scholarly journals Skeletal muscle mitochondrial density, gene expression, and enzyme activities in human heart failure: minimal effects of the disease and resistance training

2012 ◽  
Vol 112 (11) ◽  
pp. 1864-1874 ◽  
Author(s):  
Michael J. Toth ◽  
Mark S. Miller ◽  
Kimberly A. Ward ◽  
Philip A. Ades
Keyword(s):  
Gene Expression ◽  
Heart Failure ◽  
Skeletal Muscle ◽  
Resistance Training ◽  
Transcriptional Regulators ◽  
Structure And Function ◽  
Resistance Exercise Training ◽  
Mitochondrial Structure ◽  
Muscle Disuse ◽  
And Function

Impaired skeletal muscle energetics could adversely affect physical and metabolic function in patients with heart failure (HF). The effect of HF on aspects of mitochondrial structure and function, independent of muscle disuse and other disease-related confounding factors, however, is unclear. Moreover, no study has evaluated whether resistance exercise training, a modality that increases functional capacity, might derive its benefits through modulation of mitochondrial structure and function. Thirteen HF patients and 14 age- and physical activity-matched controls were evaluated for skeletal muscle mitochondrial size/content, gene expression, and enzyme activity before and after an 18-wk resistance exercise-training program. At baseline, HF patients and controls had similar mitochondrial fractional areas, although HF patients had larger average mitochondrion size ( P < 0.05) and a trend toward a reduced number of mitochondria ( P ≤ 0.10). No differences in the expression of transcriptional regulators or cytochrome oxidase subunits or the activity of mitochondrial and cytosolic enzymes were noted. Relationships among transcriptional regulators suggested that networks controlling mitochondrial content and gene expression are intact. Resistance training increased ( P < 0.01) mitochondrial transcription factor A expression in patients and controls, and this increase was related to improvements in muscle strength ( P = 0.05). Training did not, however, alter mitochondrial size/content, enzyme activities, or expression of other transcriptional regulators. In conclusion, our results suggest that the HF syndrome has minimal effects on skeletal muscle mitochondrial biology when the confounding effects of muscle disuse and other disease-related factors are removed. Moreover, the beneficial effects of resistance training on physical function in HF patients and controls are likely not related to alterations in mitochondrial biology.

scholarly journals Resistance training alters skeletal muscle structure and function in human heart failure: effects at the tissue, cellular and molecular levels

2012 ◽  
Vol 590 (5) ◽  
pp. 1243-1259 ◽  
Author(s):  
Michael J. Toth ◽  
Mark S. Miller ◽  
Peter VanBuren ◽  
Nicholas G. Bedrin ◽  
Martin M. LeWinter ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Resistance Training ◽  
Human Heart ◽  
Structure And Function ◽  
Human Heart Failure ◽  
Muscle Structure ◽  
And Function

scholarly journals Renal ischemia alters expression of mitochondria-related genes and impairs mitochondrial structure and function in swine scattered tubular-like cells

2020 ◽  
Vol 319 (1) ◽  
pp. F19-F28 ◽  
Author(s):  
Rahele A. Farahani ◽  
Xiang-Yang Zhu ◽  
Hui Tang ◽  
Kyra L. Jordan ◽  
Lilach O. Lerman ◽  
...  
Keyword(s):  
Gene Expression ◽  
Structural Damage ◽  
Nuclear Dna ◽  
Mitochondrial Genes ◽  
Structure And Function ◽  
Mitochondrial Damage ◽  
Renal Ischemia ◽  
Gene Gain ◽  
Mitochondrial Structure ◽  
And Function

Scattered tubular-like cells (STCs) are dedifferentiated surviving tubular epithelial cells that repair neighboring injured cells. Experimental renal artery stenosis (RAS) impairs STC reparative potency by inducing mitochondrial injury, but the exact mechanisms of mitochondrial damage remain unknown. We hypothesized that RAS alters expression of mitochondria-related genes, contributing to mitochondrial structural damage and dysfunction in swine STCs. CD24+/CD133+ STCs were isolated from pig kidneys after 10 wk of RAS or sham ( n = 3 each). mRNA sequencing was performed, and nuclear DNA (nDNA)-encoded mitochondrial genes and mitochondrial DNA (mtDNA)-encoded genes were identified. Mitochondrial structure, ATP generation, biogenesis, and expression of mitochondria-associated microRNAs were also assessed. There were 96 nDNA-encoded mitochondrial genes upregulated and 12 mtDNA-encoded genes downregulated in RAS-STCs versus normal STCs. Functional analysis revealed that nDNA-encoded and mtDNA-encoded differentially expressed genes were primarily implicated in mitochondrial respiration and ATP synthesis. Mitochondria from RAS STCs were swollen and showed cristae remodeling and loss and decreased ATP production. Immunoreactivity of the mitochondrial biogenesis marker peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α and expression of the mitochondria-associated microRNAs miR-15a, miR-181a, miR-196a, and miR-296-3p, which target several mtDNA genes, were higher in RAS-STCs compared with normal STCs, suggesting a potential modulation of mitochondria-related gene expression. These results demonstrate that RAS induces an imbalance in mtDNA- and nDNA-mitochondrial gene expression, impairing mitochondrial structure and function in swine STCs. These observations support development of gene gain- and loss-of-function strategies to ameliorate mitochondrial damage and preserve the reparative potency of STCs in patients with renal ischemia.

scholarly journals Moderate-intensity resistance exercise alters skeletal muscle molecular and cellular structure and function in inactive older adults with knee osteoarthritis

2017 ◽  
Vol 122 (4) ◽  
pp. 775-787 ◽  
Author(s):  
Mark S. Miller ◽  
Damien M. Callahan ◽  
Timothy W. Tourville ◽  
James R. Slauterbeck ◽  
Anna Kaplan ◽  
...  
Keyword(s):  
Older Adults ◽  
Skeletal Muscle ◽  
Resistance Training ◽  
Knee Osteoarthritis ◽  
Resistance Exercise ◽  
High Intensity ◽  
Structure And Function ◽  
Moderate Intensity ◽  
Men And Women ◽  
And Function

High-intensity resistance exercise (REX) training increases physical capacity, in part, by improving muscle cell size and function. Moderate-intensity REX, which is more feasible for many older adults with disease and/or disability, also increases physical function, but the mechanisms underlying such improvements are not understood. Therefore, we measured skeletal muscle structure and function from the molecular to the tissue level in response to 14 wk of moderate-intensity REX in physically inactive older adults with knee osteoarthritis ( n = 17; 70 ± 1 yr). Although REX training increased quadriceps muscle cross-sectional area (CSA), average single-fiber CSA was unchanged because of reciprocal changes in myosin heavy chain (MHC) I and IIA fibers. Intermyofibrillar mitochondrial content increased with training because of increases in mitochondrial size in men, but not women, with no changes in subsarcolemmal mitochondria in either sex. REX increased whole muscle contractile performance similarly in men and women. In contrast, adaptations in single-muscle fiber force production per CSA (i.e., tension) and contractile velocity varied between men and women in a fiber type-dependent manner, with adaptations being explained at the molecular level by differential changes in myosin-actin cross-bridge kinetics and mechanics and single-fiber MHC protein expression. Our results are notable compared with studies of high-intensity REX because they show that the effects of moderate-intensity REX in older adults on muscle fiber size/structure and myofilament function are absent or modest. Moreover, our data highlight unique sex-specific adaptations due to differential cellular and subcellular structural and functional changes.NEW & NOTEWORTHY Moderate-intensity resistance training causes sex-specific adaptations in skeletal muscle structure and function at the cellular and molecular levels in inactive older adult men and women with knee osteoarthritis. However, these responses were minimal compared with high-intensity resistance training. Thus adjuncts to moderate-intensity training need to be developed to correct underlying cellular and molecular structural and functional deficits that are at the root of impaired physical function in this mobility-limited population.

scholarly journals Essential Role of Septin 7 in Skeletal Muscle Structure and Function

2020 ◽  
Vol 118 (3) ◽  
pp. 258a
Author(s):  
Laszlo Csernoch ◽  
Mónika Gönczi ◽  
Zsolt Ráduly ◽  
László Szabó ◽  
Nóra Dobrosi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Essential Role ◽  
Structure And Function ◽  
Muscle Structure ◽  
And Function

scholarly journals Heterochronic Parabiosis: Old Blood Induces Changes in Mitochondrial Structure and Function of Young Mice

2020 ◽  
Author(s):  
Jenny L Gonzalez-Armenta ◽  
Ning Li ◽  
Rae-Ling Lee ◽  
Baisong Lu ◽  
Anthony J A Molina
Keyword(s):  
Mitochondrial Respiration ◽  
Complex I ◽  
Structure And Function ◽  
Muscle Performance ◽  
Mitochondrial Morphology ◽  
Positive Effects ◽  
Mitochondrial Structure ◽  
And Function ◽  
Old Mice ◽  
Young Mice

Abstract Heterochronic parabiosis models have been utilized to demonstrate the role of blood-borne circulating factors in systemic effects of aging. In previous studies, heterochronic parabiosis has shown positive effects across multiple tissues in old mice. More recently, a study demonstrated old blood had a more profound negative effect on muscle performance and neurogenesis of young mice. In this study, we used heterochronic parabiosis to test the hypothesis that circulating factors mediate mitochondrial bioenergetic decline, a well-established biological hallmark of aging. We examined mitochondrial morphology, expression of mitochondrial complexes, and mitochondrial respiration from skeletal muscle of mice connected as heterochronic pairs, as well as young and old isochronic controls. Our results indicate that young heterochronic mice had significantly lower total mitochondrial content and on average had significantly smaller mitochondria compared to young isochronic controls. Expression of complex IV followed a similar pattern: young heterochronic mice had a trend for lower expression compared to young isochronic controls. Additionally, respirometric analyses indicate that young heterochronic mice had significantly lower complex I, complex I + II, and maximal mitochondrial respiration and a trend for lower complex II-driven respiration compared to young isochronic controls. Interestingly, we did not observe significant improvements in old heterochronic mice compared to old isochronic controls, demonstrating the profound deleterious effects of circulating factors from old mice on mitochondrial structure and function. We also found no significant differences between the young and old heterochronic mice, demonstrating that circulating factors can be a driver of age-related differences in mitochondrial structure and function.

PROLONGED INTRAVENOUS INFUSION OF LABELLED IODOCOMPOUNDS IN THE RAT: [125I]IODIDE METABOLISM AND EFFECTS OF MODERATE DIETARY IODINE DEFICIENCY

1979 ◽  
Vol 82 (2) ◽  
pp. 227-234 ◽  
Author(s):  
VIPA BOONNAMSIRI ◽  
J. C. KERMODE ◽  
B. D. THOMPSON
Keyword(s):  
Skeletal Muscle ◽  
Iodine Deficiency ◽  
Intravenous Infusion ◽  
Structure And Function ◽  
Continuous Intravenous Infusion ◽  
Close Approximation ◽  
Faecal Excretion ◽  
And Function ◽  
Layer Chromatography ◽  
Secretion Rates

SUMMARY Radio-iodide was administered by prolonged continuous intravenous infusion to rats maintained under iodine-replete conditions and in moderate iodine deficiency. A close approximation to equilibrium labelling was thereby achieved. Labelled iodocompounds extracted from various tissues were analysed by thin-layer chromatography. Moderate iodine deficiency resulted in a slight increase in the ratio of mono-iodotyrosine to di-iodotyrosine in the thyroid. No change in the ratio of tri-iodothyronine (T3) to thyroxine (T4) was found in thyroid, plasma or skeletal muscle. Faecal excretion of T3 declined appreciably relative to that of T4. Under iodine-replete conditions the ratio of thyroidal secretion rates of T3 and T4 was estimated to be more than three times higher than the ratio of these iodocompounds within the thyroid. Heterogeneity of thyroglobulin structure and function may explain these observations.

Sign in / Sign up

Export Citation Format

Share Document