Skeletal Muscle Adaptations to Ischemia and Severe Exercise

Hoppeler, Hans; Hudlická, O; Uhlmann, E.; Claassen, Horst

doi:10.1097/00042752-199201000-00008

Cited by 8 publications

(6 citation statements)

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“…The type I predominance found in our study, as well as the muscle fibre areas of tibialis anterior muscle are in accordance with the findings of other authors of age-matched human subjects [24,34,35]. However, as a result of conflicting reports regarding muscle oxidative capacity in patients with peripheral occlusive arterial disease [1-3,8,10,11,13,14,21,23,34] the relationship between local pathology and clinical symptomatology remains elusive. Jennische [36] found a selective vulnerability of the fast glycolytic fibres to experimental ischemia in rats.…”

Section: Discussionsupporting

confidence: 92%

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Morphological, histochemical, and interstitial pressure changes in the tibialis anterior muscle before and after aortofemoral bypass in patients with peripheral arterial occlusive disease

Albani

Megalopoulos

Kiskinis

et al. 2002

BMC Musculoskelet Disord

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Background: Morphological and electrophysiological studies of ischemic muscles in peripheral arterial disease disclosed evidence of denervation and fibre atrophy. The purpose of the present study is to describe morphological changes in ischemic muscles before and after reperfusion surgery in patients with peripheral occlusive arterial disease, and to provide an insight into the effect of reperfusion on the histochemistry of the reperfused muscle.

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Section: Discussionsupporting

confidence: 92%

“…Structural and functional adaptations take place in working and resting muscles when the blood flow is insufficient to satisfy energy requirements [1-3]. Partial ischemia for short periods of time may cause cell damage in humans [4,5], while metabolic changes in leg muscles have been reported after 16 hours of ischemia [6].…”

Section: Introductionmentioning

confidence: 99%

Morphological, histochemical, and interstitial pressure changes in the tibialis anterior muscle before and after aortofemoral bypass in patients with peripheral arterial occlusive disease

Albani

Megalopoulos

Kiskinis

et al. 2002

BMC Musculoskelet Disord

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“…The animals could walk and their resting blood flow was not affected but it did not increase during contractions (43). The volume density of mitochondria, which is higher in muscles exposed to hypoxia (37), was significantly higher (38), but capillary growth did not occur ( Fig. 4) (40).…”

Section: Capillary Growth In Skeletal Muscle-link With Activitymentioning

confidence: 93%

Is Physiological Angiogenesis in Skeletal Muscle Regulated by Changes in Microcirculation?

HUDLICKA¹

1998

Microcirculation

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Physiological angiogenesis occurs in female reproductive organs, in growing antlers as a result of long-term exposure to cold and possibly hypoxia, and due to increased activity (training) in skeletal and cardiac muscle. The common denominator is increased blood flow, which may result in increased velocity of flow and/or diameters in arterioles and capillaries, increased capillary pressure and increased capillary hematocrit. Increased velocity would lead to increased shear stress, while increased pressure and/or diameters would increase wall tension. Either of these factors may cause a disturbance of the endothelium on the luminal side of vessels. In addition, increased contractile activity during training could cause changes on the abluminal side (for example, modification of the capillary basement membrane or the extracellular matrix induced by stretch/ relaxation). In order to elucidate the role of these individual factors in angiogenesis, microcirculation was studied in skeletal muscles which were exposed to: (a) increased activity by chronic electrical stimulation; (b) long-term increase in blood flow by various vasodilators; (c) long-term administration of CoCl 2 to increase hematocrit; and (d) long-term stretch, achieved by removal of agonist muscles. Capillary growth, demonstrated as an increased capillary/fiber ratio, as determined by histochemical staining and by electron microscopy, occurred in (a), (b), and (d), but not (c). Capillary proliferation, estimated by labeling index for bromodeoxyuridine of capillary-linked nuclei, occurred in (a), but not in (b).Chronic electrical stimulation resulted in an increase in the diameter of capillaries, a transient widening of arterioles, and no change in venules. Capillary hematocrit and the velocity of red blood cells (V rbc ) were also increased. Calculated shear stress and capillary wall tension were higher in stimulated muscles than in control muscles. Long-term increase in blood flow, induced by administration of the ␣ 1 -blocker prazosin, caused increased V rbc with no change in diameters and increased only capillary shear stress. Stretched muscles had decreased blood flow, but longer sarcomeres initially caused concomitant stretch of capillaries. Increased shear stress/wall tension/stretch may initiate angiogenesis by damaging the luminal side of endothelial cells and/or their basement membrane, or by releasing growth factors or other humoral agents (prostaglandins and/or nitric oxide). Immunohistochemistry in stimulated or stretched muscles showed no evidence for expresson of mRNA for basic fibroblast growth factor (bFGF), or the growth factor itself, but a low molecular mass endothelial cellstimulating angiogenic factor (ESAF) (77) was increased in (a), (b), and (d). The involvement of prostaglandins and nitric oxide was demonstrated by the finding of attenuated incorporation of BrdU into capillary-linked nuclei in stimulated muscles after administration of indomethacin or L-NNA. Thus, changes in the microcirculation leading to increased shear stress a...

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“…The activity of both enzymes can be increased by acute exercise: nNOS due to muscle fiber contractions and eNOS due to changes in blood flow and shear stress (17). It is also possible that chronic stimulation could increase eNOS in muscle fibers, because the expression of eNOS was found to be correlated with mitochondrial content in normal rat muscles (42), and stimulation is known to increase the proportions of mitochondria (29) and highly oxidative fibers (36).…”

Section: Table 1 Cf In Edl From Control and 7-day-stimulated L-nna-omentioning

confidence: 99%

Nitric oxide, VEGF, and VEGFR-2: interactions in activity-induced angiogenesis in rat skeletal muscle

Milkiewicz¹,

Hudlická²,

Brown³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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Vascular endothelial growth factor (VEGF) is considered to be important in promotion of capillary growth in skeletal muscles exposed to increased activity. We studied its interactions with nitric oxide (NO) by examining the expression of endothelial NO synthase (NOS), VEGF, and VEGF receptor-2 (VEGFR-2) proteins in relation to capillary growth in rat extensor digitorum longus muscles electrically stimulated for 2, 4, or 7 days with and without NOS inhibition by N(omega)-nitro-L-arginine (L-NNA, 3 mg/day). Stimulation increased all proteins from 2 days onward, concomitantly with capillary proliferation (labeling for proliferating cell nuclear antigen). Capillary-to-fiber ratio was elevated by 25% after 7 days. Concurrent oral administration of L-NNA did not affect the increase in endothelial NOS but depressed its activity, as shown by increased blood pressure and decreased arteriolar diameters in 2-day-stimulated muscles. NOS inhibition eliminated the increased expression of VEGFR-2 and VEGF proteins in muscles stimulated for 2 and 4 days but not for 7 days. However, it depressed capillary proliferation and the increase in C/F at all time points. We conclude that, in stimulated muscles, NO, generated by activation of neuronal NOS by muscle activity or endothelial NOS by increased blood flow and capillary shear stress, may increase capillary proliferation in the early stages of stimulation through upregulation of VEGFR-2 and VEGF. With longer stimulation, capillary growth appears to require NO, and high levels of VEGF and VEGFR-2 may be contributing to maintenance of the increased capillary bed.

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Skeletal Muscle Adaptations to Ischemia and Severe Exercise

Cited by 8 publications

References 0 publications

Morphological, histochemical, and interstitial pressure changes in the tibialis anterior muscle before and after aortofemoral bypass in patients with peripheral arterial occlusive disease

Morphological, histochemical, and interstitial pressure changes in the tibialis anterior muscle before and after aortofemoral bypass in patients with peripheral arterial occlusive disease

Is Physiological Angiogenesis in Skeletal Muscle Regulated by Changes in Microcirculation?

Nitric oxide, VEGF, and VEGFR-2: interactions in activity-induced angiogenesis in rat skeletal muscle

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