Effects of treadmill exercise on fuel metabolism in hepatic cirrhosis

DeLissio, M.; Goodyear, Laurie J.; Fuller, Susan P.; Krawitt, Edward L.; Devlin, John T.

doi:10.1152/jappl.1991.70.1.210

Cited by 36 publications

(25 citation statements)

References 14 publications

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“…If glycogen availfurther indirect evidence for hepatic catecholamine resisability in our patients was indeed diminished, the rate of tance in cirrhosis. 14 In contrast to the failure of epinephrine gluconeogenesis must have been reciprocally elevated, because their total hepatic output was normal. To our knowledge, direct measurement of gluconeogenesis in cirrhotic pa- attributing almost 70% of net hepatic glucose release to gluco-increase in hepatic glucose production occurred.…”

Section: Discussionmentioning

confidence: 99%

Effects of epinephrine on glucose metabolism in patients with alcoholic cirrhosis

Schricker¹,

Albuszies²,

Weidenbach³

et al. 1996

Hepatology

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liver has also been demonstrated to be resistant to the action The cirrhotic liver has been shown to be resistant to of glucagon, making cirrhotic patients especially vulnerable the actions of various glucoregulatory hormones. The to hyper-and hypoglycemia. 3 Although the metabolic effects objective of this study was to investigate the effects of of several glucoregulatory hormones have been widely studepinephrine on hepatic glucose metabolism in cirrhotic ied in liver disease, few studies have addressed the influence patients. Thirteen cirrhotic and eight healthy subjects of epinephrine on hepatic glucose metabolism in cirrhosis. 4 were studied. Hepatic glucose production and turnover Thus, the current study was undertaken to investigate the of alanine and glycerol were measured using stable isoeffects of epinephrine on hepatic glucose production in patope technique before and during 70 and 150 minutes of tients with alcoholic cirrhosis. epinephrine infusion (0.1 mg/kg/min). b-Adrenoreceptor binding sites and affinity in mononuclear leukocyte PATIENTS AND METHODS membranes also were determined. Hepatic glucose production and alanine turnover in normals significantlyWith the approval of the local ethics committee, 8 healthy volunincreased during epinephrine infusion, but did not teers and 13 cirrhotic patients were admitted to the study. The inveschange in cirrhotics. Glycerol turnover increased after tigation was conducted according to the principles established in 70 minutes of epinephrine infusion in both groups. Epi-Helsinki. All participants were instructed of the purpose and risks of the study and gave their written informed consent. nephrine induced a significant rise of high-affinity b-The volunteers were healthy men with normal body composition adrenoreceptor binding sites in normals, yielding a sig-(age, 26 { 1 years; height, 182 { 2 cm; weight, 76 { 2 kg). Medical nificant correlation between hepatic glucose production history and physical examination of the subjects revealed no pathoand receptor density (r Å .94, P õ .0001). In cirrhotic logical findings. No volunteer had a family history of diabetes mellipatients, similar changes in the number of high-affinity tus or used any medication. The subjects were asked to consume a b-adrenoreceptors were observed, but no correlation diet comparable with a standardized hospital diet and not to consume with hepatic glucose production was detected. The cir-any alcohol-or caffeine-containing beverages 3 days prior to the rhotic liver did not respond normally to the stimulatory study. effect of epinephrine on hepatic glucose production. BeAll patients were men, and cirrhosis was of alcoholic origin. The clinical condition of each patient was classified as Child B, i.e., Childcause this blunted response was not related to changes Table 1. All patients had endoscopically proven esophageal varices and were hospitalized for gastroesophageal variceal hemorrhages secondary to hepatic cirrhosis and portal hypertension. All patients The liver plays a pivotal role in p...

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Section: Discussionmentioning

confidence: 99%

Effects of epinephrine on glucose metabolism in patients with alcoholic cirrhosis

Schricker¹,

Albuszies²,

Weidenbach³

et al. 1996

Hepatology

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“…In cirrhotic patients isokinetic muscle strength and work capacity have been found to be severely reduced. [1][2][3][4][5][6] Fatigue and loss of muscle strength can be related to both central and peripheral phenomena. [7][8][9] The central components are largely unknown, but probably include psychologic factors such as the mental condition and motivation of the person, as well as metabolic disturbances, e.g., hypoglycemia, hyperammoniemia, and changes in amino acid composition.…”

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confidence: 99%

Reduced mitochondrial adenosine triphosphate synthesis in skeletal muscle in patients with child-pugh class B and C cirrhosis

et al. 2001

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Patients with cirrhosis of the liver often complain of tiredness and a lack of strength at physical exercise. Other investigators have found that muscle strength, work capacity, and maximal oxygen consumption are reduced in cirrhosis. We hypothesized that mitochondrial maximal rate of ATP synthesis in skeletal muscle may be impaired in these patients. This was tested with 31 P nuclear magnetic resonance spectroscopy in anterior tibial muscle of cirrhotic patients and healthy controls at rest, during exercise, and subsequent recovery. In patients with Child-Pugh class B and C cirrhosis resting PCr/P i ratio (8.3 ؎ 1.0; n ‫؍‬ 7) was lower than in patients with Child-Pugh class A cirrhosis (12.1 ؎ 2.1; n ‫؍‬ 7) and controls (11. 7 ؎ 1.1; n ‫؍‬ 6; P ‫؍‬ .03), while the resting P i /␥ATP ratio was higher in Child-Pugh class B and C patients (0.43, 0.30, and 0.27, respectively; P ‫؍‬ .03). Maximal rate of mitochondrial adenosine triphosphate ( Patients with cirrhosis often complain of tiredness and weakness at physical exercise. In cirrhotic patients isokinetic muscle strength and work capacity have been found to be severely reduced. [1][2][3][4][5][6] Fatigue and loss of muscle strength can be related to both central and peripheral phenomena. 7-9 The central components are largely unknown, but probably include psychologic factors such as the mental condition and motivation of the person, as well as metabolic disturbances, e.g., hypoglycemia, hyperammoniemia, and changes in amino acid composition. 9 In cirrhosis the peripheral components possibly include decreased skeletal muscle mass, hemodynamic changes, decreased hepatic glycogenolysis, and insulin resistance. 10 There may, however, also be more fundamental metabolic changes such as impaired mitochondrial function. It appears that in cirrhosis maximal oxygen consumption is decreased, 2,3 which at least to some extent is a result of the decreased muscle mass in the cirrhotic patients, but which may also be the result of decreased mitochondrial oxidative capacity and/or reduced number of mitochondria in the muscle tissue. In accordance with this notion the content of adenosine triphosphate (ATP), phosphocreatine (PCr), and total Mg 2ϩ were reported to be decreased in biopsy specimens of skeletal muscle in patients with cirrhosis. 11-13 A reduced ATP/ ADP ratio was also found. 11,12 In contrast to the static data available after biopsy the technique of 31 P nuclear magnetic resonance spectroscopy (NMRS) allows a dynamic examination of the relative concentrations of ATP, PCr, and inorganic phosphorus (P i ) at rest, during, and after exercise. We used this technique to study the hypothesis that mitochondrial capacity for ATP synthesis is reduced in the skeletal muscle of the cirrhotic patient. The study indicated that this was indeed the case for patients with cirrhosis of Child-Pugh class B and C. PATIENTS AND METHODSThe study included 14 patients with stable cirrhosis of the liver. Clinical data are shown in Table 1. The controls were 6 healthy individuals with simil...

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“…The exercise capacity of subjects with hepatic cirrhosis was assessed using oxygen consumption on maximum cardiopulmonary tests on fifteen different articles (21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35). These studies are described on table 1.…”

Section: Methodsmentioning

confidence: 99%

“…These studies are described on table 1. In only two studies (21,23) oxygen maximum consumption (VO 2max ) was tested. In most studies, authors used peak of VO 2 (VO 2peak ), which considers the maximum value achieved in an exhaustion moment.…”

Section: Methodsmentioning

confidence: 99%

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The influence that hepatic cirrhosis provides in exercise capacity and muscle strength: a review

2015

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Introduction: Hepatic cirrhosis leads to a series of physiological changes, among which stand out cardiorespiratory and muscle impairments. These changes determine a negative impact on quality of life and may cause physical inactivity. Objective: The objective of this study was to review, in the most current scientific literature, the influence that hepatic cirrhosis provides in exercise capacity and muscle strength, and the effect of exercise when applied to this situation. Materials and methods: For this review, research on original studies was carried out on Medical Literature Analysis and Retrieval System Online (assessed by PubMed), Scopus and Web of Science between the years 1990 to 2015. In order to be included, studies had to meet the following criteria: a) be from original articles; b) evaluate exercise capacity or muscle strength; and c) provide relevant results. Results and Discussion: The majority of studies concluded that the exercise capacity and muscle strength are decreased in individuals with cirrhosis when compared to control subjects.

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Effects of treadmill exercise on fuel metabolism in hepatic cirrhosis

Cited by 36 publications

References 14 publications

Effects of epinephrine on glucose metabolism in patients with alcoholic cirrhosis

Effects of epinephrine on glucose metabolism in patients with alcoholic cirrhosis

Reduced mitochondrial adenosine triphosphate synthesis in skeletal muscle in patients with child-pugh class B and C cirrhosis

The influence that hepatic cirrhosis provides in exercise capacity and muscle strength: a review

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