The Role of Intracellular pH in the Control of Adenosine Output from Red Skeletal Muscle

Ballard, HJ

doi:10.1159/000109437

Cited by 5 publications

(5 citation statements)

References 15 publications

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“…These findings suggest that in human skeletal muscle, adenosine plays a very important role in the regulation of local blood flow. Similar findings have been reported for rodent muscle 11 and canine muscle 9 ; it should be noted, however, that the level of hypoxia used in the present study is mild compared with those used in various animal models. It has been suggested, in animal preparations, that other compounds interact with adenosine to mediate the vasodilation associated with hypoxia.…”

supporting

confidence: 89%

“…However, it has been shown that during systemic hypoxia, the release of adenosine from canine skeletal muscle was increased. 9 Furthermore, it has been demonstrated in rodent muscle that adenosine largely mediates the vasodilation associated with systemic hypoxia 10,11 and that this vasodilation was dependent on nitric oxide synthesis. 10 However, whether these same substances or mechanisms are responsible for the hypoxia-induced vasodilatation in human skeletal muscle is unclear.…”

mentioning

confidence: 99%

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Systemic Hypoxia Elevates Skeletal Muscle Interstitial Adenosine Levels in Humans

1998

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Background-Adenosine is a potent vasodilator that has been shown to increase in cardiac tissue in response to hypoxia.However, peripheral vasodilatation also occurs during hypoxia, and the vasoactive substance(s) responsible for skeletal muscle vasodilation have not yet been completely identified. Therefore, the purpose of this study was to measure and quantify skeletal muscle interstitial adenosine during acute systemic hypoxia. Methods and Results-Skeletal muscle interstitial adenosine concentrations were determined by the microdialysis technique, in which 4 semipermeable microdialysis probes were inserted into the vastus lateralis muscle of 6 healthy male subjects and perfused at a rate of 5 L/min with Ringer's solution. Sixty minutes after the insertion of the microdialysis probes, systemic hypoxia was induced for 30 minutes by having the subjects breathe a mixture of 10.5% O 2 in N 2 . Arterial oxygen saturation (fingertip oximeter) was lowered (PϽ0.05) from 96Ϯ0.7% to 74.9Ϯ1.4%, and forearm blood flow was increased 28%. During normoxia, the interstitial adenosine concentration was 0.44Ϯ0.08 mol/L, and it was increased to 1.03Ϯ0.

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supporting

confidence: 89%

mentioning

confidence: 99%

Systemic Hypoxia Elevates Skeletal Muscle Interstitial Adenosine Levels in Humans

1998

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“…However, studies using experimental models other than the perfused rat hindquarter have clearly demonstrated that adenosine production is markedly enhanced during both muscle contractions (Tomaniga et al 1980; Ballard et al 1987; Achike & Ballard, 1993) and hypoxia (Marshall et al 1993; Skinner & Marshall, 1996). In fact, it has been shown that muscle adenosine release is closely correlated with venous lactate concentration and pH (Ballard, 1995; Mo & Ballard, 1997). In the current experiments, venous lactate concentration was markedly elevated during both contractions and hypoxia, whereas venous pH was significantly depressed only during hypoxia.…”

Section: Discussionmentioning

confidence: 99%

Role of adenosine in regulating glucose uptake during contractions and hypoxia in rat skeletal muscle

Derave

Hespel

1999

The Journal of Physiology

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The effect of A1‐adenosine receptor antagonism via 8‐cyclopentyl‐1,3‐dipropyl‐xanthine (CPDPX) on the stimulation of skeletal muscle glucose uptake by contractions and hypoxia was investigated in isolated perfused rat hindquarters. The standard perfusate contained either no insulin or a submaximal insulin concentration at 100 μU ml−1. Muscles were stimulated to contract for 45 min by intermittent tetanic stimulation of the sciatic nerve. Hypoxia was induced by reducing perfusate haematocrit from 30% to 10% on the one hand, and by switching the gassing of the perfusate from a 35% to a 0% O2 mixture for 60 min on the other hand. The effect of contractions and hypoxia alone, or in combination, was investigated. Hypoxia‐induced muscle glucose uptake was not altered by CPDPX in the absence or presence of insulin. In contrast, contraction‐induced glucose uptake was reduced by ≈25% (P < 0.05) by exposure of muscles to CPDPX. CPDPX did not affect hindlimb glucose uptake either before or after contractions. The increment of muscle glucose uptake during hypoxia combined with contractions was greater (P < 0.05) than the effect of hypoxia alone. The current findings provide evidence that the mechanism by which hypoxia stimulates muscle glucose uptake is, at least in part, different from the mechanism of glucose uptake stimulation by contractions, because (i) A1‐adenosine receptors regulate insulin‐mediated glucose uptake in muscle during contractions but not during hypoxia and (ii) submaximal hypoxia and contractions are additive stimuli to muscle glucose uptake.

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“…Elevated extracellular adenosine is detectable in cultures of primary rat skeletal muscle fibers activated by electrical stimulation(361, 362, 562). Lactic acid and low intracellular pH both are associated with elevated release of adenosine from skeletal muscle cells (50, 51). Endothelial cells also release adenosine (207, 208).…”

Section: Training Adaptations Within the Active Muscle: Increased mentioning

confidence: 99%

Exercise Training and Peripheral Arterial Disease

Haas

Lloyd

Yang

et al. 2012

Comprehensive Physiology

121

108

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Peripheral arterial disease (PAD) is a common vascular disease that reduces blood flow capacity to the legs of patients. PAD leads to exercise intolerance that can progress in severity to greatly limit mobility, and in advanced cases leads to frank ischemia with pain at rest. It is estimated that 12–15 million people in the United States are diagnosed with PAD, with a much larger population that is undiagnosed. The presence of PAD predicts a 50–1500% increase in morbidity and mortality, depending on severity. Treatment of patients with PAD is limited to modification of cardiovascular disease risk factors, pharmacological intervention, surgery, and exercise therapy. Extended exercise programs that involve walking ~5 times/wk, at a significant intensity that requires frequent rest periods, are most significant. Pre-clinical studies and virtually all clinical trials demonstrate the benefits of exercise therapy, including: improved walking tolerance, modified inflammatory/hemostatic markers, enhanced vasoresponsiveness, adaptations within the limb (angiogenesis, arteriogenesis, mitochondrial synthesis) that enhance oxygen delivery and metabolic responses, potentially delayed progression of the disease, enhanced quality of life indices, and extended longevity. A synthesis is provided as to how these adaptations can develop in the context of our current state of knowledge and events known to be orchestrated by exercise. The benefits are so compelling that exercise prescription should be an essential option presented to patients with PAD in the absence of contraindications. Obviously, selecting for a life style pattern, that includes enhanced physical activity prior to the advance of PAD limitations, is the most desirable and beneficial.

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The Role of Intracellular pH in the Control of Adenosine Output from Red Skeletal Muscle

Cited by 5 publications

References 15 publications

Systemic Hypoxia Elevates Skeletal Muscle Interstitial Adenosine Levels in Humans

Systemic Hypoxia Elevates Skeletal Muscle Interstitial Adenosine Levels in Humans

Role of adenosine in regulating glucose uptake during contractions and hypoxia in rat skeletal muscle

Exercise Training and Peripheral Arterial Disease

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