scholarly journals Dietary fish oil reduces skeletal muscle oxygen consumption, provides fatigue resistance and improves contractile recovery in the rat in vivo hindlimb

2010 ◽  
Vol 104 (12) ◽  
pp. 1771-1779 ◽  
Author(s):  
Gregory E. Peoples ◽  
Peter L. McLennan
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Consumption ◽  
Fish Oil ◽  
Mechanical Performance ◽  
Muscle Membrane ◽  
Membrane Composition ◽  
Pufa Ratio ◽  
Dietary Fish ◽  
Pufa Group

Dietary fish oil modulates skeletal muscle membrane fatty acid composition. Similar changes in heart membrane composition modulate myocardial oxygen consumption and enhance mechanical performance. The rat in vivo autologous perfused hindlimb was used to investigate the influence of membrane composition on skeletal muscle function. Male Wistar rats were fed either saturated fat (SF), n-6 PUFA (linoleic acid rich) or n-3 PUFA (fish oil) diets for 8 weeks. Hindlimb skeletal muscle perfused using the animal's own blood was stimulated via the sciatic nerve (1 Hz, 6-12 V, 0·05 ms) to contract in repeated 10 min bouts. The n-3 PUFA diet markedly increased 22 : 6n-3 DHA, total n-3 PUFA and decreased the n-6:n-3 PUFA ratio (P < 0·05) in red and white skeletal muscle membranes. There was no difference in initial twitch tension but the n-3 PUFA group maintained greater twitch tension within all contraction bouts and recovered better during rest to produce greater twitch tension throughout the final contraction bout (P < 0·05). Hindlimb oxygen consumption during contraction was significantly lower in the n-3 PUFA group compared with the SF group, producing a significantly higher O2 efficiency index compared with both SF and n-6 PUFA groups (P < 0·05). Resting oxygen consumption was increased in recovery in the SF group (P < 0·05) but did not change in the n-3 PUFA group. Membrane incorporation of n-3 PUFA DHA following fish oil feeding was associated with increased efficiency of muscle O2 consumption and promoted resistance to muscle fatigue.

scholarly journals Long-chain n-3 DHA reduces the extent of skeletal muscle fatigue in the rat in vivo hindlimb model

2013 ◽  
Vol 111 (6) ◽  
pp. 996-1003 ◽  
Author(s):  
Gregory E. Peoples ◽  
Peter L. McLennan
Keyword(s):  
Skeletal Muscle ◽  
Fish Oil ◽  
Muscle Fatigue ◽  
Muscle Membrane ◽  
Mammalian Skeletal Muscle ◽  
Skeletal Muscle Fatigue ◽  
Arterial Blood ◽  
Oxygen Efficiency ◽  
Long Chain

Dietary fish oil modifies skeletal muscle membrane fatty acid composition and oxygen efficiency similar to changes in the myocardium. Oxygen efficiency is a key determinant of sustained force in mammalian skeletal muscle. Therefore, in the present study, we tested the effects of a fish-oil diet on skeletal muscle fatigue under the stress of contraction using the rat in vivo autologous perfused hindlimb model. For 8 weeks, male Wistar rats were fed a diet rich in saturated fat (SF), a diet rich in n-6 PUFA or a diet rich in long-chain (LC) n-3 PUFA DHA derived from fish oil. In anaesthetised, mechanically ventilated rats, with their hindlimbs perfused with arterial blood at a constant flow, the gastrocnemius–plantaris–soleus muscle bundle was stimulated via sciatic nerve (2 Hz, 6–12 V, 0·05 ms) to contract repetitively for 30 min. Rats fed the n-3 PUFA diet developed higher maximum twitch tension than those fed the SF and n-6 PUFA diets (P< 0·05) and sustained twitch tension through more repetitions before the tension declined to 50 % of the maximum twitch tension (P< 0·05). The n-3 PUFA group used less oxygen for tension developed and produced higher venous lactate concentrations with no difference in glycogen utilisation compared with the SF and n-6 PUFA groups. These results further support that incorporation of DHA into skeletal muscle membranes increases the efficiency of oxygen use over a range of contractile force and this is expressed as a higher sustained force and prolonged time to fatigue.

Abstract 121: Development of Enzyme Replacement Therapy in Mammalian Models of Barth Syndrome

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Ana Dinca ◽  
Wei-Ming Chien ◽  
Michael Chin
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Consumption ◽  
Cell Line ◽  
Single Gene ◽  
Barth Syndrome ◽  
Protein Therapy ◽  
Knock Out ◽  
Enzyme Replacement ◽  
C Terminus

Barth Syndrome (BTHS) is caused by a single gene mutation in the mitochondrial transacylase, tafazzin (TAZ), which results in impaired lipid metabolism leading to dysfunction in highly energetic tissues such as the heart and skeletal muscle. TAZ remodels the signature mitochondrial phospholipid, cardiolipin (CL), which is responsible for providing support to the electron transport chain. BTHS patients suffer from growth deficiencies, cardiomyopathy, hypotonia and neutropenia. Currently, treatment for patients with BTHS is supportive, seeking to ameliorate rather than prevent heart problems, skeletal muscle problems and recurring infections. Protein therapy, on the other hand, might treat and even prevent cardiac, skeletal muscle as well as infection-related morbidities. We designed a recombinant TAZ protein containing a cell penetrating peptide in its C-terminus, which enables the recombinant TAZ to penetrate cells and then treated TAZ-deficient cells with it. We tested the permeability of the recombinant protein by direct delivery to H9C2 cardiomyoblasts and found that the protein is successfully taken up by the cells. We have generated a CRISPR-mediated TAZ knock out cardiomyoblast cell line and we found that TAZ knock out cells show a decrease in oxygen consumption as compared to the wild type cells; this is consistent with data from BTHS patient-derived cells. We are using this cell line to assess the enzymatic activity of the delivered protein by conducting mitochondrial respiration measurements. We have also acquired a mouse model of BTHS and are testing the recombinant TAZ in vivo. Preliminary data shows an augmentation in oxygen consumption following treatment with TAZ. These results indicate that the protein is able to reach the mitochondria, where it is enzymatically active and able to enhance respiration. As the protein is able to rescue respiration in cells in which tafazzin was absent, this suggests that our approach should not only be able to prevent onset of symptoms, but also rescue the phenotype in already affected tissues.

scholarly journals Factors determining training-induced changes in V̇O2max, critical power and V̇O2 on-kinetics in skeletal muscle

2020 ◽  
Author(s):  
Bernard Korzeniewski ◽  
Harry B. Rossiter
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Consumption ◽  
Computer Simulations ◽  
Critical Power ◽  
Slow Component ◽  
Primary Phase ◽  
Exercise Intolerance ◽  
Threshold Mechanism ◽  
Induced Changes

Computer simulations, using the "Pi double-threshold" mechanism of muscle fatigue postulated previously (the first threshold initiating progressive reduction in work efficiency and the second threshold resulting in exercise intolerance), demonstrated that several parameters of the skeletal muscle bioenergetic system can affect the maximum oxygen consumption (V̇O2max), critical power (CP) and oxygen consumption (V̇O2) on-kinetics in skeletal muscle. Simulations and experimental observations together demonstrate that endurance exercise training increases oxidative phosphorylation (OXPHOS) activity and/or each-step activation (ESA) intensity, the latter especially in the early stages of training. Here, new computer simulations demonstrate that an endurance training-induced increase in OXPHOS activity and decrease in peak Pi (Pipeak), at which exercise is terminated because of exercise intolerance, result in increased V̇O2max and CP, speeding of the primary phase II of V̇O2 on-kinetics and decrease of the V̇O2 slow component magnitude, consistent with their observed behavior in vivo. It is possible, but remains unknown, whether there is a contribution to this behavior of an increase in the critical Pi (Picrit), above which the additional ATP usage underlying the slow component begins, and decrease in the activity of the additional ATP usage (kadd). Thus, we offer a mechanism, involving Pi accumulation, Picrit and Pipeak, of the training-induced adaptations in V̇O2max, CP, and the primary and slow component phases of V̇O2 on-kinetics that was absent in the literature.

scholarly journals Dietary fish oil delays hypoxic skeletal muscle fatigue and enhances caffeine-stimulated contractile recovery in the rat in vivo hindlimb

2017 ◽  
Vol 42 (6) ◽  
pp. 613-620 ◽  
Author(s):  
Gregory E. Peoples ◽  
Peter L. McLennan
Keyword(s):  
Skeletal Muscle ◽  
Fish Oil ◽  
Muscle Fatigue ◽  
Contractile Function ◽  
Physiological Role ◽  
Muscle Bundle ◽  
Skeletal Muscle Fatigue ◽  
Dietary Fish ◽  
Contractile Recovery ◽  
Muscle Contractile

Oxygen efficiency influences skeletal muscle contractile function during physiological hypoxia. Dietary fish oil, providing docosahexaenoic acid (DHA), reduces the oxygen cost of muscle contraction. This study used an autologous perfused rat hindlimb model to examine the effects of a fish oil diet on skeletal muscle fatigue during an acute hypoxic challenge. Male Wistar rats were fed a diet rich in saturated fat (SF), long-chain (LC) n-6 polyunsaturated fatty acids (n-6 PUFA), or LC n-3 PUFA DHA from fish oil (FO) (8 weeks). During anaesthetised and ventilated conditions (normoxia 21% O2 (SaO2–98%) and hypoxia 14% O2 (SaO2–89%)) the hindlimb was perfused at a constant flow and the gastrocnemius–plantaris–soleus muscle bundle was stimulated via sciatic nerve (2 Hz, 6–12V, 0.05 ms) to established fatigue. Caffeine (2.5, 5, 10 mM) was supplied to the contracting muscle bundle via the arterial cannula to assess force recovery. Hypoxia, independent of diet, attenuated maximal twitch tension (normoxia: 82 ± 8; hypoxia: 41 ± 2 g·g−1 tissue w.w.). However, rats fed FO sustained higher peak twitch tension compared with the SF and n-6 PUFA groups (P < 0.05), and the time to decline to 50% of maximum twitch tension was extended (SF: 546 ± 58; n-6 PUFA: 522 ± 58; FO: 792 ± 96 s; P < 0.05). In addition, caffeine-stimulated skeletal muscle contractile recovery was enhanced in the FO-fed animals (SF: 41 ± 3; n-6 PUFA: 40 ± 4; FO: 52 ± 7% recovery; P < 0.05). These results support a physiological role of DHA in skeletal muscle membranes when exposed to low-oxygen stress that is consistent with the attenuation of muscle fatigue under physiologically normoxic conditions.

Effects of dietary fish oil on cardiovascular responsiveness to adrenergic agonists in spontaneously hypertensive rat

1993 ◽  
Vol 71 (7) ◽  
pp. 432-438 ◽  
Author(s):  
Jacquelyn M. Smith ◽  
Stephen J. Kopp ◽  
Dennis J. Paulson ◽  
June T. Daar
Keyword(s):  
Fish Oil ◽  
Spontaneously Hypertensive Rats ◽  
Aortic Pressure ◽  
Adrenergic Agonists ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Dietary Fish ◽  
Fish Oil Supplementation ◽  
Mean Aortic Pressure

To test the hypothesis that dietary fish oil supplementation decreases systolic blood pressure in hypertensive rats by modifying cardiovascular responsiveness to adrenergic agonists, spontaneously hypertensive rats (SHR) and Wistar–Kyoto rats (WKY) received either a corn or fish oil diet, 5% (g/kg) for 10 weeks. Mean aortic pressure was lower in fish oil treated (161 ± 7 mm Hg (1 mmHg = 133.3 Pa)) than corn oil treated (191 ± 6 mmHg) SHR. Although dietary fish oil supplementation decreased responsiveness to norepinephrine in isolated thoracic aorta from SHR, there was no change in cardiovascular responsiveness to the β1 agonist dobutamine or the α1, agonist phenylephrine when these adrenergic agonists were administered in vivo. However, dietary fish oil did decrease the spontaneous basal tone in aorta from both SHR and WKY. This study provides further evidence that dietary fish oil lowers blood pressure in an animal model genetically predisposed to hypertension. However, the mechanism for this decrease in mean aortic pressure in vivo does not appear to be related to modification of cardiovascular responsiveness to α1- or β1-adrenergic agonists and may be related to a decrease in basal vasomotor tone.Key words: fish oil, antihypertensive, spontaneously hypertensive rats, dobutamine, vascular smooth muscle.

The effect of level of dietary fish oil inclusion on intake and methane emissions of beef steers

2009 ◽  
Vol 2009 ◽  
pp. 25-25 ◽  
Author(s):  
K J Petrie ◽  
K J Hart ◽  
J Callan ◽  
T M Boland ◽  
D A Kenny
Keyword(s):  
Fish Oil ◽  
Dietary Supplementation ◽  
Manure Management ◽  
Beef Steers ◽  
Enteric Fermentation ◽  
Free Hydrogen ◽  
Dietary Fish ◽  
Ruminal Biohydrogenation ◽  
Fish Oil Supplementation

Irish livestock account for 0.55 million tonnes of methane (CH4) annually from enteric fermentation and manure management (EPA, 2006). However, recent studies have shown the potential to reduce ruminal methanogenesis through strategic dietary supplementation with polyunsaturated fatty acids (PUFA; Jordan et al. 2006). This is likely to be mediated, in part, through the unsaturated double bonds of PUFA acting as sinks for free hydrogen during ruminal biohydrogenation. Fish oil is acknowledged as the richest natural source of long chain n-3 PUFA such as eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids (Ruxton et al., 2004). Despite this, there is little published information on the effect of dietary fish oil supplementation on in vivo ruminal methanogenesis in cattle. The aim of this study was to assess the effect of a novel concentrated n-3 PUFA fish oil, on the intake and CH4 emissions of beef steers.

Effect of fish oil n-3 fatty acids on cerebral microcirculation

1990 ◽  
Vol 258 (6) ◽  
pp. H1780-H1785 ◽  
Author(s):  
E. F. Ellis ◽  
R. J. Police ◽  
L. M. Yancey ◽  
M. N. Grabeel ◽  
M. L. Heizer ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fish Oil ◽  
Cerebrovascular Reactivity ◽  
Maximal Increase ◽  
Cranial Window ◽  
Epa And Dha ◽  
Cerebrovascular Function ◽  
Dietary Fish ◽  
Arteriolar Diameter

Dietary fish oil containing the n-3 polyunsaturated fatty acids eicosapentaenoic acid (EPA, 20:5) and docosahexaenoic acid (DHA, 22:6) is being consumed by many individuals in an effort to reduce thrombosis and heart disease. However, little is known about how these fatty acids can affect cerebrovascular function. The purpose of the present study was to begin to examine the effects of these fatty acids on cerebral arteriolar diameter and to compare their effects with that of arachidonic acid (AA). Pial arteriolar diameter responses to the topically applied fatty acids [0.2-200 micrograms/ml cerebrospinal fluid (CSF)] were measured in rabbits using in vivo microscopy and the acute cranial window technique. Prostaglandin E2 (PGE2) formed by the brain in response to AA, EPA, and DHA was measured in CSF using radioimmunoassay. EPA induced a dose-dependent dilation response of which the maximum was 29%, whereas the maximal dilation produced by AA was 100%. The arteriolar effect of EPA was reduced by indomethacin or superoxide dismutase plus catalase, indicating vasoactivity due to oxygen radicals formed by cyclooxygenase metabolism of EPA. DHA itself had no effect on diameter or adenosine-induced dilation but reduced dilation by AA when coapplied with AA. AA induced a 65-fold maximal increase in PGE2, whereas EPA and DHA had comparatively little effect. These results imply that substitution of n-3 fatty acids for AA in brain phospholipids may result in less cyclooxygenase-dependent cerebrovascular reactivity. This alteration in reactivity may produce important effects with respect to the brain's blood flow response to a number of physiological and pathological challenges.

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