| 1. |
- Wyckelsma, VL, et al.
(author)
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Vitamin C and E Treatment Blocks Changes in Kynurenine Metabolism Triggered by Three Weeks of Sprint Interval Training in Recreationally Active Elderly Humans
- 2021
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In: Antioxidants (Basel, Switzerland). - : MDPI AG. - 2076-3921. ; 10:9
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Journal article (peer-reviewed)abstract
- The kynurenine pathway (KP) is gaining attention in several clinical fields. Recent studies show that physical exercise offers a therapeutic way to improve ratios of neurotoxic to neuroprotective KP metabolites. Antioxidant supplementation can blunt beneficial responses to physical exercise. We here studied the effects of endurance training in the form of sprint interval training (SIT; three sessions of 4–6 × 30 s cycling sprints per week for three weeks) in elderly (~65 years) men exposed to either placebo (n = 9) or the antioxidants vitamin C (1 g/day) and E (235 mg/day) (n = 11). Blood samples and muscle biopsies were taken under resting conditions in association with the first (untrained state) and last (trained state) SIT sessions. In the placebo group, the blood plasma level of the neurotoxic quinolinic acid was lower (~30%) and the neuroprotective kynurenic acid to quinolinic acid ratio was higher (~50%) in the trained than in the untrained state. Moreover, muscle biopsies showed a training-induced increase in kynurenine aminotransferase (KAT) III in the placebo group. All these training effects were absent in the vitamin-treated group. In conclusion, KP metabolism was shifted towards neuroprotection after three weeks of SIT in elderly men and this shift was blocked by antioxidant treatment.
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| 5. |
- Glenmark, B, et al.
(author)
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Difference in skeletal muscle function in males vs. females: role of estrogen receptor-beta
- 2004
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In: American journal of physiology. Endocrinology and metabolism. - : American Physiological Society. - 0193-1849 .- 1522-1555. ; 287:6, s. E1125-E1131
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Journal article (peer-reviewed)abstract
- Male skeletal muscles are generally faster and have higher maximum power output than female muscles. Conversely, during repeated contractions, female muscles are generally more fatigue resistant and recover faster. We studied the role of estrogen receptor-β (ERβ) in this gender difference by comparing contractile function of soleus (mainly slow-twitch) and extensor digitorum longus (fast-twitch) muscles isolated from ERβ-deficient (ERβ−/−) and wild-type mice of both sexes. Results showed generally shorter contraction and relaxation times in male compared with female muscles, and ERβ deficiency had no effect on this. Fatigue (induced by repeated tetanic contractions) and recovery of female muscles were not affected by ERβ deficiency. However, male ERβ−/− muscles were slightly more fatigue resistant and produced higher forces during the recovery period than wild-type male muscles. In fact, female muscles and male ERβ−/− muscles displayed markedly better recovery than male wild-type muscles. Gene screening of male soleus muscles showed 25 genes that were differently expressed in ERβ−/− and wild-type mice. Five of these genes were selected for further analysis: muscle ankyrin repeat protein-2, muscle LIM protein, calsequestrin, parvalbumin, and aquaporin-1. Expression of these genes showed a similar general pattern: increased expression in male and decreased expression in female ERβ−/− muscles. In conclusion, ERβ deficiency results in increased performance during fatigue and recovery of male muscles, whereas female muscles are not affected. Improved contractile performance of male ERβ−/− mouse muscles was associated with increased expression of mRNAs encoding important muscle proteins.
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| 7. |
- Holmberg, K, et al.
(author)
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Generation and phenotypic characterization of a galanin overexpressing mouse
- 2005
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In: Neuroscience. - : Elsevier BV. - 0306-4522 .- 1873-7544. ; 133:1, s. 59-77
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Journal article (peer-reviewed)abstract
- In most parts of the peripheral nervous system galanin is expressed at very low levels. To further understand the functional role of galanin, a mouse overexpressing galanin under the platelet-derived growth factor-B was generated, and high levels of galanin expression were observed in several peripheral tissues and spinal cord. Thus, a large proportion of neurons in autonomic and sensory ganglia were galanin-positive, as were most spinal motor neurons. Strong galanin-like immunoreactivity was also seen in nerve terminals in the corresponding target tissues, including skin, blood vessels, sweat and salivary glands, motor end-plates and the gray matter of the spinal cord. In transgenic superior cervical ganglia around half of all neuron profiles expressed galanin mRNA but axotomy did not cause a further increase, even if mRNA levels were increased in individual neurons. In transgenic dorsal root ganglia galanin mRNA was detected in around two thirds of all neuron profiles, including large ones, and after axotomy the percentage of galanin neuron profiles was similar in overexpressing and wild type mice. Axotomy reduced the total number of DRG neurons less in overexpressing than in wild type mice, indicating a modest rescue effect. Aging by itself increased galanin expression in the superior cervical ganglion in wild type and transgenic mice, and in the latter also in preganglionic cholinergic neurons projecting to the superior cervical ganglion. Galanin overexpressing mice showed an attenuated plasma extravasation, an increased pain response in the formalin test, and changes in muscle physiology, but did not differ from wild type mice in sudomotor function. These findings suggest that overexpressed galanin in some tissues of these mice can be released and via a receptor-mediated action influence pathophysiological processes. © 2005 Published by Elsevier Ltd on behalf of IBRO.
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| 12. |
- Westerblad, H., et al.
(author)
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Effects of ryanodine receptor agonist 4-chloro-m-cresol on myoplasmic free Ca2+ concentration and force of contraction in mouse skeletal muscle
- 1998
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In: Cell Calcium. - 0143-4160 .- 1532-1991. ; 24:2, s. 105-115
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Journal article (peer-reviewed)abstract
- In single mouse skeletal muscle fibers injected with fluorescent Ca2+ indicator Indo-1, 4-chloro-m-cresol (chlorocresol, 4-CmC) and its lipophilic analogue 4-chloro-3-ethylphenol (4-CEP) increased resting myoplasmic free [Ca2+] ([Ca2+]i) in a dose-dependent manner. In this regard, 4-CEP was more potent than 4-CmC and both were more potent than caffeine. High concentrations of 4-CmC (1 mM) or 4-CEP (500 microM) caused large and irreversible increase in resting [Ca2+]i leading to contracture. 4-CmC potentiated the [Ca2+]i increase and force of contraction induced by tetanic stimulation. Unlike caffeine, 4-CmC did not affect the activity of sarcoplasmic reticulum Ca2+ pump or the myofibrillar Ca2+ sensitivity. A low concentration of 4-CEP (20 microM) had no effect on resting [Ca2+]i on its own, but it enhanced the resting [Ca2+]i increase induced by caffeine and also potentiated the [Ca2+]i increase and contraction induced by tetanic stimulation. However, a relatively high concentration of 4-CEP (200 microM) inhibited tetanic stimulation-induced [Ca2+]i increase and contraction. Dantrolene, a muscle relaxant, inhibited 4-CmC-induced [Ca2+]i increase under resting conditions. However, when 4-CEP was applied in the presence of dantrolene, there was an exaggerated increase in [Ca2+]i. We conclude that 4-CmC and 4-CEP are potent agonists that can increase [Ca2+]i rapidly and reversibly by activating ryanodine receptors in situ in intact skeletal muscle fibers. These compounds, specially 4-CmC, may be useful for mechanistic and functional studies of ryanodine receptors and excitation-contraction coupling in skeletal muscles.
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| 13. |
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| 14. |
- Wyckelsma, VL, et al.
(author)
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Response to Mörseburg et al
- 2022
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In: American journal of human genetics. - : Elsevier BV. - 1537-6605 .- 0002-9297. ; 109:5, s. 973-973
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Journal article (other academic/artistic)
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| 15. |
- Wyckelsma, VL, et al.
(author)
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Vitamin C and E Treatment Blunts Sprint Interval Training-Induced Changes in Inflammatory Mediator-, Calcium-, and Mitochondria-Related Signaling in Recreationally Active Elderly Humans
- 2020
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In: Antioxidants (Basel, Switzerland). - : MDPI AG. - 2076-3921. ; 9:9
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Journal article (peer-reviewed)abstract
- Sprint interval training (SIT) has emerged as a time-efficient training regimen for young individuals. Here, we studied whether SIT is effective also in elderly individuals and whether the training response was affected by treatment with the antioxidants vitamin C and E. Recreationally active elderly (mean age 65) men received either vitamin C (1 g/day) and vitamin E (235 mg/day) or placebo. Training consisted of nine SIT sessions (three sessions/week for three weeks of 4-6 repetitions of 30-s all-out cycling sprints) interposed by 4 min rest. Vastus lateralis muscle biopsies were taken before, 1 h after, and 24 h after the first and last SIT sessions. At the end of the three weeks of training, SIT-induced changes in relative mRNA expression of reactive oxygen/nitrogen species (ROS)- and mitochondria-related proteins, inflammatory mediators, and the sarcoplasmic reticulum Ca2+ channel, the ryanodine receptor 1 (RyR1), were blunted in the vitamin treated group. Western blots frequently showed a major (>50%) decrease in the full-length expression of RyR1 24 h after SIT sessions; in the trained state, vitamin treatment seemed to provide protection against this severe RyR1 modification. Power at exhaustion during an incremental cycling test was increased by ~5% at the end of the training period, whereas maximal oxygen uptake remained unchanged; vitamin treatment did not affect these measures. In conclusion, treatment with the antioxidants vitamin C and E blunts SIT-induced cellular signaling in skeletal muscle of elderly individuals, while the present training regimen was too short or too intense for the changes in signaling to be translated into a clear-cut change in physical performance.
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| 20. |
- Abbate, F, et al.
(author)
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Prolonged force increase following a high-frequency burst is not due to a sustained elevation of [Ca2+]i
- 2002
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In: American journal of physiology. Cell physiology. - : American Physiological Society. - 0363-6143 .- 1522-1563. ; 283:1, s. C42-C47
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Journal article (peer-reviewed)abstract
- A brief high-frequency burst of action potentials results in a sustained force increase in skeletal muscle. The present study investigates whether this force potentiation is the result of a sustained increase of the free myoplasmic [Ca2+] ([Ca2+]i). Single fibers from mouse flexor brevis muscles were stimulated with three impulses at 150 Hz (triplet) at the start of a 350-ms tetanus or in the middle of a 700-ms tetanus; the stimulation frequency of the rest of the tetanus ranged from 20 to 60 Hz. After the triplet, force was significantly ( P < 0.05) increased between 17 and 20% when the triplet was given at the start of the tetanus and between 5 and 18% when the triplet was given in the middle ( n = 7). However, during this potentiation, [Ca2+]iwas not consistently increased. Hence, the increased force following a high-frequency burst is likely due to changes in the myofibrillar properties.
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| 21. |
- Allen, DG, et al.
(author)
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Impaired calcium release during fatigue
- 2008
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In: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 104:1, s. 296-305
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Journal article (peer-reviewed)abstract
- Impaired calcium release from the sarcoplasmic reticulum (SR) has been identified as a contributor to fatigue in isolated skeletal muscle fibers. The functional importance of this phenomenon can be quantified by the use of agents, such as caffeine, which can increase SR Ca2+release during fatigue. A number of possible mechanisms for impaired calcium release have been proposed. These include reduction in the amplitude of the action potential, potentially caused by extracellular K+accumulation, which may reduce voltage sensor activation but is counteracted by a number of mechanisms in intact animals. Reduced effectiveness of SR Ca2+channel opening is caused by the fall in intracellular ATP and the rise in Mg2+concentrations that occur during fatigue. Reduced Ca2+available for release within the SR can occur if inorganic phosphate enters the SR and precipitates with Ca2+. Further progress requires the development of methods that can identify impaired SR Ca2+release in intact, blood-perfused muscles and that can distinguish between the various mechanisms proposed.
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| 22. |
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| 23. |
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| 24. |
- Allen, DG, et al.
(author)
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Muscle fatigue: the role of intracellular calcium stores
- 2002
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In: Canadian journal of applied physiology = Revue canadienne de physiologie appliquee. - : Canadian Science Publishing. - 1066-7814. ; 27:1, s. 83-96
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Journal article (peer-reviewed)abstract
- Force declines when muscles are used repeatedly and intensively and a variety of intracellular mechanisms appear to contribute to this muscle fatigue. Intracellular calcium release declines during fatigue and has been shown to contribute to the reduction in force. Three new approaches have helped to define the role of calcium stores to this decline in calcium release. Skinned fibre experiments show that when intracellular phosphate is increased the amount of Ca2+ released from the sarcoplasmic reticulum (SR) declines. Intact fibre experiments show that the size of the calcium store declines during fatigue and recovers on rest. Intact muscles which lack the enzyme creatine kinase, do not exhibit the usual rise of phosphate during fatigue and, under these conditions, the decline of Ca2+ release is absent or delayed. These results can be explained by the "calcium phosphate precipitation" hypothesis. This proposes that if phosphate in the myoplasm rises, it enters the SR and binds to Ca2+ as Ca2+ phosphate. The resultant reduction in free Ca2+ within the SR contributes to the reduced Ca2+ release during fatigue. Key words: sarcoplasmic reticulum, myoplasmic phosphate, calcium phosphate precipitation, creatine kinase, glycogen
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| 26. |
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| 27. |
- Allen, DG, et al.
(author)
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Skeletal muscle fatigue: cellular mechanisms
- 2008
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In: Physiological reviews. - : American Physiological Society. - 0031-9333 .- 1522-1210. ; 88:1, s. 287-332
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Journal article (peer-reviewed)abstract
- Repeated, intense use of muscles leads to a decline in performance known as muscle fatigue. Many muscle properties change during fatigue including the action potential, extracellular and intracellular ions, and many intracellular metabolites. A range of mechanisms have been identified that contribute to the decline of performance. The traditional explanation, accumulation of intracellular lactate and hydrogen ions causing impaired function of the contractile proteins, is probably of limited importance in mammals. Alternative explanations that will be considered are the effects of ionic changes on the action potential, failure of SR Ca2+release by various mechanisms, and the effects of reactive oxygen species. Many different activities lead to fatigue, and an important challenge is to identify the various mechanisms that contribute under different circumstances. Most of the mechanistic studies of fatigue are on isolated animal tissues, and another major challenge is to use the knowledge generated in these studies to identify the mechanisms of fatigue in intact animals and particularly in human diseases.
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| 46. |
- Bruton, JD, et al.
(author)
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Effects of CO2-induced acidification on the fatigue resistance of single mouse muscle fibers at 28 degrees C
- 1998
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In: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 85:2, s. 478-483
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Journal article (peer-reviewed)abstract
- The role of reduced muscle pH in the development of skeletal muscle fatigue is unclear. This study investigated the effects of lowering skeletal muscle intracellular pH by exposure to 30% CO2on the number of isometric tetani needed to induce significant fatigue. Isolated single mouse muscle fibers were stimulated repetitively at intervals of 4–2.5 s by using 80-Hz, 400-ms tetani at 28°C in Tyrode solution bubbled with either 5 or 30% CO2. Stimulation continued until tetanic force had fallen to 40% of the initial value. Exposure to 30% CO2caused a significant fall in intracellular pH of ∼0.3 pH unit but did not cause any significant changes in initial peak tetanic force. During the course of repetitive stimulation, intracellular pH fell by ∼0.3 pH unit in both normal and acidified fibers. The number of tetani needed to reduce force to 40% of the initial value was not significantly different in 5 and 30% CO2Tyrode. The sole effect of acidosis was to reduce the rate of relaxation of force, especially in fatigued fibers. It is concluded that, at 28°C, acidosis per se does not accelerate the development of fatigue during repeated tetanic stimulation of isolated mouse skeletal muscle fibers.
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