Interaction of hyperoxia and blood flow during fatigue of canine skeletal muscle in situ

1979 ◽  
Vol 47 (5) ◽  
pp. 1018-1024 ◽  
Author(s):  
J. K. Barclay ◽  
C. M. Boulianne ◽  
B. A. Wilson ◽  
S. J. Tiffin

Right and left gastrocnemius-plantaris muscle preparations in 20 dogs anesthetized with pentobarbital sodium were used to investigate the effect of hyperoxia on tension maintenance. Muscles were stimulated via the sciatic nerve for 20 min at 60 200-ms tetanic contractions/min (10 impulses/contraction). Direct muscle stimulation after the experimental period resulted in no significant change in tension. In control experiments the tension developed by the right or left muscles over the 20 min was not different. The tension developed by muscles perfused with hyperoxic blood decreased 14% after 20 min, whereas tension in the normoxic muscles decreased 35%. Blood flow in the hyperoxic muscles was significantly higher at 20 min (P less than 0.05). Pump perfusion of one of a pair of normoxic muscles resulted in a tension decrease of 13% in the pump-perfused muscles, whereas tension in the control muscles decreased 34%. Tension maintenance was flow dependent. The effect of hyperoxia could be mediated through the involvement of oxygen in the long-term control of muscle blood flow.

2004 ◽  
Vol 97 (2) ◽  
pp. 764-772 ◽  
Author(s):  
Jefferson C. Frisbee

The present study tested the hypothesis that enhanced vascular α-adrenergic constriction in obese Zucker rats (OZR) impairs arteriolar dilation and perfusion of skeletal muscle at rest and with increased metabolic demand. In lean Zucker rats (LZR) and OZR, isolated gracilis arterioles were viewed via television microscopy, and the contralateral cremaster muscle or gastrocnemius muscle was prepared for study in situ. Gracilis and cremasteric arterioles were challenged with dilator stimuli under control conditions and after blockade of α-adrenoreceptors with prazosin, phentolamine, or yohimbine. Gastrocnemius muscles performed isometric twitch contractions of increasing frequency, and perfusion was continuously monitored. In OZR, dilator responses of arterioles to hypoxia (gracilis), wall shear rate (cremaster), acetylcholine, and iloprost (both) were impaired vs. LZR. Treatment with prazosin and phentolamine (and in cremasteric arterioles only, yohimbine) improved arteriolar reactivity to these stimuli in OZR, although responses remained impaired vs. LZR. Gastrocnemius muscle blood flow was reduced at rest in OZR; this was corrected with intravenous infusion of phentolamine or prazosin. At all contraction frequencies, blood flow was reduced in OZR vs. LZR; this was improved by infusion of phentolamine or prazosin at low-moderate metabolic demand only (1 and 3 Hz). At 5 Hz, adrenoreceptor blockade did not alter blood flow in OZR from levels in untreated rats. These results suggest that enhanced α-adrenergic constriction of arterioles of OZR contributes to impaired dilator responses and reduced muscle blood flow at rest and with mild-moderate (although not with large) elevations in metabolic demand.


1995 ◽  
Vol 269 (2) ◽  
pp. H717-H724 ◽  
Author(s):  
T. H. Adair ◽  
J. Hang ◽  
M. L. Wells ◽  
F. D. Magee ◽  
J. P. Montani

We tested whether chronic stimulation of skeletal muscle can increase the growth of paired arteries and veins in rabbit extensor digitorum longus muscle (EDL). The right EDL of female New Zealand White rabbits was stimulated via the common peroneal nerve at 10 Hz using 300 microseconds square waves at 3-4 V. Two-hour periods of stimulation was alternated with 4-h periods of rest, 7 days/wk for approximately 60 days. The left EDL served as control. The hindlimb vascular system was maximally dilated and perfuse-fixed with 3% glutaraldehyde and 2% paraformaldehyde at arterial and venous pressures of 80-100 and 15-20 mmHg, respectively. Muscles were postfixed in OsO4 and embedded in EPOX 812 resin. One millimeter-thick transverse sections were cut at uniform locations through the entire breadth of the muscle and analyzed using videomicroscopy along with computerized morphometric and stereological techniques. All paired arteries and veins on each full muscle section were analyzed. Chronic muscle stimulation caused the wall volume of paired arteries and veins to increase by an average of approximately twofold and the lumen volume to increase by an average of approximately threefold compared with the contralateral muscles. The wall-to-lumen area ratio of the arteries and veins was not affected. Muscle stimulation also caused the numerical density of arteries having a diameter > 100 microns to increase by approximately fourfold and the density of veins having a perimeter > 500 microns to increase by approximately 10-fold.(ABSTRACT TRUNCATED AT 250 WORDS)


2005 ◽  
Vol 98 (2) ◽  
pp. 753-761 ◽  
Author(s):  
R. M. McAllister ◽  
J. L. Jasperse ◽  
M. H. Laughlin

Endurance exercise training (Ex) has been shown to increase maximal skeletal muscle blood flow. The purpose of this study was to test the hypothesis that increased endothelium-dependent vasodilation is associated with the Ex-induced increase in muscle blood flow. Furthermore, we hypothesized that enhanced endothelium-dependent dilation is confined to vessels in high-oxidative muscles that are recruited during Ex. To test these hypotheses, sedentary (Sed) and rats that underwent Ex (30 m/min × 10% grade, 60 min/day, 5 days/wk, 8–12 wk) were studied using three experimental approaches. Training effectiveness was evidenced by increased citrate synthase activity in soleus and vastus lateralis (red section) muscles ( P < 0.05). Vasodilatory responses to the endothelium-dependent agent acetylcholine (ACh) in situ tended to be augmented by training in the red section of gastrocnemius muscle (RG; Sed: control, 0.69 ± 0.12; ACh, 1.25 ± 0.15; Ex: control, 0.86 ± 0.17; ACh, 1.76 ± 0.27 ml·min−1·100 g−1·mmHg−1; 0.05 < P < 0.10 for Ex vs. Sed during ACh). Responses to ACh in situ did not differ between Sed and Ex for either the soleus muscle or white section of gastrocnemius muscle (WG). Dilatory responses of second-order arterioles from the RG in vitro to flow (4–8 μl/min) and sodium nitroprusside (SNP; 10−7 through10−4 M), but not ACh, were augmented in Ex (vs. Sed; P < 0.05). Dilatory responses to ACh, flow, and SNP of arterioles from soleus and WG muscles did not differ between Sed and Ex. Content of the endothelial isoform of nitric oxide synthase (eNOS) was increased in second-order, fourth-order, and fifth-order arterioles from the RG of Ex; eNOS content was similar between Sed and Ex in vessels from the soleus and WG muscles. These findings indicate that Ex induces endothelial adaptations in fast-twitch, oxidative, glycolytic skeletal muscle. These adaptations may contribute to enhanced skeletal muscle blood flow in endurance-trained individuals.


2002 ◽  
Vol 92 (2) ◽  
pp. 461-468 ◽  
Author(s):  
Cheryl E. King-VanVlack ◽  
J. D. Mewburn ◽  
C. K. Chapler ◽  
P. H. MacDonald

In the present study, we determined whether endothelin (ET)-1 contributed to the observed reduction in muscle blood flow (Q˙) during contractions with nitric oxide synthase (NOS) inhibition and whether muscle O2 uptake (V˙o 2) would be affected by the decrease in muscle Q˙ with NOS inhibition at different contraction intensities. Muscle Q˙,V˙o 2, O2 extraction ratio (OER), and tension development (TD) were studied in the in situ gastrocnemius muscle preparation in anesthetized dogs. A decrease in the V˙o 2-to-TD ratio (V˙o 2/TD) was used as an indicator of O2 limitation. Three contraction protocols were used: 1) isometric twitch contractions at 2 twitches (tw)/s, 2) the same contractions at 4 tw/s, and 3) pretreatment with an ETA-receptor antagonist (BQ-123) before 2 tw/s contractions. The muscle was stimulated to contract, and measures were obtained at steady state (∼5–8 min). NOS inhibition ( N ω-nitro-l-arginine methyl ester) was then induced, and measures were repeated at 2, 5, 10, and 15 min. During 2 tw/s contractions, NOS inhibition reduced Q˙with and without ETA-receptor blockade. In both groups, OER increased in response to the fall in Q˙, with the result being no change in V˙o 2/TD. NOS inhibition also decreased Q˙ during 4 tw/s contractions, but OER did not increase, resulting in a reduction inV˙o 2/TD 5 and 15 min after N ω-nitro-l-arginine methyl ester. These data indicated that 1) a reciprocal increase in ET-1 during NOS inhibition does not influence active hyperemia in skeletal muscle, and 2) during 4 tw/s contractions, the ischemia with NOS inhibition was associated with either an O2 limitation or an alteration in the efficiency of muscle contractions.


1984 ◽  
Vol 247 (5) ◽  
pp. H869-H873
Author(s):  
G. J. Crystal ◽  
H. F. Downey ◽  
F. A. Bashour

Active and reactive hyperemias have been observed in the skeletal muscle circulation tachyphylactic to exogenous adenosine following 3-h supramaximal doses of the vasodilator. These findings failed to support a need for adenosine in metabolic control of skeletal muscle blood flow. The present study was conducted to determine if the coronary circulation also develops tachyphylaxis to adenosine while remaining sensitive to other metabolically linked vasodilator mechanisms. Experiments were conducted in eight pentobarbital-anesthetized, open-chest dogs whose blood flow in the left anterior descending coronary artery (LAD) was measured electromagnetically during 3-h infusion of adenosine into the LAD. Measurements of regional myocardial blood flow (radioactive microspheres), myocardial O2 consumption (Fick principle), and percent segment shortening (ultrasonic crystals) were also obtained. Adenosine was infused into the LAD at a rate of 27.0-72.0 mumol/min, depending on blood flow rate. Calculated concentration of adenosine in LAD blood averaged 0.484 +/- 0.111 mumol/ml, which was well in excess of that required for maximal coronary vasodilation. LAD blood flow averaged 21.5 +/- 2.2 ml/min during the preadenosine control condition. LAD blood flow after 3 h adenosine (123.3 +/- 23.0 ml/min) was not significantly different from that after 1-3 min adenosine (105.8 +/- 17.9 ml/min). There was no significant transmural variation in LAD blood flow during adenosine infusion. Adenosine had no significant effect on myocardial O2 consumption or percent segment shortening. Our results demonstrate persistent transmural vasodilation in the canine coronary circulation during long-term, supramaximal doses of adenosine and are consistent with a role for endogenous adenosine in maintenance of coronary vasodilation during sustained elevations in myocardial energy demands.


1983 ◽  
Vol 55 (3) ◽  
pp. 976-982 ◽  
Author(s):  
B. R. MacIntosh ◽  
W. N. Stainsby ◽  
L. B. Gladden

The purpose of this study was to investigate the contractile response of skeletal muscle in situ when stimulation results in an unfused tetanic contraction. The left gastrocnemius-plantaris muscle group of anesthetized (pentobarbital sodium) dogs (n = 16) was connected to an isometric lever and stimulated indirectly for 30 min. During 10-Hz stimulation, total tension (the peak of each oscillation in tension) increased during the first 2 min of stimulation (staircase), then decreased during the remaining 28 min of stimulation. Since relaxation was incomplete at this rate of stimulation, the developed tension, the difference between peak tension and the lowest tension between successive contractions, did not follow the same pattern of staircase and fatigue as the peak tension did. Developed tension (delta T) decreased during the staircase response then increased from 2 to 10 min before finally decreasing again during the last 20 min, ending at 56 +/- 15 (mean +/- SE) % of the initial (first contraction) delta T. At 2 min of 10-Hz contractions, half-relaxation time (1/2 RT) was too long to measure (insufficient relaxation between contractions), but later, 1/2 RT decreased from greater than 65 ms to less than 40 ms. Increased 1/2 RT has been associated with reduced energy availability. If an increased 1/2 RT is an indication of insufficient energy, then it can be concluded that fatigue continued in spite of a recovery of energy supplies. This suggests a possible dissociation of fatigue and energy availability.


1995 ◽  
Vol 268 (2) ◽  
pp. R492-R497 ◽  
Author(s):  
C. H. Lang ◽  
M. Ajmal ◽  
A. G. Baillie

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.


1990 ◽  
Vol 69 (3) ◽  
pp. 830-836 ◽  
Author(s):  
M. C. Hogan ◽  
D. E. Bebout ◽  
A. T. Gray ◽  
P. D. Wagner ◽  
J. B. West ◽  
...  

In the present study we investigated the effects of carboxyhemoglobinemia (HbCO) on muscle maximal O2 uptake (VO2max) during hypoxia. O2 uptake (VO2) was measured in isolated in situ canine gastrocnemius (n = 12) working maximally (isometric twitch contractions at 5 Hz for 3 min). The muscles were pump perfused at identical blood flow, arterial PO2 (PaO2) and total hemoglobin concentration [( Hb]) with blood containing either 1% (control) or 30% HbCO. In both conditions PaO2 was set at 30 Torr, which produced the same arterial O2 contents, and muscle blood flow was set at 120 ml.100 g-1.min-1, so that O2 delivery in both conditions was the same. To minimize CO diffusion into the tissues, perfusion with HbCO-containing blood was limited to the time of the contraction period. VO2max was 8.8 +/- 0.6 (SE) ml.min-1.100 g-1 (n = 12) with hypoxemia alone and was reduced by 26% to 6.5 +/- 0.4 ml.min-1.100 g-1 when HbCO was present (n = 12; P less than 0.01). In both cases, mean muscle effluent venous PO2 (PVO2) was the same (16 +/- 1 Torr). Because PaO2 and PVO2 were the same for both conditions, the mean capillary PO2 (estimate of mean O2 driving pressure) was probably not much different for the two conditions, even though the O2 dissociation curve was shifted to the left by HbCO. Consequently the blood-to-mitochondria O2 diffusive conductance was likely reduced by HbCO.(ABSTRACT TRUNCATED AT 250 WORDS)


2005 ◽  
Vol 61 (2) ◽  
Author(s):  
M. A. Gregory ◽  
M. N. Deane ◽  
M. Marsh

Objective: The precise mechanisms by which massage promotes repair in injured soft tissue are unknown. Various authorshave attributed the beneficial effects of massage to vasodilation and increased skin and muscle blood flow. The aim of this study was to determine whether deep transverse friction massage (DTF) causes capillary vasodilation in untraumatised skeletal muscle. Setting: Academic institution.Interventions: Twelve New Zealand white rabbits were anaesthetised and the left biceps femoris muscle received 10 minutes of DTF. Following treatment, wedge biopsies were taken from the musclewithin 10 minutes of treatment (R1 - 4), 24 hours (R5 - 8) and 6 days(R9 - 12) after treatment. To serve as controls, similar biopsies weretaken from the right biceps femoris of animals. The samples were fixed, dehydrated and embedded in epoxy resin.Transverse sections (1µm) of muscle were cut, stained with 1% aqueous alkaline toluidine blue and examined with a light microscope using a 40X objective. Images containing capillaries were captured using an image analyser with SIS software and the cross sectional diameters of at least 60 capillaries were measured from each specimen. Main Outcome Measures: Changes in capillary diameter. Results: The mean capillary diameters in control muscle averaged 4.76 µm. DTF caused a significant immediate increase of 17.3% in cross sectional area (p<0.001), which was not significantly increased by 10.0% after 24 hours (p>0.05). Six days after treatment the cross-sectional area of the treated muscle was 7.6% smaller than the controls. Conclusions: This confirms the contention that DTF stimulates muscle blood flow immediately after treatment and this may account for its beneficial effects in certain conditions. 


1996 ◽  
Vol 80 (6) ◽  
pp. 1978-1983 ◽  
Author(s):  
S. S. Kurdak ◽  
B. Grassi ◽  
P. D. Wagner ◽  
M. C. Hogan

The purpose of this study was to determine whether reduction in apparent muscle O2 diffusing capacity (Dmo2) calculated during reduced blood flow conditions in maximally working muscle is a reflection of alterations in blood flow distribution. Isolated dog gastrocnemius muscle (n = 6) was stimulated for 3 min to achieve peak O2 uptake (VO2) at two levels of blood flow (controlled by pump perfusion): control (C) conditions at normal perfusion pressure (blood flow = 111 +/- 10 ml.100 g-1.min-1) and reduced blood flow treatment [ischemia (I); 52 +/- 6 ml.100 g-1.min-1]. In addition, maximal vasodilation was achieved by adenosine (A) infusion (10(-2)M) at both levels of blood flow, so that each muscle was subjected randomly to a total of four conditions (C, CA, I, and IA; each separated by 45 min of rest). Muscle blood flow distribution was measured with 15-microns-diameter colored microspheres. A numerical integration technique was used to calculate Dmo2 for each treatment with use of a model that calculates O2 loss along a capillary on the basis of Fick's law of diffusion. Peak VO2 was reduced significantly (P < 0.01) with ischemia and was unchanged by adenosine infusion at either flow rate (10.6 +/- 0.9, 9.7 +/- 1.0, 6.7 +/- 0.2, and 5.9 +/- 0.8 ml.100 g-1.min-1 for C, CA, I, and IA, respectively). Dmo2 was significantly lower by 30-35% (P < 0.01) when flow was reduced (except for CA vs. I; 0.23 +/- 0.03, 0.20 +/- 0.02, 0.16 +/- 0.01, and 0.13 +/- 0.01 ml.100 g-1.min-1.Torr-1 for C, CA, I, and IA, respectively). As expressed by the coefficient of variation (0.45 +/- 0.04, 0.47 +/- 0.04, 0.55 +/- 0.03, and 0.53 +/- 0.04 for C, CA, I, and IA, respectively), blood flow heterogeneity per se was not significantly different among the four conditions when examined by analysis of variance. However, there was a strong negative correlation (r = 0.89, P < 0.05) between Dmo2 and blood flow heterogeneity among the four conditions, suggesting that blood flow redistribution (likely a result of a decrease in the number of perfused capillaries) becomes an increasingly important factor in the determination of Dmo2 as blood flow is diminished.


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