Effect of blood flow and muscle contraction on noradrenaline spillover in the canine gracilis muscle

1999 ◽  
Vol 78 (1) ◽  
pp. 75-80
Author(s):  
Julie L Lavoie ◽  
François Trudeau ◽  
Louise Béliveau

Many authors have reported that, during exercise, noradrenaline spillover increases and fractional extraction decreases. It has been suggested that the increase in blood flow to active muscles may contribute to these effects. Muscle contraction also causes changes in many factors that may affect noradrenaline spillover and fractional extraction. In this experiment, we studied the effect of muscle contraction and blood flow on noradrenaline and adrenaline spillover and fractional extraction in the in situ canine gracilis muscle. The low intensity stimulation protocol enabled us to have muscle contractions without any effect on the local concentration of noradrenaline, as measured by microdialysis, and noradrenaline spillover. Fractional extraction of both noradrenaline and adrenaline was unaffected by increasing blood flow three and four times its resting value. In addition, noradrenaline spillover was increased by the higher blood flow, from 188 to 452 pg·min-1 at rest and from 246 to 880 pg·min-1 during stimulation. Stimulation of muscle contraction caused a significant increase in fractional extraction of noradrenaline and a nonsignificant increase in adrenaline extraction. In addition, an adrenaline spillover was observed in certain conditions. In light of our results, it seems that blood flow may not be the main factor decreasing fractional extraction of noradrenaline during exercise. However, blood flow could contribute to the increase in noradrenaline spillover observed in the active muscles during exercise.Key words: skeletal muscle, spillover, fractional extraction, stimulation, adrenaline.

2001 ◽  
Vol 79 (10) ◽  
pp. 831-835
Author(s):  
Julie L Lavoie ◽  
Louise Béliveau

Noradrenaline spillover from skeletal muscle vascular areas increases during exercise but the underlying mechanisms are not well understood. Muscle contraction itself causes changes in many factors that could affect noradrenaline spillover. For instance, it has been reported that bradykinin is synthesized in skeletal muscle areas during contraction. Because the B2 bradykinin receptor facilitates noradrenaline spillover, it may be involved in the increase associated with contraction. In this experiment, we studied the effect of bradykinin on noradrenaline spillover in the in situ canine gracilis muscle, using the specific B2 antagonist HOE 140. The drug did not modify noradrenaline spillover at rest, but did cause a significant decrease during muscle contraction, from 558 to 181 pg·min–1. As reported previously in the literature, fractional extraction of noradrenaline decreased during muscle contraction. This effect was independent of HOE 140 treatment. In light of our results, it seems that bradykinin formation during muscle contraction may play an important part in the observed increase in noradrenaline spillover but does not affect fractional extraction.Key words: skeletal muscle, fractional extraction, stimulation, HOE 140, B2 receptors.


2012 ◽  
Vol 303 (11) ◽  
pp. R1110-R1126 ◽  
Author(s):  
Jessica Spires ◽  
L. Bruce Gladden ◽  
Bruno Grassi ◽  
Gerald M. Saidel ◽  
Nicola Lai

On the basis of experimental studies, the intracellular O2 (iPo2)-work rate (WR) relationship in skeletal muscle is not unique. One study found that iPo2 reached a plateau at 60% of maximal WR, while another found that iPo2 decreased linearly at higher WR, inferring capillary permeability-surface area ( PS) and blood-tissue O2 gradient, respectively, as alternative dominant factors for determining O2 diffusion changes during exercise. This relationship is affected by several factors, including O2 delivery and oxidative and glycolytic capacities of the muscle. In this study, these factors are examined using a mechanistic, mathematical model to analyze experimental data from contracting skeletal muscle and predict the effects of muscle contraction on O2 transport, glycogenolysis, and iPo2. The model describes convection, O2 diffusion, and cellular metabolism, including anaerobic glycogenolysis. Consequently, the model simulates iPo2 in response to muscle contraction under a variety of experimental conditions. The model was validated by comparison of simulations of O2 uptake with corresponding experimental responses of electrically stimulated canine muscle under different O2 content, blood flow, and contraction intensities. The model allows hypothetical variation of PS, glycogenolytic capacity, and blood flow and predictions of the distinctive effects of these factors on the iPo2-contraction intensity relationship in canine muscle. Although PS is the main factor regulating O2 diffusion rate, model simulations indicate that PS and O2 gradient have essential roles, depending on the specific conditions. Furthermore, the model predicts that different convection and diffusion patterns and metabolic factors may be responsible for different iPo2-WR relationships in humans.


2020 ◽  
Vol 43 (10) ◽  
Author(s):  
Yao Yang ◽  
Jiahui Xiang ◽  
Zhaoli Zhang ◽  
Ekene Christopher Umego ◽  
Guoping Huang ◽  
...  

1993 ◽  
Vol 265 (1) ◽  
pp. H123-H130 ◽  
Author(s):  
H. Y. Chang ◽  
M. E. Ward ◽  
S. N. Hussain

The role of endogenous nitric oxide (NO) in the regulation of phrenic blood flow (Qphr) and O2 consumption (VO2) of the in situ isolated left hemidiaphragms was assessed in two groups of anesthetized, mechanically ventilated dogs. Saline was infused into the phrenic artery for 20 min in one group, whereas N omega-nitro-L-arginine (L-NNA, 6 x 10(-4) M) was infused in the other (L-NNA) group. Qphr and diaphragmatic VO2 were measured at rest and during 2 min of continuous 3-Hz stimulation of the left phrenic nerve. The animals were progressively hemorrhaged, and the measurements were repeated at various arterial pressures (Pa). For the resting diaphragm, Qphr at a mean Pa of 145 mmHg was lower in the L-NNA group than in the saline group; however, diaphragmatic VO2 values were similar in both groups. Qphr decreased with the decline in Pa in both groups, but O2 extraction ratios obtained at mean Pa of 25–45 mmHg were similar in both groups (71 vs. 73%). For the contracting diaphragm, Qphr and diaphragmatic VO2 values at a given Pa were lower in the L-NNA group than in the saline group (except at mean Pa < 75 mmHg). O2 extraction ratios obtained at a given Pa were similar in both groups. We concluded that 1) EDRF inhibition limits diaphragmatic blood flow both at rest and during 3-Hz stimulation; 2) diaphragmatic O2 extraction is unaffected by EDRF inhibition; and 3) the effect of EDRF release on diaphragmatic VO2 is dependent on the level of metabolic demands.


1999 ◽  
Vol 87 (5) ◽  
pp. 1741-1746 ◽  
Author(s):  
Jay S. Naik ◽  
Zoran Valic ◽  
John B. Buckwalter ◽  
Philip S. Clifford

To test the hypothesis that vasodilation occurs because of the release of a vasoactive substance after a brief muscle contraction and to determine whether acetylcholine spillover from the motor nerve is involved in contraction-induced hyperemia, tetanic muscle contractions were produced by sciatic nerve stimulation in anesthetized dogs ( n = 16), instrumented with flow probes on both external iliac arteries. A 1-s stimulation of the sciatic nerve at 1.5, 3, and 10 times motor threshold increased blood flow above baseline ( P < 0.01) for 20, 25, and 30 s, respectively. Blood flow was significantly greater 1 s after the contraction ended for 3 and 10 × motor threshold ( P < 0.01) and did not peak until 6–7 s after the contraction. The elevations in blood flow to a 1-s stimulation of the sciatic nerve and a 30-s train of stimulations were abolished by neuromuscular blockade (vecuronium). The delayed peak blood flow response and the prolonged hyperemia suggest that a vasoactive substance is rapidly released from the contracting skeletal muscle and can affect blood flow with removal of the mechanical constraint imposed by the contraction. In addition, acetylcholine spillover from the motor nerve is not responsible for the increase in blood flow in response to muscle contraction.


1983 ◽  
Vol 244 (4) ◽  
pp. H546-H551 ◽  
Author(s):  
E. L. Bockman

The results of the present study indicate that, although there are quantitative differences, there are no fundamental, qualitative differences in the vascular and metabolic responses to muscle contraction between slow-twitch soleus muscle and fast-twitch gracilis muscle in cats. Vascularly isolated muscles were perfused under free-flow conditions and were stimulated to contract isometrically for 12 min. Venous outflow was measured with a drop counter. Resting blood flow (6.3 +/- 1.3 ml . min-1 . 100 g-1) and oxygen consumption (0.27 +/- 0.04 ml O2 . min-1 . 100g-1) in soleus muscle did not differ significantly from the respective values in gracilis muscle. Blood flow increased by as much as sixfold above control values in both soleus and gracilis muscles in response to muscle contraction. Oxygen consumption increased linearly as a function of muscle performance in both muscles. However, the oxygen cost per kilogram of force developed was about threefold greater in gracilis compared with soleus muscle. The lower oxygen cost of contraction, coupled with an apparent maximal oxygen consumption twice that of gracilis muscle, enabled soleus muscle to maintain a greater level of muscle performance.


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