EFFECTS OF EXERCISE ON BLOOD PRESSURE, SYMPATHETIC NERVE ACTIVITY, AND MUSCLE BLOOD FLOW RESPONSES TO HYPERINSULINEMIA IN MEN.

1998 ◽  
Vol 30 (Supplement) ◽  
pp. 213
Author(s):  
C. L.M. Forjaz ◽  
P. R. Ramires ◽  
T. Tinucci ◽  
K. C. Ortega ◽  
H. E.H. Salom??o ◽  
...  
2004 ◽  
Vol 97 (2) ◽  
pp. 731-738 ◽  
Author(s):  
Gail D. Thomas ◽  
Steven S. Segal

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.


2009 ◽  
Vol 12 (1) ◽  
pp. 58-65 ◽  
Author(s):  
Ligia M. Antunes-Correa ◽  
Ruth C. Melo ◽  
Thais S. Nobre ◽  
Linda M. Ueno ◽  
Fabio G.M. Franco ◽  
...  

2006 ◽  
Vol 290 (4) ◽  
pp. H1601-H1609 ◽  
Author(s):  
Jian Cui ◽  
Mithra Sathishkumar ◽  
Thad E. Wilson ◽  
Manabu Shibasaki ◽  
Scott L. Davis ◽  
...  

Skin sympathetic nerve activity (SSNA) exhibits low- and high-frequency spectral components in normothermic subjects. However, spectral characteristics of SSNA in heat-stressed subjects are unknown. Because the main components of the integrated SSNA during heat stress (sudomotor/vasodilator activities) are different from those during normothermia and cooling (vasoconstrictor activity), we hypothesize that spectral characteristics of SSNA in heat-stressed subjects will be different from those in subjects subjected to normothermia or cooling. In 17 healthy subjects, SSNA, electrocardiogram, arterial blood pressure (via Finapres), respiratory activity, and skin blood flow were recorded during normothermia and heat stress. In 7 of the 17 subjects, these variables were also recorded during cooling. Spectral characteristics of integrated SSNA, R-R interval, beat-by-beat mean blood pressure, skin blood flow variability, and respiratory excursions were assessed. Heat stress and cooling significantly increased total SSNA. SSNA spectral power in the low-frequency (0.03–0.15 Hz), high-frequency (0.15–0.45 Hz), and very-high-frequency (0.45–2.5 Hz) regions was significantly elevated by heat stress and cooling. Interestingly, heat stress caused a greater relative increase of SSNA spectral power within the 0.45- to 2.5-Hz region than in the other spectral ranges; cooling did not show this effect. Differences in the SSNA spectral distribution between normothermia/cooling and heat stress may reflect different characteristics of central modulation of vasoconstrictor and sudomotor/vasodilator activities.


Physiology ◽  
1995 ◽  
Vol 10 (6) ◽  
pp. 274-280
Author(s):  
JM Marshall

Studies involving recordings of gross muscle blood flow and intravital microscopy have been used to analyze the behavior of muscle vasculature during systemic hypoxia. The roles of sympathetic nerve activity, circulating hormones (e.g., catecholamines, angiotensin, vasopressin), and locally released adenosine and K+ in determining the behavior of arterial and venous vessels are considered.


2005 ◽  
Vol 98 (3) ◽  
pp. 866-871 ◽  
Author(s):  
V. A. F. Bisquolo ◽  
C. G. Cardoso ◽  
K. C. Ortega ◽  
J. L. Gusmão ◽  
T. Tinucci ◽  
...  

Insulin infusion causes muscle vasodilation, despite the increase in sympathetic nerve activity. In contrast, a single bout of exercise decreases sympathetic activity and increases muscle blood flow during the postexercise period. We tested the hypothesis that muscle sympathetic activity would be lower and muscle vasodilation would be higher during hyperinsulinemia performed after a single bout of dynamic exercise. Twenty-one healthy young men randomly underwent two hyperinsulinemic euglycemic clamps performed after 45 min of seated rest (control) or bicycle exercise (50% of peak oxygen uptake). Muscle sympathetic nerve activity (MSNA, microneurography), forearm blood flow (FBF, plethysmography), blood pressure (BP, oscillometric method), and heart rate (HR, ECG) were measured at baseline (90 min after exercise or seated rest) and during hyperinsulinemic euglycemic clamps. Baseline glucose and insulin concentrations were similar in the exercise and control sessions. Insulin sensitivity was unchanged by previous exercise. During the clamp, insulin levels increased similarly in both sessions. As expected, insulin infusion increased MSNA, FBF, BP, and HR in both sessions (23 ± 1 vs. 36 ± 2 bursts/min, 1.8 ± 0.1 vs. 2.2 ± 0.2 ml·min−1·100 ml−1, 89 ± 2 vs. 92 ± 2 mmHg, and 58 ± 1 vs. 62 ± 1 beats/min, respectively, P < 0.05). BP and HR were similar between sessions. However, MSNA was significantly lower (27 ± 2 vs. 31 ± 2 bursts/min), and FBF was significantly higher (2.2 ± 0.2 vs. 1.8 ± 0.1 ml·min−1·100 ml−1, P < 0.05) in the exercise session compared with the control session. In conclusion, in healthy men, a prolonged bout of dynamic exercise decreases MSNA and increases FBF. These effects persist during acute hyperinsulinemia performed after exercise.


2016 ◽  
Author(s):  
◽  
Shenghua Yuan Sinkler

Rapid onset vasodilation (ROV) occurs immediately in response to skeletal muscle contraction and initiates a prompt increase in blood flow and oxygen delivery that facilitate the transition to exercise. Muscle blood flow is attenuated during aging which limits physical activity. Understanding the mechanisms that attenuate ROV requires invasive measurements that cannot be performed in human subjects. Published studies indicate that the effects of aging on muscle blood flow are similar in mice and in humans. Using our established mouse model to study the actual blood vessels that control blood flow in living skeletal muscle, the focus of my research is to understand where and how aging affects ROV in light of enhanced sympathetic nerve activity and endothelium dysfunction. A mouse was anesthetized and a skeletal muscle was prepared for studying individual microvessels using a microscope. The muscle was stimulated to contract with the amount and speed of vessel opening (vasodilation) recorded. I used selective interventions to modulate sympathetic or endothelial function and compared ROV for each vessel branch between Young (4 months) and Old (24 months) mice to resolve the effects of aging. I found that sympathetic activation attenuates ROV and that endothelium is integral to ROV. Thus, enhanced sympathetic nerve activity and endothelium dysfunction with aging attenuates ROV. These effects are greater effects in larger upstream vessels, which can restrict blood flow into active muscles. My research provides new insight for improving muscle blood flow, thereby promoting physical activity to improve the quality of life for aging individuals.


2007 ◽  
Vol 293 (1) ◽  
pp. H846-H852 ◽  
Author(s):  
Andrea Di Vanna ◽  
Ana Maria F. W. Braga ◽  
Mateus C. Laterza ◽  
Linda M. Ueno ◽  
Maria Urbana P. B. Rondon ◽  
...  

Chemoreflex control of sympathetic nerve activity is exaggerated in heart failure (HF) patients. However, the vascular implications of the augmented sympathetic activity during chemoreceptor activation in patients with HF are unknown. We tested the hypothesis that the muscle blood flow responses during peripheral and central chemoreflex stimulation would be blunted in patients with HF. Sixteen patients with HF (49 ± 3 years old, Functional Class II-III, New York Heart Association) and 11 age-paired normal controls were studied. The peripheral chemoreflex control was evaluated by inhalation of 10% O2 and 90% N2 for 3 min. The central chemoreflex control was evaluated by inhalation of 7% CO2 and 93% O2 for 3 min. Muscle sympathetic nerve activity (MSNA) was directly evaluated by microneurography. Forearm blood flow was evaluated by venous occlusion plethysmography. Baseline MSNA were significantly greater in HF patients (33 ± 3 vs. 20 ± 2 bursts/min, P = 0.001). Forearm vascular conductance (FVC) was not different between the groups. During hypoxia, the increase in MSNA was significantly greater in HF patients than in normal controls (9.0 ± 1.6 vs. 0.8 ± 2.0 bursts/min, P = 0.001). The increase in FVC was significantly lower in HF patients (0.00 ± 0.10 vs. 0.76 ± 0.25 units, P = 0.001). During hypercapnia, MSNA responses were significantly greater in HF patients than in normal controls (13.9 ± 3.2 vs. 2.1 ± 1.9 bursts/min, P = 0.001). FVC responses were significantly lower in HF patients (−0.29 ± 0.10 vs. 0.37 ± 0.18 units, P = 0.001). In conclusion, muscle vasodilatation during peripheral and central chemoreceptor stimulation is blunted in HF patients. This vascular response seems to be explained, at least in part, by the exaggerated MSNA responses during hypoxia and hypercapnia.


Author(s):  
Michael M. Tymko ◽  
Lindsey F. Berthelsen ◽  
Rachel J. Skow ◽  
Andrew R. Steele ◽  
Graham M. Fraser ◽  
...  

The relationship between sympathetic nerve activity and the vasculature has been of great interest due to its potential role in various cardiovascular-related disease. This relationship, termed "sympathetic transduction", has been quantified using several different laboratory and analytical techniques. The most common method is to assess the association between relative changes in muscle sympathetic nerve activity, measured via microneurography, and physiological outcomes (e.g., blood pressure, total peripheral resistance, and blood flow etc.) in response to a sympathetic stressor (e.g. exercise, cold stress, orthostatic stress). This approach, however, comes with its own caveats. For instance, elevations in blood pressure and heart rate during a sympathetic stressor can have an independent impact on muscle sympathetic nerve activity. Another assessment of sympathetic transduction was developed by Wallin and Nerhed in 1982, where alterations in blood pressure and heart rate were assessed immediately following bursts of muscle sympathetic nerve activity at rest. This approach has since been characterized and further innovated by others, including the breakdown of consecutive burst sequences (e.g., singlet, doublet, triplet, and quadruplet), and burst height (quartile analysis) on specific vascular outcomes (e.g., blood pressure, blood flow, vascular resistance). The purpose of this review is to provide an overview of the literature that has assessed sympathetic transduction using microneurography and various sympathetic stressors (static sympathetic transduction) and using the same or similar approach established by Wallin and Nerhed at rest (dynamic neurovascular transduction). Herein, we discuss the overlapping literature between these two methodologies and highlight the key physiological questions that remain.


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