Journal articles on the topic 'Muscle blood flow'
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1
Hussain, Sabah N. A. "Regulation of ventilatory muscle blood flow." Journal of Applied Physiology 81, no. 4 (October 1, 1996): 1455–68. http://dx.doi.org/10.1152/jappl.1996.81.4.1455.
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Hussain, Sabah N. A. Regulation of ventilatory muscle blood flow. J. Appl. Physiol. 81(4): 1455–1468, 1996.—The ventilatory muscles perform various functions such as ventilation of the lungs, postural stabilization, and expulsive maneuvers (e.g., coughing). They are classified in functional terms as inspiratory muscles, which include the diaphragm, parasternal intercostal, external intercostal, scalene, and sternocleidomastoid muscles; and expiratory muscles, which include the abdominal muscles, internal intercostal, and triangularis sterni. The ventilatory muscles require high-energy phosphate compounds such as ATP to fuel the biochemical and physical processes of contraction and relaxation. Maintaining adequate intracellular concentrations of these compounds depends on adequate intracellular substrate levels and delivery of these substrates by arterial blood flow. In addition to the delivery of substrates, blood flow influences muscle function through the removal of metabolic by-products, which, if accumulated, could exert negative effects on several excitatory and contractile processes. Skeletal muscle substrate utilization is also dependent on the ability to extract substrates from arterial blood, which, in turn, is accomplished by increasing the total number of perfused capillaries. It follows that matching perfusion to metabolic demands is critical for the maintenance of normal muscle contractile function. In this article, I review the factors that influence ventilatory muscle blood flow. Major emphasis is placed on the diaphragm because a large number of published reports deal with diaphragmatic blood flow. The second reason for focusing on the diaphragm is because it is the largest and most important inspiratory muscle.
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Delp, Michael D., Changping Duan, Chester A. Ray, and R. B. Armstrong. "Rat hindlimb muscle blood flow during level and downhill locomotion." Journal of Applied Physiology 86, no. 2 (February 1, 1999): 564–68. http://dx.doi.org/10.1152/jappl.1999.86.2.564.
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During eccentrically biased exercise (e.g., downhill locomotion), whole body oxygen consumption and blood lactate concentrations are lower than during level locomotion. These general systemic measurements indicate that muscle metabolism is lower during downhill exercise. This study was designed to test the hypothesis that hindlimb muscle blood flow is correspondingly lower during downhill vs. level exercise. Muscle blood flow (determined by using radioactive microspheres) was measured in rats after 15 min of treadmill exercise at 15 m/min on the level (L, 0°) or downhill (D, −17°). Blood flow to ankle extensor muscles was either lower (e.g., white gastrocnemius muscle: D, 9 ± 2; L, 15 ± 1 ml ⋅ min−1 ⋅ 100 g−1) or not different (e.g., soleus muscle: D, 250 ± 35; L, 230 ± 21 ml ⋅ min−1 ⋅ 100 g−1) in downhill vs. level exercise. In contrast, blood flow to ankle flexor muscles was higher (e.g., extensor digitorum longus muscle: D, 53 ± 5; L, 31 ± 6 ml ⋅ min−1 ⋅ 100 g−1) during downhill vs. level exercise. When individual extensor and flexor muscle flows were summed, total flow to the leg was lower during downhill exercise (D, 3.24 ± 0.08; L, 3.47 ± 0.05 ml/min). These data indicate that muscle blood flow and metabolism are lower during eccentrically biased exercise but are not uniformly reduced in all active muscles; i.e., flows are equivalent in several ankle extensor muscles and higher in ankle flexor muscles.
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Elia, M., and A. Kurpad. "What is the Blood Flow to Resting Human Muscle?" Clinical Science 84, no. 5 (May 1, 1993): 559–63. http://dx.doi.org/10.1042/cs0840559.
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1. An investigation was carried out in five healthy lean adults to assess whether forearm and calf plethysmography largely reflect muscle blood flow as measured by 133Xe and whether there is substantial variability in the blood flow to muscles located at different sites in the body. 2. Blood flow to forearm and calf flexors and extensors, biceps, triceps and quadriceps was assessed using the 133Xe clearance technique. Blood flow to forearm skin and subcutaneous adipose tissue was also measured using the 133Xe clearance technique, whereas blood flow to the forearm and calf was measured using strain gauge plethysmography. 3. The mean blood flow to different muscles ranged from 1.4 ± 0.6 (gastrocnemius) to 1.8 ± 0.7 (forearm extensor) ml min−1 100 g−1 muscle (1.4 ± 0.6 and 1.9 ± 0.8 ml min−1 100 ml−1 muscle, respectively) but there were no significant differences between them. Forearm and calf blood flows (2.7 ± 0.3 and 3.0 ± 0.7 ml min−1 100 ml−1 limb tissue, respectively) were about 50% to more than 100% greater (P <0.025) than blood flow to the muscles within them (1.7 ± 0.5 and 1.4 ± 0.5ml min−1 100g−1 muscle, respectively, or 1.8 ± 0.6 and 1.5 ± 0.5 ml min−1 100 ml−1 muscle, respectively). In contrast, the blood flows to 100 g of forearm skin (9.1 ± 2.6 ml min−1 100 g−1) and adipose tissue (3.8 ± 1.1 ml min−1 100 g−1) were higher than the blood flow to 100 g of forearm (P <0.01 and not significant, respectively). 4. Although several possibilities can explain the discrepancy between muscle blood flow measured by 133Xe and blood flow to the distal limbs measured by plethysmography, the results suggest that non-muscular blood flow, especially that to skin, is substantially greater than muscular blood flow. Indeed, the overall blood flow to the forearm could be accounted for by summation of blood flows to individual constituent tissues, which were assumed to be present in proportions typical of lean subjects. The results have important implications in the use of arteriovenous catheterization studies for assessing flux of oxygen, carbon dioxide and metabolites across muscle.
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Armstrong, R. B., M. D. Delp, E. F. Goljan, and M. H. Laughlin. "Distribution of blood flow in muscles of miniature swine during exercise." Journal of Applied Physiology 62, no. 3 (March 1, 1987): 1285–98. http://dx.doi.org/10.1152/jappl.1987.62.3.1285.
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The purpose of this study was to determine how the distribution of blood flow within and among the skeletal muscles of miniature swine (22 +/- 1 kg body wt) varies as a function of treadmill speed. Radiolabeled microspheres were used to measure cardiac output (Q) and tissue blood flows in preexercise and at 3–5 min of treadmill exercise at 4.8, 8.0, 11.3, 14.5, and 17.7 km/h. All pigs (n = 8) attained maximal O2 consumption (VO2max) (60 +/- 4 ml X min-1 X kg-1) by the time they ran at 17.7 km/h. At VO2max, 87% of Q (9.9 +/- 0.5 l/min) was to skeletal muscle, which constituted 36 +/- 1% of body mass. Average total muscle blood flow at VO2max was 127 +/- 14 ml X min-1 X 100 g-1; average limb muscle flow was 135 +/- 17 ml X min-1 X 100 g-1. Within the limb muscles, blood flow was distributed so that the deep red parts of extensor muscles had flows about two times higher than the more superficial white portions of the same muscles; the highest muscle blood flows occurred in the elbow flexors (brachialis: 290 +/- 44 ml X min-1 X 100 g-1). Peak exercise blood flows in the limb muscles were proportional (P less than 0.05) to the succinate dehydrogenase activities (r = 0.84), capillary densities (r = 0.78), and populations of oxidative (slow-twitch oxidative + fast-twitch oxidative-glycolytic) fiber types (r = 0.93) in the muscles. Total muscle blood flow plotted as a function of exercise intensity did not peak until the pigs attained VO2max, although flows in some individual muscles showed a plateau in this relationship at submaximal exercise intensities. The data demonstrate that blood flow in skeletal muscles of miniature swine is distributed heterogeneously and varies in relation to fiber type composition and exercise intensity.
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Supinski, Gerald S. "Respiratory Muscle Blood Flow." Clinics in Chest Medicine 9, no. 2 (June 1988): 211–23. http://dx.doi.org/10.1016/s0272-5231(21)00500-1.
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Glenn, G. M., M. H. Laughlin, and R. B. Armstrong. "Muscle blood flow and fiber activity in partially curarized rats during exercise." Journal of Applied Physiology 63, no. 4 (October 1, 1987): 1450–56. http://dx.doi.org/10.1152/jappl.1987.63.4.1450.
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We previously reported that low doses of d-tubocurarine attenuated glycogen loss in red muscles of rats during treadmill walking but that the initial hyperemia in the muscles was normal. The present studies were performed to 1) determine with electromyography (EMG) whether red muscle fiber activity is reduced in walking, curarized rats and 2) study muscle blood flow and glycogen loss during running with different doses of curare (dose response). At 0.5 min of treadmill walking (15 m/min), integrated EMG in vastus intermedius (VI) muscle was reduced by an average of 18% in curarized (60 micrograms/kg) rats, although blood flow (measured with microspheres) was the same as in saline control rats. Comparison of blood flows and glycogen loss in quadriceps muscles at 1 min of treadmill running (30 m/min) with different curare doses (20–60 micrograms/kg) demonstrated that red muscle glycogen loss was inversely related to curare dose but that blood flows in the same muscles were unaffected by curare. These findings provide support for our previous conclusion that at the initiation of low to moderate treadmill exercise, red muscle blood flow is not proportional to the activity or metabolism of the muscle fibers.
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Armstrong, R. B., and M. H. Laughlin. "Rat muscle blood flows during high-speed locomotion." Journal of Applied Physiology 59, no. 4 (October 1, 1985): 1322–28. http://dx.doi.org/10.1152/jappl.1985.59.4.1322.
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We previously studied blood flow distribution within and among rat muscles as a function of speed from walking (15 m/min) through galloping (75 m/min) on a motor-driven treadmill. The results showed that muscle blood flows continued to increase as a function of speed through 75 m/min. The purpose of the present study was to have rats run up to maximal treadmill speeds to determine if blood flows in the muscles reach a plateau as a function of running speed over the animals' normal range of locomotory speeds. Muscle blood flows were measured with radiolabeled microspheres at 1 min of running at 75, 90, and 105 m/min in male Sprague-Dawley rats. The data indicate that even at these relatively high treadmill speeds there was still no clear evidence of a plateau in blood flow in most of the hindlimb muscles. Flows in most muscles continued to increase as a function of speed. These observed patterns of blood flow vs. running speed may have resulted from the rigorous selection of rats that were capable of performing the high-intensity exercise and thus only be representative of a highly specific population of animals. On the other hand, the data could be interpreted to indicate that the cardiovascular potential during exercise is considerably higher in laboratory rats than has normally been assumed and that inadequate blood flow delivery to the muscles does not serve as a major limitation to their locomotory performance.
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Laughlin, M. H. "Skeletal muscle blood flow capacity: role of muscle pump in exercise hyperemia." American Journal of Physiology-Heart and Circulatory Physiology 253, no. 5 (November 1, 1987): H993—H1004. http://dx.doi.org/10.1152/ajpheart.1987.253.5.h993.
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An appreciation for the potential of skeletal muscle vascular beds for blood flow (blood flow capacity) is required if one is to understand the limits of the cardiorespiratory system in exercise. To assess this potential, an index of blood flow capacity that can be objectively measured is required. One obvious index would be to measure maximal muscle blood flow (MBF). However, a unique value for maximal MBF cannot be measured, since once maximal vasodilation is attained MBF is a function of perfusion pressure. Another approach would be to measure maximal or peak vascular conductance. However, peak vascular conductance is different among skeletal muscles composed of different fiber types and is a function of perfusion pressure during peak vasodilation within muscle composed of a given fiber type. Also, muscle contraction can increase or decrease blood flow and/or the apparent peak vascular conductance depending on the experimental preparation and the type of muscle contraction. Blood flows and calculated values of conductance appear to be greater during rhythmic contractions (with the appropriate frequency and duration) than observed in resting muscle during what is called "maximal" vasodilation. Moreover, dynamic exercise in conscious subjects produces the greatest skeletal muscle blood flows. The purpose of this review is to consider the interaction of the determinants of muscle blood flow during locomotory exercise. Emphasis is directed toward the hypothesis that the "muscle pump" is an important determinant of perfusion of active skeletal muscle. It is concluded that, during normal dynamic exercise, MBF is determined by skeletal muscle vascular conductance, the perfusion pressure gradient, and the efficacy of the muscle pump.
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Klabunde, R. E., M. H. Laughlin, and R. B. Armstrong. "Systemic adenosine deaminase administration does not reduce active hyperemia in running rats." Journal of Applied Physiology 64, no. 1 (January 1, 1988): 108–14. http://dx.doi.org/10.1152/jappl.1988.64.1.108.
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The importance of adenosine in controlling the magnitude and distribution of blood flow among and within skeletal muscles in rats during slow locomotor exercise was tested by systemic infusion of adenosine deaminase (ADA). Blood flows were measured using labeled microspheres before exercise and at 0.5, 15, and 30 min of fast treadmill walking at 15 m/min. An initial infusion of ADA (1,000 U/kg) was given 30 min before the first blood flow measurement and a second injection (1,000 U/kg) was given 5 min into exercise. These infusions maintained ADA activity above 5 U/ml blood throughout the experimental period. This plasma concentration of ADA was shown to be sufficient to result in a 64% decrease in muscle adenosine levels during ischemic contraction. Blood flows were measured in all of the muscles of the hindlimb (28 samples) and in various nonmuscular tissues in ADA-treated and control rats. Preexercise blood flows were primarily directed to slow-twitch muscles and exercise blood flows were highest in muscles with fast-twitch oxidative fibers. ADA treatment did not reduce total muscle blood flow or exercise blood flows in any of the muscles at any time. These findings do not support the hypothesis that adenosine plays an essential role in controlling muscle blood flow in skeletal muscles during normal locomotor activity.
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Musch, T. I., D. B. Friedman, K. H. Pitetti, G. C. Haidet, J. Stray-Gundersen, J. H. Mitchell, and G. A. Ordway. "Regional distribution of blood flow of dogs during graded dynamic exercise." Journal of Applied Physiology 63, no. 6 (December 1, 1987): 2269–77. http://dx.doi.org/10.1152/jappl.1987.63.6.2269.
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The regional blood flow response to progressive treadmill exercise was measured with radioactive microspheres in 25 untrained mongrel dogs. Incremental increases in work intensity resulted in corresponding increases in blood flows to the gracilis, gastrocnemius, semimembranosus, and semitendinosus muscles of the hindlimb and to the heart. During maximal exercise, blood flow was greatest in the semimembranosus muscle and lowest in the semitendinosus muscle (342 and 134 ml–1.100 g tissue-1.min-1, respectively). Exercise produced a decrease in blood flow to the temporalis muscle, which was classified as nonlocomotive in function. Blood flows to the stomach, pancreas, and large intestine decreased at the lowest exercise work load and remained diminished throughout the continuum to maximal exercise. Blood flows to the small intestine and spleen were maintained during submaximal exercise but were reduced by 50% at maximal O2 consumption (VO2max). No changes in blood flows to the kidneys, adrenal glands, liver, and brain were found. These results demonstrate that 1) renal blood flow is maintained at resting levels during exercise in untrained dogs; 2) blood flow changes in the various organs of the splanchnic region of dogs during exercise are heterogeneous; and 3) blood flows to the working skeletal muscles of dogs progressively increase with increasing work loads up to VO2max.
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Kawagoe, Y., S. Permutt, and H. E. Fessler. "Hyperinflation with intrinsic PEEP and respiratory muscle blood flow." Journal of Applied Physiology 77, no. 5 (November 1, 1994): 2440–48. http://dx.doi.org/10.1152/jappl.1994.77.5.2440.
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Increased end-expiratory lung volume and intrinsic positive end-expiratory pressure (PEEP) are common in obstructive lung disease, especially during exacerbations or exercise. This loads the respiratory muscles and may also stress the circulatory system, causing a reduction or redistribution of cardiac output. We measured the blood flow to respiratory muscles and systemic organs using colored microspheres in 10 spontaneously breathing anesthetized tracheotomized dogs. Flows during baseline breathing (BL) were compared with those during hyperinflation (HI) induced by a mechanical analogue of airway closure and with those during an inspiratory resistive load (IR) that produced an equivalent increase in inspiratory work and time-integrated transdiaphragmatic pressure. Cardiac output was unchanged during IR (3.19 +/- 0.27 l/min at BL, 3.09 +/- 0.34 l/min during IR) but was reduced during HI (2.14 +/- 0.29 l/min; P < 0.01). Among the organs studied, flow was unaltered by IR but decreased to the liver and pancreas and increased to the brain during HI. For the respiratory muscles, flow to the diaphragm increased during IR. However, despite a 1.9-fold increase in inspiratory work per minute and a 2.5-fold increase in integrated transdiaphragmatic pressure during HI, blood flow to the diaphragm was unchanged and flow to the scalenes and sternomastoid fell. The only respiratory muscle to which flow increased during HI was the transversus abdominis, an expiratory muscle. We conclude that the circulatory effects of hyperinflation in this model impair inspiratory muscle perfusion and speculate that this may contribute to respiratory muscle dysfunction in hyperinflated states.
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Thomas, Gail D., and Steven S. Segal. "Neural control of muscle blood flow during exercise." Journal of Applied Physiology 97, no. 2 (August 2004): 731–38. http://dx.doi.org/10.1152/japplphysiol.00076.2004.
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Activation of skeletal muscle fibers by somatic nerves results in vasodilation and functional hyperemia. Sympathetic nerve activity is integral to vasoconstriction and the maintenance of arterial blood pressure. Thus the interaction between somatic and sympathetic neuroeffector pathways underlies blood flow control to skeletal muscle during exercise. Muscle blood flow increases in proportion to the intensity of activity despite concomitant increases in sympathetic neural discharge to the active muscles, indicating a reduced responsiveness to sympathetic activation. However, increased sympathetic nerve activity can restrict blood flow to active muscles to maintain arterial blood pressure. In this brief review, we highlight recent advances in our understanding of the neural control of the circulation in exercising muscle by focusing on two main topics: 1) the role of motor unit recruitment and muscle fiber activation in generating vasodilator signals and 2) the nature of interaction between sympathetic vasoconstriction and functional vasodilation that occurs throughout the resistance network. Understanding how these control systems interact to govern muscle blood flow during exercise leads to a clear set of specific aims for future research.
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Peterson, D. F., R. B. Armstrong, and M. H. Laughlin. "Sympathetic neural influences on muscle blood flow in rats during submaximal exercise." Journal of Applied Physiology 65, no. 1 (July 1, 1988): 434–40. http://dx.doi.org/10.1152/jappl.1988.65.1.434.
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These experiments were designed to estimate the involvement of the sympathetic innervation in regulation of hindlimb muscle blood flow distribution among and within muscles during submaximal locomotory exercise in rats. Blood flows to 32 hindlimb muscles and 13 other selected tissues were measured using the radiolabeled microsphere technique, before exercise and at 0.5, 2, 5, and 15 min of treadmill exercise at 15 m/min. The two groups of rats studied were 1) intact control, and 2) acutely sympathectomized (hindlimb sympathectomy accomplished by bilateral section of the lumbar sympathetic chain and its connections to the spinal cord at L2-L3). There were no differences in total hindlimb muscle blood flow among the two groups during preexercise or at 30 s or 2 min of exercise. However, flow was higher in eight individual muscles at 2 min of exercise in the sympathectomized rats. At 5 and 15 min of exercise there was higher total hindlimb muscle blood flow in the denervated group compared with control. These differences were also present in many individual muscles. Our results suggest that 1) sympathetic nerves do not exert a net influence on the initial elevations in muscle blood flow at the beginning of exercise, 2) sympathetic nerves are involved in regulating muscle blood flow during steady-state submaximal exercise in conscious rats, and 3) these changes are seen in muscles of all fiber types.
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Burton, H. W., T. R. Stevenson, R. C. Dysko, K. P. Gallagher, and J. A. Faulkner. "Total and regional blood flows in vascularized skeletal muscle grafts in rabbits." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 5 (November 1, 1988): H1043—H1049. http://dx.doi.org/10.1152/ajpheart.1988.255.5.h1043.
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The transplantation of whole skeletal muscles is a common clinical procedure. Although atypical blood flows have been reported in small free muscle grafts, the blood flow of large neurovascular-intact (NVI) and neurovascular-anastomosed (NVA) grafts have not been measured. Because the maximum specific force (N/cm2) of NVI and NVA grafts is 65% that of control muscles, we hypothesized that total and regional blood flows (ml.min-1.100g-1) of NVI and NVA grafts at rest and during twitch contractions are significantly lower than lower flows of control muscles. In rabbits, blood flows of control rectus femoris (RFM) muscles and NVI and NVA grafts of RFM muscles were measured by the radioactive-microsphere technique. In control muscles, blood flow increased linearly from 6.8 +/- 1 ml.min-1.100 g-1 at rest to 64.4 +/- 7 ml.min-1. 100 g-1 at a stimulation frequency of 3 Hz with no further increase at 4 Hz. Total blood flows in grafts were not different from the control RFM muscle values, except for a higher resting flow in NVA grafts and a lower flow at 3 Hz in NVI grafts. Minor variations in regional flows were observed. We conclude that the operative procedures of grafting and repair of blood vessels affect the vascular bed of muscles minimally, and the deficits observed in grafts do not arise from inadequate perfusion.
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McAllister, R. M., M. D. Delp, K. A. Thayer, and M. H. Laughlin. "Muscle blood flow during exercise in sedentary and trained hypothyroid rats." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 6 (December 1, 1995): H1949—H1954. http://dx.doi.org/10.1152/ajpheart.1995.269.6.h1949.
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Hypothyroidism is characterized by exercise intolerance. We hypothesized that active muscle blood flow during in vivo exercise is inadequate in the hypothyroid state. Additionally, we hypothesized that endurance exercise training would restore normal blood flow during acute exercise. To test these hypotheses, rats were made hypothyroid (Hypo) over 3-4 mo with propylthiouracil. A subset of Hypo rats was trained (THypo) on a treadmill at 30 m/min (15% grade) for 60 min/day 5 days/wk over 10-15 wk. Hypothyroidism was evidenced by approximately 80% reductions in plasma triiodothyronine levels in Hypo and THypo and by 40-50% reductions in citrate synthase activities in high oxidative muscles in Hypo compared with euthyroid (Eut) rats. Training efficacy was indicated by increased (25-100%) citrate synthase activities in muscles of THypo vs. Hypo. Regional blood flows were determined by the radiolabeled microsphere method before exercise and at 1-2 min of treadmill running at 15 m/min (0% grade). Preexercise muscle blood flows were generally similar among groups. During exercise, however, flows were lower in Hypo than in Eut for high oxidative muscles such as the red section of vastus lateralis [277 +/- 24 and 153 +/- 13 (SE) ml.min-1.100 g-1 for Eut and Hypo, respectively; P < 0.01] and vastus intermedius (317 +/- 32 and 187 +/- 20 ml.min-1.100 g-1 for Eut and Hypo, respectively; P < 0.01) muscles. Training (THypo) did not normalize these flows (168 +/- 24 and 181 +/- 24 ml.min-1.100 g-1 for red section of vastus lateralis and vastus intermedius muscles, respectively). Blood flows to low oxidative muscle, such as the white section of vastus lateralis muscle, were similar among groups (21 +/- 5, 25 +/- 4, and 34 +/- 7 ml.min-1.100 g-1 for Eut, Hypo, and THypo, respectively; P = NS). These findings indicate that hypothyroidism is associated with reduced blood flow to skeletal muscle during exercise, suggesting that impaired delivery of nutrients to and/or removal of metabolites from skeletal muscle contributes to the poor exercise tolerance characteristic of hypothyroidism.
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Joyner, Michael J., and Darren P. Casey. "Regulation of Increased Blood Flow (Hyperemia) to Muscles During Exercise: A Hierarchy of Competing Physiological Needs." Physiological Reviews 95, no. 2 (April 2015): 549–601. http://dx.doi.org/10.1152/physrev.00035.2013.
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This review focuses on how blood flow to contracting skeletal muscles is regulated during exercise in humans. The idea is that blood flow to the contracting muscles links oxygen in the atmosphere with the contracting muscles where it is consumed. In this context, we take a top down approach and review the basics of oxygen consumption at rest and during exercise in humans, how these values change with training, and the systemic hemodynamic adaptations that support them. We highlight the very high muscle blood flow responses to exercise discovered in the 1980s. We also discuss the vasodilating factors in the contracting muscles responsible for these very high flows. Finally, the competition between demand for blood flow by contracting muscles and maximum systemic cardiac output is discussed as a potential challenge to blood pressure regulation during heavy large muscle mass or whole body exercise in humans. At this time, no one dominant dilator mechanism accounts for exercise hyperemia. Additionally, complex interactions between the sympathetic nervous system and the microcirculation facilitate high levels of systemic oxygen extraction and permit just enough sympathetic control of blood flow to contracting muscles to regulate blood pressure during large muscle mass exercise in humans.
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Laughlin, M. H., and R. B. Armstrong. "Adrenoreceptor effects on rat muscle blood flow during treadmill exercise." Journal of Applied Physiology 62, no. 4 (April 1, 1987): 1465–72. http://dx.doi.org/10.1152/jappl.1987.62.4.1465.
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The purpose of this study was to examine the effects of the adrenergic receptors on the distribution of blood flow within and among skeletal muscles in rats. Blood flow was measured with the radiolabeled microsphere technique before exercise and during treadmill exercise at 15 or 60 m/min. Alpha- (phentolamine) or beta- (propranolol) adrenergic blocking drugs were administered, and then blood flow was measured and results compared with those from saline-treated rats. Before exercise, alpha-blockade caused increases in total muscle blood flow and in all fast-twitch muscles, whereas muscles composed of greater than 20% slow-twitch fibers showed no effect. During exercise at 15 m/min, the normal increase in total muscle blood flow was attenuated by alpha-blockade. Compared with controls, blood flow was less in the high-oxidative (fast and slow) muscle fiber areas of extensor muscles, whereas blood flow to white areas of extensor muscles was increased. beta-Blockade tended to decrease muscle blood flow before exercise and during exercise at 15 m/min with no apparent relationship between the effects of blockade on blood flow and muscle fiber type. These effects of beta-blockade were not apparent during exercise at 60 m/min. We conclude that before exercise alpha-receptor effects are limited to fast muscle, whereas beta-receptor influences are independent of fiber type, beta-receptors contribute to the initial hyperemia of exercise at 15 m/min, and beta-receptor influence is inversely related to metabolic rate.
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Joyner, Michael J., and Darren P. Casey. "Muscle blood flow, hypoxia, and hypoperfusion." Journal of Applied Physiology 116, no. 7 (April 1, 2014): 852–57. http://dx.doi.org/10.1152/japplphysiol.00620.2013.
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Blood flow increases to exercising skeletal muscle, and this increase is driven primarily by vasodilation in the contracting muscles. When oxygen delivery to the contracting muscles is altered by changes in arterial oxygen content, the magnitude of the vasodilator response to exercise changes. It is augmented during hypoxia and blunted during hyperoxia. Because the magnitude of the increased vasodilation during hypoxic exercise tends to keep oxygen delivery to the contracting muscles constant, we have termed this phenomenon “compensatory vasodilation.” In a series of studies, we have explored metabolic, endothelial, and neural mechanisms that might contribute to compensatory vasodilation. These include the contribution of vasodilating substances like nitric oxide (NO) and adenosine, along with altered interactions between sympathetic vasoconstriction and metabolic vasodilation. We have also compared the compensatory vasodilator responses to hypoxic exercise with those seen when oxygen delivery to contracting muscles is altered by acute reductions in perfusion pressure. A synthesis of our findings indicate that NO contributes to the compensatory dilator responses during both hypoxia and hypoperfusion, while adenosine appears to contribute only during hypoperfusion. During hypoxia, the NO-mediated component is linked to a β-adrenergic receptor mechanism during lower intensity exercise, while another source of NO is engaged at higher exercise intensities. There are also subtle interactions between α-adrenergic vasoconstriction and metabolic vasodilation that influence the responses to hypoxia, hyperoxia, and hypoperfusion. Together our findings emphasize both the tight linkage of oxygen demand and supply during exercise and the redundant nature of the vasomotor responses to contraction.
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Laughlin, M. H., R. E. Klabunde, M. D. Delp, and R. B. Armstrong. "Effects of dipyridamole on muscle blood flow in exercising miniature swine." American Journal of Physiology-Heart and Circulatory Physiology 257, no. 5 (November 1, 1989): H1507—H1515. http://dx.doi.org/10.1152/ajpheart.1989.257.5.h1507.
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The purpose of this study was to determine whether a vasodilator reserve exists in respiratory muscles and forelimb skeletal muscles in miniature swine during treadmill exercise. Blood flow (BF) was measured with radiolabeled microspheres during preexercise and before and after dipyridamole (DYP; 1 mg/kg iv) at 2 min of treadmill exercise at 11.2 (70% Vo2 max) and 17.6 km/h (Vo2 max). Muscle BFs were increased during exercise, and the relationship between exercise intensity and BF varied among the muscles. The high-oxidative extensor muscles and the flexor muscles attained peak BFs at 11.2 km/h, whereas the more superficial, lower oxidative extensor muscles showed increases in BF up to maximal exercise. During running at 11.2 km/h, DYP produced increases in BF only in cardiac muscle, respiratory muscle and the medial head of the triceps muscle (MHT), which is composed of 91% slow-twitch oxidative (SO) fibers. During maximal exercise (17.6 km/h), DYP produced a 31-mmHg decrease in mean arterial pressure (MAP) and increases in vascular conductance in all muscles studied. BF was only increased in MHT and cardiac muscle. We conclude that vasodilator reserve remains in skeletal muscle and respiratory muscle even during maximal exercise in swine. If it is assumed that DYP-induced vasodilation in a muscle sample is indicative of adenosine production, these results suggest that SO skeletal muscle (MHT) and respiratory muscle are similar to cardiac muscle in that they produce adenosine even when adequately perfused. Furthermore, during maximal exercise, all skeletal muscle appears to produce adenosine, suggesting that muscle BF is restricted under these conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
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Sheriff, Don D., and Richard Van Bibber. "Flow-generating capability of the isolated skeletal muscle pump." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 5 (May 1, 1998): H1502—H1508. http://dx.doi.org/10.1152/ajpheart.1998.274.5.h1502.
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We sought to test directly whether the mechanical forces produced during rhythmic muscle contraction and relaxation act on the muscle vasculature in a manner sufficient to initiate and sustain blood flow. To accomplish this goal, we evaluated the mechanical performance of the isolated skeletal muscle pump. The hindlimb skeletal muscle pump was isolated by reversibly connecting the inferior vena cava and terminal aorta with extracorporeal tubing in 15- to 20-kg anesthetized pigs ( n = 5). During electrically evoked contractions (1/s), hindlimb muscles were made to perfuse themselves by diverting the venous blood propelled out of the muscles into the shunt tubing, which had been prefilled with fresh arterial blood. This caused arterial blood to be pushed into the distal aorta and then through the muscles (shunt open, proximal aorta and vena cava clamped). In essence, the muscles perfused themselves for brief periods by driving blood around a “short-circuit” that isolates muscle from the remainder of the circulation, analogous to isolated heart-lung preparations. Because the large, short shunt offers a negligible resistance to flow, the arterial-venous pressure difference across the limbs was continuously zero, and thus the energy to drive flow through muscle could come only from the muscle pump. The increase in blood flow during normal heart-perfused contractions (with only the shunt tubing clamped) was compared with shunt-perfused contractions in which the large veins were preloaded with extra blood volume. Muscle blood flow increased by 87 ± 11 and 110 ± 21 (SE) ml/min in the first few seconds after the onset of shunt-perfused and heart-perfused contractions, respectively ( P > 0.4). We conclude that the mechanical forces produced by muscle contraction and relaxation act on the muscle vasculature in a manner sufficient to generate a significant flow of blood.
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Copp, Steven W., K. Sue Hageman, Brad J. Behnke, David C. Poole, and Timothy I. Musch. "Effects of Type II diabetes on exercising skeletal muscle blood flow in the rat." Journal of Applied Physiology 109, no. 5 (November 2010): 1347–53. http://dx.doi.org/10.1152/japplphysiol.00668.2010.
Full textAbstract:
The purpose of the present investigation was to examine the muscle hyperemic response to steady-state submaximal running exercise in the Goto-Kakizaki (GK) Type II diabetic rat. Specifically, the hypothesis was tested that Type II diabetes would redistribute exercising blood flow toward less oxidative muscles and muscle portions of the hindlimb. GK diabetic ( n = 10) and Wistar control ( n = 8, blood glucose concentration, 13.7 ± 1.6 and 5.7 ± 0.2 mM, respectively, P < 0.05) rats were run at 20 m/min on a 10% grade. Blood flows to 28 hindlimb muscles and muscle portions as well as the abdominal organs and kidneys were measured in the steady state of exercise using radiolabeled 15-μm microspheres. Blood flow to the total hindlimb musculature did not differ between GK diabetic and control rats (161 ± 16 and 129 ± 15 ml·min−1·100g−1, respectively, P = 0.18). Moreover, there was no difference in blood flow between GK diabetic and control rats in 20 of the individual muscles or muscle parts examined. However, in the other eight muscles examined that typically are comprised of a majority of fast-twitch glycolytic (IIb/IIdx) fibers, blood flow was significantly greater (i.e., ↑31–119%, P < 0.05) in the GK diabetic rats. Despite previously documented impairments of several vasodilatory pathways in Type II diabetes these data provide the first demonstration that a reduction of exercising muscle blood flow during submaximal exercise is not an obligatory consequence of this condition in the GK diabetic rat.
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Volianitis, Stefanos, and Niels H. Secher. "Cardiovascular control during whole body exercise." Journal of Applied Physiology 121, no. 2 (August 1, 2016): 376–90. http://dx.doi.org/10.1152/japplphysiol.00674.2015.
Full textAbstract:
It has been considered whether during whole body exercise the increase in cardiac output is large enough to support skeletal muscle blood flow. This review addresses four lines of evidence for a flow limitation to skeletal muscles during whole body exercise. First, even though during exercise the blood flow achieved by the arms is lower than that achieved by the legs (∼160 vs. ∼385 ml·min−1·100 g−1), the muscle mass that can be perfused with such flow is limited by the capacity to increase cardiac output (42 l/min, highest recorded value). Secondly, activation of the exercise pressor reflex during fatiguing work with one muscle group limits flow to other muscle groups. Another line of evidence comes from evaluation of regional blood flow during exercise where there is a discrepancy between flow to a muscle group when it is working exclusively and when it works together with other muscles. Finally, regulation of peripheral resistance by sympathetic vasoconstriction in active muscles by the arterial baroreflex is critical for blood pressure regulation during exercise. Together, these findings indicate that during whole body exercise muscle blood flow is subordinate to the control of blood pressure.
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Delp, M. D., and R. B. Armstrong. "Blood flow in normal and denervated muscle during exercise in conscious rats." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 6 (December 1, 1988): H1509—H1515. http://dx.doi.org/10.1152/ajpheart.1988.255.6.h1509.
Full textAbstract:
The purpose of this study was to test the hypothesis that extrinsic mechanical factors, i.e., the dynamic shortening and lengthening imposed on a muscle during limb movements and the rhythmic compressions as surrounding muscles contract and relax, contribute to the initial muscle hyperemia during locomotion in conscious male Sprague-Dawley rats. Soleus and lateral head of gastrocnemius muscles were surgically denervated in one hindlimb several hours before exercise to remove 1) local metabolic vasodilator effects, 2) vasoconstrictor or vasodilatory influences mediated through sympathetic postganglionic fibers, and 3) intrinsic mechanical pumping. Blood flow was measured with radioactive microspheres during preexercise and at 30 s and 5 min of exercise in rats walking at 15 m/min or a motor-driven treadmill. Glycogen concentrations were also measured as an indicator of muscular activity to verify the denervation. Blood flows to control muscles in the normal limb were similar to previously reported values during preexercise and exercise. Denervation, however, decreased preexercise blood flow (69–88%) to muscle composed predominantly of oxidative fibers and increased flow (53%) to muscle composed predominantly of glycolytic fibers. During exercise, blood flow to denervated muscles either remained unchanged or decreased. These data suggest that extrinsic mechanical factors do not significantly contribute to the initial hyperemic response at the onset of low-intensity exercise in normal muscle.
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Athanasopoulos, Dimitris, Zafeiris Louvaris, Evgenia Cherouveim, Vasilis Andrianopoulos, Charis Roussos, Spyros Zakynthinos, and Ioannis Vogiatzis. "Expiratory muscle loading increases intercostal muscle blood flow during leg exercise in healthy humans." Journal of Applied Physiology 109, no. 2 (August 2010): 388–95. http://dx.doi.org/10.1152/japplphysiol.01290.2009.
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We investigated whether expiratory muscle loading induced by the application of expiratory flow limitation (EFL) during exercise in healthy subjects causes a reduction in quadriceps muscle blood flow in favor of the blood flow to the intercostal muscles. We hypothesized that, during exercise with EFL quadriceps muscle blood flow would be reduced, whereas intercostal muscle blood flow would be increased compared with exercise without EFL. We initially performed an incremental exercise test on eight healthy male subjects with a Starling resistor in the expiratory line limiting expiratory flow to ∼ 1 l/s to determine peak EFL exercise workload. On a different day, two constant-load exercise trials were performed in a balanced ordering sequence, during which subjects exercised with or without EFL at peak EFL exercise workload for 6 min. Intercostal (probe over the 7th intercostal space) and vastus lateralis muscle blood flow index (BFI) was calculated by near-infrared spectroscopy using indocyanine green, whereas cardiac output (CO) was measured by an impedance cardiography technique. At exercise termination, CO and stroke volume were not significantly different during exercise, with or without EFL (CO: 16.5 vs. 15.2 l/min, stroke volume: 104 vs. 107 ml/beat). Quadriceps muscle BFI during exercise with EFL (5.4 nM/s) was significantly ( P = 0.043) lower compared with exercise without EFL (7.6 nM/s), whereas intercostal muscle BFI during exercise with EFL (3.5 nM/s) was significantly ( P = 0.021) greater compared with that recorded during control exercise (0.4 nM/s). In conclusion, increased respiratory muscle loading during exercise in healthy humans causes an increase in blood flow to the intercostal muscles and a concomitant decrease in quadriceps muscle blood flow.
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Sheel, A. William, Robert Boushel, and Jerome A. Dempsey. "Competition for blood flow distribution between respiratory and locomotor muscles: implications for muscle fatigue." Journal of Applied Physiology 125, no. 3 (September 1, 2018): 820–31. http://dx.doi.org/10.1152/japplphysiol.00189.2018.
Full textAbstract:
Sympathetically induced vasoconstrictor modulation of local vasodilation occurs in contracting skeletal muscle during exercise to ensure appropriate perfusion of a large active muscle mass and to maintain also arterial blood pressure. In this synthesis, we discuss the contribution of group III-IV muscle afferents to the sympathetic modulation of blood flow distribution to locomotor and respiratory muscles during exercise. This is followed by an examination of the conditions under which diaphragm and locomotor muscle fatigue occur. Emphasis is given to those studies in humans and animal models that experimentally changed respiratory muscle work to evaluate blood flow redistribution and its effects on locomotor muscle fatigue, and conversely, those that evaluated the influence of coincident limb muscle contraction on respiratory muscle blood flow and fatigue. We propose the concept of a “two-way street of sympathetic vasoconstrictor activity” emanating from both limb and respiratory muscle metaboreceptors during exercise, which constrains blood flow and O2 transport thereby promoting fatigue of both sets of muscles. We end with considerations of a hierarchy of blood flow distribution during exercise between respiratory versus locomotor musculatures and the clinical implications of muscle afferent feedback influences on muscle perfusion, fatigue, and exercise tolerance.
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McAllister, R. M., J. C. Sansone, and M. H. Laughlin. "Effects of hyperthyroidism on muscle blood flow during exercise in rats." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 1 (January 1, 1995): H330—H335. http://dx.doi.org/10.1152/ajpheart.1995.268.1.h330.
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Hyperthyroidism is associated with exercise intolerance. Previous research, however, has shown that cardiac output is either normal or enhanced during exercise in the hyperthyroid state. We therefore hypothesized that blood flow to working skeletal muscle is augmented in hyperthyroid animals during in vivo submaximal exercise and, consequently, that noncardiovascular factors are responsible for intolerance to exercise. To test this hypothesis, rats were made hyperthyroid (Hyper) over 6–12 wk with injections of triiodothyronine (300 micrograms/kg). Hyperthyroidism was evidenced by left ventricular hypertrophy [euthyroid (Eut), 2.12 +/- 0.05 mg/g body wt; Hyper, 2.78 +/- 0.06; P < 0.005], 25–60% increases in citrate synthase activities in Hyper hindlimb muscles over those of Eut rats, and higher preexercise heart rates (Eut, 415 +/- 18 beats/min; Hyper, 479 +/- 19; P < 0.025). Regional blood flows were determined by the radiolabeled microsphere method, preexercise, and at 1–2 min of treadmill running at 15 m/min (0% grade). Total hindlimb muscle blood flow preexercise was unaffected (Eut, 31 +/- 4 ml.min-1.(100) g-1, n = 11; Hyper, 40 +/- 6, n = 9; not significant) but was higher (P < 0.025) in Hyper (127 +/- 17, n = 9) compared with Eut (72 +/- 11, n = 9) during treadmill running. During exercise, flows to individual muscles and muscle sections were approximately 50–150% higher in Hyper compared with Eut rats. Visceral blood flows were largely similar between groups. These findings indicate that hyperthyroidism is associated with augmented blood flow to skeletal muscle during submaximal exercise. Thus hypoperfusion of skeletal muscle does not account for the poor exercise tolerance characteristic of hyperthyroidism.
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Eisenberg, H. A., and D. A. Hood. "Blood flow, mitochondria, and performance in skeletal muscle after denervation and reinnervation." Journal of Applied Physiology 76, no. 2 (February 1, 1994): 859–66. http://dx.doi.org/10.1152/jappl.1994.76.2.859.
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Tibialis anterior (TA) muscles of rats underwent bilateral peroneal nerve crush (NC) or denervation (D) and were compared with sham-operated (SO) animals to determine the effect of reinnervation on blood flow, mitochondria, metabolites, and muscle performance. After surgery, animals were left for 2, 7, 21, or 42 days (NC and SO groups) or 2, 7, or 21 days (D group; n = 7–11.day-1.group-1), after which TA muscles were stimulated in situ at 1 Hz. alpha-Motoneuron reinnervation of muscle was complete 21 days after NC. Blood flow increased 10-fold above SO values in nonstimulated TA muscle 7 days after NC and D (P < 0.05). By 21 days, blood flow to nonstimulated TA muscle in NC animals returned to SO values but remained elevated (P < 0.05) in D muscle. Thus restoration of neural control of blood flow to resting muscle likely occurred by 21 days post-NC. Blood flow to stimulated muscle was not affected by NC or D, indicating the probable importance of metabolic factors in regulating blood flow during 1-Hz contractions. Cytochrome-c oxidase activity decreased (P < 0.05) below SO values 7 days after NC and D. By 21 days, cytochrome-c oxidase activity in TA muscles of NC animals returned to SO values, while values in denervated TA muscle continued to decrease. Despite these changes, endurance performance of TA muscle was not affected by D or NC at any time. These results suggest that reinnervation processes controlling blood flow and muscle function occur along similar time courses and that muscle blood flow is more closely related to endurance performance than is muscle oxidative capacity under these contraction conditions.
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Pang, L. M., Y. J. Kim, and A. R. Bazzy. "Blood flow to respiratory muscles and major organs during inspiratory flow resistive loads." Journal of Applied Physiology 74, no. 1 (January 1, 1993): 428–34. http://dx.doi.org/10.1152/jappl.1993.74.1.428.
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To determine whether diaphragmatic fatigue in the intact animal subjected to loaded breathing is associated with a decrease in diaphragmatic blood flow, seven unanesthetized sheep were subjected to severe inspiratory flow resistive (IFR) loads that led to a decrease in transdiaphragmatic pressure (Pdi) and a rise in arterial PCO2 (PaCO2). Blood flow to the diaphragm, other respiratory muscles, limb muscles, and major organs was measured using the radionuclide-labeled microsphere method. With these loads blood flow increased to the diaphragm (621 +/- 242%) and all the other inspiratory and expiratory diaphragm (621 +/- 242%) and all the other inspiratory and expiratory muscles; there was no statistically significant change in blood flow to these muscles at the time when Pdi decreased and PaCO2 rose. Blood flow also increased to the heart (103 +/- 34%), brain (212 +/- 39%), and adrenals (76 +/- 9%), whereas pancreatic flow decreased (-66 +/- 14%). Limb muscle blood flow remained unchanged. We conclude that in unanesthetized sheep subjected to IFR loads 1) we did not demonstrate a decrease in respiratory muscle blood flow associated with diaphragmatic fatigue and ventilatory failure, and 2) there is a redistribution of blood flow among major organs.
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Turinsky, Jiri, Alice Damrau-Abney, and Daniel J. Loegering. "Blood flow and glucose uptake in denervated, insulin-resistant muscles." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 274, no. 2 (February 1, 1998): R311—R317. http://dx.doi.org/10.1152/ajpregu.1998.274.2.r311.
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To investigate whether changes in blood flow contribute to the insulin resistance in denervated muscles, basal and insulin-stimulated 2-deoxy-d-glucose (2-DG) uptake in vivo and blood flow were measured in soleus (slow twitch), plantaris (fast twitch), and gastrocnemius (fast twitch) muscles at 1 and 3 days after a right hindlimb denervation in the rat. Muscles of the contralateral sham hindlimb served as an internal control. Sham plantaris and gastrocnemius muscles showed 32 and 60% lower basal 2-DG uptake, 46 and 66% lower insulin-stimulated 2-DG uptake, and 79 and 81% lower blood flow, respectively, compared with sham soleus muscle. At 1 day after denervation, soleus, plantaris, and gastrocnemius muscles exhibited an 80, 64, and 42% decrease in insulin-stimulated 2-DG uptake, respectively, in the presence of 63, 323, and 304% higher blood flow, respectively. At 3 days after denervation, soleus muscle showed a 60% decrease in basal 2-DG uptake, complete unresponsiveness to insulin, and an 86% decrease in blood flow. In contrast, the denervated plantaris and gastrocnemius muscles exhibited a 262 and 105% increase in basal 2-DG uptake, respectively, no change in insulin-stimulated 2-DG uptake, and no change in blood flow compared with corresponding contralateral sham muscles. The results demonstrate that muscle blood flow is influenced by muscle fiber population and time after denervation and that changes in blood flow do not contribute to the insulin resistance in the denervated muscles.
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Hsia, C. C., M. Ramanathan, J. L. Pean, and R. L. Johnson. "Respiratory muscle blood flow in exercising dogs after pneumonectomy." Journal of Applied Physiology 73, no. 1 (July 1, 1992): 240–47. http://dx.doi.org/10.1152/jappl.1992.73.1.240.
Full textAbstract:
In three foxhounds after left pneumonectomy, the relationships of ventilatory work and respiratory muscle (RM) blood flow to ventilation (VE) during steady-state exercise were examined. VE was measured using a specially constructed respiratory mask and a pneumotach; work of breathing was measured by the esophageal balloon technique. Blood flow to RM was measured by the radionuclide-labeled microsphere technique. Lung compliance after pneumonectomy was 55% of that before pneumonectomy; compliance of the thorax was unchanged. O2 uptake (VO2) of RM comprised only 5% of total body VO2 at exercise. At rest, inspiratory muscles received 62% and expiratory muscles 38% of the total O2 delivered to the RM (QO2RM). During exercise, inspiratory muscles received 59% and expiratory muscles 41% of total QO2RM. Blood flow per gram of muscle to the costal diaphragm was significantly higher than that to the crural diaphragm. The diaphragm, parasternals, and posterior cricoarytenoids were the most important inspiratory muscles, and internal intercostals and external obliques were the most important expiratory muscles for exercise. Up to a VE of 120 l/min through one lung, QO2RM constituted only a small fraction of total body VO2 during exercise and maximal vasodilation in the diaphragm was never approached.
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Jatav, Minakshi. "Blood Flow Restriction (BFR) Therapy to Rehabilitate Muscle Injuries in Post-operative Knee Patient." Chettinad Health City Medical Journal 11, no. 02 (June 30, 2022): 51–61. http://dx.doi.org/10.24321/2278.2044.202216.
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KAATSU is a blood flow restriction training that was developed in Japan in the 1960s as a low-intensity strengthening exercise. It involves the wrapping of a tourniquet or pneumatic cuff over the muscle at a quick repetition rate during low-intensity muscle contractions. It is a muscle-strengthening technique used in physical therapy clinics to help patients regain muscle function following an injury or surgery. This is performed by temporarily cutting off blood flow to the muscles during the exercise. There were no linguistic or regional limitations in the literature searches for this article. This review contains a total of 25 records. Other resources were used to define additional elements. 4 records were duplicated and removed from the database. A total of 21 documents were found, with two being ruled out based on the title and abstract. Only 19 full-text items were authorised, and among these, 7 were eliminated because they were urgent research, case studies, and in a few studies, physical characteristics were not examined. This review article finally contained a total of 12 papers. Low-intensity exercise is used in blood flow restriction strengthening to achieve strength improvements similar to those seen in high-intensity training. BFR is a novel approach to physical therapy (PT). According to a preliminary study, this can result in adequate strength improvements during low-intensity exercise.
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Lavoie, Julie L., François Trudeau, and Louise Béliveau. "Effect of blood flow and muscle contraction on noradrenaline spillover in the canine gracilis muscle." Canadian Journal of Physiology and Pharmacology 78, no. 1 (December 22, 1999): 75–80. http://dx.doi.org/10.1139/y99-116.
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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.
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Musch, T. I., and D. C. Poole. "Blood flow response to treadmill running in the rat spinotrapezius muscle." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 6 (December 1, 1996): H2730—H2734. http://dx.doi.org/10.1152/ajpheart.1996.271.6.h2730.
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The rat spinotrapezius muscle has been utilized to investigate the microcirculatory consequences of exercise training. It was the purpose of this investigation to determine whether, and to what extent, this muscle is recruited during treadmill exercise. Radioactive 15-micron microspheres were used to measure blood flow to the spinotrapezius and hind limb musculature as well as to the abdominal organs of female Wistar rats. Blood flows were measured at rest and during two levels of treadmill-running exercise (i.e., 0% grade, 15 m/min and 10% grade, 24 m/min). As expected, exercise increased blood flow to the soleus, plantaris, red gastrocnemius, mixed gastrocnemius, and white gastrocnemius muscles, whereas blood flow to the stomach, intestines, pancreas, spleen, and kidneys was decreased (P < 0.05). However, contrary to our expectation, blood flow to the spinotrapezius muscle decreased from 61 +/- 6 ml.100 g-1.min-1 at rest to 39 +/- 2 ml.100 g-1.min-1 at 0% grade, 15 m/min and 46 +/- 4 ml.100 g-1.min-1 at 10% grade, 24 m/min (P < 0.05). These findings support the premise that treadmill running does not recruit the spinotrapezius muscle and suggest that previous training-induced arteriolar adaptations produced in this muscle may result from mechanisms unrelated to augmented exercise blood flow or muscle metabolism.
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Olive, Jennifer L., Jill M. Slade, Gary A. Dudley, and Kevin K. McCully. "Blood flow and muscle fatigue in SCI individuals during electrical stimulation." Journal of Applied Physiology 94, no. 2 (February 1, 2003): 701–8. http://dx.doi.org/10.1152/japplphysiol.00736.2002.
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Our purpose was to measure blood flow and muscle fatigue in chronic, complete, spinal cord-injured (SCI) and able-bodied (AB) individuals during electrical stimulation. Electrical stimulation of the quadriceps muscles was used to elicit similar activated muscle mass. Blood flow was measured in the femoral artery by Doppler ultrasound. Muscle fatigue was significantly greater (three- to eightfold, P ≤ 0.001) in the SCI vs. the AB individuals. The magnitude of blood flow was not significantly different between groups. A prolonged half-time to peak blood flow at the beginning of exercise (fivefold, P = 0.001) and recovery of blood flow at the end of exercise (threefold, P = 0.009) was found in the SCI vs. the AB group. In conclusion, the magnitude of the muscle blood flow to electrical stimulation was not associated with increased muscle fatigue in SCI individuals. However, the prolonged time to peak blood flow may be an explanation for increased fatigue in SCI individuals.
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Armstrong, R. B., C. D. Ianuzzo, and M. H. Laughlin. "Blood flow and glycogen use in hypertrophied rat muscles during exercise." Journal of Applied Physiology 61, no. 2 (August 1, 1986): 683–87. http://dx.doi.org/10.1152/jappl.1986.61.2.683.
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Previous findings suggest that skeletal muscle that has enlarged as a result of removal of synergistic muscles has a similar metabolic capacity and improved resistance to fatigue compared with normal muscle. The purpose of the present study was to follow blood flow and glycogen loss patterns in hypertrophied rat plantaris plantaris and soleus muscles during treadmill exercise to provide information on the adequacy of perfusion of the muscles during in vivo exercise. Thirty days following surgical removal of gastrocnemius muscle, blood flows (determined with radiolabeled microspheres) and glycogen concentrations were determined in all of the ankle extensor muscles of experimental and sham-operated control rats during preexercise and after 5–6 min of treadmill exercise at 15 m/min. There were no differences (P greater than 0.05) in blood flows per unit mass or glycogen concentrations between control and hypertrophied plantaris or soleus muscles at either time, although both muscles were larger (P less than 0.05) in the experimental group (plantaris: 95%; soleus: 40%). None of the other secondary ankle extensor muscles (tibialis posterior, flexor digitorum longus or flexor hallicus longus) hypertrophied in response to removal of gastrocnemius. These results provide indirect evidence that O2 delivery in the enlarged muscles is not compromised during low-intensity treadmill exercise due to limited perfusion.
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EGAR, E. I. "Muscle blood flow and neuromuscular block." British Journal of Anaesthesia 73, no. 5 (November 1994): 726. http://dx.doi.org/10.1093/bja/73.5.726-c.
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ABDULATIF, M. "Muscle blood flow and neuromuscular block." British Journal of Anaesthesia 73, no. 5 (November 1994): 726. http://dx.doi.org/10.1093/bja/73.5.726-d.
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Cherepanova, Vera, Tatyana Neshumova, and Robert Elsner. "Muscle blood flow in diving mammals." Comparative Biochemistry and Physiology Part A: Physiology 106, no. 1 (September 1993): 1–6. http://dx.doi.org/10.1016/0300-9629(93)90029-4.
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Craig, Bruce W. "Can Blood Flow Influence Muscle Growth?" Strength and Conditioning Journal 24, no. 2 (April 2002): 13–14. http://dx.doi.org/10.1519/00126548-200204000-00003.
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LAUGHLIN, M. HAROLD, and R. B. ARMSTRONG. "Muscle Blood Flow During Locomotory Exercise." Exercise and Sport Sciences Reviews 13 (1985): 95???136. http://dx.doi.org/10.1249/00003677-198500130-00006.
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Pilegaard, H., J. Bangsbo, P. Henningsen, C. Jeul, and EA Richter. "Blood Flow and Muscle Lactate Release." Clinical Science 87, s1 (January 1, 1994): 72. http://dx.doi.org/10.1042/cs087s072.
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Armstrong, R. B., C. B. Vandenakker, and M. H. Laughlin. "Muscle blood flow patterns during exercise in partially curarized rats." Journal of Applied Physiology 58, no. 3 (March 1, 1985): 698–701. http://dx.doi.org/10.1152/jappl.1985.58.3.698.
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We studied the distribution of blood flow within and among muscles of partially curarized (40–100 micrograms/kg body wt) rats during preexercise and at 1 min of low-speed treadmill exercise (15 m/min). Glycogen loss in the deep red muscles and parts of muscles was significantly reduced in the curarized animals during exercise, indicating the fibers in these muscles were recruited to a lesser extent and/or had lower metabolisms than fibers in the same muscles of control rats. However, elevations in blood flow in the red muscles of the curarized rats were as great or greater than those in the control rats. Thus reduced recruitment and/or metabolism of the deep red muscle fibers of the curarized animals was not accompanied by reduced blood flow. These findings suggest a dissociation between red fiber metabolism and blood flow in the curarized rats during the 1st min of slow treadmill exercise and indicate that release of vasodilator substances or local physical factors associated with muscle fiber activity are not solely responsible for the initial hyperemia during exercise.
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Laughlin, M. H., R. J. Korthuis, W. L. Sexton, and R. B. Armstrong. "Regional muscle blood flow capacity and exercise hyperemia in high-intensity trained rats." Journal of Applied Physiology 64, no. 6 (June 1, 1988): 2420–27. http://dx.doi.org/10.1152/jappl.1988.64.6.2420.
Full textAbstract:
The purpose of this study was to determine the effects of high-intensity treadmill exercise training on 1) the regional distribution of muscle blood flow within and among muscles in rats during high-intensity treadmill exercise (phase I) and 2) on the total and regional hindlimb skeletal muscle blood flow capacities as measured in isolated perfused rat hindquarters during maximal papaverine vasodilation (phase II). Two groups of male Sprague-Dawley rats were trained 5 days/wk for 6 wk with a program consisting of 6 bouts/day of 2.5-min runs at 60 m/min up a 15% grade with 4.5-min rest periods between bouts. After training, blood flows were measured with the radiolabeled microsphere technique (phase I) in pair-weighted sedentary control and exercise-trained rats while they ran at 60 m/min (0% grade). In phase II of the study, regional vascular flow capacities were determined at three perfusion pressures (30, 40, and 50 mmHg) in isolated perfused hindquarters of control and trained rats maximally vasodilated with papaverine. The results indicate that this exercise training program produces increases in the vascular flow capacity of fast-twitch glycolytic muscle tissue of rats. However, these changes were not apparent in the magnitude or distribution of muscle blood flow in conscious rats running at 60 m/min, since blood flows within and among muscles during exercise were the same in trained and control rats.
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Schmid-Scho¨nbein, G. W. "A Theory of Blood Flow in Skeletal Muscle." Journal of Biomechanical Engineering 110, no. 1 (February 1, 1988): 20–26. http://dx.doi.org/10.1115/1.3108401.
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A theoretical analysis of blood flow in the microcirculation of skeletal muscle is provided. The flow in the microvessels of this organ is quasi steady and has a very low Reynolds number. The blood is non-Newtonian and the blood vessels are distensible with viscoelastic properties. A formulation of the problem is provided using a viscoelastic model for the vessel wall which was recently derived from measurements in the rat spinotrapezius muscle (Skalak and Schmid-Scho¨nbein, 1986b). Closed form solutions are derived for several physiologically important cases, such as perfusion at steady state, transient and oscillatory flows. The results show that resting skeletal muscle has, over a wide range of perfusion pressures an almost linear pressure-flow curve. At low flow it exhibits nonlinearities. Vessel distensibility and the non-Newtonian properties of blood both have a strong influence on the shape of the pressure-flow curve. During oscillatory flow the muscle exhibits hysteresis. The theoretical results are in qualitative agreement with experimental observations.
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McDonald, K. S., M. D. Delp, and R. H. Fitts. "Effect of hindlimb unweighting on tissue blood flow in the rat." Journal of Applied Physiology 72, no. 6 (June 1, 1992): 2210–18. http://dx.doi.org/10.1152/jappl.1992.72.6.2210.
Full textAbstract:
The purpose of this study was to characterize the distribution of blood flow in the rat during hindlimb unweighting (HU) and post-HU standing and exercise and examine whether the previously reported (Witzmann et al., J. Appl. Physiol. 54: 1242–1248, 1983) elevation in anaerobic metabolism observed with contractile activity in the atrophied soleus muscle was caused by a reduced hindlimb blood flow. After either 15 days of HU or cage control, blood flow was measured with radioactive microspheres during unweighting, normal standing, and running on a treadmill (15 m/min). In another group of control and experimental animals, blood flow was measured during preexercise (PE) treadmill standing and treadmill running (15 m/min). Soleus muscle blood flow was not different between groups during unweighting, PE standing, and running at 15 m/min. Chronic unweighting resulted in the tendency for greater blood flow to muscles composed of predominantly fast-twitch glycolytic fibers. With exercise, blood flow to visceral organs was reduced compared with PE values in the control rats, whereas flow to visceral organs in 15-day HU animals was unaltered by exercise. These higher flows to the viscera and to muscles composed of predominantly fast-twitch glycolytic fibers suggest an apparent reduction in the ability of the sympathetic nervous system to distribute cardiac output after chronic HU. In conclusion, because 15 days of HU did not affect blood flow to the soleus during exercise, the increased dependence of the atrophied soleus on anerobic energy production during contractile activity cannot be explained by a reduced muscle blood flow.
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Copp, Steven W., Peter J. Schwagerl, Daniel M. Hirai, David C. Poole, and Timothy I. Musch. "Acute ascorbic acid and hindlimb skeletal muscle blood flow distribution in old rats: rest and exercise." Canadian Journal of Physiology and Pharmacology 90, no. 11 (November 2012): 1498–505. http://dx.doi.org/10.1139/y2012-109.
Full textAbstract:
Excess reactive oxygen species are implicated in the impaired peripheral vascular function evident during exercise in older individuals. We tested the hypothesis that an acute infusion of the antioxidant ascorbic acid (AA) in old rats would improve antioxidant capacity and reduce oxidative stress and, therefore, elevate hindlimb muscle blood flow at rest and during treadmill exercise in muscles containing principally type I and IIa muscle fibers. Total and individual hindlimb skeletal muscle blood flow was measured (radiolabeled microspheres) in old rats (26–28 months) at rest (n = 8) and during treadmill exercise (n = 8; 20 m·min–1, 5% grade) before and after AA treatment (76 mg·(kg body mass)–1 intra-arterial (i.a.) injection). AA elevated total antioxidant capacity (rest, ∼37%; and exercise, 31%) and reduced oxidative stress (∼26%, exercise only). AA reduced resting total hindlimb muscle blood flow (control, 25 ± 3; AA, 16 ± 2 mL·min–1·(100 g)–1; p < 0.05) and blood flow to 8 of 28 individual muscles with no fiber-type correlation (p > 0.05). During exercise there was no effect of AA on total hindlimb muscle blood flow (control, 154 ± 14; AA, 162 ± 13 mL·min–1·(100 g)–1; p > 0.05) or blood flow to any individual muscle. This disconnect between whole-body antioxidant status and skeletal muscle blood flow in old rats mandates consideration when pursuing antioxidant treatments experimentally or clinically in older populations.
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Mittelstadt, S. W., L. B. Bell, K. P. O'Hagan, and P. S. Clifford. "Muscle chemoreflex alters vascular conductance in nonischemic exercising skeletal muscle." Journal of Applied Physiology 77, no. 6 (December 1, 1994): 2761–66. http://dx.doi.org/10.1152/jappl.1994.77.6.2761.
Full textAbstract:
Previous studies have shown that the muscle chemoreflex causes an augmented blood pressure response to exercise and partially restores blood flow to ischemic muscle. The purpose of this study was to investigate the effects of the muscle chemoreflex on blood flow to nonischemic exercising skeletal muscle. During each experiment, dogs ran at 10 kph for 8–16 min and the muscle chemoreflex was evoked by reducing hindlimb blood flow at 4-min intervals (0–80%). Arterial blood pressure, hindlimb blood flow, forelimb blood flow, and forelimb vascular conductance were averaged over the last minute at each level of occlusion. Stimulation of the muscle chemoreflex caused increases in arterial blood pressure and forelimb blood flow and decreases in forelimb vascular conductance. The decrease in forelimb vascular conductance demonstrates that the muscle chemoreflex causes vasoconstriction in the nonischemic exercising forelimb. Despite the decrease in vascular conductance, the increased driving pressure caused by the pressor response was large enough to produce an increased forelimb blood flow.
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Dobson, John L., and L. Bruce Gladden. "Effect of rhythmic tetanic skeletal muscle contractions on peak muscle perfusion." Journal of Applied Physiology 94, no. 1 (January 1, 2003): 11–19. http://dx.doi.org/10.1152/japplphysiol.00339.2002.
Full textAbstract:
The purpose of this investigation was to examine the effect of rhythmic tetanic skeletal muscle contractions on peak muscle perfusion by using spontaneously perfused canine gastrocnemii in situ. Simultaneous pulsatile blood pressures were measured by means of transducers placed in the popliteal artery and vein, and pulsatile flow was measured with a flow-through-type transit-time ultrasound probe placed in the venous return line. Two series of experiments were performed. In series 1, maximal vasodilation of the muscles' vascular beds was elicited by infusing a normal saline solution containing adenosine (29.3 mg/min) and sodium nitroprusside (180 μg/min) for 15 s and then simultaneously occluding both the popliteal artery and vein for 5 min. The release of occlusion initiated a maximal hyperemic response, during which time four tetanic contractions were induced with supramaximal voltage (6–8 V, 0.2-ms stimuli for 200-ms duration at 50 Hz, 1/s). In series 2, the muscles were stimulated for 3 min before the muscle contractions were stopped for a period of 3 s; stimulation was then resumed. The results of series 1 indicate that, although contractions lowered venous pressure, muscle blood flow was significantly reduced from 2,056 ± 246 to 1,738 ± 225 ml · kg−1 · min−1when contractions were initiated and then increased significantly to 1,925 ± 225 ml · kg−1 · min−1during the first 5 s after contractions were stopped. In series 2, blood flow after 3 min of contractions averaged 1,454 ± 149 ml · kg−1 · min−1. Stopping the contractions for 3 s caused blood flow to increase significantly to 1,874 ± 172 ml · kg−1 · min−1; blood flow declined significantly to 1,458 ± 139 ml · kg−1 · min−1when contractions were resumed. We conclude that the mechanical action of rhythmic, synchronous, maximal isometric tetanic skeletal muscle contractions inhibits peak muscle perfusion during maximal and near-maximal vasodilation of the muscle's vascular bed. This argues against a primary role for the muscle pump in achieving peak skeletal muscle blood flow.
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Bond Jr., Vernon, Arthur T. Johnson, Paul Vaccaro, Paul Wang, Richard G. Adams, Russell J. Tearney, Richard M. Millis, B. Don Franks, and David R. Bassett Jr. "Lower Leg High-Intensity Resistance Training and Peripheral Hemodynamic Adaptations." Canadian Journal of Applied Physiology 21, no. 3 (June 1, 1996): 209–17. http://dx.doi.org/10.1139/h96-017.
Full textAbstract:
High-intensity resistance (HIR) training has been associated with muscle hypertrophy and decreased microvascular density that might produce a blood flow limitation. The effect of HIR training on lower leg maximal blood flow and minimum vascular resistance (Rmin) during reactive hyperemia were investigated in 7 healthy males. The gastrocnemius-soleus muscles of one leg were trained using maximal isokinetic concentric contractions for 4 weeks; the nontrained leg was the control. Lower leg blood flow was measured by venous occlusion plethysmography. Lower leg muscle volume was determined using magnetic resonance imaging. Peak isokinetic torque increased in both the trained (T) and nontrained (NT) legs (p <.05). Lower leg muscle volume increased by 2% in the T leg only (p <.05). In the T leg, maximal blood flow decreased and Rmin increased (p <.05); no hemodynamic change was detected in the NT leg. It is concluded that HIR training of the calf muscles is associated with a decrease in hyperemia-induced blood flow; thereby, indicating a blood flow limitation to the calf muscles. Key words: Isokinetic strength training, reactive hyperemia
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Blaak, E. E., M. A. van Baak, G. J. Kemerink, M. T. W. Pakbiers, G. A. K. Heidendal, and W. H. M. Saris. "Total Forearm Blood Flow as an Indicator of Skeletal Muscle Blood Flow: Effect of Subcutaneous Adipose Tissue Blood Flow." Clinical Science 87, no. 5 (November 1, 1994): 559–66. http://dx.doi.org/10.1042/cs0870559.
Full textAbstract:
1. In studying forearm skeletal muscle substrate exchange, an often applied method for estimating skeletal muscle blood flow is strain gauge plethysmography. A disadvantage of this method is that it only measures total blood flow through a segment of forearm and not the flow through the individual parts such as skin, adipose tissue and muscle. 2. In the present study the contribution of forearm subcutaneous adipose tissue blood flow to total forearm blood flow was evaluated in lean (% body fat 17.0 ± 2.2) and obese males (% body fat 30.9 ± 1.6) during rest and during infusion of the non-selective β-agonist isoprenaline. Measurements were obtained of body composition (hydrostatic weighing), forearm composition (magnetic resonance imaging) and of total forearm (venous occlusion plethysmography), skin (skin blood flow, laser Doppler), and subcutaneous adipose tissue blood flow (133Xe washout technique). 3. The absolute forearm area and the relative amount of fat (% of forearm area) were significantly higher in obese as compared to lean subjects, whereas the relative amounts of muscle and skin were similar. 4. During rest, the percentage contribution of adipose tissue blood flow to total forearm blood flow was significantly higher in lean compared with obese subjects (19 vs 12%, P < 0.05), whereas there were no differences in percentage contribution between both groups during isoprenaline infusion (10 vs 13%). Furthermore, the contribution of adipose tissue blood flow to total forearm blood flow was significantly lower during isoprenaline infusion than during rest in lean subjects (P < 0.05), whereas in the obese this value was similar during rest and during isoprenaline infusion. 5. In conclusion, although the overall contribution of adipose tissue blood flow to total forearm blood flow seems to be relatively small, the significance of this contribution may vary with degree of adiposity. Calculations on the contribution of adipose tissue blood flow and SBF to total forearm blood flow indicate that the contribution of non-muscular flow to total forearm blood flow may be of considerable importance and may amount in lean subjects to 35–50% of total forearm blood flow in the resting state.