The Experts below are selected from a list of 306 Experts worldwide ranked by ideXlab platform
Stamatis Adamopoulos - One of the best experts on this subject based on the ideXlab platform.
-
Rat skeletal Muscle Metabolism in experimental heart failure: effects of physical training
Acta Physiologica Scandinavica, 1995Co-Authors: Franois Brunotte, George K. Radda, Campbell H. Thompson, Stamatis Adamopoulos, Andrew J.s. Coats, John F. Unitt, Dc Lindsay, L. Kaklamanis, Bheeshma RajagopalanAbstract:Skeletal Muscle metabolic abnormalities exist in chronic heart failure. The influence of physical training on Muscle Metabolism after myocardial infarction was studied in a rat model. 31 P magnetic resonance spectroscopy and enzyme assays were performed in Wistar rats 12 weeks after coronary artery ligation. Infarcted rats were allocated randomly to either 6 weeks of training or non-training. Spectra were collected from the calf Muscles during sciatic nerve stimulation at 2 Hz. Fibre typing and enzymatic assays were performed on the Muscles of the contralateral non stimulated leg. Post-mortem rats were also divided into severe and moderate heart failure according to the lung weight per body weight. At 200 g twitch tension, phosphocreatine and pH were found to be significantly lower in the non-trained severe heart failure group compared with the other groups. Phosphocreatine recovery half-time was significantly longer in the non-trained group with severe heart failure and correlated with the citrate synthase activity in the Muscle. The training did not induce a change in the enzyme activities in the infarcted animals with moderate heart failure but did correct the lower citrate synthase activity in the non-trained severe heart failure animals. This normalization of Muscle Metabolism was achieved by training without any change in calf Muscle mass, making atrophy unlikely to be the sole cause of the metabolic changes in heart failure. Training in rats with severe heart failure can reverse the abnormalities of skeletal Muscle Metabolism, implicating decreased physical activity in the aetiology of these changes.
-
physical training improves skeletal Muscle Metabolism in patients with chronic heart failure
Journal of the American College of Cardiology, 1993Co-Authors: Campbell H. Thompson, Franois Brunotte, Stamatis Adamopoulos, Andrew J.s. Coats, Leonard F Arnolda, T E Meyer, Jeff F Dunn, John R StrattonAbstract:Objectives. This study investigated the effects of physical training on skeletal Muscle Metabolism in patients with chronic heart failure. Background. Skeletal Muscle metabolic abnormalities in patients with chronic heart failure have been associated with exercise intolerance. Muscle deconditioning is a possible mechanism for the intrinsic skeletal Muscle metabolic changes seen in chronic heart failure. Methods. We used phosphorus-31 nuclear magnetic resonance spectroscopy to study Muscle Metabolism during exercise in 12 patients with stable ischemic chronic heart failure undergoing 8 weeks of home-based bicycle exercise training in a randomized crossover controlled trial. Changes in Muscle pH and concentrations of phosphocreatine and adenosine diphosphate (ADP) were measured in phosphorus-31 spectra of calf Muscle obtained at rest, throughout incremental work load plantar flexion until exhaustion and during recovery from exercise. Results were compared with those in 15 age-matched control subjects who performed a single study only. Results. Before training, phosphocreatine depletion, Muscle acidification and the increase in ADP during the 1st 4 min of plantar flexion exercise were all increased (p < 0.04) compared with values in control subjects. Training produced an increase (p < 0.002) in incremental plantar flexion exercise tolerance. After training, phosphocreatine depletion and the increase in ADP during exercise were reduced significantly (p < 0.003) at all matched submaximal work loads and at peak exercise, although there was no significant change in the response of Muscle pH to exercise. After training, changes in ADP were not significantly different from those in control subjects, although phosphocreatine depletion was still greater (p < 0.05) in trained patients than in control subjects. The phosphocreatine recovery half-time was significantly (p < 0.05) shorter after training, althrough there was no significant change in the half-time of adenosine diphosphate recovery. In untrained subjects, the initial rate of phosphocreatine resynthesis after exercise (a measure of the rate of oxidative adenosine triphosphate [ATP]synthesis) and the inferred maximal rate of mitochondrial ATP synthesis were reduced compared with rates in control subjects (p < 0.003) and both were significantly increased (p < 0.05) by training, so that they were not significantly different from values in control subjects. Conclusions. The reduction in phosphocreatine depletion and in the increase in ADP during exercise, and the enhanced rate of phosphocreatine resynthesis in recovery (which is independent of Muscle mass) indicate that a substantial correction of the impaired oxidative capacity of skeletal Muscle in chronic heart failure can be achieved by exercise training.
Andrew J.s. Coats - One of the best experts on this subject based on the ideXlab platform.
-
Rat skeletal Muscle Metabolism in experimental heart failure: effects of physical training
Acta Physiologica Scandinavica, 1995Co-Authors: Franois Brunotte, George K. Radda, Campbell H. Thompson, Stamatis Adamopoulos, Andrew J.s. Coats, John F. Unitt, Dc Lindsay, L. Kaklamanis, Bheeshma RajagopalanAbstract:Skeletal Muscle metabolic abnormalities exist in chronic heart failure. The influence of physical training on Muscle Metabolism after myocardial infarction was studied in a rat model. 31 P magnetic resonance spectroscopy and enzyme assays were performed in Wistar rats 12 weeks after coronary artery ligation. Infarcted rats were allocated randomly to either 6 weeks of training or non-training. Spectra were collected from the calf Muscles during sciatic nerve stimulation at 2 Hz. Fibre typing and enzymatic assays were performed on the Muscles of the contralateral non stimulated leg. Post-mortem rats were also divided into severe and moderate heart failure according to the lung weight per body weight. At 200 g twitch tension, phosphocreatine and pH were found to be significantly lower in the non-trained severe heart failure group compared with the other groups. Phosphocreatine recovery half-time was significantly longer in the non-trained group with severe heart failure and correlated with the citrate synthase activity in the Muscle. The training did not induce a change in the enzyme activities in the infarcted animals with moderate heart failure but did correct the lower citrate synthase activity in the non-trained severe heart failure animals. This normalization of Muscle Metabolism was achieved by training without any change in calf Muscle mass, making atrophy unlikely to be the sole cause of the metabolic changes in heart failure. Training in rats with severe heart failure can reverse the abnormalities of skeletal Muscle Metabolism, implicating decreased physical activity in the aetiology of these changes.
-
physical training improves skeletal Muscle Metabolism in patients with chronic heart failure
Journal of the American College of Cardiology, 1993Co-Authors: Campbell H. Thompson, Franois Brunotte, Stamatis Adamopoulos, Andrew J.s. Coats, Leonard F Arnolda, T E Meyer, Jeff F Dunn, John R StrattonAbstract:Objectives. This study investigated the effects of physical training on skeletal Muscle Metabolism in patients with chronic heart failure. Background. Skeletal Muscle metabolic abnormalities in patients with chronic heart failure have been associated with exercise intolerance. Muscle deconditioning is a possible mechanism for the intrinsic skeletal Muscle metabolic changes seen in chronic heart failure. Methods. We used phosphorus-31 nuclear magnetic resonance spectroscopy to study Muscle Metabolism during exercise in 12 patients with stable ischemic chronic heart failure undergoing 8 weeks of home-based bicycle exercise training in a randomized crossover controlled trial. Changes in Muscle pH and concentrations of phosphocreatine and adenosine diphosphate (ADP) were measured in phosphorus-31 spectra of calf Muscle obtained at rest, throughout incremental work load plantar flexion until exhaustion and during recovery from exercise. Results were compared with those in 15 age-matched control subjects who performed a single study only. Results. Before training, phosphocreatine depletion, Muscle acidification and the increase in ADP during the 1st 4 min of plantar flexion exercise were all increased (p < 0.04) compared with values in control subjects. Training produced an increase (p < 0.002) in incremental plantar flexion exercise tolerance. After training, phosphocreatine depletion and the increase in ADP during exercise were reduced significantly (p < 0.003) at all matched submaximal work loads and at peak exercise, although there was no significant change in the response of Muscle pH to exercise. After training, changes in ADP were not significantly different from those in control subjects, although phosphocreatine depletion was still greater (p < 0.05) in trained patients than in control subjects. The phosphocreatine recovery half-time was significantly (p < 0.05) shorter after training, althrough there was no significant change in the half-time of adenosine diphosphate recovery. In untrained subjects, the initial rate of phosphocreatine resynthesis after exercise (a measure of the rate of oxidative adenosine triphosphate [ATP]synthesis) and the inferred maximal rate of mitochondrial ATP synthesis were reduced compared with rates in control subjects (p < 0.003) and both were significantly increased (p < 0.05) by training, so that they were not significantly different from values in control subjects. Conclusions. The reduction in phosphocreatine depletion and in the increase in ADP during exercise, and the enhanced rate of phosphocreatine resynthesis in recovery (which is independent of Muscle mass) indicate that a substantial correction of the impaired oxidative capacity of skeletal Muscle in chronic heart failure can be achieved by exercise training.
Campbell H. Thompson - One of the best experts on this subject based on the ideXlab platform.
-
Supplemental oxygen and Muscle Metabolism in mitochondrial myopathy patients
European Journal of Applied Physiology, 2007Co-Authors: Michael I. Trenell, Campbell H. Thompson, Graham J. KempAbstract:Patients with mitochondrial myopathy (MM) have a reduced capacity to perform exercise due to a reduced oxidative capacity. We undertook this study to determine whether skeletal Muscle Metabolism could be improved with oxygen therapy in patients with MM. Six patients with MM and six controls, matched for age, gender and physical activity, underwent 31P-magnetic resonance spectroscopy (31P-MRS) examination. 31P-MR spectra were collected at rest and in series during exercise and recovery whilst breathing normoxic (0.21 O2) or hyperoxic (1.0 O2) air. At rest, MM showed an elevated [ADP] (18 ± 3 μmol/l) and pH (7.03 ± 0.01) in comparison to the control group (12 ± 1 μmol/l, 7.01 ± 0.01) (P 0.05). Inferred maximal ATP synthesis rate improved by 33% with oxygen in MM (21 ± 3 vs. 28 ± 5 mmol/(l min), P 0.05). We conclude that oxygen therapy is associated with significant improvements in Muscle Metabolism in patients with MM. These data suggest that patients with MM could benefit from therapies which improve the provision of oxygen.
-
The effect of propionyl L-carnitine on skeletal Muscle Metabolism in renal failure.
Clinical Nephrology, 1997Co-Authors: Campbell H. Thompson, Graham J. Kemp, A. B. Irish, D. J. Taylor, George K. RaddaAbstract: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 31 P 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 (Q max ) remained below normal (28 ± 3 mM/min before and 24 ± 3 mM/min after PLC; controls 49 ± 3 mM/min). Q max correlated positively with hemoglobin concentration ([Hb]) after PLC (p 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.
-
Skeletal Muscle Metabolism before and after gemfibrozil treatment in dialysed patients with chronic renal failure
Clinical Nephrology, 1996Co-Authors: Campbell H. Thompson, Graham J. Kemp, A. B. Irish, D. J. Taylor, George K. RaddaAbstract:Patients with chronic renal failure appear at greater risk for skeletal Muscle side effects from the fibric acid group of lipid lowering agents. In order to determine whether sub-clinical defects of skeletal Muscle Metabolism can be detected in dyslipidaemic dialysis-dependent patients receiving fibrates, we studied nine patients before and after three months of gemfibrozil therapy (300-600 mg daily). Aerobic and anaerobic Metabolism of the right calf Muscle was examined at rest and during exercise using 31 P magnetic resonance spectroscopy. Near infra-red spectroscopy was used to assess skeletal Muscle re-oxygenation following ischaemic exercise of the arm. Following gemfibrozil treatment, plasma triglycerides fell significantly 3.0 ± 0.5 mM (SEM) to 1.5 ± 0.2 mM. Gemfibrozil did not affect the established metabolic defects that exist in the skeletal Muscle of the dialysed patient. Skeletal Muscle re-oxygenation was not significantly lower in renal failure and was not altered by gemfibrozil. Gemfibrozil (600 mg daily) significantly improved the lipid profile of chronic renal failure and was not associated with clinical or bioenergetic impairment of skeletal Muscle Metabolism.
-
Rat skeletal Muscle Metabolism in experimental heart failure: effects of physical training
Acta Physiologica Scandinavica, 1995Co-Authors: Franois Brunotte, George K. Radda, Campbell H. Thompson, Stamatis Adamopoulos, Andrew J.s. Coats, John F. Unitt, Dc Lindsay, L. Kaklamanis, Bheeshma RajagopalanAbstract:Skeletal Muscle metabolic abnormalities exist in chronic heart failure. The influence of physical training on Muscle Metabolism after myocardial infarction was studied in a rat model. 31 P magnetic resonance spectroscopy and enzyme assays were performed in Wistar rats 12 weeks after coronary artery ligation. Infarcted rats were allocated randomly to either 6 weeks of training or non-training. Spectra were collected from the calf Muscles during sciatic nerve stimulation at 2 Hz. Fibre typing and enzymatic assays were performed on the Muscles of the contralateral non stimulated leg. Post-mortem rats were also divided into severe and moderate heart failure according to the lung weight per body weight. At 200 g twitch tension, phosphocreatine and pH were found to be significantly lower in the non-trained severe heart failure group compared with the other groups. Phosphocreatine recovery half-time was significantly longer in the non-trained group with severe heart failure and correlated with the citrate synthase activity in the Muscle. The training did not induce a change in the enzyme activities in the infarcted animals with moderate heart failure but did correct the lower citrate synthase activity in the non-trained severe heart failure animals. This normalization of Muscle Metabolism was achieved by training without any change in calf Muscle mass, making atrophy unlikely to be the sole cause of the metabolic changes in heart failure. Training in rats with severe heart failure can reverse the abnormalities of skeletal Muscle Metabolism, implicating decreased physical activity in the aetiology of these changes.
-
Uraemic Muscle Metabolism at rest and during exercise
Nephrology Dialysis Transplantation, 1994Co-Authors: Campbell H. Thompson, Bheeshma Rajagopalan, Peter Styles, Graham J. Kemp, D. J. Taylor, P. R. J. Barnes, G. K. RaddaAbstract:The effect of chronic renal failure and the accompanying hyperphosphataemia on Muscle Metabolism at rest and during exercise was examined in a group of undialysed patients suffering from chronic renal failure. 31P magnetic resonance spectroscopy was used to measure intracellular high-energy phosphates in resting Muscle as well as changes in the concentrations of these metabolites during exercise and recovery from exercise. In resting Muscle, cell [Pi] rose with plasma [Pi], and free [ADP] changed such that the phosphorylation potential ([ATP]/([ADP] x [Pi])), which probably controls mitochondrial oxidation in resting Muscle, was preserved despite a wide variation in cell [Pi]. The maximal oxidative capacity of the Muscle was calculated from the kinetics of phosphocreatine recovery after exercise. There was no reduction in uraemic Muscle oxidative capacity compared to control Muscle. This contrasts with our finding of a reduction in the mitochondrial oxidative capacity in the Muscle of patients established on dialysis, suggesting that a substance crucial for mitochondrial function or substrate supply to mitochondria is removed by dialysis.
John R Stratton - One of the best experts on this subject based on the ideXlab platform.
-
physical training improves skeletal Muscle Metabolism in patients with chronic heart failure
Journal of the American College of Cardiology, 1993Co-Authors: Campbell H. Thompson, Franois Brunotte, Stamatis Adamopoulos, Andrew J.s. Coats, Leonard F Arnolda, T E Meyer, Jeff F Dunn, John R StrattonAbstract:Objectives. This study investigated the effects of physical training on skeletal Muscle Metabolism in patients with chronic heart failure. Background. Skeletal Muscle metabolic abnormalities in patients with chronic heart failure have been associated with exercise intolerance. Muscle deconditioning is a possible mechanism for the intrinsic skeletal Muscle metabolic changes seen in chronic heart failure. Methods. We used phosphorus-31 nuclear magnetic resonance spectroscopy to study Muscle Metabolism during exercise in 12 patients with stable ischemic chronic heart failure undergoing 8 weeks of home-based bicycle exercise training in a randomized crossover controlled trial. Changes in Muscle pH and concentrations of phosphocreatine and adenosine diphosphate (ADP) were measured in phosphorus-31 spectra of calf Muscle obtained at rest, throughout incremental work load plantar flexion until exhaustion and during recovery from exercise. Results were compared with those in 15 age-matched control subjects who performed a single study only. Results. Before training, phosphocreatine depletion, Muscle acidification and the increase in ADP during the 1st 4 min of plantar flexion exercise were all increased (p < 0.04) compared with values in control subjects. Training produced an increase (p < 0.002) in incremental plantar flexion exercise tolerance. After training, phosphocreatine depletion and the increase in ADP during exercise were reduced significantly (p < 0.003) at all matched submaximal work loads and at peak exercise, although there was no significant change in the response of Muscle pH to exercise. After training, changes in ADP were not significantly different from those in control subjects, although phosphocreatine depletion was still greater (p < 0.05) in trained patients than in control subjects. The phosphocreatine recovery half-time was significantly (p < 0.05) shorter after training, althrough there was no significant change in the half-time of adenosine diphosphate recovery. In untrained subjects, the initial rate of phosphocreatine resynthesis after exercise (a measure of the rate of oxidative adenosine triphosphate [ATP]synthesis) and the inferred maximal rate of mitochondrial ATP synthesis were reduced compared with rates in control subjects (p < 0.003) and both were significantly increased (p < 0.05) by training, so that they were not significantly different from values in control subjects. Conclusions. The reduction in phosphocreatine depletion and in the increase in ADP during exercise, and the enhanced rate of phosphocreatine resynthesis in recovery (which is independent of Muscle mass) indicate that a substantial correction of the impaired oxidative capacity of skeletal Muscle in chronic heart failure can be achieved by exercise training.
Franois Brunotte - One of the best experts on this subject based on the ideXlab platform.
-
Rat skeletal Muscle Metabolism in experimental heart failure: effects of physical training
Acta Physiologica Scandinavica, 1995Co-Authors: Franois Brunotte, George K. Radda, Campbell H. Thompson, Stamatis Adamopoulos, Andrew J.s. Coats, John F. Unitt, Dc Lindsay, L. Kaklamanis, Bheeshma RajagopalanAbstract:Skeletal Muscle metabolic abnormalities exist in chronic heart failure. The influence of physical training on Muscle Metabolism after myocardial infarction was studied in a rat model. 31 P magnetic resonance spectroscopy and enzyme assays were performed in Wistar rats 12 weeks after coronary artery ligation. Infarcted rats were allocated randomly to either 6 weeks of training or non-training. Spectra were collected from the calf Muscles during sciatic nerve stimulation at 2 Hz. Fibre typing and enzymatic assays were performed on the Muscles of the contralateral non stimulated leg. Post-mortem rats were also divided into severe and moderate heart failure according to the lung weight per body weight. At 200 g twitch tension, phosphocreatine and pH were found to be significantly lower in the non-trained severe heart failure group compared with the other groups. Phosphocreatine recovery half-time was significantly longer in the non-trained group with severe heart failure and correlated with the citrate synthase activity in the Muscle. The training did not induce a change in the enzyme activities in the infarcted animals with moderate heart failure but did correct the lower citrate synthase activity in the non-trained severe heart failure animals. This normalization of Muscle Metabolism was achieved by training without any change in calf Muscle mass, making atrophy unlikely to be the sole cause of the metabolic changes in heart failure. Training in rats with severe heart failure can reverse the abnormalities of skeletal Muscle Metabolism, implicating decreased physical activity in the aetiology of these changes.
-
physical training improves skeletal Muscle Metabolism in patients with chronic heart failure
Journal of the American College of Cardiology, 1993Co-Authors: Campbell H. Thompson, Franois Brunotte, Stamatis Adamopoulos, Andrew J.s. Coats, Leonard F Arnolda, T E Meyer, Jeff F Dunn, John R StrattonAbstract:Objectives. This study investigated the effects of physical training on skeletal Muscle Metabolism in patients with chronic heart failure. Background. Skeletal Muscle metabolic abnormalities in patients with chronic heart failure have been associated with exercise intolerance. Muscle deconditioning is a possible mechanism for the intrinsic skeletal Muscle metabolic changes seen in chronic heart failure. Methods. We used phosphorus-31 nuclear magnetic resonance spectroscopy to study Muscle Metabolism during exercise in 12 patients with stable ischemic chronic heart failure undergoing 8 weeks of home-based bicycle exercise training in a randomized crossover controlled trial. Changes in Muscle pH and concentrations of phosphocreatine and adenosine diphosphate (ADP) were measured in phosphorus-31 spectra of calf Muscle obtained at rest, throughout incremental work load plantar flexion until exhaustion and during recovery from exercise. Results were compared with those in 15 age-matched control subjects who performed a single study only. Results. Before training, phosphocreatine depletion, Muscle acidification and the increase in ADP during the 1st 4 min of plantar flexion exercise were all increased (p < 0.04) compared with values in control subjects. Training produced an increase (p < 0.002) in incremental plantar flexion exercise tolerance. After training, phosphocreatine depletion and the increase in ADP during exercise were reduced significantly (p < 0.003) at all matched submaximal work loads and at peak exercise, although there was no significant change in the response of Muscle pH to exercise. After training, changes in ADP were not significantly different from those in control subjects, although phosphocreatine depletion was still greater (p < 0.05) in trained patients than in control subjects. The phosphocreatine recovery half-time was significantly (p < 0.05) shorter after training, althrough there was no significant change in the half-time of adenosine diphosphate recovery. In untrained subjects, the initial rate of phosphocreatine resynthesis after exercise (a measure of the rate of oxidative adenosine triphosphate [ATP]synthesis) and the inferred maximal rate of mitochondrial ATP synthesis were reduced compared with rates in control subjects (p < 0.003) and both were significantly increased (p < 0.05) by training, so that they were not significantly different from values in control subjects. Conclusions. The reduction in phosphocreatine depletion and in the increase in ADP during exercise, and the enhanced rate of phosphocreatine resynthesis in recovery (which is independent of Muscle mass) indicate that a substantial correction of the impaired oxidative capacity of skeletal Muscle in chronic heart failure can be achieved by exercise training.
