Oxygen uptake and blood flow in canine skeletal muscle during moderate and severe anemia

1983 ◽  
Vol 61 (2) ◽  
pp. 178-182 ◽  
Author(s):  
C. K. Chapler ◽  
S. M. Cain
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Oxygen Uptake ◽  
Oxygen Transport ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Arterial Oxygen ◽  
Acute Anemia ◽  
Moderate Anemia ◽  
The Mean

The metabolic and cardiovascular adjustments of the whole body and skeletal muscle were studied during moderate and severe acute anemia. In 15 anesthetized dogs, venous outflow from the gastrocnemius–plantaris muscle group was isolated. Cardiac output [Formula: see text], muscle blood flow [Formula: see text], total body and muscle oxygen uptake [Formula: see text] were determined during a control period, and at 30 and 60 min of either (i) moderate anemia (n = 8) in which the mean hematocrit (Hct) was 25% or (ii) progressive anemia (n = 7) in which the mean Hct values were 25% at 30 min and 16% at 60 min of anemia. Muscle [Formula: see text], [Formula: see text], and [Formula: see text] were increased in both groups at 30 min of anemia. By 60 min, [Formula: see text] and [Formula: see text] declined to preanemic control values in the moderate anemia group; whole body [Formula: see text] was maintained at the control level. Arterial oxygen transport was the same in the two groups at both 30 and 60 min of anemia despite the difference in Hct at 60 min. Muscle [Formula: see text] showed a further and similar rise in both groups between 30 and 60 min of anemia. These data show that the rise in muscle [Formula: see text] during acute anemia was not directly proportional to the degree of the hematocrit reduction. Further, the findings suggest that the muscle [Formula: see text] response was related to the decrease in arterial oxygen transport.

Neural control of glucose uptake by skeletal muscle after central administration of NMDA

1995 ◽  
Vol 268 (2) ◽  
pp. R492-R497 ◽  
Author(s):  
C. H. Lang ◽  
M. Ajmal ◽  
A. G. Baillie
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Glucose Uptake ◽  
Neural Control ◽  
Plasma Insulin ◽  
Regional Blood Flow ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Glucose Disposal ◽  
Central Administration

Intracerebroventricular injection of N-methyl-D-aspartate (NMDA) produces hyperglycemia and increases whole body glucose uptake. The purpose of the present study was to determine in rats which tissues are responsible for the elevated rate of glucose disposal. NMDA was injected intracerebroventricularly, and the glucose metabolic rate (Rg) was determined for individual tissues 20-60 min later using 2-deoxy-D-[U-14C]glucose. NMDA decreased Rg in skin, ileum, lung, and liver (30-35%) compared with time-matched control animals. In contrast, Rg in skeletal muscle and heart was increased 150-160%. This increased Rg was not due to an elevation in plasma insulin concentrations. In subsequent studies, the sciatic nerve in one leg was cut 4 h before injection of NMDA. NMDA increased Rg in the gastrocnemius (149%) and soleus (220%) in the innervated leg. However, Rg was not increased after NMDA in contralateral muscles from the denervated limb. Data from a third series of experiments indicated that the NMDA-induced increase in Rg by innervated muscle and its abolition in the denervated muscle were not due to changes in muscle blood flow. The results of the present study indicate that 1) central administration of NMDA increases whole body glucose uptake by preferentially stimulating glucose uptake by skeletal muscle, and 2) the enhanced glucose uptake by muscle is neurally mediated and independent of changes in either the plasma insulin concentration or regional blood flow.

Regulation of canine skeletal muscle and hindlimb blood flow in acute anemia

1988 ◽  
Vol 66 (1) ◽  
pp. 101-105 ◽  
Author(s):  
P. Kubes ◽  
C. K. Chapler ◽  
S. M. Cain
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Nerve Stimulation ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Sympathetic Stimulation ◽  
Arterial Blood ◽  
Measured Resistance ◽  
Muscle Groups

Redistribution of blood flow away from resting skeletal muscle does not occur during anemic hypoxia even when whole body oxygen uptake is not maintained. In the present study, the effects of sympathetic nerve stimulation on both skeletal muscle and hindlimb blood flow were studied prior to and during anemia in anesthetized, paralyzed, and ventilated dogs. In one series (skeletal muscle group, n = 8) paw blood flow was excluded by placing a tourniquet around the ankle; in a second series (hindlimb group, n = 8) no tourniquet was placed at the ankle. The distal end of the transected left sciatic nerve was stimulated to produce a maximal vasoconstrictor response for 4-min intervals at normal hematocrit (Hct.) and at 30 min of anemia (Hct. = 14%). Arterial blood pressure and hindlimb or muscle blood flow were measured; resistance and vascular hindrance were calculated. Nerve stimulation decreased blood flow (p < 0.05) in the hindlimb and muscle groups at normal Hct. Blood flow rose (p < 0.05) during anemia and was decreased (p < 0.05) in both groups during nerve stimulation. However, the blood flow values in both groups during nerve stimulation in anemic animals were greater (p < 0.05) than those at normal Hct. Hindlimb and muscle vascular resistance fell significantly during anemia and nerve stimulation produced a greater increase in vascular resistance at normal Hct. Vascular hindrance in muscle, but not hindlimb, was less during nerve stimulation in anemia than at normal Hct. The data indicate that (i) maximal sympathetic stimulation produced a significant decrease in both skeletal muscle and hindlimb blood flow during anemia, (ii) the reduction in blood flow in these areas was less with sympathetic stimulation during anemia than at normal Hct., and (iii) the anemic stimulus (Hct. = 14%) does not activate maximal sympathetic vasoconstrictor tone in the skeletal muscle.

Hydrogen ion concentration and oxygen uptake in an isolated canine hindlimb

1976 ◽  
Vol 40 (1) ◽  
pp. 1-5 ◽  
Author(s):  
A. H. Harken
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Lactate Production ◽  
Hydrogen Ion ◽  
Arterial Oxygen ◽  
Hydrogen Ion Concentration ◽  
Membrane Lung ◽  
Arterial Blood ◽  
The Mean

Oxygen utilization (VO2) and lactate production by an isolated perfused canine hindlimb was evaluated at various hydrogen ion concentrations. A membrane lung perfusion system was established such that blood flow and temperature could be fixed at normal levels. Oxygen, nitrogen, and carbon dioxide (CO2) gas flows to the membrane lung were independently regulated to provide a fixed arterial oxygen content (CaO2). By changing CO2 flow, the pH of the arterial blood was varied between 6.9 and 7.6 at 10-min intervals. The mean O2 delivery (CaO2 X blood flow) was between 16.3 ML O2/min and 20.5 ml O2/min. Standard error of the mean in each dog, however, was less than 0.4 ml O2/min. VO2 was linearly related to the pH of the perfusing blood: VO2% = 100.1 pH - 643 (r = 0.866). Oxygen consumption was inversely related to PCO2: VO2% = -0.62 PCO2 + 124, but the correlation was less good (r = 0.729). Lactate production was linearly related to the pH of the perfusing blood (above a pH of 7.4): lactate produced = 22.5 pH - 162.5 (r = 0.75). At a pH below 7.4, lactate was not produced. Oxygen consumption of skeletal muscle appears critically dependent on extracellular fluid pH. A change in pH of 0.1 alters VO2 almost exactly 10%. Alkalosis is a potent stimulus to lactic acid production by skeletal muscle.

scholarly journals Local, but not indirect whole body heating, increases human skeletal muscle blood flow

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Illka Heinonen ◽  
R. Matthew Brothers ◽  
Jukka Kemppainen ◽  
Juhani Knuuti ◽  
Kari K. Kalliokoski ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Human Skeletal Muscle ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Skeletal Muscle Blood Flow

Glucose-Induced Thermogenesis in Splanchnic and Leg Tissues in Man

1995 ◽  
Vol 88 (5) ◽  
pp. 543-550 ◽  
Author(s):  
Lene Simonsen ◽  
Camilla Ryge ◽  
Jens Bülow
Keyword(s):  
Carbon Dioxide ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Oxygen Uptake ◽  
Tap Water ◽  
Whole Body ◽  
Constant Infusion ◽  
Initial Increase ◽  
Glucose Intake ◽  
Splanchnic Oxygen

1. Fourteen healthy subjects were investigated before and for 4 hours after oral intake of 75 g of glucose (n = 8) or tap water (n = 6). Whole-body energy expenditure was measured by an open-circuit ventilated hood system. Blood samples for determination of oxygen, carbon dioxide, glucose and lactate were taken from an artery, a hepatic vein and a femoral vein. Blood flow in the splanchnic region was measured by constant infusion of Indocyanine Green. Leg blood flow was measured by venous occlusion strain-gauge plethysmography. Oxygen uptake and carbon dioxide output in the splanchnic and leg tissues were calculated as the product of blood flow and arteriovenous differences in oxygen or carbon dioxide concentrations. Net exchanges of glucose and lactate across the splanchnic and leg tissues were calculated as the product of blood flow and arteriovenous differences in whole-blood glucose or lactate concentrations. 2. Splanchnic oxygen uptake had a biphasic course with an initial increase from 2.35 ± 0.88 (SD) mmol/min to 2.85 ± 1.20 mmol/min 30 min after the glucose intake (P < 0.005) and a later decrease below the basal value to around 2.02 mmol/min 90–180 min after the glucose intake (P < 0.05). The integrated increase in the splanchnic oxygen uptake during the 4 h after the glucose intake was −32.6 ± 49.7 mmol/240 min. Leg oxygen uptake increased from 4.3 ± 1.4 μmol min−1 100 g−1 to 7.0 ± 3.2 μmol min−1 100 g−1 90 min after the glucose intake (P < 0.01). The integrated increase in leg oxygen uptake was 305.1 ± 394.3 μmol 240 min−1 100 g−1. Assuming leg oxygen uptake mainly represents average skeletal muscle, the skeletal muscle mass can explain around 45% of the whole-body glucose-induced thermogenesis. 3. It is concluded that the splanchnic tissues do not contribute to the integrated glucose-induced thermogenesis owing to a biphasic response in oxygen uptake, with an initial increase and a later decrease. Measurements across a leg give the same information as measurements across a forearm with respect to estimation of glucose-induced thermogenesis in skeletal muscle.

Muscle Blood Flow and Mitochondrial Function: Influence of Aging

2002 ◽  
Vol 12 (3) ◽  
pp. 368-378 ◽  
Author(s):  
Ronald L. Terjung ◽  
Ryszard Zarzeczny ◽  
H.T. Yang
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Exercise Training ◽  
Muscle Blood Flow ◽  
The Elderly ◽  
Exchange Capacity ◽  
Oxygen Exchange ◽  
Whole Body ◽  
Tissue Blood Flow ◽  
Fiber Types

Skeletal muscle mitochondrial capacity (mito), tissue blood flow (BF) capacity, and oxygen exchange capacity (e.g., DO2) appear to be well matched. The different skeletal muscle fiber types and muscle remodeled, due to inactivity >(e.g., related to aging or disease) or exercise training, exhibit widely differing aerobics capacities (V̇O2max). Yet, there are remarkably coordinated alterations in these 3 parameters in each of these conditions. With such a balance, there is likely shared control among these parameters in limiting (V̇O2max) of muscle, although this is a matter of considerable debate. The reduction in aerobic capacity in elderly can be improved by submaximal aerobic exercise training; this is related to increases in muscle mitochondria concentration and capillarity, but probably not BF capacity, as this is limited by central cardiovascular function. Thus, exercise-induced biochemical adaptations and angiogenesis occur in the elderly. The increase in muscle capillarity likely contributes to the increased oxygen exchange capacity, typical of endurance type training. The increase in [mito] appears essential to realize the increased in muscle V̇O2max with training and amplifies the rate-limiting influence of the muscle’s oxygen exchange capacity. Further, vascular remodeling induced by exercise in the elderly could be effective at improving flow capacity, if limited by peripheral obstruction. Thus, the limits to aerobic function specific to aged muscle appear most influenced by inactivity, whereas central cardiovascular changes impact whole body performance. Some may consider the aged myocyte as a small, inactive, normal myocyte in need of activity!

scholarly journals Local heating, but not indirect whole body heating, increases human skeletal muscle blood flow

2011 ◽  
Vol 111 (3) ◽  
pp. 818-824 ◽  
Author(s):  
Ilkka Heinonen ◽  
R. Matthew Brothers ◽  
Jukka Kemppainen ◽  
Juhani Knuuti ◽  
Kari K. Kalliokoski ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Heat Stress ◽  
Local Heating ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Skeletal Muscle Blood Flow ◽  
Whole Body Heat Stress ◽  
Body Heat ◽  
Indirect Heating

For decades it was believed that direct and indirect heating (the latter of which elevates blood and core temperatures without directly heating the area being evaluated) increases skin but not skeletal muscle blood flow. Recent results, however, suggest that passive heating of the leg may increase muscle blood flow. Using the technique of positron-emission tomography, the present study tested the hypothesis that both direct and indirect heating increases muscle blood flow. Calf muscle and skin blood flows were evaluated from eight subjects during normothermic baseline, during local heating of the right calf [only the right calf was exposed to the heating source (water-perfused suit)], and during indirect whole body heat stress in which the left calf was not exposed to the heating source. Local heating increased intramuscular temperature of the right calf from 33.4 ± 1.0°C to 37.4 ± 0.8°C, without changing intestinal temperature. This stimulus increased muscle blood flow from 1.4 ± 0.5 to 2.3 ± 1.2 ml·100 g−1·min−1 ( P < 0.05), whereas skin blood flow under the heating source increased from 0.7 ± 0.3 to 5.5 ± 1.5 ml·100 g−1·min−1 ( P < 0.01). While whole body heat stress increased intestinal temperature by ∼1°C, muscle blood flow in the calf that was not directly exposed to the water-perfused suit (i.e., indirect heating) did not increase during the whole body heat stress (normothermia: 1.6 ± 0.5 ml·100 g−1·min−1; heat stress: 1.7 ± 0.3 ml·100 g−1·min−1; P = 0.87). Whole body heating, however, reflexively increased calf skin blood flow (to 4.0 ± 1.5 ml·100 g−1·min−1) in the area not exposed to the water-perfused suit. These data show that local, but not indirect, heating increases calf skeletal muscle blood flow in humans. These results have important implications toward the reconsideration of previously accepted blood flow distribution during whole body heat stress.

Hindlimb vascular responses to sympathetic augmentation during acute anemia

1985 ◽  
Vol 63 (7) ◽  
pp. 782-786 ◽  
Author(s):  
Stephen M. Cain ◽  
C. K. Chapler
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Sympathetic Activity ◽  
Carotid Arteries ◽  
Muscle Blood Flow ◽  
Recovery Period ◽  
Control Period ◽  
Whole Body ◽  
Block Group ◽  
Limb Blood Flow

The effect of increased sympathetic activity on skeletal muscle blood flow during acute anemic hypoxia was studied in 16 anesthetized dogs. Sympathetic activity was altered by clamping the carotid arteries bilaterally below the carotid sinus. One group (n = 8) was beta blocked by administration of propranolol (1 mg/kg); a second group (n = 8) was untreated. Venous outflow from the left hindlimb was isolated for measurement of blood flow and O2 uptake [Formula: see text]. After a 20-min control period, both carotid arteries were clamped (CC) for 20 min followed by a 20-min recovery period. The sequence was repeated after hematocrit was lowered to about 15% by dextran exchange for blood. Prior to anemia, CC did not alter cardiac output or limb blood flow in either group. After induction of anemia, hindlimb resistance was higher with CC in the beta block than in the no block group. Both limb blood flow and [Formula: see text] fell in the β-block group with CC during anemia. Beta block also prevented the additive increases in whole body [Formula: see text] seen with CC and induction of anemia. The data showed that the increased vasoconstrictor tone that was obtained with beta block during anemia was successful in redistributing the lower viscosity blood away from resting skeletal muscle, even to the point that muscle [Formula: see text] was decreased.

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