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PubMed2001

Analysis of stimulus-evoked pain in patients with myofascial temporomandibular pain disorders.

The pathophysiological mechanisms of myofascial temporomandibular disorders (TMD) are still under investigation. The hypothesis that TMD pain is caused by a generalized sensitization of higher order neurons in the nociceptive pathways combined with a decreased efficacy of endogenous inhibitory systems has recently gained support in the literature. This study was designed to further investigate the somatosensory sensibility within and outside the craniofacial region. Twenty-two patients fulfilled the research diagnostic criteria for TMD for myofascial pain (Dworkin and LeResche, J Craniomandib Disord Facial Oral Pain 6 (1992) 301) and 21 age- and sex-matched subjects served as a control group. The somatosensory sensibility to a deep tonic input was tested by standardized infusions of hypertonic saline into the masseter and anterior tibialis muscle. Furthermore, pressure pain thresholds (PPTs) and heat pain thresholds (HPTs) were assessed with phasic stimuli at the same sites before and following the infusions. Myofascial TMD patients reported infusion of hypertonic saline to be more painful on 10 cm visual analogue scales (peak pain 8.8 +/- 0.4 cm) than control subjects (6.8 +/- 0.5 cm, t-test: P = 0.003) in the masseter but not in the anterior tibialis (7.4 +/- 0.5 vs. 6.6 +/- 0.5 cm, P=0.181). The perceived area of experimental masseter pain measured on drawings was marginally larger in TMD patients (2.6+/-0.5 arbitrary units (a.u.)) than in control subjects (1.4 +/- 0.2 a.u., Mann-Whitney: P = 0.048) but no differences were observed for the anterior tibialis (P = 0.771). The PPTs were lower in the myofascial TMD patients compared to the control group, both in the masseter (analysis of variance (ANOVA): P = 0.002) and in the anterior tibialis (P = 0.005), whereas there were no significant differences in HPT (ANOVAs: P = 0.357, P = 0.101). There were no significant correlations between measures of somatosensory sensibility and measures of clinical pain intensity, pain duration, graded chronic pain scores or somatization or depression scores (Pearson: R < 0.304, P > 0.172). The present study in a well-defined group of myofascial TMD patients found that the responsiveness to both tonic and phasic deep stimuli, but not to phasic superficial inputs at the pain threshold level, in the craniofacial region was higher compared with a control group. These findings suggest that myofascial TMD pain is associated with a facilitation of stimulus-evoked pain primarily, but not exclusively related to the painful region.

Adult↗

PubMed1998

Myocyte recovery after mechanical circulatory support in humans with end-stage heart failure.

BACKGROUND: The failing myocardium is characterized by decreased force production, slowed relaxation, and depressed responses to beta-adrenergic stimulation. In some heart failure patients, heart function is so poor that a left ventricular assist device (LVAD) is inserted as a bridge to transplantation. In the present research, we investigated whether circulatory support with an LVAD influenced the functional properties of myocytes from the failing heart. METHODS AND RESULTS: Myocytes were isolated from human explanted failing hearts (HF-myocytes) and failing hearts with antecedent LVAD support (HF-LVAD-myocytes). Studies of myocyte function indicated that the magnitude of contraction was greater (9.6+/-0.7% versus 6.9+/-0.5% shortening), the time to peak contraction was significantly abbreviated (0.37+/-0.01 versus 0.75+/-0.04 seconds), and the time to 50% relaxation was reduced (0.55+/-0.02 versus 1.45+/-0.11 seconds) in the HF-LVAD-myocytes compared with the HF-myocytes (P<0.05). The HF-LVAD-myocytes had larger contractions than the HF-myocytes at all frequencies of stimulation tested. The negative force-frequency relationship of the HF-myocytes was improved in HF-LVAD-myocytes but was not reversed. Responses to beta-adrenergic stimulation (by isoproterenol) were greater in HF-LVAD-myocytes versus HF-myocytes. CONCLUSIONS: The results of the study strongly support the idea that circulatory support with an LVAD improves myocyte contractile properties and increases beta-adrenergic responsiveness.

Adrenergic beta-Agonists↗

PubMed2000

The Menopause Rating Scale (MRS): comparison with Kupperman index and quality-of-life scale SF-36.

OBJECTIVE: To evaluate further the Menopause Rating Scale (MRS) for scoring menopausal symptoms by comparison with other instruments relevant for women in their menopausal transition: the Kupperman index and the quality-of-life scale SF-36. METHOD: A population sample of 306 women, who had been randomly selected from an initially representative survey of German women (aged 40-60), completed three questionnaires in 1997: the Menopause Rating Scale (MRS), the Kupperman index and the short form-36 (SF-36). RESULTS: A comparison of the MRS with the Kupperman index produced a high correlation of raw scores (r = 0.91). The highest association of scores (80%) was found in the highest quartile of the MRS. The terms 'mild', 'moderate' and 'severe', relating to the degree of severity of menopausal symptoms, reflect different contents and spread in each scale, i.e. are not directly comparable. There is a strikingly good association between the subscales of the SF-36 and the MRS. The MRS correlates best with those dimensions of the SF-36 that are highly relevant for women in the menopausal transition. For this reason, the MRS can be utilized as an age- and condition-specific quality-of-life instrument. CONCLUSIONS: The Menopause Rating Scale is a valuable modern tool for the assessment of menopausal complaints. It combines in practice excellent applicability and good reliability, and there are normal values for the population available. The MRS could serve as an adequate diagnostic instrument for menopausal quality of life.

Adult↗

PubMed2002

Defining 'relative' androgen deficiency in aging men: how should testosterone be measured and what are the relationships between androgen levels and physical, sexual and emotional health?

In men, bioavailable and free testosterone levels decline by about 1.0 and 1.2% per year, respectively, after the age of 40. The definition of clinically relevant androgen deficiency in the aging male remains uncertain. Clinical features common to both aging and androgen deficiency include decreased muscle mass and strength, and increased fatigue, increased fat mass, loss of libido, erectile dysfunction, impaired cognitive function and depression. It is, however, difficult to separate the effect on plasma testosterone of concomitant disease, compared with the effects of a decrease in testosterone levels alone. Testosterone supplementation has been shown to be effective in improving many of the clinical features of androgen deficiency in the older male, and is safe, at least in the short term. The maximum benefit occurs in those men with the lowest testosterone levels.

Adipose Tissue↗

PubMed1990

[Clinical significance of serum cardiac myosin light chain I in patients with muscular dystrophy].

We examined serum cardiac myosin light chain I (LCI), serum creatine kinase (CK) levels and left ventricular function in patients with muscular dystrophy and secondary cardiac involvement. LCI levels were determined by a two-site immunoradiometric assay method in 25 patients with muscular dystrophy and 10 normal subjects. This study included 15 patients with Duchenne muscular dystrophy (DMD), 8 patients with Fukuyama type congenital muscular dystrophy (FCMD) and 2 sisters with non-Fukuyama type congenital muscular dystrophy (nFCMD). We measured the value of left ventricular fractional shortening (FS) using echocardiography. All patients with DMD and FCMD showed moderate or severe skeletal muscle weakness. The mean values of LCI were significantly higher in patients with DMD (11.0 +/- 8.3 ng/ml, p less than 0.01) and in patients with FCMD (1.6 +/- 1.4 ng/ml, p less than 0.05) than in normal subjects (0.3 +/- 0.2 ng/ml). In patients with DMD, LCI level correlated closely with CK level (r = 0.81, p less than 0.01) but not with FS (r = 0.35, n.s.). In patients with FCMD, LCI level correlated significantly with CK level (r = 0.75, p less than 0.05) but not with FS (r = 0.44, n.s.). Close correlation between LCI and CK levels was thought to result from the cross reaction between cardiac LCI and myosin light chains of skeletal muscle in the assay method we used. Two siblings with nFCMD showed mild skeletal muscle weakness. A 22-year-old sister with mild left ventricular dysfunction (FS = 0.41) showed high level of CK (4794/U/L) and mild elevation of LCI (7.3 ngml).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed2006

Palmitate induced mitochondrial deoxyribonucleic acid damage and apoptosis in l6 rat skeletal muscle cells.

A major characteristic of type 2 diabetes mellitus (T2DM) is insulin resistance in skeletal muscle. A growing body of evidence indicates that oxidative stress that results from increased production of reactive oxygen species and/or reactive nitrogen species leads to insulin resistance, tissue damage, and other complications observed in T2DM. It has been suggested that muscular free fatty acid accumulation might be responsible for the mitochondrial dysfunction and insulin resistance seen in T2DM, although the mechanisms by which increased levels of free fatty acid lead to insulin resistance are not well understood. To help resolve this situation, we report that saturated fatty acid palmitate stimulated the expression of inducible nitric oxide (NO) synthase and the production of reactive oxygen species and NO in L6 myotubes. Additionally, palmitate caused a significant dose-dependent increase in mitochondrial DNA (mtDNA) damage and a subsequent decrease in L6 myotube viability and ATP levels at concentrations as low as 0.5 mM. Furthermore, palmitate induced apoptosis, which was detected by DNA fragmentation, caspase-3 cleavage, and cytochrome c release. N-acetyl cysteine, a precursor compound for glutathione formation, aminoguanidine, an inducible NO synthase inhibitor, and 5,10,15,20-tetrakis(4-sulphonatophenyl) porphyrinato iron (III), a peroxynitrite inhibitor, all prevented palmitate-induced mtDNA damage and diminished palmitate-induced cytotoxicity. We conclude that exposure of L6 myotubes to palmitate induced mtDNA damage and triggered mitochondrial dysfunction, which caused apoptosis. Additionally, our findings indicate that palmitate-induced mtDNA damage and cytotoxicity in skeletal muscle cells were caused by overproduction of peroxynitrite.

Adenosine Triphosphate↗

PubMed2002

The cardiospecificity of the third-generation cTnT assay after exercise-induced muscle damage.

PURPOSE: The purpose of the present study was to examine the cardiospecificity of cTnI and the new third-generation cTnT assay, in the presence of exercise-induced muscle damage in highly trained individuals, and to examine the impact of a maximal-ramping treadmill test on cardiac function. METHODS: Eight highly trained male triathletes (mean +/- SD; age: 29 +/- 9 yr; height: 1.79 +/- 0.10 m; body mass: 77 +/- 10 kg; .VO(2max): 67.4 +/- 6.3 mL.kg(-1).min(-1)) completed two bouts of exercise. On the first occasion, subjects completed a maximal-ramping treadmill test. On a separate occasion, the subjects completed 30 min of downhill running (15% gradient) at a speed equivalent to 70% of maximal running velocity attained during the maximal-ramping treadmill test. All subjects were assessed using ECG, echocardiography, and blood analysis. Measurements were taken at rest, immediately after, and 48 h postexercise for each bout of exercise. Echocardiographic analysis was used to determine left ventricular systolic and diastolic function. Blood samples were analyzed for markers of myocyte damage. RESULTS: Echocardiographic results indicated normal left ventricular function before and after both exercise bouts. Total CK and CKMB were significantly elevated 48 h after the downhill run. cTnT and cTnI were not elevated at any stage of the study. CONCLUSIONS: Neither the maximal-ramping treadmill test nor the 30-min downhill run produced cardiac dysfunction or myocardial damage in young, healthy trained subjects. The elevated total CK and CKMB within the downhill study are noncardiac in origin as demonstrated by the lack of cTnT and cTnI. The cTnI and new third-generation cTnT assays may be used to detect cardiac damage in the presence of elevated total CK and CKMB associated with exercise-induced skeletal muscle damage.

Adult↗

PubMed1995

Influence of variation in jaw posture on sternocleidomastoid and trapezius electromyographic activity.

This study was conducted in order to determine the influence of variation in the occlusal contacts on electromyographic (EMG) cervical activity in 20 patients with myogenic cranio-cervical-mandibular dysfunction. EMG recordings during maximal voluntary clenching were performed by placing surface electrodes on the left sternocleidomastoid and upper trapezius muscles in the following conditions: intercuspal position; edge to edge left laterotrusive contacts (ipsilateral); edge to edge right laterotrusive contacts (contralateral); edge to edge protrusive contacts; and retrusive occlusal contacts. A significant higher EMG activity was recorded in both muscles during maximal voluntary clenching in retrusive occlusal contact position, whereas no significant differences in EMG activity were observed between intercuspal position, ipsilateral, contralateral and protrusive contact positions. The EMG pattern observed suggests that a more frequent intensity and duration of tooth clenching in retrusive occlusal contact position could result in more clinical symptomatology in these cervical muscles in patients with myogenic cranio-cervical-mandibular dysfunction.

Adolescent↗

PubMed2003

Dynamic cardiomyoplasty: impact of effective pacing.

Dynamic cardiomyoplasty, in which the transposed latissimus dorsi muscle is wrapped around the heart and then electrically stimulated to augment systolic dysfunction, is an alternative surgical treatment for severe cardiomyopathies. Critical to success of this operation is to provide the wrapped skeletal muscle with more fatigue-resistant structure through repetitive electrical stimulation. A cardiostimulating device is important in this regard to perform synchronised contraction contributing to symptomatic improvement. Here in, we present a case with dynamic cardiomyoplasty improving following renewal of impaired myostimulator device.

Aged↗

PubMed2006

Increased apoptosis, Huntingtin inclusions and altered differentiation in muscle cell cultures from Huntington's disease subjects.

Mutated huntingtin (htt) is ubiquitously expressed in tissues of Huntington's disease (HD) patients. In the brain, the mutated protein leads to neuronal cell dysfunction and death, associated with formation of htt-positive inclusions. Given increasing evidence of abnormalities in HD skeletal muscle, we extensively analyzed primary muscle cell cultures from seven HD subjects (including two unaffected mutation carriers). Myoblasts from presymptomatic and symptomatic HD subjects showed cellular abnormalities in vitro, namely mitochondrial depolarization, cytochrome c release, increased caspase-3, -8, and -9 activities, and defective cell differentiation. Another notable feature was the formation of htt inclusions in differentiated myotubes. This study helps to advance current knowledge about the downstream effects of the htt mutation in human tissues. Further applications may include drug screening using this human cellular model.

Apoptosis↗

PubMed2006

Melatonin reduces ischemia/reperfusion-induced superoxide generation in arterial wall and cell death in skeletal muscle.

The purpose of this study was to determine the effect of melatonin on superoxide generation in arterial wall at an early phase of reperfusion and on endothelial dysfunction of microvasculature and cell viability of cremaster muscle at late phase of reperfusion (24 hr) after prolonged ischemia. Bilateral vascular pedicles which supply blood flow to the cremaster muscle were exposed. After surgical preparation, microvascular clamps were applied on the right iliac, femoral and spermatic arteries to create 4 hr of ischemia in both feeding vessels and the unexposed cremaster muscle. The vascular clamping was omitted on the left iliac, femoral and spermatic arteries and served as an internal control. Melatonin or Vehicle was via by intravenous injection at 10 min prior to reperfusion and 10 min after reperfusion. In the first experiment, the vascular pedicle was harvested after reperfusion to measure superoxide generation in real time by lucigenin-derived chemiluminescence. In the second experiment, endothelial-dependent and -independent vasodilatation was examined in the terminal arteriole of cremaster muscle which was then harvested to examine cell viability by WST-1 assay on day 2. Superoxide generation in arterial wall peaked at first 5-min of reperfusion and declined to near baseline after 60 min of reperfusion. Melatonin treatment significantly reduced superoxide generation in arterial walls and improved cell viability in cremaster muscles. Melatonin treatment also significantly reduced microvascular endothelial dysfunction which was still observable in the microcirculation of cremaster muscle after 24 hr of reperfusion. Melatonin reduces superoxide generation in the early phase of reperfusion resulting in attenuating endothelial dysfunction and muscle cell death in the late phase of reperfusion.

Animals↗

PubMed2005

Enhanced resistance to fatigue and altered calcium handling properties of sarcalumenin knockout mice.

Sarcalumenin is a Ca2+-binding protein located in the sarcoplasmic reticulum of striated muscle cells, the physiological function of which has not been fully determined yet. Using sarcalumenin knockout (sar(-/-)) mice, we showed that sar ablation altered store-operated Ca2+ entry (SOCE) and enhanced muscle fatigue resistance. Sar(-/-) mice fatigued less with treadmill exercise, and intact isolated soleus and extensor digitorum longus muscles from sar(-/-) mice were more resistant to intermittent fatiguing stimulation than those from wild-type mice. Enhanced SOCE was observed in the sar(-/-) muscles. Biochemical analysis revealed that sar(-/-) muscles contained significantly elevated expression of mitsugumin 29 (MG29), a synaptophysin-related membrane protein located in the triad junction of skeletal muscle. Because the ablation of mg29 has been shown to cause increased fatigability and dysfunction of SOCE, the enhanced SOCE activity seen in sar(-/-) muscle may be correlated with the increased expression of MG29. Our data suggest that systemic ablation of sarcalumenin caused enhanced resistance to muscle fatigue by compensatory changes in Ca2+ regulatory proteins that effect SOCE.

Animals↗

PubMed1996

The creatinine approach to estimate skeletal muscle mass in patients with cirrhosis.

The creatinine-method to estimate muscle mass is frequently used in clinical studies, although the validity of this approach is uncertain in patients with cirrhosis. In this study 102 patients with cirrhosis differing in cause, clinical state, liver, and renal function were investigated to determine whether reduced liver or renal function may explain in part the low levels of urinary creatinine excretion frequently observed in these patients. Muscle mass assessed by 24-hour urinary creatinine excretion was compared with anthropometrically obtained muscle mass calculated from arm muscle area (AMA), and with body cell mass (BCM) estimated by bioelectrical impedance analysis and total body potassium counting. In cirrhosis, the 24-hour urinary creatinine excretion was 10.4% and AMA was 19% lower than predicted values. The differences between the results obtained by different methods did not show any relation to parameters of liver function (ICG-t1/2, caffeine-t1/2, MEGX-test, cholinesterase) or the severity of liver disease (i.e., Child-Pugh score). In contrast, renal function was strongly correlated with the differences between creatinine- and anthropometric-muscle mass (r = .64, P < .001). At the same time, patients with normal renal function (62% of the whole population) had significantly higher creatinine (29.1 +/- 8.5 vs. 15.8 +/- 6 kg, P < .001) and anthropometric-muscle mass (22.4 +/- 6 vs. 17.9 +/- 5.3 kg; P < .01) than patients with reduced renal function (38% of the patients). In addition, significantly higher differences between measured and predicted values of urinary creatinine excretion (-0.389 +/- 0.33 vs. 0.06 +/- 0.31 g/24 h; P < .001) and of AMA (13.2 +/- 12 vs. 7.2 +/- 12 cm2; P < .03) were found in the subgroup with impaired renal function. In conclusion, renal dysfunction but not reduced liver function systematically affects the urinary creatinine method for the estimation of skeletal muscle mass in cirrhosis.

Adult↗

PubMed2004

Effect of dietary creatine on skeletal muscle myosin heavy chain isoform expression in an animal model of uremia.

BACKGROUND: Chronic renal failure is accompanied with muscle dysfunction and myopathy, characterized by muscle weakness and increased fatigue. Myosin heavy chain (MHC) is the principal structural protein that controls the intrinsic contractile properties of striated muscle. Creatine is widely used as an ergogenic nutritional supplement in sportsmen. This study investigates the effect of creatine supplementation on MHC expression in the setting of uremic myopathy. METHODS: Male Wistar rats were either sham operated or subtotally nephrectomized and received a control diet or creatine (2% w/w)-supplemented diet. After 4 weeks of treatment, serum creatinine, creatine, urea and creatinine clearances were determined. MHC isoforms were determined electrophoretically in the extensor digitorum longus and soleus muscles. RESULTS: Creatinine clearances were lower in nephrectomized animals, but similar in creatine-supplemented and control diet animals. Nephrectomized animals had significantly higher MHC IIb and lower MHC IIx isoform expression in the extensor digitorum longus muscle compared to sham-operated animals. In the soleus muscle, MHC IIb expression was increased in nephrectomized animals. Creatine supplementation reversed the MHC transitions observed in uremia in the soleus muscle, but not in the extensor digitorum longus muscle. CONCLUSION: We observed altered expression of MHC isoforms in uremia. In uremic animals, fast MHC IIb isoforms were increased, whereas MHC I and IIx isoforms predominate in control animals. Dietary creatine supplementation reversed the altered MHC expression during uremia in slow-twitch, but not in fast-twitch muscles.

Administration, Oral↗

PubMed1999

Adhesion molecule expression in postischemic microvascular dysfunction: activity of a micronized purified flavonoid fraction.

Ischemia and reperfusion (I/R) induces neutrophil infiltration in skeletal muscle that is localized to the ischemic region. To transmigrate at ischemic regions, granulocytes must first arrest in the postcapillary venular segment of the microcirculation. Initially, leukocytes roll along the endothelium of these venules, a weak adhesive interaction that is mediated by the selectins (L-, E-, and P-selectin). Leukocyte rolling functions to slow the neutrophil during its transit through the microcirculation, thereby allowing it to monitor its local environment for the presence of activating factors arising from the ischemic tissues. When activated, the rolling granulocyte is rendered capable of forming the stronger adhesive interactions that allow the cell to become arrested in postcapillary venules in the ischemic region. These adhesive interactions are mediated by a leukocyte glycoprotein complex designated CD11/CD18 and intercellular adhesion molecule-1 (ICAM-1) expressed on endothelial cells. The stationary neutrophil uses the gradient in concentration of soluble chemoattractants liberated from ischemic tissues as a directional cue to move from the vascular to extravascular compartment, being guided in its transit across the endothelium by interactions with platelet endothelial cell adhesion molecule-1 (PECAM-1), an adhesive molecule localized to the interendothelial cleft. This paper reviews current understanding of the mechanisms underlying the establishment of leukocyte/endothelial cell interactions in postischemic skeletal muscle in terms of specific adhesion molecules that participate in neutrophil sequestration after I/R. Discovery of the molecular determinants of neutrophil/endothelial cell adhesion has uncovered potential mechanisms whereby agents exhibiting anti-adhesive properties may act. The micronized purified flavonoid fraction (450 mg diosmin, 50 mg hesperidin) prevents I/R-induced leukocyte adhesion in skeletal muscle. This anti-adhesive effect appears to be mediated at least in part by inhibition of induced expression of ICAM-1.

Animals↗

PubMed2003

Paroxysms of excitement: sodium channel dysfunction in heart and brain.

Inherited disorders of ion-channels are associated with paroxysmal dysfunction of excitable tissues and manifest as diseases of the brain, heart and skeletal muscle. These so-called channelopathies have now been described for most of the major categories of voltage-dependent ion-channels including those selectively permeable to sodium. Sodium channelopathies affecting the heart and brain are reviewed in this essay. They show striking differences and similarities including, for example, their responsiveness to changes in body temperature and sleep state. They represent a paradigm for efforts to trace disturbed behaviour of physiological systems back to its molecular origins and understanding their molecular basis may provide clues to important health issues such as cardiac side effects of drugs and response to medication used to treat epilepsy.

Animals↗

PubMed2000

Toward a wholly nutritional therapy for type 2 diabetes.

It may now be feasible to target specific supplemental nutrients to each of the key dysfunctions which conspire to maintain hyperglycemia in type 2 diabetes: bioactive chromium for skeletal muscle insulin resistance, conjugated linoleic acid for adipocyte insulin resistance, high-dose biotin for excessive hepatic glucose output, and coenzyme Q(10) for beta cell failure. Nutritional strategies which disinhibit hepatic fatty acid oxidation (involving hydroxycitrate, carnitine, pyruvate, and other adjuvants) may likewise prove beneficial - in the short term, by decreasing serum free fatty acids and, in the longer term, by promoting regression of visceral obesity. The nutrients and food factors recommended here appear to be safe and well tolerated, and thus may have particular utility for diabetes prevention.

Biotin↗

PubMed1994

Canine mitochondrial myopathy associated with reduced mitochondrial mRNA and altered cytochrome c oxidase activities in fibroblasts and skeletal muscle.

Skeletal muscle and fibroblast biopsies obtained from a normal dog and an old English sheep dog with exertional myopathy and lactic acidosis were examined for mitochondrial enzyme activities and mitochondrially coded mRNAs. The fibroblast cultures of the affected dog showed reduced cytochrome c oxidase (COX) I+II mRNA content (25% of control) and COX enzyme activities (23% of control). The skeletal muscle of the affected dog was similarly affected and showed not only decreased COX I+II mRNA content, but also decreased ATPase6 mRNA level. Apart from COX enzyme activity (62% of control), the oligomycin sensitive ATPase and NADH-Ferricyanide reductase activities were also reduced in the skeletal muscle of the affected dog (12-20% of control). These results suggest that a mitochondrial dysfunction may be the causative factor of the exertional metabolic myopathy with lactic acidosis in this affected old English sheep dog. These animals may serve as an excellent model for mitochondrial myopathies.

Adenosine Triphosphatases↗