scholarly journals Bilateral NIRS measurements of muscle mitochondrial capacity: Feasibility and repeatability

2021 ◽  
Vol 9 (8) ◽  
Author(s):  
Rewais Hanna ◽  
Jigar Gosalia ◽  
Alaina Demalis ◽  
Zachary Hobson ◽  
Kevin K. McCully ◽  
...  
Keyword(s):  
Mitochondrial Capacity

scholarly journals Limited Mitochondrial Capacity of Visceral Versus Subcutaneous White Adipocytes in Male C57BL/6N Mice

Endocrinology ◽  
2015 ◽  
Vol 156 (3) ◽  
pp. 923-933 ◽  
Author(s):  
Theresa Schöttl ◽  
Lisa Kappler ◽  
Katharina Braun ◽  
Tobias Fromme ◽  
Martin Klingenspor
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Mitochondrial Respiratory Chain ◽  
Metabolic Risk ◽  
Oxygen Species ◽  
White Adipocyte ◽  
White Adipocytes ◽  
Fat Depot ◽  
Mitochondrial Capacity

Abstract Accumulation of visceral fat is associated with metabolic risk whereas excessive amounts of peripheral fat are considered less problematic. At the same time, altered white adipocyte mitochondrial bioenergetics has been implicated in the pathogenesis of insulin resistance and type 2 diabetes. We therefore investigated whether the metabolic risk of visceral vs peripheral fat coincides with a difference in mitochondrial capacity of white adipocytes. We assessed bioenergetic parameters of subcutaneous inguinal and visceral epididymal white adipocytes from male C57BL/6N mice employing a comprehensive respirometry setup of intact and permeabilized adipocytes as well as isolated mitochondria. Inguinal adipocytes clearly featured a higher respiratory capacity attributable to increased mitochondrial respiratory chain content compared with epididymal adipocytes. The lower capacity of mitochondria from epididymal adipocytes was accompanied by an increased generation of reactive oxygen species per oxygen consumed. Feeding a high-fat diet (HFD) for 1 week reduced white adipocyte mitochondrial capacity, with stronger effects in epididymal when compared with inguinal adipocytes. This was accompanied by impaired body glucose homeostasis. Therefore, the limited bioenergetic performance combined with the proportionally higher generation of reactive oxygen species of visceral adipocytes could be seen as a candidate mechanism mediating the elevated metabolic risk associated with this fat depot.

ATGL-mediated triglyceride turnover and the regulation of mitochondrial capacity in skeletal muscle

2015 ◽  
Vol 308 (11) ◽  
pp. E960-E970 ◽  
Author(s):  
Ruth C. R. Meex ◽  
Andrew J. Hoy ◽  
Rachael M. Mason ◽  
Sheree D. Martin ◽  
Sean L. McGee ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Lipid Droplets ◽  
Target Genes ◽  
Control Point ◽  
Hormone Sensitive Lipase ◽  
Acid Oxidation ◽  
Minor Importance ◽  
Transcriptional Responses ◽  
Mitochondrial Capacity

Emerging evidence indicates that skeletal muscle lipid droplets are an important control point for intracellular lipid homeostasis and that regulating fatty acid fluxes from lipid droplets might influence mitochondrial capacity. We used pharmacological blockers of the major triglyceride lipases, adipose triglyceride lipase (ATGL) and hormone-sensitive lipase, to show that a large proportion of the fatty acids that are transported into myotubes are trafficked through the intramyocellular triglyceride pool. We next tested whether increasing lipolysis from intramyocellular lipid droplets could activate transcriptional responses to enhance mitochondrial and fatty acid oxidative capacity. ATGL was overexpressed by adenoviral and adenoassociated viral infection in C2C12 myotubes and the tibialis anterior muscle of C57Bl/6 mice, respectively. ATGL overexpression in C2C12 myotubes increased lipolysis, which was associated with increased peroxisome proliferator-activated receptor (PPAR)-∂ activity, transcriptional upregulation of some PPAR∂ target genes, and enhanced mitochondrial capacity. The transcriptional responses were specific to ATGL actions and not a generalized increase in fatty acid flux in the myotubes. Marked ATGL overexpression (20-fold) induced modest molecular changes in the skeletal muscle of mice, but these effects were not sufficient to alter fatty acid oxidation. Together, these data demonstrate the importance of lipid droplets for myocellular fatty acid trafficking and the capacity to modulate mitochondrial capacity by enhancing lipid droplet lipolysis in vitro; however, this adaptive program is of minor importance when superimposing the normal metabolic stresses encountered in free-moving animals.

Impaired energy metabolism in rat myocardium during phosphate depletion

1982 ◽  
Vol 242 (6) ◽  
pp. F699-F704 ◽  
Author(s):  
N. Brautbar ◽  
R. Baczynski ◽  
C. Carpenter ◽  
S. Moser ◽  
P. Geiger ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Adenine Nucleotides ◽  
Creatine Phosphate ◽  
Inorganic Phosphorus ◽  
High Energy ◽  
Deficient Diet ◽  
Myocardial Energetics ◽  
Phosphate Depletion ◽  
Myocardial Biopsies ◽  
Mitochondrial Capacity

The effects of phosphate depletion (PD) of 4, 8, and 12 wk duration on myocardial energy metabolism were studied in rats fed a phosphate-deficient diet and compared with rats pair-fed a normal phosphate diet. Myocardial biopsies were examined for high-energy phosphate bonds. The results show that PD causes a significant reduction in myocardial concentration of inorganic phosphorus at 4 wk of PD and creatine phosphate at 8 wk of PD, while adenine nucleotides were significantly reduced only after 12 wk of PD. The changes in cellular inorganic phosphorus and creatine phosphate displayed a significant correlation with serum phosphorus levels. Mitochondrial respiration was impaired early in PD. Total cellular, mitochondrial, and myofibrillar creatine kinase activities were significantly reduced at 4 wk of PD and fell further at 8 and 12 wk. These data show that chronic PD is associated with reduced mitochondrial capacity to produce ATP, impaired transport via the creatine phosphate shuttle, and reduced myofibrillar ability to utilize ATP. These abnormalities indicate that all steps of myocardial energetics are impaired in PD and provide the molecular basis for the altered myocardial function seen in PD.

88 Differing Mitochondrial Capacity in Two Separate Skeletal Muscles from Calm and Temperamental Brahman Heifers.

2018 ◽  
Vol 96 (suppl_1) ◽  
pp. 46-47
Author(s):  
S H White ◽  
C M Latham ◽  
C R Long ◽  
R D Randel ◽  
T H Welsh, Jr
Keyword(s):  
Skeletal Muscles ◽  
Mitochondrial Capacity

scholarly journals Decreased Mitochondrial Dynamics Is Associated with Insulin Resistance, Metabolic Rate, and Fitness in African Americans

2019 ◽  
Vol 105 (4) ◽  
pp. 1210-1220 ◽  
Author(s):  
John J Dubé ◽  
Michael L Collyer ◽  
Sara Trant ◽  
Frederico G S Toledo ◽  
Bret H Goodpaster ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Metabolic Rate ◽  
African American Women ◽  
Racial Differences ◽  
Mitochondrial Dynamics ◽  
Resting Metabolic Rate ◽  
Gene Array ◽  
Mitochondrial Capacity

Abstract Context African American women (AAW) have a higher incidence of insulin resistance and are at a greater risk for the development of obesity and type 2 diabetes than Caucasian women (CW). Although several factors have been proposed to mediate these racial disparities, the mechanisms remain poorly defined. We previously demonstrated that sedentary lean AAW have lower peripheral insulin sensitivity, reduced maximal aerobic fitness (VO2max), and lower resting metabolic rate (RMR) than CW. We have also demonstrated that skeletal muscle mitochondrial respiration is lower in AAW and appears to play a role in these racial differences. Objective The goal of this study was to assess mitochondrial pathways and dynamics to examine the potential mechanisms of lower insulin sensitivity, RMR, VO2max, and mitochondrial capacity in AAW. Design To achieve this goal, we assessed several mitochondrial pathways in skeletal muscle using gene array technology and semiquantitative protein analysis. Results We report alterations in mitochondrial pathways associated with inner membrane small molecule transport genes, fusion–fission, and autophagy in lean AAW. These differences were associated with lower insulin sensitivity, RMR, and VO2max. Conclusions Together these data suggest that the metabolic racial disparity of insulin resistance, RMR, VO2max, and mitochondrial capacity may be mediated by perturbations in mitochondrial pathways associated with membrane transport, fission–fusion, and autophagy. The mechanisms contributing to these differences remain unknown.

scholarly journals Cell-autonomous and non-autonomous roles of daf-16 in muscle function and mitochondrial capacity in aging C. elegans

Aging ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 2295-2311 ◽  
Author(s):  
Hongning Wang ◽  
Phillip Webster ◽  
Lizhen Chen ◽  
Alfred L. Fisher
Keyword(s):  
Muscle Function ◽  
C Elegans ◽  
Mitochondrial Capacity

Near infrared spectroscopy-guided exercise training for claudication in peripheral arterial disease

2018 ◽  
Vol 26 (5) ◽  
pp. 471-480 ◽  
Author(s):  
Jonathan R Murrow ◽  
Jared T Brizendine ◽  
Bill Djire ◽  
Hui-Ju Young ◽  
Stephen Rathbun ◽  
...  
Keyword(s):  
Blood Flow ◽  
Infrared Spectroscopy ◽  
Near Infrared Spectroscopy ◽  
Near Infrared ◽  
Muscle Blood Flow ◽  
Arterial Disease ◽  
Walking Program ◽  
Peripheral Arterial ◽  
Walking Time ◽  
Mitochondrial Capacity

Rationale Supervised treadmill exercise for claudication in peripheral arterial disease is effective but poorly tolerated because of ischemic leg pain. Near infrared spectroscopy allows non-invasive detection of muscle ischemia during exercise, allowing for characterization of tissue perfusion and oxygen utilization during training. Objective We evaluated walking time, muscle blood flow, and muscle mitochondrial capacity in patients with peripheral artery disease after a traditional pain-based walking program and after a muscle oxygen-guided walking program. Method and results Patients with peripheral artery disease trained thrice weekly in 40-minute-long sessions for 12 weeks, randomized to oxygen-guided training ( n = 8, age 72 ± 9.7 years, 25% female) versus traditional pain-based training ( n = 10, age 71.6 ± 8.8 years, 20% female). Oxygen-guided training intensity was determined by maintaining a 15% reduction in skeletal muscle oxygenation by near infrared spectroscopy rather than relying on symptoms of pain to determine exercise effort. Pain free and maximal walking times were measured with a 12-minute Gardner treadmill test. Gastrocnemius mitochondrial capacity and blood flow were measured using near infrared spectroscopy. Baseline pain-free walking time was similar on a Gardner treadmill test (2.5 ± 0.9 vs. 3.6 ± 1.0 min, p = 0.5). After training, oxygen-guided cohorts improved similar to pain-guided cohorts (pain-free walking time 6.7 ± 0.9 vs. 6.9 ± 1.1 min, p < 0.01 for change from baseline and p = 0.97 between cohorts). Mitochondrial capacity improved in both groups but more so in the pain-guided cohort than in the oxygen-guided cohort (38.8 ± 8.3 vs. 14.0 ± 9.3, p = 0.018). Resting muscle blood flow did not improve significantly in either group with training. Conclusions Oxygen-guided exercise training improves claudication comparable to pain-based training regimens. Adaptations in mitochondrial function rather than increases in limb perfusion may account for functional improvement. Increases in mitochondrial oxidative capacity may be proportional to the degree of tissue hypoxia during exercise.

scholarly journals Sea Cucumber Peptides Improved the Mitochondrial Capacity of Mice: A Potential Mechanism to Enhance Gluconeogenesis and Fat Catabolism during Exercise for Improved Antifatigue Property

2020 ◽  
Vol 2020 ◽  
pp. 1-17
Author(s):  
Yihao Yu ◽  
Guoqing Wu ◽  
Yuge Jiang ◽  
Bowen Li ◽  
Chuanxing Feng ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Antioxidant Capacity ◽  
Sea Cucumber ◽  
Lactic Dehydrogenase ◽  
Mrna Levels ◽  
Energy Regulation ◽  
Lipid Catabolism ◽  
Swimming Test ◽  
Grip Test ◽  
Mitochondrial Capacity

Sea cucumber promotes multifaceted health benefits. However, the mechanisms of sea cucumber peptides (Scp) regulating the antifatigue capacity is still unknown. The present study is aimed at further elucidating the effects and mechanisms of Scp on the antifatigue capacity of mice. At first, C57BL/6J mice were assigned into four groups named Con, L-Scp, M-Scp, and H-Scp and received diets containing Scp (0%, 0.15%, 0.3%, and 0.5%, respectively) for continuous 30 days. On the 21th day, a fore grip test was conducted on mice. On the 25th day, a rotating rod test was conducted on mice. On the 30th day, the quantities of glycogen and mitochondrial DNA (mtDNA) were determined in 8 random mice and another 8 mice were forced to swim for 1 hour before slaughter for detecting biochemical indicators. It was observed that the Scp groups significantly prolonged the running time in rotarod, increased forelimb grip strength, improved lactic acid (LD) and urea nitrogen (BUN) levels in the serum, decreased lactic dehydrogenase (LDH) and glutamic oxalacetic transaminase (GOT) activities in the serum, increased blood glucose (BG) and glycogen (GN) levels in the liver and skeletal muscle after swimming, increased the activity of Na+-K+-ATPase and Ca2+-Mg2+-ATPase in the skeletal muscle and heart, and improved antioxidant capacity. Furthermore, Scp treatment significantly elevated the mRNA and protein relative levels of power-sensitive factors, lipid catabolism, and mitochondrial biogenesis and significantly upregulated mRNA levels of gluconeogenesis. Besides, mtDNA before the swimming test was increased in the three Scp groups. These results show that Scp treatment has antifatigue capacity. Furthermore, these results suggest that improved energy regulation and antioxidant capacity may be the result of improved mitochondrial function.

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