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PubMed1998

Local relation between oxidative metabolism and perfusion in leg muscles of patients with heart failure studied by magnetic resonance imaging and spectroscopy.

BACKGROUND: We studied the local relation of muscle perfusion and metabolism in patients with severe chronic heart failure. Alterations of skeletal muscle blood flow and oxidative capacity contribute to exercise intolerance in these patients. The interdependence of both parameters has often been questioned. METHODS AND RESULTS: With the use of nuclear magnetic resonance, we quantified leg and muscle perfusion during reactive hyperemia in 7 patients with heart failure (New York Heart Association class III and IV) and 7 age-matched control subjects from the difference in longitudinal relaxation rate (1/T1). By using 31P nuclear magnetic resonance spectroscopy, we assessed oxidative metabolism from the creatine rephosphorylation time constant after a short ischemic exercise. Phosphocreatine recovery is slowed (74.6 +/- 11.3 vs 49.9 +/- 13.9 seconds, p = .002) and reactive hyperemic flow is reduced (48.5 +/- 24.9 vs 113 +/- 30.4 mL/100 mL per minute, p = .0005). CONCLUSIONS: By using a totally noninvasive protocol, we demonstrated that reactive hyperemic flow correlates with oxidative capacity in calf muscles from patients with heart failure, showing that exercise performance and local circulatory dysfunction are decreased in parallel in severe heart failure.

Aged↗
PubMed1997

The effect of propionyl L-carnitine on skeletal muscle metabolism in renal failure.

The effect of propionyl L-carnitine on skeletal muscle metabolism in chronic renal failure. Carnitine deficiency, resulting in defective oxidative ATP synthesis, has been implicated in the myopathy of chronic renal failure. Using 31P magnetic resonance spectroscopy we examined calf muscle metabolism in 10 dialysed patients before and after 8 weeks of propionyl L-carnitine (PLC) 2 g.p.o. daily. Resting phosphocreatine/ATP (4.41 +/- 0.20 [SEM]) decreased to normal control levels on PLC (3.98 +/- 0.14; controls 4.00 +/- 0.06). In contrast, there was no effect of PLC on aerobic and anaerobic metabolism of muscle during or following 2-10 min exercise. The maximal calculated oxidative capacity (Qmax) remained below normal (28 +/- 3 mM/min before and 24 +/- 3 mM/min after PLC; controls 49 +/- 3 mM/min). Qmax correlated positively with hemoglobin concentration ([Hb]) after PLC (p < 0.03). Oxidative capacity assessed by phosphocreatine recovery T significantly improved with PLC administration (0.93 +/- 0.1 to 0.74 +/- 0.08 min) in those patients (n = 6) with [Hb] > 10 g/dl. [Hb] was rate limiting to oxidative metabolism in recovery from exercise but only following treatment with PLC. Patients with anemia or those subjects who use relatively more non-oxidatively synthesized ATP during exercise, do not respond to PLC. Oxidative metabolism did not normalize on PLC suggesting that anemia and carnitine deficiency are not the only causes of mitochondrial dysfunction in renal failure.

Adenosine Triphosphate↗
PubMedDate not supplied

A kinematic study of the upper-limb motion of wheelchair basketball shooting in tetraplegic adults.

Kinematic aspects of the reduced shooting ability of tetraplegic (TP) wheelchair basketball players were investigated and compared with those of able-bodied (AB) basketball players. TP showed significantly smaller values for the vertical component of ball release velocity (4.26 (degree/s) versus 5.45 (degree/s)) and maximum wrist flexion angular velocity (878.4 (degree/s) versus 1445.9 degrees) than AB. Moreover, for a specific shoulder horizontal adduction motion, a larger range of shoulder abduction motion and larger displacements of the right shoulder were observed in TP. The reduced ball velocity of TP subjects with lesions at the C7 to C8 levels depended on an insufficient wrist flexion angular velocity, where dysfunction of available musculature may be a causal determinant. Further, the specific motions observed in TP subjects most likely maximize the function of available musculature, thereby partially compensating for the dysfunction of the wrist flexor muscles and contributing to resultant ball release velocity.

Adult↗
PubMed1995

Mitochondrial abnormalities in human immunodeficiency virus-associated myopathy.

There is controversy as to whether zidovudine (ZDV) induces a mitochondrial myopathy that is distinguishable from human immunodeficiency virus (HIV)-associated myopathy in ZDV-naive patients. Mitochondrial abnormalities were evaluated in skeletal muscle obtained from 18 HIV-positive, ZDV-exposed patients, and 9 who were drug naive. All patients had clinical myopathy, and underwent neuromuscular evaluation with information recorded on timing and dosage of ZDV. All underwent muscle biopsies and samples were examined without knowledge of clinical history or ZDV status. Biopsy samples were evaluated by light and electron microscopy. Mitochondrial abnormalities were seen in ZDV-treated and -naive groups, and did not correlate with ZDV exposure or cumulative ZDV dosage. Mitochondrial abnormalities displayed significant correlation with the presence and severity of myofiber degeneration on biopsy, regardless of ZDV status. As mitochondrial abnormalities reflect myofiber degeneration, present in both patient groups, they may not be used as evidence of primary mitochondrial dysfunction. The etiology of myofiber degeneration in patients with HIV infection, whether ZDV-exposed or -naive, remains unclear.

Adult↗
PubMed2005

Acute and severe hypobaric hypoxia increases oxidative stress and impairs mitochondrial function in mouse skeletal muscle.

Severe high-altitude hypoxia exposure is considered a triggering stimulus for redox disturbances at distinct levels of cellular organization. The effect of an in vivo acute and severe hypobaric hypoxic insult (48 h at a pressure equivalent to 8,500 m) on oxidative damage and respiratory function was analyzed in skeletal muscle mitochondria isolated from vitamin E-supplemented (60 mg/kg ip, 3 times/wk for 3 wk) and nonsupplemented mice. Forty male mice were randomly divided into four groups: control + placebo, hypoxia + placebo (H + P), control + vitamin E, and hypoxia + vitamin E. Significant increases in mitochondrial heat shock protein 60 expression and protein carbonyls group levels and decreases in aconitase activity and sulfhydryl group content were found in the H + P group when compared with the control + placebo group. Mitochondrial respiration was significantly impaired in animals from the H + P group, as demonstrated by decreased state 3 respiratory control ratio and ADP-to-oxygen ratio and by increased state 4 with both complex I- and II-linked substrates. Using malate + pyruvate as substrates, hypoxia decreased the respiratory rate in the presence of carbonyl cyanide m-chlorophenylhydrazone and also stimulated oligomycin-inhibited respiration. However, vitamin E treatment attenuated the effect of hypoxia on the mitochondrial levels of heat shock protein 60 and markers of oxidative stress. Vitamin E was also able to prevent most mitochondrial alterations induced by hypobaric hypoxia. In conclusion, hypobaric hypoxia increases mitochondrial oxidative stress while decreasing mitochondrial capacity for oxidative phosphorylation. Vitamin E was an effective preventive agent, which further supports the oxidative character of mitochondrial dysfunction induced by hypoxia.

Acute Disease↗
PubMed2003

Myocardial dysfunction and male mortality in peroxisome proliferator-activated receptor alpha knockout mice overexpressing lipoprotein lipase in muscle.

Free fatty acids (FFA) are liberated from triglyceride-rich lipoproteins by lipoprotein lipase (LPL) and are considered to be a principal energy source for the heart. The peroxisome proliferator-activated receptor alpha (PPARalpha) is a key regulator of FFA catabolism. To investigate its role in cardiac muscle metabolism, transgenic mice overexpressing LPL in skeletal and cardiac muscle were bred on a PPARalpha knockout background. Fifty-five percent of male animals lacking PPARalpha and overexpressing LPL died within 4 months after birth. In contrast, females of this genotype stayed alive. Deceased animals exhibited cardiopulmonary congestion but had no increase of neutral lipids in the heart. Changes in plasma glucose, FFA, lactate, and triglycerides did not clearly account for gender-specific differences in mortality; however, they indicated a critical role for PPARalpha during fasting. Analysis of cardiac function revealed that in isolated perfused hearts, left ventricular developed pressure (a measure of contractility) was markedly lower in PPARalpha knockout mice overexpressing LPL compared with controls. Glucose uptake of isolated perfused hearts was significantly higher in PPARalpha knockout mice with both normal or increased LPL expression. However, uptake of FFA was not different among genotypes. In contrast, fasted FFA levels were significantly lower in cardiac muscle of PPARalpha knockout mice with normal LPL expression (-26%) and PPARalpha knockout mice overexpressing LPL (-38%) compared with controls. Our results indicate a critical role for PPARalpha in myocardial pump function and suggest that mouse models combining different genetic effects such as PPARalpha knockout mice overexpressing muscle LPL may be useful to study cardiomyopathies.

Animals↗
PubMed2000

Reconstruction of the lower urinary tract using autologous muscle transfer and cell seeding: current status and future perspectives.

Functioning free-muscle transfer has established itself for the treatment of skeletal muscle deficiency over the last two decades. The capability of skeletal muscle to empty a spherical reservoir has been shown to be lessened if the muscle has contracted due to dissection. Currently there is no established curative treatment for bladder acontractility. Experimental data and preliminary clinical results have shown that innervated free latissimus dorsi muscle (LD) may serve as a substitute for a dysfunctional detrusor. In a clinical protocol, latissimus dorsi detrusor myoplasty (LDDM) was applied in 11 patients (age 9-68 years) with bladder acontractility due to spinal cord injury (seven patients), congenital malformations (two patients), detrusor myopathy (one patient), and idiopathic causes (one patient) who had required catheterization for bladder emptying for a minimum of 2 years. In all, 10 of 11 patients were capable of voiding volitionally, with eight of them no longer requiring catheterization, throughout the follow-up period of 12-46 months. Transplanted LD activity was confirmed by ultrasonography and flow-mode computerized tomography. It can thus be concluded that emptying of the bladder can be induced through the contractility of reinnervated free LD that has been wrapped around the bladder. An innervated free-LD flap does not undergo the severe muscle fibrosis, contracture, and atrophy that occur after transfer of completely or partially denervated pedicled muscle. Apart from the restoration of deficient detrusor function, microneurovascular transfer of a free-LD flap may be combined with tissue engineering to serve as a basis for bladder augmentation and substitution.

Adolescent↗
PubMed2003

Anatomical and biomechanical mechanisms of subacromial impingement syndrome.

Subacromial impingement syndrome is the most common disorder of the shoulder, resulting in functional loss and disability in the patients that it affects. This musculoskeletal disorder affects the structures of the subacromial space, which are the tendons of the rotator cuff and the subacromial bursa. Subacromial impingement syndrome appears to result from a variety of factors. Evidence exists to support the presence of the anatomical factors of inflammation of the tendons and bursa, degeneration of the tendons, weak or dysfunctional rotator cuff musculature, weak or dysfunctional scapular musculature, posterior glenohumeral capsule tightness, postural dysfunctions of the spinal column and scapula and bony or soft tissue abnormalities of the borders of the subacromial outlet. These entities may lead to or cause dysfunctional glenohumeral and scapulothoracic movement patterns. These various mechanisms, singularly or in combination may cause subacromial impingement syndrome.

Biomechanical Phenomena↗
PubMed2001

Experimental use of the obturator internus muscle as a functioning pelvic floor muscle in dogs.

OBJECTIVE: To investigate the possibility of using the obturator internus muscle instead of the levator ani as a pelvic floor muscle. DESIGN: Experimental study. SETTING: Teaching hospital, Egypt. ANIMALS: 7 male and 3 female mongrel dogs. INTERVENTIONS: Through a para-anal incision both muscles were exposed; the levator ani was excised and the lower border of the obturator internus was mobilised and sutured to the anorectal junction, the vesical neck, and the vaginal fornix. MAIN OUTCOME MEASURES: Rectal and anal pressures and electromyographic (EMG) activity recorded before and during transposition, and 1, 3, and 6 months later. Histological examination of biopsy specimens taken from the levator ani before, and from the obturator internus before, and 3, 6, and 12 months after, transposition. RESULTS: Stimulation of the levator ani caused anal pressure to decline significantly (p < 0.05). Stimulation of the obturator internus did not change anal pressure before transposition but caused a decline after it. There was EMG activity in the levator ani at rest, but not in the obturator internus before transposition though it was evident by 6 months afterwards. Levator ani consisted of skeletal muscle fibres with smooth muscle fibres in places, whereas the obturator internus consisted of skeletal fibres alone. Six months after operation examination of the obturator internus showed the presence of some smooth muscle fibres. CONCLUSION: These results suggest that the obturator internus might be suitable both anatomically and physiologically to replace the levator ani. However, before it can be suggested as a treatment for levator dysfunction syndrome further experimental studies are necessary.

Anal Canal↗
PubMed1998

Neurophysiologic studies in peripheral arterial disease.

The purpose of the study was to compare the electrophysiological parameters (nerve conduction studies and quantitative electromyography [EMG]) between patients with chronic peripheral arterial disease (PAD) and normal control subjects. Forty patients with PAD and 30 control subjects (40 legs) were evaluated clinically and electrophysiologically using previously described methods. The amplitude of compound muscle action potentials (CMAPs) and the motor conduction velocities (MCVs) of peroneal and tibial nerve for most patients with PAD were within normal limits but compared with those of the controls, it was found that the peroneal and tibial MCVs as well as the amplitude of sural nerve were significantly decreased. The EMG testing of patients with PAD and controls of the anterior tibialis and the gastrocnemius muscle did not show evidence of denervation or myopathic abnormalities. However, the mean amplitude and duration of both muscles were significantly larger compared with the controls. Routine electrophysiological studies are not the appropriate (sensitive enough) tests for detecting peripheral nerve or muscle dysfunction associated with PAD.

Action Potentials↗
PubMed2005

A single-fibre EMG study of neuromuscular transmission in migraine patients.

It is known that mutations of CACNA1A, which encodes a neuronal P/Q Ca(2+) channel, are present in patients with familial hemiplegic migraine, and possibly in other types of migraine as well. This calcium channel is also involved in neuromuscular transmission. To assess if the single-fibre EMG (SFEMG) method can demonstrate a neuromuscular transmission deficit in migraine, a group of 26 patients with different types of migraine and 20 healthy control subjects were studied. The migraine patients were divided into three groups: 8 patients with migraine without aura (MoA), 12 with migraine with aura excluding visual aura (MA) and 6 with visual aura (VA). A SFEMG of the voluntarily activated extensor digitorum communis muscle was performed. The SFEMG results were normal in the healthy controls and the MoA group (migraine without aura). Slight neuromuscular transmission disturbances were present in 6/12 (50%) of patients with MA and in 1/6 (17%) of patients with VA. We suggest that abnormal neuromuscular transmission detectable by SFEMG may reflect a genetically determined dysfunction of the P/Q Ca(2+) channels in a subgroup of migraineurs with aura.

Adult↗
PubMed1996

Assessment of quadriceps muscle performance by hand-held, isometric, and isokinetic dynamometry in patients with knee dysfunction.

One component of patient evaluation is muscle performance assessment. The purpose of this study was: 1) to determine the difference and correlation between hand-held, isometric, and isokinetic dynamometry test results in patients with knee dysfunction and 2) to determine the effect of pain during such testing. Bilateral quadriceps strength in 23 subjects with unilateral knee dysfunction was tested using concentric and eccentric isokinetic dynamometry at 60 degrees/sec, isometric dynamometry, and hand-held dynamometry, both at 60 degrees of knee flexion. Pain ratings were obtained before, during, and after each test. Statistical analysis revealed a significant difference between involved and uninvolved limbs for eccentric isokinetic dynamometry (p = 0.002) and hand-held dynamometry (p = 0.005); no difference was found between limbs for the concentric isokinetic and isometric dynamometry (p > 0.05). Mean percent deficits in quadriceps strength ranged from 11 to 18%, with no significant difference found between testing modes. Pearson product moment correlations ranged from 0.34 to 0.76 when comparing testing modes. No significant difference existed in pain scores before, during, and after each mode of testing. It was concluded that large variation existed between different testing modes, which results in different conclusions regarding the strength of the quadriceps in patients with knee dysfunction.

Adolescent↗
PubMed1995

Cytochrome c oxidase deficiency in zidovudine myopathy affects perifascicular muscle fibres and arterial smooth muscle cells.

In order to assess the pathogenesis of myopathological alterations induced by zidovudine, we studied muscle samples from 21 patients infected by human immunodeficiency virus with zidovudine myopathy. Cytochrome c oxidase histoenzymatic reaction was evaluated in skeletal muscle fibres and arterial smooth muscle cells. Other investigations included immunocytochemistry for membrane attack complex and endomysial capillary counts. All patients had partial cytochrome c oxidase deficiency. A perifascicular distribution of cytochrome c oxidase-deficient fibres was found in 14 of 21 patients. Cytochrome c oxidase-deficient fibres were significantly more frequent in perifascicular areas than in the complete muscle sections (28% vs 12%, P < 0.001). Cytochrome c oxidase-deficient arteries were found in 11 patients, of whom 10 also had a perifascicular deficiency. Mononuclear microvascular inflammation was observed in four patients and membrane attack complex deposition in capillary walls in two patients. The capillary counts were not significantly different in the patients and in the controls. These results suggest that, in addition to a direct action of zidovudine on mitochondrial DNA, chronic muscle ischaemia related to zidovudine-induced vascular dysfunction might be implicated at the inception of muscle damage in zidovudine myopathy.

Adult↗
PubMed2003

Changing stimulation patterns improves performance during electrically elicited contractions.

The clinical efficacy of functional electrical stimulation (FES) is limited by the rapid onset of fatigue. FES applications use electrical stimuli separated by regular interpulse intervals (constant-frequency trains or CFTs) to activate muscles. However, doublet-frequency trains (DFTs) may produce greater forces than CFTs, but also produce more fatigue. DFTs contain a series of doublets, two pulses separated by a short (5-ms) interpulse interval. We hypothesized that a combination of CFTs followed by DFTs would improve performance compared to either train type alone. Quadriceps muscles of 15 normal subjects were fatigued with either 150 DFTs, or initially fatigued with CFTs until the targeted isometric force was no longer produced and then switched to DFTs. The combination reached the targeted isometric force (mean +/- SEM) more times (59.80 +/- 4.03) than either the CFTs alone (51.20 +/- 3.50) or DFTs alone (55.33 +/- 3.81). This finding suggests that combining train types may be a useful strategy to offset the rapid fatigue that persons with neurological dysfunction, such as spinal cord injury, experience when using FES.

Adult↗
PubMed1999

Dysfunction of nitric oxide mediation in isolated rat arterioles with methionine diet-induced hyperhomocysteinemia.

In humans, increased plasma homocysteine (Hcy) has been shown to be correlated with occlusive arterial diseases and atherosclerosis. Studies of isolated conductance vessels of experimental animals suggest that Hcy may interfere with local vasoregulatory mechanisms, yet the effect of hyperhomocysteinemia (HHcy) on the function of microvessels, such as skeletal muscle arterioles, has not been investigated. Male Wistar rats were divided into 2 groups: control rats (C; plasma Hcy, 7.1+/-0.3 micromol/L; n=25), and rats made HHcy by 1 g/kg body weight daily intake of methionine in the drinking water for 4 weeks (plasma Hcy, 23.6+/-2.9 micromol/L; P<0.01 versus C; n=25). First-order arterioles ( approximately 130 micrometer in diameter) were isolated from gracilis muscle, cannulated, and pressurized (80 mm Hg, no-flow conditions). Changes in diameter were observed by videomicroscopy. Arteriolar constrictions to norepinephrine (NE; 3x10(-7) mol/L) were significantly (P<0.01) greater in HHcy compared with C rats (C, 37.7+/-4.9%; HHcy, 59.5+/-5. 2%). Removal of the endothelium (-E) augmented NE-induced constrictions only in arterioles from C rats, whereas it had no effect on responses of arterioles from HHcy rats (C-E, 55.9+/-6.9%; HHcy-E, 56.5+/-7.0%). Dilations to cumulative doses of acetylcholine (ACh; 10(-8) mol/L) were significantly reduced in arterioles from HHcy rats (C, 64.0+/-5.2%; HHcy, 24.1+/-6.8%). Inhibition of nitric oxide (NO) synthesis with N(omega)-nitro-L-arginine (L-NNA; 10(-4) mol/L) significantly decreased ACh-induced dilations of C arterioles, whereas it did not affect HHcy arterioles. Similar alterations were found in arteriolar dilations to histamine, another known NO-dependent agonist. Endothelium-independent dilations to the NO donor sodium nitroprusside were not different in arterioles from C and HHcy rats, either in the presence or absence of L-NNA. Presence of superoxide dismutase and catalase (scavenger of reactive oxygen metabolites) did not affect HHcy-induced alterations in the ACh response. We conclude that hyperhomocysteinemia reduces rat skeletal muscle arteriolar dilations in response to ACh and histamine, and enhances constrictions to NE, alterations that are likely to be caused by the reduced mediation of these responses by NO. The reduced activity of NO in arterioles may contribute to the microvascular impairment described in HHcy.

Acetylcholine↗
PubMed2005

Decline in skeletal muscle mitochondrial function with aging in humans.

Cumulative mtDNA damage occurs in aging animals, and mtDNA mutations are reported to accelerate aging in mice. We determined whether aging results in increased DNA oxidative damage and reduced mtDNA abundance and mitochondrial function in skeletal muscle of human subjects. Studies performed in 146 healthy men and women aged 18-89 yr demonstrated that mtDNA and mRNA abundance and mitochondrial ATP production all declined with advancing age. Abundance of mtDNA was positively related to mitochondrial ATP production rate, which in turn, was closely associated with aerobic capacity and glucose tolerance. The content of several mitochondrial proteins was reduced in older muscles, whereas the level of the oxidative DNA lesion, 8-oxo-deoxyguanosine, was increased, supporting the oxidative damage theory of aging. These results demonstrate that age-related muscle mitochondrial dysfunction is related to reduced mtDNA and muscle functional changes that are common in the elderly.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1994

Delayed recovery of endothelium-dependent vasodilation in regenerating arterioles of skeletal muscle autografts.

This study investigated the responses of regenerating arterioles in grafted skeletal muscle to the endothelium-dependent dilator acetylcholine (ACh); the substrate for endothelium-derived relaxing factor (EDRF), L-arginine (L-Arg); and sodium nitroprusside (SNP). Additionally, responses of graft arterioles to the endothelium-independent substances adenosine (Ado) and norepinephrine (NE) were measured. The retractor muscle of hamsters was removed, placed in a myotoxic solution, and grafted into its original site. The graft revascularized spontaneously by sprouting of vessels in surrounding tissue. Quantification of changes in arteriolar luminal diameter was accomplished using in vivo video microscopy at 30, 45, and 60 days postgrafting. In 30-day grafts, there was little or no response to topically applied ACh or L-Arg. By 45 days, arteriole response to 10(-6), 10(-5), and 10(-4) M ACh and 10(-4) L-Arg was 0, 4, 20, and 17% of the control response, respectively. SNP (10(-6)-10(-4) M) produced approximately 50% of the control response at both 30 and 45 days. By 60 days the response of graft arterioles to ACh, L-Arg, and SNP was not different from controls. Arteriolar response in 30-day grafts to Ado (10(-6)-10(-4) M) was significantly attenuated, but was not different from control by 45 days. Responsiveness of arterioles to NE had recovered to control levels by 30 days postgrafting. These data indicate that the restoration of endothelium-dependent regulation of arteriolar dilation lags behind endothelium-independent, receptor-mediated mechanisms. The diminished response of regenerating arterioles may be related to dysfunctions in both the synthetic pathway for EDRF and the guanylate cyclase/cGMP mechanism for vascular smooth muscle cell relaxation and/or flow-dependent mechanisms of blood flow regulation.

Acetylcholine↗