Muscle blood-flow studies by the technetium (99mTc) clearance technique in normal subjects and in patients with intermittent claudication

1971 ◽  
Vol 58 (7) ◽  
pp. 532-537 ◽  
Author(s):  
C. L. Cutajar ◽  
N. J. G. Brown ◽  
Adrian Marston
Keyword(s):  
Blood Flow ◽  
Intermittent Claudication ◽  
Muscle Blood Flow ◽  
Normal Subjects ◽  
Clearance Technique

Pressure-time product, work rate, and endurance during resistive breathing in humans

1988 ◽  
Vol 64 (4) ◽  
pp. 1397-1404 ◽  
Author(s):  
D. S. Dodd ◽  
S. Kelly ◽  
P. W. Collett ◽  
L. A. Engel
Keyword(s):  
Blood Flow ◽  
Respiratory Muscle ◽  
Muscle Blood Flow ◽  
Normal Subjects ◽  
Work Rate ◽  
Available Energy ◽  
Pressure Time ◽  
Mouth Pressure ◽  
Resistive Breathing ◽  
Pressure Time Product

We examined the effect of increasing work rate, without a corresponding increase in the pressure-time product, on energy cost and inspiratory muscle endurance (Tlim) in five normal subjects during inspiratory resistive breathing. Tidal volume, mean inspiratory mouth pressure, duty cycle, and hence the pressure-time product were kept constant, whereas work rate was varied by changing the frequency of breathing. There was a linear decrease in Tlim of -2.1 ± 0.5 s.J-1.min-1 (r = 0.87 ± 0.06) with increasing work rate. The data satisfied a model of energy balance during fatiguing runs (Monod and Scherrer. Ergonomics 8: 329-337, 1965) and were consistent with the hypothesis that the rate of energy supply, or respiratory muscle blood flow, is fixed when the pressure-time product is constant. Our results indicate that during inspiratory resistive breathing against fatiguing loads, work rate determines endurance independently of the pressure-time product. On the basis of the model, our results lead to estimates of respiratory muscle blood flow and available energy stores under the conditions of our experiment.

scholarly journals Experimental Models of Chronic Lower Extremity Arterial Occlusive Disease: Lessons for Drug Development

1996 ◽  
Vol 1 (1) ◽  
pp. 43-49 ◽  
Author(s):  
CD Nicholson
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Vascular Disease ◽  
Peripheral Vascular Disease ◽  
Intermittent Claudication ◽  
Physical Training ◽  
Muscle Blood Flow ◽  
Lower Limbs ◽  
Peripheral Vascular ◽  
Vascular Insufficiency

Peripheral vascular disease is the result of chronic vascular insufficiency. As the vascular insufficiency of the lower limbs progressively deteriorates, the condition progresses from intermittent claudication (pain upon exercise) to pain at rest and gangrene. In very severe cases amputation of the leg may be necessary. Whilst dieting, cessation of smoking and physical exercise all beneficially affect the progression of the disorder, the available drug therapy is of limited benefit. Very effective pharmacological agents capable of alleviating the symptoms of chronic peripheral vascular disease have not been developed. In order to mimic the vascular insufficiency of intermittent claudication, an animal model was developed in rats. This involves short-term and long-term 6–10 weeks ligation of the femoral artery of the rat. As demonstrated using measurements of hindlimb skeletal muscle, blood flow, pO2, metabolism and function, a model of intermittent claudication was produced. Using this model, the beneficial effects of physical training was demonstrated. Physical training induced an increase in blood flow and a greater capacity for aerobic metabolism in the partially ischaemic skeletal muscle. The effect of vasodilators has also been examined in this model; in contrast to agents such as Ca2+ antagonists, K+ channel openers appear to improve nutritional blood flow and metabolism in the afflicted skeletal muscle. This model can also be utilized to demonstrate the effects of haemorrheological interventions and of agents modulating muscle metabolism. However, additional effort is required to develop models for the evaluation of efficacy of antiatherothrombotic drugs.

Does the pressor response to ischemic exercise improve blood flow to contracting muscles in humans?

1991 ◽  
Vol 71 (4) ◽  
pp. 1496-1501 ◽  
Author(s):  
M. J. Joyner
Keyword(s):  
Blood Flow ◽  
Pressor Response ◽  
Muscle Blood Flow ◽  
Normal Subjects ◽  
Arterial System ◽  
Forearm Muscles ◽  
Rhythmic Exercise ◽  
Altered Blood ◽  
Deep Vein ◽  
Improve Blood Flow

The purpose of this study was to determine in humans 1) the gain for the reflex pressor response that occurs when perfusion pressure to rhythmically contracting muscles is reduced and 2) whether the pressor response improves blood flow to the contracting muscles. Six normal subjects performed light, moderate, and heavy rhythmic forearm contractions (30/min) with the forearm enclosed in a Plexiglas box. Pressure in the box was increased 10 mmHg each minute up to 50 mmHg to reduce transmural pressure in the arterial system of the forearm. Mean arterial pressure (MAP) was measured continuously. During light exercise no reflex increase in MAP occurred until box pressure was 50 mmHg. During moderate and heavy exercise MAP began to increase with only 10- to 20-mmHg increases in box pressure. The slope of this increase was 3.5–3.9 mmHg per 10 mmHg of box pressure (approximately 60% of that in dogs). In a further study on six subjects a deep vein draining the active forearm muscles was cannulated and deep venous O2 saturation measured to assess how a 50-mmHg increase in box pressure and subsequent reflex increase in MAP altered blood flow to the contracting muscles during heavy rhythmic exercise. The increase in box pressure reduced blood flow to contracting forearm muscles by 20–25% and was followed by a 19-mmHg increase in MAP that did not appear to improve perfusion of the active muscles. This finding was unexpected, because studies in dogs suggest that the pressor response to rhythmic exercise with restricted muscle blood flow can improve perfusion of the active muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Minimal influence of blood flow on interstitial glucose and lactate-normal and insulin-resistant muscle

1998 ◽  
Vol 274 (3) ◽  
pp. E446-E452 ◽  
Author(s):  
A. Holmäng ◽  
M. Müller ◽  
O. K. Andersson ◽  
P. Lönnroth
Keyword(s):  
Blood Flow ◽  
Glucose Concentration ◽  
Muscle Blood Flow ◽  
Normal Subjects ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Insulin Resistant ◽  
Control Subjects ◽  
Femoral Muscle ◽  
Interstitial Glucose

To study the regulation of the interstitial glucose concentration in skeletal muscle, nine control subjects and nine older and overweight non-insulin-dependent diabetes mellitus (NIDDM) subjects with extreme insulin resistance were investigated with microdialysis in the medial femoral muscle before and during a euglycemic insulin clamp. After an overnight fast, arterial plasma glucose concentration was 4.9 ± 0.1 and 8.5 ± 0.6 mmol/l ( P < 0.001), respectively. The arterial-interstitial concentration ([a-i]) differences of glucose and lactate were 0.43 ± 0.16 ( P < 0.05) and −0.13 ± 0.05 mmol/l, respectively, in normal subjects. In NIDDM subjects, [a-i] differences for glucose and lactate were nonsignificant. Muscle blood flow was similar in controls and NIDDM subjects. During the glucose clamp, the glucose [a-i] differences increased and the lactate [a-i] differences decreased significantly in both groups. The glucose 170 infusion rate was 8.0 ± 0.77 vs. 3.2 ± 0.51 mg ⋅ kg−1 ⋅ min−1( P < 0.001), and blood flow was 9.9 ± 1.6 vs. 6.7 ± 0.9 ml ⋅ 100 g−1 ⋅ min−1( P < 0.05) in controls and NIDDM subjects, respectively. These results show that 1) the capillary wall is rate limiting for muscle glucose uptake and lactate release in control subjects but not in postabsorptive hyperglycemic insulin-resistant subjects, 2) vasodilation during insulin infusion does not prevent the increase in [a-i] difference of glucose in normal subjects, and 3) in severely insulin-resistant muscle, the [a-i] difference of glucose is not extended despite lack of vasodilation.

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