The effects of pulmonary hypertension on skeletal muscle oxygen pressures in contracting rat spinotrapezius muscle

2021 ◽  
Author(s):  
Kiana M. Schulze ◽  
Ramona E. Weber ◽  
Trenton D. Colburn ◽  
Andrew G. Horn ◽  
Carl J. Ade ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Pulmonary Hypertension ◽  
Muscle Oxygen

scholarly journals Impairment of skeletal muscle oxygen extraction and cardiac output are matched in precapillary pulmonary hypertension

2021 ◽  
pp. 00449-2021
Author(s):  
Harrison Stubbs ◽  
Colin Church ◽  
Martin Johnson ◽  
Stephen Thomson
Keyword(s):  
Skeletal Muscle ◽  
Pulmonary Hypertension ◽  
Cardiac Output ◽  
Oxygen Extraction ◽  
Muscle Oxygen

A comparison of exercise type and intensity on the noninvasive assessment of skeletal muscle mitochondrial function using near-infrared spectroscopy

2013 ◽  
Vol 114 (2) ◽  
pp. 230-237 ◽  
Author(s):  
Terence E. Ryan ◽  
Jared T. Brizendine ◽  
Kevin K. McCully
Keyword(s):  
Skeletal Muscle ◽  
Infrared Spectroscopy ◽  
Near Infrared Spectroscopy ◽  
Mitochondrial Function ◽  
Rate Constants ◽  
Near Infrared ◽  
Clinical Settings ◽  
Muscle Oxygen ◽  
Muscle Oxygen Consumption ◽  
Intensity Of Exercise

Near-infrared spectroscopy (NIRS) can be used to measure muscle oxygen consumption (mVO2) using arterial occlusions. The recovery rate of mVO2after exercise can provide an index of skeletal muscle mitochondrial function. The purpose of this study was to test the influence of exercise modality and intensity on NIRS measurements of mitochondrial function. Three experiments were performed. Thirty subjects (age: 18–27 yr) were tested. NIRS signals were corrected for blood volume changes. The recovery of mVO2after exercise was fit to a monoexponential curve, and a rate constant was calculated (directly related to mitochondrial function). No differences were found in NIRS rate constants for VOL and ES exercises (2.04 ± 0.57 vs. 2.01 ± 0.59 min−1for VOL and ES, respectively; P = 0.317). NIRS rate constants were independent of the contraction frequency for both VOL and ES (VOL: P = 0.166 and ES: P = 0.780). ES current intensity resulted in significant changes to the normalized time-tension integral (54 ± 11, 82 ± 7, and 100 ± 0% for low, medium, and high currents, respectively; P < 0.001) but did not influence NIRS rate constants (2.02 ± 0.54, 1.95 ± 0.44, 2.02 ± 0.46 min−1for low, medium, and high currents, respectively; P = 0.771). In summary, NIRS measurements of skeletal muscle mitochondrial function can be compared between VOL and ES exercises and were independent of the intensity of exercise. NIRS represents an important new technique that is practical for testing in research and clinical settings.

Soothing the sleeping giant: improving skeletal muscle oxygen kinetics and exercise intolerance in HFpEF

2015 ◽  
Vol 119 (6) ◽  
pp. 734-738 ◽  
Author(s):  
Satyam Sarma ◽  
Benjamin D. Levine
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Oxygen Consumption ◽  
Functional Capacity ◽  
Oxidative Capacity ◽  
Exercise Intolerance ◽  
Aerobic Performance ◽  
Muscle Oxygen ◽  
Oxygen Kinetics ◽  
Patients With Heart Failure

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.

scholarly journals TAKling GDF-15 and skeletal muscle atrophy in pulmonary hypertension: are we there yet?

Thorax ◽  
2018 ◽  
Vol 74 (2) ◽  
pp. 103-105
Author(s):  
Yen-Chun Lai ◽  
Steeve Provencher ◽  
Elena A Goncharova
Keyword(s):  
Skeletal Muscle ◽  
Pulmonary Hypertension ◽  
Muscle Atrophy ◽  
Skeletal Muscle Atrophy

Haemodynamic changes and skeletal muscle oxygen tension during complete blood exchange with ultrapurified polymerized bovine haemoglobin

1997 ◽  
Vol 23 (8) ◽  
pp. 865-872 ◽  
Author(s):  
T. G. Standl ◽  
E. Kochs ◽  
W. Reeker ◽  
G. Redmann ◽  
C. Werner ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Tension ◽  
Muscle Oxygen ◽  
Bovine Haemoglobin ◽  
Blood Exchange ◽  
Haemodynamic Changes

Abstract 2769: Impaired Skeletal Muscle Oxygen Utilization Contributes to Exercise Intolerance in Barth Syndrome

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Carolyn T Spencer ◽  
Randall M Bryant ◽  
Barry Byrne ◽  
Elisabeth Heal ◽  
Renee Margossian ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Function ◽  
Mitochondrial Dysfunction ◽  
Near Infrared ◽  
Vastus Lateralis ◽  
Barth Syndrome ◽  
Exercise Intolerance ◽  
Peak Exercise ◽  
Indirect Measure ◽  
Muscle Oxygen

Objective s: Barth Syndrome (BTHS) is an X-linked mutation in the TAZ gene characterized by cardiolipin deficiency, mitochondrial dysfunction and cardio-skeletal myopathy. We hypothe- sized that abnormal skeletal muscle oxygen (O 2 ) utilization contributes to exercise intolerance in BTHS. Methods : Boys with BTHS (n=13) and healthy male controls (n=7) performed a graded exercise test on a cycle ergometer with continuous metabolic and EKG monitoring. Near infrared spectroscopy (NIRS), an indirect measure of tissue O 2 saturation and index of skeletal muscle O 2 utilization, was applied to the vastus lateralis during exercise. Cardiac function in BTHS was assessed by echocardiography and serum BNP to examine the relationship between resting cardiac function and exercise capacity in BTHS. Results : Age (16±5 vs 13±3 years; p=0.22), BMI (17±3 vs. 20±5; p=0.14) and BSA (1.0±0.5 vs 1.2±0.6 m 2 ; p=0.3) were not different between BTHS and controls. BTHS had lower peak VO 2 (19±6 vs. 52±6 ml/kg/min, p < 0.001), lower % of predicted peak VO 2 (40±10% vs. 115±12%, p=0.0004), lower peak work rate (58±18 vs. 205±69 watts, p=0.0004), and lower peak O 2 pulse (4.6±1.6 vs. 14±6 ml O 2 /kg/beat, p< 0.00001) than controls. Peak HR in BTHS was lower but remained within normal peak predicted rate (172±14 vs. 197±11 bpm, p=0.001). Vastus lateralis tissue O 2 saturation at peak exercise decreased from baseline in controls as expected (-18±16%, p<0.001) but paradoxically increased from baseline in BTHS (+17±14%, p<0.03, p=0.0005 BTHS vs. controls) indicating impaired muscle O 2 utilization. Absolute (r= - 0.70, p<0.0001) and percent (r= - 0.70, p<0.001) change in NIRS from baseline was negatively associated with peak VO 2 . There was no correlation between peak VO 2 and resting EF (55±7%; r=0.12), SF (30±4%; r= -.26), myocardial performance index (0.4±0.1; r= -.3) or serum BNP (232±381; r=0.1). Conclusion : O 2 consumption during exercise in BTHS is severely reduced and caused, at least in part, by impaired skeletal muscle O 2 utilization. Resting cardiac function is not related to O 2 consumption in BTHS but cardiac dysfunction during exercise in BTHS is not excluded without further studies. Mitochondrial dysfunction likely mediates skeletal muscle O 2 utilization deficits during exercise in BTHS.

INCREASE OF SKELETAL MUSCLE OXYGEN TENSION BY HELP-LDL-APHERESIS IN CARDIAC ALLOGRAFT RECIPIENTS WITH SEVERE HYPERCHOLESTEROLEMIA.

2000 ◽  
Vol 69 (Supplement) ◽  
pp. S235 ◽  
Author(s):  
Jai-Wun Park ◽  
C. Morowietz ◽  
Florian M. Wagner ◽  
C. A. Labarrere ◽  
Stephan Schueler ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Tension ◽  
Cardiac Allograft ◽  
Ldl Apheresis ◽  
Muscle Oxygen

scholarly journals Skeletal Muscle Oxygen Kinetics During Exercise In Adults With Obstructive Sleep Apnea.

2019 ◽  
Vol 51 (Supplement) ◽  
pp. 301
Author(s):  
Jeffrey E. Herrick ◽  
Shirpa Puri ◽  
Monira Aldhahi ◽  
Vivek Jain ◽  
Lisa MK Chin
Keyword(s):  
Skeletal Muscle ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Muscle Oxygen ◽  
Obstructive Sleep ◽  
Oxygen Kinetics
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