Effects of Endotoxin on Canine Skeletal Muscle Oxygen Delivery-Uptake Relations During Progressive Hypoxic Hypoxia

1992 ◽  
pp. 751-757 ◽  
Author(s):  
Scott E. Curtis ◽  
W. E. Bradley ◽  
Stephen M. Cain
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Delivery ◽  
Hypoxic Hypoxia ◽  
Muscle Oxygen

In vivo effects on human skeletal muscle oxygen delivery and metabolism of cardiopulmonary bypass and perioperative hemodilution

2011 ◽  
Vol 38 (3) ◽  
pp. 413-421 ◽  
Author(s):  
R. A. De Blasi ◽  
E. Tonelli ◽  
R. Arcioni ◽  
M. Mercieri ◽  
L. Cigognetti ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cardiopulmonary Bypass ◽  
Oxygen Delivery ◽  
Human Skeletal Muscle ◽  
Muscle Oxygen ◽  
In Vivo Effects

Determinants of VO2 max decline with aging: an integrated perspective

2008 ◽  
Vol 33 (1) ◽  
pp. 130-140 ◽  
Author(s):  
Andrew C. Betik ◽  
Russell T. Hepple
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Output ◽  
Oxygen Delivery ◽  
Dominant Role ◽  
Oxidative Capacity ◽  
Oxygen Utilization ◽  
Critical Perspective ◽  
Progressive Decline ◽  
Muscle Oxygen ◽  
Capillary Bed

Aging is associated with a progressive decline in the capacity for physical activity. Central to this decline is a reduction in the maximal rate of oxygen utilization, or VO2 max. This critical perspective examines the roles played by the factors that determine the rate of muscle oxygen delivery versus those that determine the utilization of oxygen by muscle as a means of probing the reasons for VO2 max decline with aging. Reductions in muscle oxygen delivery, principally due to reduced cardiac output and perhaps also a maldistribution of cardiac output, appear to play the dominant role up until late middle age. On the other hand, there is a decline in skeletal muscle oxidative capacity with aging, due in part to mitochondrial dysfunction, which appears to play a particularly important role in extreme old age (senescence) where skeletal muscle VO2 max is observed to decline by approximately 50% even under conditions of similar oxygen delivery as young adult muscle. It is noteworthy that at least the structural aspects of the capillary bed do not appear to be reduced in a manner that would compromise the capacity for muscle oxygen diffusion even in senescence.

scholarly journals Fatigue-independent alterations in muscle activation and effort perception during forearm exercise: role of local oxygen delivery

2019 ◽  
Vol 127 (1) ◽  
pp. 111-121 ◽  
Author(s):  
P. J. Drouin ◽  
Z. I. N. Kohoko ◽  
O. K. Mew ◽  
M. J. T. Lynn ◽  
A. M. Fenuta ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Delivery ◽  
Muscle Activation ◽  
Voluntary Exercise ◽  
Force Output ◽  
Muscle Oxygen ◽  
Perception Of Effort ◽  
Forearm Exercise ◽  
Exercise Muscle

The oxygen-conforming response (OCR) of skeletal muscle refers to a downregulation of muscle force for a given muscle activation when oxygen delivery (O2D) is reduced, which is rapidly reversed when O2D is restored. We tested the hypothesis that the OCR exists in voluntary human exercise and results in compensatory changes in muscle activation to maintain force output, thereby altering perception of effort. In eight men and eight women, electromyography (EMG), oxyhemoglobin (O2Hb) and deoxyhemoglobin (HHb), forearm blood flow (FBF), and task effort awareness (TEA) were measured. Participants completed two nonfatiguing rhythmic handgrip tests consisting of 5-min steady state (SS) followed by two bouts of 2-min brachial artery compression to reduce FBF by ~50% of SS (C1 and C2), separated by 2 min of no compression (NC1) and ending with 2 min of no compression (NC2). When FBF was compromised during C1, EMG/Force (1.58 ± 0.39) increased compared with SS (1.31 ± 0.33, P = 0.001). However, EMG/Force was not restored upon FBF restoration at NC1 (1.48 ± 0.38, P = 0.479), consistent with C1 evoking skeletal muscle fatigue. When FBF was compromised during C2, EMG/Force increased (1.73 ± 0.50) compared with NC1 (1.48 ± 0.38, P = 0.013). EMG/Force returned to NC1 levels during NC2 (1.50 ± 0.39, P = 0.016), consistent with an OCR in C2. TEA (SS 2.2 ± 2.3, C1 3.9 ± 2.5, NC1 3.4 ± 2.7, C2 4.6 ± 2.7, NC2 3.9 ± 2.8) mirrored changes in EMG. It is noteworthy that during the second compromise and then restoration of muscle oxygenation EMG and TEA were rapidly restored to precompromise levels. We interpreted these findings to support the existence of an OCR and its ability to rapidly modify perception of effort during voluntary exercise. NEW & NOTEWORTHY In healthy individuals, when force output is maintained during rhythmic handgrip exercise, muscle activation and perception of effort rapidly increase with compromised muscle oxygen delivery (O2D) and then return to precompromised levels when muscle O2D is restored. These findings suggest that an oxygen-conforming response (OCR) exists and is able to modify perception of effort during voluntary exercise. Therefore, similar to fatigue, an OCR may have implications for exercise tolerance.

Resuscitation of severe but brief haemorrhagic shock with PFC in rabbits restores skeletal muscle oxygen delivery and does not alter skeletal muscle metabolism

Resuscitation ◽  
2006 ◽  
Vol 70 (1) ◽  
pp. 124-132 ◽  
Author(s):  
Sandra Audonnet-Blaise ◽  
Marie-Pierre Krafft ◽  
Younes Smani ◽  
Paul-Michel Mertes ◽  
Pierre-Yves Marie ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Delivery ◽  
Muscle Metabolism ◽  
Haemorrhagic Shock ◽  
Skeletal Muscle Metabolism ◽  
Muscle Oxygen

Control of oxygen delivery within skeletal muscle

2005 ◽  
pp. 23-24
Author(s):  
Paul McDonough ◽  
Brad Behnke ◽  
Danielle Padilla ◽  
Timothy Musch ◽  
David Poole
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Delivery

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.

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