Region-specific adaptations in determinants of rat skeletal muscle oxygenation to chronic hypoxia

Wüst, Rob C I; Jaspers, Richard T.; Heijst, Arno van; Hopman, Maria T. E.; Hoofd, Louis; Laarse, Willem J. van der; Degens, Hans

doi:10.1152/ajpheart.00272.2009

Cited by 31 publications

(45 citation statements)

References 77 publications

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“…Experiments using intrathecal fentanyl in humans during cycling have shown that opioid-mediated muscle afferents inhibit central motor drive (Amann et al, 2009;Gagnon et al, 2012); thus changes in afferent discharge with fatigue or oxygenation are expected to alter the pattern of muscle activation. Although a comparative analysis of the metabolic responses of the different portions of the quadriceps muscle in man has not been performed, rodent studies have shown that the metabolic response to hypoxia are region specific, depending on the predominant muscle fiber type and the degree of capillarization (Wust et al, 2009). …”

Section: Discussionmentioning

confidence: 99%

Muscle Activation During Exercise in Severe Acute Hypoxia: Role of Absolute and Relative Intensity

Torres‐Peralta

Losa‐Reyna²,

González-Izal³

et al. 2014

High Altitude Medicine & Biology

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Torres-Peralta, Rafael, José Losa-Reyna, Miriam González-Izal, Ismael Perez-Suarez, Jaime Calle-Herrero, Mikel Izquierdo, and José A.L. Calbet. Muscle activation during exercise in severe acute hypoxia: Role of absolute and relative intensity. High Alt Med Biol 15:472-482, 2014.-The aim of this study was to determine the influence of severe acute hypoxia on muscle activation during whole body dynamic exercise. Eleven young men performed four incremental cycle ergometer tests to exhaustion breathing normoxic (F I o 2 = 0.21, two tests) or hypoxic gas (F I o 2 = 0.108, two tests). Surface electromyography (EMG) activities of rectus femoris (RF), vastus medialis (VL), vastus lateralis (VL), and biceps femoris (BF) were recorded. The two normoxic and the two hypoxic tests were averaged to reduce EMG variability. Peak Vo 2 was 34% lower in hypoxia than in normoxia ( p < 0.05). The EMG root mean square (RMS) increased with exercise intensity in all muscles ( p < 0.05), with greater effect in hypoxia than in normoxia in the RF and VM ( p < 0.05), and a similar trend in VL ( p = 0.10). At the same relative intensity, the RMS was greater in normoxia than in hypoxia in RF, VL, and BF ( p < 0.05), with a similar trend in VM ( p = 0.08). Median frequency increased with exercise intensity ( p < 0.05), and was higher in hypoxia than in normoxia in VL ( p < 0.05). Muscle contraction burst duration increased with exercise intensity in VM and VL ( p < 0.05), without clear effects of F I o 2 . No significant F I o 2 effects on frequency domain indices were observed when compared at the same relative intensity. In conclusion, muscle activation during whole body exercise increases almost linearly with exercise intensity, following a muscle-specific pattern, which is adjusted depending on the F I o 2 and the relative intensity of exercise. Both VL and VM are increasingly involved in power output generation with the increase of intensity and the reduction in F I o 2 .

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Section: Discussionmentioning

confidence: 99%

Muscle Activation During Exercise in Severe Acute Hypoxia: Role of Absolute and Relative Intensity

Torres‐Peralta

Losa‐Reyna²,

González-Izal³

et al. 2014

High Altitude Medicine & Biology

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“…The SDH activity in individual muscle fibers in histological sections was determined as described previously (55). Sections were incubated at 37°C in the dark for 20 min in a medium consisting of 37 mM sodium phosphate buffer pH 7.6, containing 74 mM sodium succinate and 0.4 mM tetranitroblue tetrazolium (TNBT).…”

Section: Methodsmentioning

confidence: 99%

“…However, an alternative view is that atrophy in large, type II, fibers may be protective against developing an anoxic core (and, hence, cell damage) under conditions where local capillary blood flow (and O 2 delivery) is reduced (24) or in hypoxia (55); whereas hypoxic/anoxic cell damage might be more prevalent following only small reductions in capillary contacts in highly oxidative, type I, fibers. The interaction between fiber size, capillarity and mitochondrial volume density is, therefore, far more complex than whole-muscle averages suggest (11).…”

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confidence: 99%

“…The interaction between fiber size, capillarity and mitochondrial volume density is, therefore, far more complex than whole-muscle averages suggest (11). For example, type I fibers have fewer capillary contacts when surrounded by type IIx/b fibers, compared with those proximal to other type I fibers (55). Human locomotor muscles, such as the vastus lateralis, are not homogeneous (consisting of a superficial glycolytic, and a deep oxidative region (29)).…”

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confidence: 99%

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Regional skeletal muscle remodeling and mitochondrial dysfunction in right ventricular heart failure

Wüst¹,

Myers

Stones³

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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ance is a cardinal symptom of right ventricular heart failure (RV HF) and skeletal muscle adaptations play a role in this limitation. We determined regional remodeling of muscle structure and mitochondrial function in a rat model of RV HF induced by monocrotaline injection (MCT; 60 mg·kg Ϫ1 ; n ϭ 11). Serial sections of the plantaris were stained for fiber type, succinate dehydrogenase (SDH) activity and capillaries. Mitochondrial function was assessed in permeabilized fibers using respirometry, and isolated complex activity by blue native gel electrophoresis (BN PAGE). All measurements were compared with saline-injected control animals (CON; n ϭ 12). Overall fiber cross-sectional area was smaller in MCT than CON: 1,843 Ϯ 114 vs. 2,322 Ϯ 120 m 2 (P ϭ 0.009). Capillary-to-fiber ratio was lower in MCT in the oxidative plantaris region (1.65 Ϯ 0.09 vs. 1.93 Ϯ 0.07; P ϭ 0.03), but not in the glycolytic region. SDH activity (P ϭ 0.048) and maximal respiratory rate (P ϭ 0.012) were each ϳ15% lower in all fibers in MCT. ADP sensitivity was reduced in both skeletal muscle regions in MCT (P ϭ 0.032), but normalized by rotenone. A 20% lower complex I/IV activity in MCT was confirmed by BN PAGE. MCT-treatment was associated with lower mitochondrial volume density (lower SDH activity), quality (lower complex I activity), and fewer capillaries per fiber area in oxidative skeletal muscle. These features are consistent with structural and functional remodeling of the determinants of oxygen supply potential and utilization that may contribute to exercise intolerance and reduced quality of life in patients with RV HF. bioenergetics; exercise; mitochondrial complex I; respirometry; monocrotaline AN INCREASE IN PULMONARY ARTERIAL pressure increases the loading on the right ventricle of the heart. If sustained, pulmonary arterial hypertension (PAH) results in right ventricular hypertrophy and ultimately to right ventricular heart failure (RV HF), the major cause of death in sufferers of PAH (5, 21). Mortality rates of patients with PAH and RV HF are very high: 20 to 40% in the first 3 years after diagnosis (5). PAH and HF are characterized by a reduced tolerance to muscular exercise despite new therapies (2,19,21,33). Interestingly, the reduction in the maximal oxygen uptake (V O 2max ) is a better predictor of mortality than the central hemodynamic deficit or other traditional risk factors (36). Consequently, correction of the central blood flow limitation by heart transplantation does not consistently resolve functional limitations in patients with HF (43), supporting the view that skeletal muscle remodeling plays an important role in exercise intolerance and mortality in many chronic disease states including PAH and RV HF (17,33,54).A common observation in patients with LV (32) and RV (33) HF is muscle atrophy and weakness, that contributes to a loss of power generating capacity. This may be accompanied by a shift in muscle fiber type expression away from fatigueresistant type I fibers, towards type II (33, 42, 44) and changes i...

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“…Skeletal muscle has the capacity to adapt to sustained hypoxia by way of modulation of skeletal muscle vasculature [1,2], muscle enzyme activities [3][4][5][6], muscle fibre size and distribution [7][8][9][10] and contractile performance [11][12][13]. Moreover, sustained hypoxia has been shown to elicit functional plasticity in respiratory muscles [9,10] in a manner that differs from the phenotypic changes occurring in limb muscles [10,14,15].…”

Section: Introductionmentioning

confidence: 99%

Effects of sustained hypoxia on sternohyoid and diaphragm muscle during development

Carberry

McMorrow

Bradford

et al. 2013

European Respiratory Journal

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Sustained hypoxia is a dominant feature of respiratory disease. Despite the clinical significance, the effects of sustained hypoxia on the form and function of respiratory muscle during development are relatively underexplored.Wistar rats were exposed to 1 week of sustained hypoxia (ambient pressure 450 mmHg) or normoxia at various time points during development. Sternohyoid and diaphragm muscle contractile and endurance properties were assessed in vitro. Muscle succinate dehydrogenase and myosin heavy chain composition were determined. The role of reactive oxygen species in hypoxia-induced muscle remodelling was assessed.Sustained hypoxia increased sternohyoid muscle force and fatigue in early but not late development, effects that persisted after return to normoxia. Hypoxia-induced sternohyoid muscle fatigue was not attributable to fibre type transitions or to a decrease in oxidative capacity. Chronic supplementation with the superoxide scavenger tempol did not prevent hypoxia-induced sternohyoid muscle fatigue, suggesting that mechanisms unrelated to oxidative stress underpin hypoxia-induced maladaptation in sternohyoid muscle. Sustained hypoxia had no effect on diaphragm muscle fatigue.We conclude that there are critical windows during development for hypoxia-induced airway dilator muscle maladaptation. Sustained hypoxia-induced impairment of upper airway muscle endurance may persist into later life. Upper airway muscle dysfunction could have deleterious consequences for the control of pharyngeal airway calibre in vivo. @ERSpublications There are critical windows during development for hypoxia-induced airway dilator muscle maladaptation

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Region-specific adaptations in determinants of rat skeletal muscle oxygenation to chronic hypoxia

Cited by 31 publications

References 77 publications

Muscle Activation During Exercise in Severe Acute Hypoxia: Role of Absolute and Relative Intensity

Muscle Activation During Exercise in Severe Acute Hypoxia: Role of Absolute and Relative Intensity

Regional skeletal muscle remodeling and mitochondrial dysfunction in right ventricular heart failure

Effects of sustained hypoxia on sternohyoid and diaphragm muscle during development

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