Effects of Exercise, Training, and Diet on Muscle Citric Acid Cycle Enzyme Activity

Dohm, G. Lynis; Huston, R. L.; Askew, E. W.; Fleshood, H.Lee

doi:10.1139/o73-105

Cited by 51 publications

(18 citation 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: 84%

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: 84%

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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“…Terjung et al (1972) found that mitochondria respiratory function from trained rats run to exhaustion and trained rested rats were similar, but failed to compare the results to untrained rats subjected to the same treatment. Dohm et al (1972Dohm et al ( , 1973 observed depressed mitochondrial respiration only in trained exhausted groups, but trained rats were typically run to exhaustion at almost three times the speed and for twice as long as untrained rats, limiting comparison with the current study. Chronic exercise, however, is recognized as offering cross-tolerance protection in cardiac muscle via a calciumdependent mechanism since endurance exercise is able to revert hyperglycemic-related increased sensitivity of heart mitochondria to calcium-induced mPTP opening (LuminiOliveira et al 2011).…”

Section: Discussioncontrasting

confidence: 55%

Specific training improves skeletal muscle mitochondrial calcium homeostasis after eccentric exercise

et al. 2012

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There is limited understanding of the mitochondrial adaptation following repeated eccentric exercise bouts, a model resulting in muscle adaptation known as the repeat bout effect. It was hypothesized that downhill training would reduce mitochondrial calcium content (MCC) post an acute eccentric bout with concurrent improvements in mitochondrial respiratory function. Thirty-four Sprague-Dawley rats were divided into four groups: control (N), control with acute eccentric exercise (N (ecc)), trained control (X) and trained with acute eccentric exercise (X (ecc)). Training for X and X (ecc) consisted of 30 min per day for five consecutive days of downhill treadmill running. The acute eccentric exercise bout was a -14° treadmill exercise for 90 min performed 2 weeks after the training period. Animals were killed 48 h post-exercise. Isolated mitochondria from the red quadriceps allowed for the measure of mitochondrial respiratory indices and MCC. Calpain activity and heat shock protein 72 expression (HSP72) were also measured. MCC dramatically increased following the acute bout of eccentric exercise in N (ecc) (p < 0.001), but did not change in X (ecc). Mitochondrial respiratory function tended to be slightly depressed in N (ecc) (state 3 respiration, p = 0.053; respiratory control ratio, p = 0.098) and unaltered in X (ecc). Previous training altered the calpain and heat shock protein response to an acute bout of eccentric exercise. The results suggest that downhill exercise training improves mitochondrial calcium homeostasis following an acute bout of prolonged eccentric exercise and may stabilize mitochondrial respiratory function. These improvements coincide with a reduction in calpain activity and heat shock protein upregulation.

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“…Data from the human studies suggested that CS activities elevate in response to acute exercise, whereas conflicting findings in the CS activity changes after an acute bout of exercise were reported in the rat studies (5,9,12,13,26). Unaltered or even decreased CS activities have been reported in skeletal muscles shortly after a single bout of exercise.…”

mentioning

confidence: 97%

“…Transient changes in skeletal muscle mitochondrial enzyme activities have been investigated after a single bout of exercise in both animals (5,9,21) and humans (14,27). Data from the human studies suggested that CS activities elevate in response to acute exercise, whereas conflicting findings in the CS activity changes after an acute bout of exercise were reported in the rat studies (5,9,12,13,26).…”

mentioning

confidence: 99%

Citrate synthase expression and enzyme activity after endurance training in cardiac and skeletal muscles

Siu

Donley

Bryner

2003

Journal of Applied Physiology

117

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. Citrate synthase expression and enzyme activity after endurance training in cardiac and skeletal muscles. J Appl Physiol 94: 555-560, 2003; 10.1152/ japplphysiol.00821.2002.-The present study was designed to examine the acute and chronic effects of endurance treadmill training on citrate synthase (CS) gene expression and enzymatic activity in rat skeletal and cardiac muscles. Adult rats were endurance trained for 8 wk on a treadmill. They were killed 1 h (T1, n ϭ 8) or 48 h (T48, n ϭ 8) after their last bout of exercise training. Eight rats were sedentary controls (C) during the training period. CS mRNA levels and enzymatic activities of the soleus and ventricle muscles were determined. Training resulted in higher CS mRNA levels in both the soleus muscles (21% increase in T1; 18% increase in T48, P Ͻ 0.05) and ventricle muscles (23% increase in T1; 17% increase in T48, P Ͻ 0.05) when compared with the C group. The CS enzyme activities were 42 (P Ͻ 0.01) and 25% (P Ͻ 0.01) greater in the soleus muscles of T1 and T48 groups, respectively, when compared with that of the C group. Soleus CS enzyme activity was significantly greater in the T1 vs. T48 groups (P Ͻ 0.05). However, no appreciable alterations in CS enzyme activities were observed in the ventricle muscles in both training groups. These findings suggest differential responses of skeletal and cardiac muscles in CS enzymatic activity but similar responses in CS gene expression at 1 and 48 h after the last session of endurance training. Moreover, our data support the existence of an acute effect of exercise on the training-induced elevation in CS activity in rat soleus but not ventricle muscles. physical activity; oxidative enzyme; gene transcriptional expression; soleus muscle; heart muscle CITRATE SYNTHASE (CS) is one of the key regulatory enzymes in the energy-generating metabolic pathway that catalyzes the condensation of oxaloacetate and acetyl coenzyme A to form citrate in the tricarboxylic acid cycle. It has been extensively used as a metabolic marker in assessing oxidative and respiratory capacity (22). More than 30 years ago, Holloszy and his colleagues (8) reported that endurance exercise training increases the oxidative enzyme activities in skeletal muscle. After that, numerous studies were conducted to examine the effect of exercise training on muscle oxidative capacity and metabolic characteristics (7,15,20,22,29). It is generally recognized that the skeletal muscle oxidative capacity and the activities of mitochondrial enzymes are elevated by endurance exercise training.

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Effects of Exercise, Training, and Diet on Muscle Citric Acid Cycle Enzyme Activity

Cited by 51 publications

References 0 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

Specific training improves skeletal muscle mitochondrial calcium homeostasis after eccentric exercise

Citrate synthase expression and enzyme activity after endurance training in cardiac and skeletal muscles

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