scholarly journals Quantitative and simultaneous measurement of oxygen consumption rates in rat brain and skeletal muscle using 17 O MRS imaging at 16.4T

2020 ◽  
Vol 85 (4) ◽  
pp. 2232-2246
Author(s):  
Hannes M. Wiesner ◽  
Dávid Z. Balla ◽  
Klaus Scheffler ◽  
Kâmil Uğurbil ◽  
Xiao‐Hong Zhu ◽  
...  
2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
José Adan Arevalo ◽  
Marvin L. Miller ◽  
José Pablo Vazquez-Medina ◽  
George A. Brooks

2012 ◽  
Vol 302 (6) ◽  
pp. R712-R719 ◽  
Author(s):  
Rosemary A. Schuh ◽  
Kathryn C. Jackson ◽  
Ramzi J. Khairallah ◽  
Christopher W. Ward ◽  
Espen E. Spangenburg

Measurement of mitochondrial function in skeletal muscle is a vital tool for understanding regulation of cellular bioenergetics. Currently, a number of different experimental approaches are employed to quantify mitochondrial function, with each involving either mechanically or chemically induced disruption of cellular membranes. Here, we describe a novel approach that allows for the quantification of substrate-induced mitochondria-driven oxygen consumption in intact single skeletal muscle fibers isolated from adult mice. Specifically, we isolated intact muscle fibers from the flexor digitorum brevis muscle and placed the fibers in culture conditions overnight. We then quantified oxygen consumption rates using a highly sensitive microplate format. Peak oxygen consumption rates were significantly increased by 3.4-fold and 2.9-fold by simultaneous stimulation with the uncoupling agent, carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone (FCCP), and/or pyruvate or palmitate exposure, respectively. However, when calculating the total oxygen consumed over the entire treatment, palmitate exposure resulted in significantly more oxygen consumption compared with pyruvate. Further, as proof of principle for the procedure, we isolated fibers from the mdx mouse model, which has known mitochondrial deficits. We found significant reductions in initial and peak oxygen consumption of 51% and 61% compared with fibers isolated from the wild-type (WT) animals, respectively. In addition, we determined that fibers isolated from mdx mice exhibited less total oxygen consumption in response to the FCCP + pyruvate stimulation compared with the WT mice. This novel approach allows the user to make mitochondria-specific measures in a nondisrupted muscle fiber that has been isolated from a whole muscle.


1995 ◽  
Vol 268 (3) ◽  
pp. E433-E438 ◽  
Author(s):  
M. D. Jensen ◽  
C. M. Johnson ◽  
P. E. Cryer ◽  
M. J. Murray

To determine the relative contribution of splanchnic and leg tissues to postprandial thermogenesis, systemic and regional oxygen consumption rates were measured in nine women and eight men before and for 6 h after the consumption of a mixed meal that provided one-third of the daily energy needs. In women, the increase in splanchnic oxygen uptake accounted for 63 +/- 12% of the postprandial increase in oxygen consumption, whereas in men it accounted for 35 +/- 14% (P = not significant between women and men). Leg oxygen uptake accounted for 11 +/- 4 and 10 +/- 3% of the increase in postprandial oxygen consumption in women and men, respectively. The combined data suggest that approximately 48% of postprandial thermogenesis over 6 h occurs in splanchnic tissues, whereas 30-35% occurs in skeletal muscle. Thus the increase in oxygen consumption after a mixed meal is primarily localized to splanchnic tissues, and major reductions in postprandial thermogenesis are unlikely to be attributable solely to abnormalities of skeletal muscle metabolism.


2015 ◽  
Vol 119 (6) ◽  
pp. 734-738 ◽  
Author(s):  
Satyam Sarma ◽  
Benjamin D. Levine

Patients with heart failure with preserved ejection fraction (HFpEF) have similar degrees of exercise intolerance and dyspnea as patients with heart failure with reduced EF (HFrEF). The underlying pathophysiology leading to impaired exertional ability in the HFpEF syndrome is not completely understood, and a growing body of evidence suggests “peripheral,” i.e., noncardiac, factors may play an important role. Changes in skeletal muscle function (decreased muscle mass, capillary density, mitochondrial volume, and phosphorylative capacity) are common findings in HFrEF. While cardiac failure and decreased cardiac reserve account for a large proportion of the decline in oxygen consumption in HFrEF, impaired oxygen diffusion and decreased skeletal muscle oxidative capacity can also hinder aerobic performance, functional capacity and oxygen consumption (V̇o2) kinetics. The impact of skeletal muscle dysfunction and abnormal oxidative capacity may be even more pronounced in HFpEF, a disease predominantly affecting the elderly and women, two demographic groups with a high prevalence of sarcopenia. In this review, we 1) describe the basic concepts of skeletal muscle oxygen kinetics and 2) evaluate evidence suggesting limitations in aerobic performance and functional capacity in HFpEF subjects may, in part, be due to alterations in skeletal muscle oxygen delivery and utilization. Improving oxygen kinetics with specific training regimens may improve exercise efficiency and reduce the tremendous burden imposed by skeletal muscle upon the cardiovascular system.


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