Effect of exhausting exercise on rat heart mitochondria

Terjung, RL; Klinkerfuss, GH; Baldwin, K. M.; Winder, W. W.; Holloszy, J. O.

doi:10.1152/ajplegacy.1973.225.2.300

Cited by 34 publications

(13 citation statements)

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“…Previous studies of acute effects of exhaustive endurance exercise in various animal models have demonstrated varying degrees of changes and damage to the cardiac mitochondrial ultrastructure; ranging from no detected alterations [35, 45], mitochondrial hypertrophy with preserved structural integrity [46], to swelling and more extensive disruption [47–50]. The discrepancies in findings have been suggested to be a result of a combination of different animal models, various exercise modes and diverse exercise intensities and durations.…”

Section: Discussionmentioning

confidence: 99%

Acute exhaustive aerobic exercise training impair cardiomyocyte function and calcium handling in Sprague-Dawley rats

Ljones¹,

Ness²,

Solvang-Garten³

et al. 2017

PLoS ONE

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IntroductionRecent data from long-distance endurance participants suggest that cardiac function is impaired after completion. Existing data further indicate that right ventricular function is more affected than left ventricular function. The cellular mechanisms underpinning cardiac deterioration are limited and therefore the aim of this study was to examine cardiomyocyte and molecular responses of the right and left ventricle to an acute bout of exhaustive endurance exercise.Materials and methodsMale Sprague-Dawley rats were assigned to sedentary controls or acute exhaustive endurance exercise consisting of a 120 minutes long forced treadmill run. The contractile function and Ca2+ handling properties in isolated cardiomyocytes, protein expression levels of sarcoplasmic reticulum Ca2+-ATPase and phospholamban including two of its phosphorylated states (serine 16 and threonine 17), and the mitochondrial respiration in permeabilized cardiac muscle fibers were analyzed.ResultsThe exercise group showed a significant reduction in cardiomyocyte fractional shortening (right ventricle 1 Hz and 3 Hz p<0.001; left ventricle 1 Hz p<0.05), intracellular Ca2+ amplitude (right ventricle 1 and 3 Hz p<0.001; left ventricle 1 Hz p<0.01 and 3 Hz p<0.05) and rate of diastolic Ca2+ decay (right ventricle 1 Hz p<0.001 and 3 Hz p<0.01; left ventricle 1 and 3 Hz p<0.01). Cardiomyocyte relaxation during diastole was only significantly prolonged at 3 Hz in the right ventricle (p<0.05) compared to sedentary controls. We found an increase in phosphorylation of phospholamban at serine 16 and threonine 17 in the left (p<0.05), but not the right, ventricle from exhaustively exercised animals. The protein expression levels of sarcoplasmic reticulum Ca2+-ATPase and phospholamban was not changed. Furthermore, we found a reduction in maximal oxidative phosphorylation and electron transport system capacities of mitochondrial respiration in the right (p<0.01 and p<0.05, respectively), but not the left ventricle from rats subjected to acute exhaustive treadmill exercise.ConclusionAcute exhaustive treadmill exercise is associated with impairment of cardiomyocyte Ca2+ handling and mitochondrial respiration that causes depression in both contraction and diastolic relaxation of cardiomyocytes.

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Section: Discussionmentioning

confidence: 99%

Acute exhaustive aerobic exercise training impair cardiomyocyte function and calcium handling in Sprague-Dawley rats

Ljones¹,

Ness²,

Solvang-Garten³

et al. 2017

PLoS ONE

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“…The subject has been controversial because only limited data are available and the various studies use different animal models and exercise regimens (cf. Terjung et al 1973). Meanwhile, considerable literature has accumulated indicating a detrimental role of strenuous exercise on mitochondrial function in skeletal muscle and liver (Davies et al 1982, Ji 1994 Recently, we proposed that ROS might also be involved in the pathology of heart mitochondrial dysfunction as a result of physical exercise .…”

Section: Discussionmentioning

confidence: 99%

Rigorous swim training impairs mitochondrial function in post‐ischaemic rat heart

Leichtweis

Leeuwenburgh

Parmelee

et al. 1997

Acta Physiologica Scandinavica

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The effect of rigorous swim training (6 h day-1, 5 days week-1 for an average of 191 h) on mitochondrial respiratory function was investigated in rat heart subjected to in vivo ischaemia reperfusion (I-R). Mitochondria was isolated from the risk region of the left ventricle subjected to 60 min occlusion of the main left coronary artery followed by 30 min reperfusion. Heart weight and heart-to-body weight ratio was increased by 21 and 28% (P < 0.01), respectively, in the trained (T, n = 15) vs. control rats (C, n = 20). I-R per se showed minimal effect on heart mitochondria regardless of training status. In sham, state 4 respiration rate was 26 and 32% (P < 0.05) lower in T vs. C rats, using malate-pyruvate (M-P) and 2-oxoglutarate (OG) as substrates, respectively. Training also reduced state 3 respiration by 28% (M-P) and 50% (OG) (P < 0.01). The respiratory control index (RCI) was unaltered in T with M-P, but decreased with OG (P < 0.01). In vitro exposure to superoxide radicals severely reduced state 4 and 3 respiration and RCI, but T hearts showed greater reductions of state 4 and 3 rates than C. Mitochondria from T hearts also revealed a greater state 4 inhibition by H2O2 and HO. compared with C. A lower glutathione content and a higher gamma-glutamyl transpeptidase activity (P < 0.05) was observed in T vs. C. It is concluded that rigorous swim training impairs heart mitochondrial function, making them more susceptible to in vivo and in vitro oxidative stress, and that this damaging effect may be related to a diminished glutathione reserve.

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“…Studies on myocardial mitochondria of endurance-trained animals are controver sial. Several studies have failed to show significant effects of endurance training [Bozner and Meessen, 1969;Gollnick et al, 1971;Guski et al, 1980;Kainulainen et al, 1979;Paniagua et al, 1977;Terzung et al, 1973]. In other cases changes in mitochon dria resulting from endurance training are very localized and have been attributed to focal areas of hypoxia [Arcos et al, 1967], It is possible that some ultrastructural degener ative changes in myocardial mitochondria are evident only in the early stages of train ing [Banister et al, 1971], which may be fol lowed by recovery and conditioning to stress with the result that significant changes in mitochondria of endurance-trained animals may be less easily detected [Arcos et al, 1967], Giant mitochondria have been reported in human myocardium [Harmjanz et al, 1971;Kraus and Cain, 1980] and in dogs subjected to brief periods of hypoxia [Ghadially, 1975] or experimental aortic stenosis [Wollenberger and Schulze, 1961], It is still not clear if giant mitochondria are formed by a simple enlargement of preexisting mito chondria, or by a process of fusion of several mitochondria, or by a combination of both processes [Ghadially, 1975], Our present studies indicate that a fusion of adjacent mitochondria occurs in the formation of the giant mitochondria.…”

Section: Discussionmentioning

confidence: 99%

Giant Mitochondria in the Myocardium of Aging and Endurance-Trained Mice

et al. 1987

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During the course of an ultrastructural study on the apex region of the left ventricular myocardium of experimental female C57BL/6J mice, aged between 6 and 27 months, and that had been subjected to long-term daily enforced endurance running schedules, we encountered some instances of unusual giant mitochondria. These mitochondria showed degenerative changes including the disruption, disorganization and loss of cristae and the development of a very electron-lucent matrix. In many instances, these giant mitochondria showed dense inclusions within the matrix. The giant mitochondria appear to have developed as a result of fusion between adjacent hypertrophic mitochondria followed by a sequence of progressive degenerative changes. These giant mitochondria were most common in the myocardium of mice that had followed endurance training schedules for 10 or 15 months and were not encountered in age-matched nonrunning control mice.

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Effect of exhausting exercise on rat heart mitochondria

Cited by 34 publications

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Acute exhaustive aerobic exercise training impair cardiomyocyte function and calcium handling in Sprague-Dawley rats

Acute exhaustive aerobic exercise training impair cardiomyocyte function and calcium handling in Sprague-Dawley rats

Rigorous swim training impairs mitochondrial function in post‐ischaemic rat heart

Giant Mitochondria in the Myocardium of Aging and Endurance-Trained Mice

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