  
Production Reserve ◽  
Energy Status ◽  
Tissue Samples ◽  
Atp Production ◽  
Mechanic Energy

Background: Many heart diseases can develop a reduced pumping capacity of the heart muscle. A mismatch between ATP demand and ATP production of cardiomyocytes is one of the possible causes. Assessment of the relation between the myocardial ATP production (MV ATP ) and cardiac workload is important for better understanding disease development and choice of nutritional or pharmacological treatment strategies. As there is currently no method for the measurement of MV ATP in vivo , the use of physiology-based metabolic models in conjunction with protein abundance data is an attractive approach. Methods: We developed a comprehensive kinetic model of the cardiac energy metabolism (CARDIOKIN1), which recapitulates numerous experimental findings on cardiac metabolism obtained with isolated cardiomyocytes, perfused animal hearts and in vivo studies with humans. We used the model to assess the energy status of the left ventricle (LV) of healthy subjects and patients with aortic stenosis (AS) and mitral valve insufficiency (MI). Maximal enzyme activities were individually scaled by means of protein abundances in LV tissue samples. The energy status of the LV was quantified by the ATP consumption at rest (MV ATP (rest)), at maximal workload (MV ATP (max)), and by the myocardial ATP production reserve (MAPR) representing the span between MV ATP (rest) and MV ATP (max). Results: Compared with controls, in both groups of patients, MV ATP (rest) was increased and MV ATP (max) was decreased resulting in a decreased MAPR, although all patients had preserved ejection fraction. Notably, the variance of the energetic status was high ranging from decreased to normal values. In both patient groups, the energetic status was tightly associated with mechanic energy demand. Moreover, a decrease of MV ATP (max) was associated with a decrease of the cardiac output indicating that cardiac functionality and energetic performance of the ventricle are closely coupled. Conclusions: Our analysis suggests that the ATP producing capacity of the LV of patients with valvular dysfunction is generally diminished and correlates positively with mechanic energy demand and cardiac output. However, large differences exist in the energetic state of the myocardium even in patients with similar clinical or image-based markers of hypertrophy and pump function.

scholarly journals Effect of muscle action and metabolic strain on oxidative metabolic responses in human skeletal muscle

1999 ◽  
Vol 87 (5) ◽  
pp. 1768-1775 ◽  
Author(s):  
C. A. Combs ◽  
A. H. Aletras ◽  
R. S. Balaban
Keyword(s):  
Free Energy ◽  
Atp Hydrolysis ◽  
Tibialis Anterior Muscle ◽  
Respiratory Control ◽  
Oxidative Capacity ◽  
Resonance Spectroscopy ◽  
Muscle Action ◽  
Pooled Data ◽  
Muscle Actions

A recent report suggests that differences in aerobic capacity exist between concentric and eccentric muscle action in human muscle (T. W. Ryschon, M. D. Fowler, R. E. Wysong, A. R. Anthony, and R. S. Balaban. J. Appl. Physiol. 83: 867–874, 1997). This study compared oxidative response, in the form of phosphocreatine (PCr) resynthesis rates, with matched levels of metabolic strain (i.e., changes in ADP concentration or the free energy of ATP hydrolysis) in tibialis anterior muscle exercised with either muscle action in vivo ( n = 7 subjects). Exercise was controlled and metabolic strain measured by a dynamometer and 31P-magnetic resonance spectroscopy, respectively. Metabolic strain was varied to bring cytosolic ADP concentration up to 55 μM or decrease the free energy of ATP hydrolysis to −55 kJ/mol with no change in cytoplasmic pH. PCr resynthesis rates after exercise ranged from 31.9 to 462.5 and from 21.4 to 405.4 μmol PCr/s for concentric and eccentric action, respectively. PCr resynthesis rates as a function of metabolic strain were not significantly different between muscle actions ( P > 0.40), suggesting that oxidative capacity is dependent on metabolic strain, not muscle action. Pooled data were found to more closely conform to previous biochemical measurements when a term for increasing oxidative capacity with metabolic strain was added to models of respiratory control.

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

2016 ◽  
Vol 41 (11) ◽  
pp. 1137-1145 ◽  
Author(s):  
Liam F. Fitzgerald ◽  
Anita D. Christie ◽  
Jane A. Kent
Keyword(s):  
Physical Activity ◽  
Systematic Review ◽  
Old Age ◽  
Meta Analysis ◽  
Oxidative Capacity ◽  
Muscle Group ◽  
Resonance Spectroscopy ◽  
Muscle Oxidative Capacity ◽  
Study Results

Despite 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 = 3561 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 (age, ≥55 years) adults had higher muscle oxidative capacity than younger (age, 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; I2 = ∼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.

scholarly journals The effects of therapeutic hypothermia on cerebral metabolism in neonates with hypoxic-ischemic encephalopathy: An in vivo 1H-MR spectroscopy study

2015 ◽  
Vol 36 (6) ◽  
pp. 1075-1086 ◽  
Author(s):  
Jessica L Wisnowski ◽  
Tai-Wei Wu ◽  
Aaron J Reitman ◽  
Claire McLean ◽  
Philippe Friedlich ◽  
...  
Keyword(s):  
Therapeutic Hypothermia ◽  
Energy Demand ◽  
Cerebral Metabolism ◽  
Brain Regions ◽  
Hypoxic Ischemic Encephalopathy ◽  
Cerebral White Matter ◽  
Similar Degree ◽  
Resonance Spectroscopy ◽  
Ischemic Encephalopathy

Therapeutic hypothermia has emerged as the first empirically supported therapy for neuroprotection in neonates with hypoxic-ischemic encephalopathy (HIE). We used magnetic resonance spectroscopy (1H-MRS) to characterize the effects of hypothermia on energy metabolites, neurotransmitters, and antioxidants. Thirty-one neonates with HIE were studied during hypothermia and after rewarming. Metabolite concentrations (mmol/kg) were determined from the thalamus, basal ganglia, cortical grey matter, and cerebral white matter. In the thalamus, phosphocreatine concentrations were increased by 20% during hypothermia when compared to after rewarming (3.49 ± 0.88 vs. 2.90 ± 0.65, p < 0.001) while free creatine concentrations were reduced to a similar degree (3.00 ± 0.50 vs. 3.74 ± 0.85, p < 0.001). Glutamate (5.33 ± 0.82 vs. 6.32 ± 1.12, p < 0.001), aspartate (3.39 ± 0.66 vs. 3.87 ± 1.19, p < 0.05), and GABA (0.92 ± 0.36 vs. 1.19 ± 0.41, p < 0.05) were also reduced, while taurine (1.39 ± 0.52 vs. 0.79 ± 0.61, p < 0.001) and glutathione (2.23 ± 0.41 vs. 2.09 ± 0.33, p < 0.05) were increased. Similar patterns were observed in other brain regions. These findings support that hypothermia improves energy homeostasis by decreasing the availability of excitatory neurotransmitters, and thereby, cellular energy demand.

scholarly journals In Vivo Metabolism of [1,6-13C2]Glucose Reveals Distinct Neuroenergetic Functionality between Mouse Hippocampus and Hypothalamus

Metabolites ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 50
Author(s):  
Antoine Cherix ◽  
Rajesh Sonti ◽  
Bernard Lanz ◽  
Hongxia Lei
Keyword(s):  
Metabolic Flux ◽  
Aerobic Glycolysis ◽  
Resonance Spectroscopy ◽  
Flux Analysis ◽  
Gamma Aminobutyric Acid ◽  
Atp Production ◽  
Functional Features ◽  
Metabolic Dependence ◽  
The Brain

Glucose is a major energy fuel for the brain, however, less is known about specificities of its metabolism in distinct cerebral areas. Here we examined the regional differences in glucose utilization between the hypothalamus and hippocampus using in vivo indirect 13C magnetic resonance spectroscopy (1H-[13C]-MRS) upon infusion of [1,6-13C2]glucose. Using a metabolic flux analysis with a 1-compartment mathematical model of brain metabolism, we report that compared to hippocampus, hypothalamus shows higher levels of aerobic glycolysis associated with a marked gamma-aminobutyric acid-ergic (GABAergic) and astrocytic metabolic dependence. In addition, our analysis suggests a higher rate of ATP production in hypothalamus that is accompanied by an excess of cytosolic nicotinamide adenine dinucleotide (NADH) production that does not fuel mitochondria via the malate-aspartate shuttle (MAS). In conclusion, our results reveal significant metabolic differences, which might be attributable to respective cell populations or functional features of both structures.

Metabolic response to halothane in piglets susceptible to malignant hyperthermia: an in vivo 31P-NMR study

1993 ◽  
Vol 75 (2) ◽  
pp. 955-962 ◽  
Author(s):  
C. Decanniere ◽  
P. Van Hecke ◽  
F. Vanstapel ◽  
H. Ville ◽  
R. Geers
Keyword(s):  
Malignant Hyperthermia ◽  
Intracellular Ph ◽  
Metabolic Response ◽  
Stress Test ◽  
Recovery Period ◽  
Muscle Metabolism ◽  
Resonance Spectroscopy ◽  
Intracellular Acidosis ◽  
Nmr Study

Using in vivo 31P-nuclear magnetic resonance spectroscopy, we studied the skeletal muscle metabolism of 17 anesthetized malignant hyperthermia-susceptible piglets and 25 control piglets during and after a halothane stress test. At rest, the phosphocreatine- (PCr) to-ATP ratio was 12% higher in the anesthetized piglets than in the control piglets, which may reflect a higher proportion of fast glycolytic fibers in the former. About 15 min of halothane administration sufficed to provoke onset of a reaction, which was characterized by a reciprocal drop in PCr and an increase in Pi with commencing intracellular acidosis. Halothane was withdrawn after a 20% drop in PCr. Within the next few minutes, intracellular pH dropped sharply and phosphomonoesters (PME) accumulated excessively. ATP was observed to decrease in 8 of the 17 animals. Halothane inhalation provoked a switch of metabolism toward glycolysis. Accumulation of PME suggests a mismatch between glycogenolysis and glycolysis. Despite severe acidification, glycolysis was not completely halted. Recovery of PCr and Pi started approximately 5 min after halothane withdrawal, with a longer time constant for recovery of the former. PME and intracellular pH aberrations lingered and started to recover later. Lost ATP was never restored within the observed recovery period of approximately 20 min.

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