Exercise-Induced Ultrastructural Changes in Skeletal Muscle*

Hoppeler, H.

doi:10.1055/s-2008-1025758

Cited by 288 publications

(217 citation statements)

References 135 publications

(194 reference statements)

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“…Chronic contractile activity leads to an improvement in muscular endurance performance (13,16). Increases in muscular activity, induced by either electrical stimulation or treadmill running, have been shown to increase the expression of oxidative enzymes and to result in an elevation in mitochondrial content (14,16).…”

Section: Discussionmentioning

confidence: 99%

“…In particular, chronic contractile activity is known to alter the expression of a variety of proteins from the nuclear and mitochondrial genomes (15). These changes in protein expression result in an increase in mitochondrial volume and density (6,16). In skeletal muscle, two distinct subfractions of mitochondria exist that are characterized by their anatomic localization.…”

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confidence: 99%

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Effect of prior chronic contractile activity on mitochondrial function and apoptotic protein expression in denervated muscle

O'Leary

Hood²

2008

Journal of Applied Physiology

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O'Leary MF, Hood DA. Effect of prior chronic contractile activity on mitochondrial function and apoptotic protein expression in denervated muscle. J Appl Physiol 105: 114 -120, 2008. First published May 1, 2008 doi:10.1152/japplphysiol.00724.2007.-Skeletal muscle is highly adaptable in response to increases and decreases in contractile activity. The purpose of this study was to determine whether the preconditioning of skeletal muscle has a protective effect against subsequent denervation-induced apoptotic protein expression. To investigate this, we chronically stimulated the tibialis anterior and extensor digitorum longus muscles for 7 days (10 Hz, 3 h/day) before 7 days of denervation. Denervation reduced total cytochrome-c oxidase activity by 39%, which was likely a consequence of a decrease in subsarcolemmal (SS) mitochondria. This decrease in the SS subfraction was prevented by prior chronic stimulation and, as a result, maintained total mitochondrial content at control levels. The expression of Bax was elevated 2.2-fold by denervation, and prior chronic stimulation did not attenuate this increase. This produced a increase in the Bax-to-Bcl-2 ratio, indicating greater muscle apoptotic susceptibility. Denervation also decreased state 3 respiration in SS and intermyofibrillar mitochondria and elevated state 4 reactive oxygen species production within both mitochondrial subfractions. These changes were not prevented by prior chronic stimulation. Furthermore, the antioxidant protein MnSOD was also reduced by denervation, whereas Beclin-1 was markedly elevated. This suggests that autophagic cell death could also play a significant part in denervationinduced muscle atrophy. Thus, despite prior chronic stimulation, denervation increases the apoptotic susceptibility of skeletal muscle by altering the Bax-to-Bcl-2 ratio, by increasing reactive oxygen species production, and by reducing the expression of MnSOD. Whether a more extensive stimulation paradigm would be more effective in attenuating apoptosis before muscle disuse remains to be determined. mitochondrial biogenesis; muscle atrophy; reactive oxygen species; autophagy; protein degradation SKELETAL MUSCLE IS AN ADAPTABLE tissue that exhibits a remarkable range of plasticity in response to different levels of contractile activity (15). In particular, chronic contractile activity is known to alter the expression of a variety of proteins from the nuclear and mitochondrial genomes (15). These changes in protein expression result in an increase in mitochondrial volume and density (6, 16). In skeletal muscle, two distinct subfractions of mitochondria exist that are characterized by their anatomic localization. Subsarcolemmal (SS) mitochondria are located just beneath the sarcolemmal membrane, whereas intermyofibrillar (IMF) mitochondria are intertwined between skeletal muscle myofibrils (8). SS and IMF mitochondrial subfractions are significantly increased in response to chronic contractile activity. However, SS mitochondria are more sensitive to endurance training a...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Effect of prior chronic contractile activity on mitochondrial function and apoptotic protein expression in denervated muscle

O'Leary

Hood²

2008

Journal of Applied Physiology

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“…However, in our study, we used pyruvate/malate as substrate rather than glutamate/malate because pyruvate is a physiological substrate which allows to investigate the whole mitochondrial activity (Krebs cycle and all complexes of the respiratory chain). The second was the measurement of CS activity which is a well-recognized marker of mitochondrial density in skeletal muscle [27]. Both techniques evidence an improvement of muscle oxidative capacity, proportional to the increase in the ability to oxidize lipids.…”

Section: Discussionmentioning

confidence: 99%

Training-induced improvement in lipid oxidation in type 2 diabetes mellitus is related to alterations in muscle mitochondrial activity. Effect of endurance training in type 2 diabetes

Bordenave

Metz

Flavier

et al. 2008

Diabetes & Metabolism

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Training-induced improvement in lipid oxidation in type 2 diabetes mellitus is related to alterations in muscle mitochondrial activity. Effect of endurance training in type 2 diabetes.. Diabetes and Metabolism, Elsevier Masson, 2008, 34 (2) AbstractAim: We investigated in type 2 diabetic patients (T2D) if an individualized training effect on whole body lipid oxidation is associated with changes in muscle oxidative capacities.Methods: Eleven T2D participated in this study. Whole body lipid oxidation during exercise was assessed by graded exercise indirect calorimetry. Blood samples for measuring blood glucose and free fatty acids during exercise and muscle oxidative capacities measured from a skeletal muscle biopsy (i.e., mitochondrial respiration and citrate synthase activity) were investigated in T2D before and after a 10-week individualized training targeted at LIPOXmax, which corresponds to the power at which the highest rate of lipids is oxidized (lipid oxidation at LIPOXmax).Results: Training induced both a shift to a higher power intensity of LIPOXmax (+9.1 ± 4.2 Watts, P<0.05) and an improvement of lipid oxidation at LIPOXmax (+51.27 ± 17.93 mg.min -1 , P<0.05). The improvement in lipid oxidation was correlated with training-induced improvement of mitochondrial respiration (r=0.78, P<0.01) and citrate synthase activity (r=0.63, P<0.05).Conclusion: This study shows that a quite moderate training protocol targeted at the LIPOXmax in T2D mellitus improves the ability to oxidize lipids during exercise, and that this improvement is associated with an enhancement of muscle oxidative capacities.

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“…Citrate synthase activity (U•μg -1 •min -1 ) in the gastrocnemius muscle (n = 10/group) was studied as it is used as a marker of aerobic capacity and mitochondrial density in skeletal muscle (Hoppeler, 1986). Citrate synthase activity was measured from the same muscle homogenates that were used to determine the total protein content (Citrate Synthase Assay Kit Sigma-Aldrich) with an automated KoneLab instrument (Thermo Scientific).…”

Section: Citrate Synthase Activitymentioning

confidence: 99%

Effects of intrinsic aerobic capacity, aging and voluntary running on skeletal muscle sirtuins and heat shock proteins

Karvinen

Silvennoinen

Vainio

et al. 2016

Experimental Gerontology

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Exercise-Induced Ultrastructural Changes in Skeletal Muscle*

Cited by 288 publications

References 135 publications

Effect of prior chronic contractile activity on mitochondrial function and apoptotic protein expression in denervated muscle

Effect of prior chronic contractile activity on mitochondrial function and apoptotic protein expression in denervated muscle

Training-induced improvement in lipid oxidation in type 2 diabetes mellitus is related to alterations in muscle mitochondrial activity. Effect of endurance training in type 2 diabetes

Effects of intrinsic aerobic capacity, aging and voluntary running on skeletal muscle sirtuins and heat shock proteins

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