Regulation of Blood Flow at the Onset of Exercise by Feed Forward and Feedback Mechanisms

2003 ◽  
Vol 28 (5) ◽  
pp. 774-787 ◽  
Author(s):  
Richard L. Hughson

Blood flow adapts quickly after the onset of exercise to meet the metabolic demands of skeletal muscle. This review approaches the issue of how rapidly blood flow adapts and what the mechanisms for adaptation are primarily from a control theory perspective. Several recent papers have suggested that O2 transport proceeds at a rate that anticipates the metabolic demand over a very wide range of work rates. When considered from a control theory perspective, this implies involvement of feed forward control. Although there is one very important feed forward mechanism in the muscle pump that is activated with the onset of exercise, other evidence suggests that adjustment of blood flow to match the metabolic demand relies on feedback control from local dilator factors released in proportion to the metabolic demand. These distinct mechanisms with different onset times mean that blood flow adapts to the exercise demand with at least two distinct phases. The time course of the adaptation varies greatly between work rates, showing that blood flow control cannot be described by a linear control system and that the mechanisms responsible for vasodilation are dependent on work rate. Key words: oxygen uptake, kinetics, vasodilation, muscle metabolism

Physiology ◽  
1992 ◽  
Vol 7 (4) ◽  
pp. 152-156 ◽  
Author(s):  
SS Segal

Peripheral blood flow control during exercise is coordinated among several vascular locations. The locus of control shifts upstream from distal arterioles into feeding arteries as metabolic demand increases. This shift occurs by cell-to-cell conduction and by flow-dependent endothelial cell-mediated relaxation of smooth muscle cells.


2004 ◽  
Vol 97 (1) ◽  
pp. 393-403 ◽  
Author(s):  
Philip S. Clifford ◽  
Ylva Hellsten

Skeletal muscle blood flow is closely coupled to metabolic demand, and its regulation is believed to be mainly the result of the interplay of neural vasoconstrictor activity and locally derived vasoactive substances. Muscle blood flow is increased within the first second after a single contraction and stabilizes within ∼30 s during dynamic exercise under normal conditions. Vasodilator substances may be released from contracting skeletal muscle, vascular endothelium, or red blood cells. The importance of specific vasodilators is likely to vary over the time course of flow, from the initial rapid rise to the sustained elevation during steady-state exercise. Exercise hyperemia is therefore thought to be the result of an integrated response of more than one vasodilator mechanism. To date, the identity of vasoactive substances involved in the regulation of exercise hyperemia remains uncertain. Numerous vasodilators such as adenosine, ATP, potassium, hypoxia, hydrogen ion, nitric oxide, prostanoids, and endothelium-derived hyperpolarizing factor have been proposed to be of importance; however, there is little support for any single vasodilator being essential for exercise hyperemia. Because elevated blood flow cannot be explained by the failure of any single vasodilator, a consensus is beginning to emerge for redundancy among vasodilators, where one vasoactive compound may take over when the formation of another is compromised. Conducted vasodilation or flow-mediated vasodilation may explain dilation in vessels (i.e., feed arteries) not directly exposed to vasodilator substances in the interstitium. Future investigations should focus on identifying novel vasodilators and the interaction between vasodilators by simultaneous inhibition of multiple vasodilator pathways.


2008 ◽  
Vol 22 (2) ◽  
pp. 81-90 ◽  
Author(s):  
Natalie Werner ◽  
Neval Kapan ◽  
Gustavo A. Reyes del Paso

The present study explored modulations in cerebral blood flow and systemic hemodynamics during the execution of a mental calculation task in 41 healthy subjects. Time course and lateralization of blood flow velocities in the medial cerebral arteries of both hemispheres were assessed using functional transcranial Doppler sonography. Indices of systemic hemodynamics were obtained using continuous blood pressure recordings. Doppler sonography revealed a biphasic left dominant rise in cerebral blood flow velocities during task execution. Systemic blood pressure increased, whereas heart period, heart period variability, and baroreflex sensitivity declined. Blood pressure and heart period proved predictive of the magnitude of the cerebral blood flow response, particularly of its initial component. Various physiological mechanisms may be assumed to be involved in cardiovascular adjustment to cognitive demands. While specific contributions of the sympathetic and parasympathetic systems may account for the observed pattern of systemic hemodynamics, flow metabolism coupling, fast neurogenic vasodilation, and cerebral autoregulation may be involved in mediating cerebral blood flow modulations. Furthermore, during conditions of high cardiovascular reactivity, systemic hemodynamic changes exert a marked influence on cerebral blood perfusion.


2021 ◽  
Vol 7 (2) ◽  
pp. 205521732110227
Author(s):  
Friederike Held ◽  
Sudhakar Reddy Kalluri ◽  
Achim Berthele ◽  
Ana-Katharina Klein ◽  
Markus Reindl ◽  
...  

Background Myelin oligodendrocyte glycoprotein (MOG) antibody disease (MOG-AD) is recognized as a distinct nosological entity. IgG antibodies against MOG (MOG-Ab) overlap with neuromyelitis optica spectrum disorders (NMOSD) phenotype in adults. However, an increasing number of clinical phenotypes have been reported to be associated with MOG-Ab. Objective To investigate the seroprevalence of MOG-Ab under consideration of demographics, disease entities and time course in a large cohort of unselected neurological patients. Methods Blood samples of 2.107 consecutive adult neurologic patients admitted to our department between 2016-2017 were tested for MOG-Ab using a cell-based assay. MOG-Ab persistence was analyzed in follow-up samples. External validation was performed in two independent laboratories. Results We found MOG-Ab in 25 of 2.107 (1.2%) patients. High antibody ratios were mostly associated with NMOSD and MOG-AD phenotype (5/25). Low ratios occurred in a wide range of neurological diseases, predominantly in other demyelinating CNS diseases (5/25) and stroke (6/25). MOG-Ab persistence over time was not confined to NMOSD and MOG-AD phenotype. Conclusion The present study demonstrates the occurrence of MOG-Ab in a wide range of neurological diseases. Only high MOG-Ab ratios were associated with a defined clinical phenotype, but low MOG-Ab ratios were not. The diagnostic value of low MOG-Ab is thus highly limited.


1996 ◽  
Vol 81 (4) ◽  
pp. 1516-1521 ◽  
Author(s):  
J. K. Shoemaker ◽  
H. L. Naylor ◽  
Z. I. Pozeg ◽  
R. L. Hughson

Shoemaker, J. K., H. L. Naylor, Z. I. Pozeg, and R. L. Hughson. Failure of prostaglandins to modulate the time course of blood flow during dynamic forearm exercise in humans. J. Appl. Physiol. 81(4): 1516–1521, 1996.—The time course and magnitude of increases in brachial artery mean blood velocity (MBV; pulsed Doppler), diameter ( D; echo Doppler), mean perfusion pressure (MPP; Finapres), shear rate (γ˙ = 8 ⋅ MBV/ D), and forearm blood flow (FBF = MBV ⋅ π r 2) were assessed to investigate the effect that prostaglandins (PGs) have on the hyperemic response on going from rest to rhythmic exercise in humans. While supine, eight healthy men performed 5 min of dynamic handgrip exercise by alternately raising and lowering a 4.4-kg weight (∼10% maximal voluntary contraction) with a work-to-rest cycle of 1:1 (s/s). When the exercise was performed with the arm positioned below the heart, the rate of increase in MBV and γ˙ was faster compared with the same exercise performed above the heart. Ibuprofen (Ibu; 1,200 mg/day, to reduce PG-induced vasodilation) and placebo were administered orally for 2 days before two separate testing sessions in a double-blind manner. Resting heart rate was reduced in Ibu (52 ± 3 beats/min) compared with placebo (57 ± 3 beats/min) ( P < 0.05) without change to MPP. With placebo, D increased in both arm positions from ∼4.3 mm at rest to ∼4.5 mm at 5 min of exercise ( P < 0.05). This response was not altered with Ibu ( P > 0.05). Ibu did not alter the time course of MBV or forearm blood flow ( P > 0.05) in either arm position. The γ˙ was significantly greater in Ibu vs. placebo at 30 and 40 s of above the heart exercise and for all time points after 25 s of below the heart exercise ( P < 0.05). Because PG inhibition altered the time course ofγ˙ at the brachial artery, but not FBF, it was concluded that PGs are not essential in regulating the blood flow responses to dynamic exercise in humans.


1965 ◽  
Vol 209 (4) ◽  
pp. 705-710 ◽  
Author(s):  
Michael D. Klein ◽  
Lawrence S. Cohen ◽  
Richard Gorlin

Myocardial blood flow in human subjects was assessed by comparative simultaneous measurement of krypton 85 radioactive decay from coronary sinus and precordial scintillation. Empirical correction of postclearance background from precordial curves yielded a high degree of correlation between flows derived from the two sampling sites (r = .889, P < .001). Comparison of left and right coronary flows in nine subjects revealed similarity in flow through the two vessels over a wide range of actual flow values (r = .945, P < .001).


1979 ◽  
Vol 47 (6) ◽  
pp. 1228-1233 ◽  
Author(s):  
D. S. Simon ◽  
J. F. Murray ◽  
N. C. Staub

We evaluated the attenuation of the 122 keV gamma ray of cobalt-57 across the thorax of anesthetized dogs as a method for following the time course of lung water changes in acute pulmonary edema induced by either increased microvascular permeability or increased microvascular hydrostatic pressure. The gamma rays traversed the thorax centered on the seventh rib laterally where the lung mass in the beam path was greatest. Calibration measurements in isolated lung lobes demonstrated the high sensitivity and inherent accuracy of the method over a wide range of lung water contents. In control dogs reproducibility averaged +/-3%. Increased permeability edema led to large rapid increases in the transthoracic gamma ray attenuation (TGA), while increased pressure caused an immediate, modest increase in TGA (vascular congestion) followed by a slow further increase over 2 h. There was a fairly good correlation between the increase in extravascular lung water and the change in TGA. The method is simple, safe, and noninvasive and appears to be useful for following the time course of lung water accumulation in generalized lung edema in anesthetized animals.


Author(s):  
Jenifer M Brown ◽  
Wunan Zhou ◽  
Brittany Weber ◽  
Sanjay Divakaran ◽  
Leanne Barrett ◽  
...  

Abstract Aims The transition from hypertension to heart failure (HF) remains poorly understood. We hypothesized that insufficient perfusion to match global metabolic demand, reflected by a low ratio of myocardial blood flow to global myocardial mass, may be a HF risk marker. Methods and results A retrospective cohort (n = 346) of patients with hypertension who underwent clinical positron emission tomography (PET) myocardial perfusion imaging for chest pain and/or dyspnoea at Brigham and Women’s Hospital (Boston, MA, USA) were studied. Patients without obstructive coronary artery disease by history or PET perfusion (summed stress score &lt;3), HF, cardiomyopathy, or ejection fraction (EF) &lt;40% were followed for HF hospitalization (primary outcome), all-cause death, and their composite. Myocardial blood flow, left ventricular (LV) mass, volumes, and EF were obtained from PET, and a ‘flow/mass ratio’ was determined as hyperaemic myocardial blood flow over LV mass indexed to body surface area. A lower flow/mass ratio was independently associated with larger end-diastolic (β = −0.44, P &lt; 0.001) and end-systolic volume (β = −0.48, P &lt; 0.001) and lower EF (β = 0.33, P &lt; 0.001). A flow/mass ratio below the median was associated with an adjusted hazard ratio of 2.47 [95% confidence interval (CI) 1.24–4.93; P = 0.01] for HF hospitalization, 1.95 (95% CI 1.12–3.41; P = 0.02) for death, and 2.20 (95% CI 1.39–3.49; P &lt; 0.001) for the composite. Conclusion An integrated physiological measure of insufficient myocardial perfusion to match global metabolic demand identifies subclinical hypertensive heart disease and elevated risk of HF and death in symptomatic patients with hypertension but without flow-limiting coronary artery disease.


2010 ◽  
Vol 108 (3) ◽  
pp. 705-712 ◽  
Author(s):  
Andrés Hernández ◽  
Matthew L. Goodwin ◽  
Nicola Lai ◽  
Marco E. Cabrera ◽  
James R. McDonald ◽  
...  

The purpose of this research was to develop new techniques to 1) rapidly sample venous O2 saturation to determine contraction-by-contraction oxygen uptake (V̇o2), and 2) precisely control the rate and pattern of blood flow adjustment from one chosen steady state to another. An indwelling inline oximeter probe connected to an Oximetrix 3 meter was used to sample venous oxygen concentration ([O2]) (via fractional saturation of Hb with O2). Data from the Oximetrix 3 were filtered, deconvolved, and processed by a moving average second by second. Computer software and a program written in-house were used to control blood flow with a peristaltic pump. The isolated canine gastrocnemius muscle complex (GS) in situ was utilized to test these techniques. A step change in metabolic rate was elicited by stimulating GS muscles via their sciatic nerves (supramaximal voltage, 8 V; 50 Hz, 0.2-ms pulse width; train duration 200 ms) at a rate of either 1 contraction/2 s, or 2 contractions/3 s. With arterial [O2] maintained constant, blood flow and calculated venous [O2] were averaged over each contraction cycle and used in the Fick equation to calculate contraction-by-contraction V̇o2. About 5–8 times more data points were obtained with this method compared with traditional manual sampling. Software-controlled pump perfusion enabled the ability to mimic spontaneous blood flow on-kinetics (τ: 14.3 s) as well as dramatically speed (τ: 2.0 s) and slow (τ: 63.3 s) on-kinetics. These new techniques significantly improve on existing methods for mechanistically altering blood flow kinetics as well as accurately measuring muscle oxygen consumption kinetics during transitions between metabolic rates.


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