Bioenergetic changes during contraction and recovery in diabetic rat skeletal muscle

Challiss, R. A. J.; Vranić, Mladen; Radda, George K.

doi:10.1152/ajpendo.1989.256.1.e129

Cited by 36 publications

(47 citation statements)

References 26 publications

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“…During electrical stimulation, phosphocreatine concentration falls to a greater extent in muscles of diabetic rats, and this is associated with a reduced ability to maintain submaximal force production during contractions (6). This finding is consistent with a lower oxidative enzyme capacity (15) and a reduced O 2 availability to muscle mitochondria (13).…”

supporting

confidence: 54%

“…Moreover, it is known that streptozotocin-induced diabetes in rats elicits marked skeletal muscle structural (7,19,27), hemodynamic (8,12,19), and metabolic perturbations (6,7). For instance, streptozotocin-induced diabetes causes marked muscle fiber atrophy (7,19,27), slows arteriolar vasodilation and capillary red blood cell (RBC) velocity (V RBC ) (8,12,19), and reduces citrate synthase activity (19) and pyruvate-stimulated O 2 consumption (6,11).…”

mentioning

confidence: 99%

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Dynamics of microvascular oxygen pressure during rest-contraction transition in skeletal muscle of diabetic rats

Behnke

Kindig

McDonough

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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Dynamics of microvascular oxygen pressure during rest-contraction transition in skeletal muscle of diabetic rats. Am J Physiol Heart Circ Physiol 283: H926-H932, 2002. First published May 16, 2002 10.1152/ajpheart.00059.2002.-Type I diabetes reduces dramatically the capacity of skeletal muscle to receive oxygen (Q O2). In control (C; n ϭ 6) and streptozotocininduced diabetic (D: n ϭ 6, plasma glucose ϭ 25.3 Ϯ 3.9 mmol/l and C: 8.3 Ϯ 0.5 mmol/l) rats, phosphorescence quenching was used to test the hypothesis that, in D rats, the decline in microvascular PO2 [PmO 2 , which reflects the dynamic balance between O2 utilization (V O2) and Q O2] of the spinotrapezius muscle after the onset of electrical stimulation (1 Hz) would be faster compared with that of C rats. PmO 2 data were fit with a one or two exponential process (contingent on the presence of an undershoot) with independent time delays using least-squares regression analysis. In D rats, PmO 2 at rest was lower (C: 31.2 Ϯ 3.2 mmHg; D: 24.3 Ϯ 1.3 mmHg, P Ͻ 0.05) and at the onset of contractions decreased after a shorter delay (C: 13.5 Ϯ 1.8 s; D: 7.6 Ϯ 2.1 s, P Ͻ 0.05) and with a reduced mean response time (C: 31.4 Ϯ 3.3 s; D: 23.9 Ϯ 3.1 s, P Ͻ 0.05). PmO 2 exhibited a marked undershoot of the end-stimulation response in D muscles (D: 3.3 Ϯ 1.1 mmHg, P Ͻ 0.05), which was absent in C muscles. These results indicate an altered V O2-to-Q O2 matching across the rest-exercise transition in muscles of D rats. streptozotocin diabetes; oxygen uptake kinetics; exercise intolerance; muscle oxygen delivery; phosphorescence quenching PULMONARY GAS EXCHANGE DYNAMICS (i.e., oxygen uptake, V O 2 kinetics) at exercise onset are slowed profoundly in diabetic patients (5, 23). Slowed V O 2 kinetics in response to a given metabolic challenge will mandate generation of a greater O 2 deficit and exacerbate intracellular perturbations of phosphocreatine, free ADP, and P i , for example, that accelerate glycogenolysis and utilization of finite glycogen reserves (33). This phenomenon is likely to contribute to the reduced exercise tolerance that is present in the diabetic condition.

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supporting

confidence: 54%

mentioning

confidence: 99%

Dynamics of microvascular oxygen pressure during rest-contraction transition in skeletal muscle of diabetic rats

Behnke

Kindig

McDonough

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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“…The energy metabolism of skeletal muscles was affected by a variety of factors, such as training [16], ageing [17], metabolic disorders associated with diabetes [4], global ischaemia [6] or denervation from multiple causes including trauma [5]. Diabetic patients in this study were neither athletic nor sedentary with disuse atrophy of foot muscles following immobilisation.…”

Section: Discussionmentioning

confidence: 99%

“…A combination of various factors, such as metabolic disorders associated with diabetes [4], peripheral neuropathy [5] and occlusive arterial diseases [6] possibly contribute to the impairment of energy metabolism in skeletal muscles. Ultrasonography can detect focal lesions but technical limitations hamper the global depiction due to the compact bone structure of the foot [7].…”

Section: : 165±172]mentioning

confidence: 99%

1 H- and 31 P-magnetic resonance spectroscopy and imaging as a new diagnostic tool to evaluate neuropathic foot ulcers in Type II diabetic patients

et al. 2000

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Diabetic foot ulcers are frequently severe at the plantar aspect of the first metatarsal head, and mechanical forces on the sole of the foot while standing and walking contribute to the development and progression of the wound [1,2]. Sensory neuropathy associated with loss of protective sensation allows abnormal mechanical forces to cause painless injury including skin wound and asymptomatic bone fracture [3]. Furthermore, plantar muscles play an important part in protecting the foot against these mechanical forces. Therefore, weakness or atrophy of plantar muscles may lead to diabetic foot ulcers although no study concerning abnormalities in these muscles has yet been reported. Diabetologia (2000) Abstract Aims/hypothesis. We studied 36 Type II (non-insulindependent) diabetic patients without occlusive arterial diseases in the lower extremities and 12 agematched and sex-matched non-diabetic subjects to clarify the association between diabetic polyneuropathy and foot ulcers using 1 H-and 31 P-magnetic resonance spectroscopy and imaging. Methods. The 36 diabetic patients consisted of 12 patients with superficial foot ulcers and 24 patients free from this disease. We measured fat to water and phosphocreatine to inorganic phosphate (PCr:Pi) ratios and calculated the intracellular pH of resting plantar muscles by depth-resolved surface-coil spectroscopy using an 1 H-31 P double tuned coil. Furthermore, foot vasculature, fat and PCr contents of plantar muscles were visualised by phase-contrast angiography, T 1 -weighted spin-echo imaging and 31 P-chemical shift imaging. Results. The 12 foot ulcer patients showed a reduced PCr to Pi ratio (p < 0.001) and peripheral nerve functions (p < 0.01±0.001) but an increased fat to water ratio (p < 0.001) and intracellular pH (p < 0.001) compared with the 24 patients without ulcers. From stepwise multiple regression analyses, motor nerve function as well as severity of nephropathy was associated with both fat to water and PCr to Pi ratios. When these patients were categorised into three groups based on their level of motor nerve function, the frequency of foot ulcers of the lowest group was higher than that of the highest group. Conclusion/interpretation. Our findings indicated that motor nerve dysfunction in diabetic patients was closely associated with impaired energy metabolism, fatty infiltration and increased intracellular pH of plantar muscles and high frequency of foot ulcers. These new techniques could contribute to help clarify the predisposing factors for foot ulcers. [Diabetologia (2000) 43: 165±172]

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“…Basal glucose uptake in diabetic muscle cells is reported to be lower than in non-diabetic muscle cells [32]. The higher lactate increments in the diabetic rats [22,33,34] suggest that glucose transport into the exercising muscles is normal [35]. When high levels of lactate are available, as in the diabetic rats, hepatic lactate uptake [36] and gluconeogenesis are increased [20].…”

Section: Discussionmentioning

confidence: 99%

Islet transplantation in diabetic rats normalizes basal and exercise-induced energy metabolism

et al. 1995

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Summary Transplantation of islets of Langerhans in diabetic rats normalizes resting glucose and insulin levels, but it remains unclear whether islet transplantation restores resting and exercise-induced energy metabolism. Therefore, we compared energy metabolism in islet transplanted rats with energy metabolism in normal controls and in streptozotocin-induced diabetic rats. Indirect calorimetry was applied before, during, and after moderate swimming exercise. Blood was sampled by means of a heart catheter for determination of nutrient and hormone concentrations. In islet transplanted rats, the results from indirect calorimetry and the nutrient and hormone concentrations were similar to the results in normal controls. In resting diabetic rats, insulin levels were very low, while glucose levels were exaggerated. Compared to resting controls, fat oxidation and energy expenditure were elevated, but carbohydrate oxidation was similar. Exercise increased energy expenditure and was similar in diabetic and control rats. Carbohydrate oxidation was lower and fat oxidation was higher in diabetic than in control rats. Exercise-induced increments in glucose, lactate and non-esterified fatty acid levels were the highest in diabetic rats. Thus, at rest, but not during exercise, insulin influences energy expenditure. Insulin reduces lipolysis and glycogenolysis. It enhances the relative contribution of carbohydrate oxidation and reduces fat oxidation to total energy expenditure, at rest and during exercise. Absence of insulin enhances anaerobic glycolytic pathways during exercise. It is concluded that in diabetic rats, islet transplantation of 50 % of the normal pancreatic endocrine volume successfully normalizes insulin levels and hence energy metabolism at rest and during exercise. [Diabetologia (1995) 38: 919-9261 Key words Islet transplantation, fuel oxidation, energy expenditure, glucose, non-esterified fatty acids, lactate, insulin.Poorly-treated insulin-dependent diabetes mellitus is characterized by a decrease in body weight despite an enhanced food intake. This negative energy balance is not only due to an excessive loss of glucose

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Bioenergetic changes during contraction and recovery in diabetic rat skeletal muscle

Cited by 36 publications

References 26 publications

Dynamics of microvascular oxygen pressure during rest-contraction transition in skeletal muscle of diabetic rats

Dynamics of microvascular oxygen pressure during rest-contraction transition in skeletal muscle of diabetic rats

1 H- and 31 P-magnetic resonance spectroscopy and imaging as a new diagnostic tool to evaluate neuropathic foot ulcers in Type II diabetic patients

Islet transplantation in diabetic rats normalizes basal and exercise-induced energy metabolism

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