Fatty acid oxidation by liver and muscle preparations of exhaustively exercised rats

Barakat, Hisham A.; Kasperek, George J.; Dohm, G. Lynis; Tapscott, Edward B.; Snider, R. D.

doi:10.1042/bj2080419

Cited by 27 publications

(14 citation statements)

References 25 publications

(23 reference statements)

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“…Effects may be reversible in ways that prevent later detection. Animal studies have been made with rats [2,11,12,30] and horses [7,17], and they indicate impaired function of isolated mitochondria, in agreement with the morphological observations mentioned above. On the other hand, studies of human isolated mitochondria showed no impairment upon exhaustion [32,52,53,54].…”

Section: Introductionsupporting

confidence: 77%

“…As much as 55% inhibition was detected after five track runs. Studies of trained rats showed that the specific respiratory activities of isolated mitochondria with pyruvate + malate [12] and palmitoyl-carnitine + malate [2] were lowered after exhaustion. The observation of decreased succinate respiration [12] was apparently not confirmed later [11].…”

Section: Discussionmentioning

confidence: 99%

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The effect of high-intensity exhaustive exercise studied in isolated mitochondria from human skeletal muscle

Rasmussen

Krustrup

Bangsbo

et al. 2001

Pflügers Arch - Eur J Physiol

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Six young men performed five 1-min bicycle exercise bouts to exhaustion. Muscle lactate increased to congruent with 114 mmol x kg(-1) dwt and pH decreased to congruent with 6.6. Mitochondria were prepared from a needle biopsy sample taken from m. vastus lateralis immediately after the last exercise bout. No significant effect of exhaustion on the proton permeability and amount of cytochromes c and aa3 in isolated mitochondria was detected. The activities of the following enzymes and systems were not altered either: citrate synthase, succinate dehydrogenase, cytochrome oxidase, succinate + glutamate respiration, malate + glutamate respiration, the respiratory chain, and the reactions involved in ATP synthesis. Thus, the mitochondria did not appear globally altered upon exhaustion. However, the following NAD-linked activities were significantly lowered: pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, glutamate dehydrogenase and fatty acid beta-oxidation. The activities of alpha-glycerophosphate dehydrogenase and exo-NADH oxidase, enzymes that might catalyze the oxidation of sarcoplasmic NADH, were increased. These changes may be due to the action of reactive oxygen species, protons and Ca2+. Transient opening of the permeability transition pore may also be involved. Some effects may have been reversed during isolation of the mitochondria and the changes in mitochondrial function in situ upon exhaustion may have been more extensive than observed.

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Section: Introductionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

The effect of high-intensity exhaustive exercise studied in isolated mitochondria from human skeletal muscle

Rasmussen

Krustrup

Bangsbo

et al. 2001

Pflügers Arch - Eur J Physiol

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“…As oxidative stress is commonly reported following eccentric exercise (Nikolaidis et al 2008), we suggest that it could be involved in reducing state 3 in the current study. Depressed mitochondrial RCR has been reported previously postexercise (Barakat et al 1982;Davies et al 1982;Fernstrom et al 2007) although this is not a consistent Wnding (Madsen et al 1996a) and has only been observed immediately post-exercise. The hypothesis that RCR would be depressed 48 h post-exercise was based on the substantial increases in MCC observed at this time point (Duan et al 1990).…”

Section: Discussionmentioning

confidence: 81%

Heat exposure does not alter eccentric exercise-induced increases in mitochondrial calcium and respiratory dysfunction

et al. 2011

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Eccentric exercise can lead to muscle damage including dramatic changes to mitochondrial calcium content (MCC) and impaired respiratory function. Heat acclimation can create a cross-tolerance to a number of stresses including eccentric exercise but little is known about any protection to mitochondria. We hypothesised that intermittent heat exposure will lead to improved control of MCC and to preserved mitochondrial function following eccentric exercise. Sprague-Dawley rats were exposed to 3 weeks of intermittent heat exposure (36°C, 40% relative humidity, 6 h/day, 5 days a week) or kept in cool conditions (20°C). Animals were then assigned to a control or exercise group (-14°C decline treadmill exercise for 90 min). MCC, mitochondrial respiration and mitochondrial permeability transition pore opening (mPTP) were measured in mitochondria isolated from the red quadriceps in animals killed immediately, 2 h and 48 h post-exercise. Results showed that heat exposure was associated with lower plasma creatine kinase levels (p < 0.05) post-exercise suggesting lower levels of muscle damage. There was a significant (~500%) rise in MCC (p < 0.001) and a reduction in mitochondrial respiratory control ratio (p < 0.001) 48 h post-exercise. mPTP displayed increased (p < 0.05) sensitivity to calcium immediately and 48 h post-exercise. Thus, decline running led to significant impairment of mitochondria respiration and calcium loading which was more pronounced 48 h post-exercise compared with earlier time points. MCC levels and mitochondrial function were not altered by heat exposure. In conclusion, intermittent heat exposure does not appear to provide protection against mitochondrial dysfunction resulting from eccentric exercise.

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“…Thus, although there is rodent data indicating that hepatic -oxidation may increase acutely with exercise (Barakat et al 1982) and direct human evidence that lipoprotein-derived fatty acids are oxidized by skeletal muscle during exercise (Kiens 1993) and that VLDL clearance may increase (Malkova et al 2000), the current Wndings may suggest that the level of lipoprotein export and oxidation is insuYcient to induce a reduction in HTGC during exercise or in the post-exercise period. Namely, unlike IMTG, the exercise-induced increase in adipose lipolysis (as suggested by our FFA, glycerol and TG data) and subsequent inXux of FFA into the liver may outweigh the capacity of the liver to oxidize and/or export fatty acids resulting in their accumulation in the triglyceride pool.…”

Section: Discussionmentioning

confidence: 84%

Effect of prolonged exercise and pre-exercise dietary manipulation on hepatic triglycerides in trained men

et al. 2011

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The purpose of this study was to examine the effect of exercise and pre-exercise dietary manipulation on hepatic triglyceride concentration (HTGC). HTGC was measured by proton magnetic resonance spectroscopy ((1)H-MRS) before and after 90 min of moderate intensity cycling in six endurance trained males following 67 h of mixed diet (M) and an isocaloric minimal carbohydrate (2%) high fat (83%) diet (HF). Diets were administered by balanced crossover design. Whole-body fat oxidation, plasma-free fatty acid (FFA), glycerol and triglyceride concentrations were significantly elevated during exercise in HF versus M (P < 0.05 for all). There was no significant treatment × time interaction for HTGC (P = 0.368). However, there was a significant net increase in HTGC (time effect) during the combined 6 h exercise and post-exercise period (P = 0.037). In conclusion, we observed no measurable net change in the hepatic triglyceride pool across a period involving a prolonged exercise bout. Furthermore, manipulation of pre-exercise dietary intake did not influence the interaction between the hepatic triglyceride concentration and exercise in lean trained men. This supports the contention that hepatic triglycerides do not meaningfully contribute to the high rate of fat oxidation observed during acute exercise, or the enhancement of this with regular exercise training and/or pre-exercise dietary manipulation.

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Fatty acid oxidation by liver and muscle preparations of exhaustively exercised rats

Cited by 27 publications

References 25 publications

The effect of high-intensity exhaustive exercise studied in isolated mitochondria from human skeletal muscle

The effect of high-intensity exhaustive exercise studied in isolated mitochondria from human skeletal muscle

Heat exposure does not alter eccentric exercise-induced increases in mitochondrial calcium and respiratory dysfunction

Effect of prolonged exercise and pre-exercise dietary manipulation on hepatic triglycerides in trained men

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