Enhanced vagal baroreflex response during 24 h after acute exercise

1991 ◽  
Vol 260 (3) ◽  
pp. R570-R575 ◽  
Author(s):  
V. A. Convertino ◽  
W. C. Adams

We evaluated carotid-cardiac baroreflex responses in eight normotensive men (25-41 yr) on two different test days, each separated by at least 1 wk. On one day, baroreflex response was tested before and at 3, 6, 12, 18, and 24 h after graded supine cycle exercise to volitional exhaustion. On another day, this 24-h protocol was repeated with no exercise (control). Beat-to-beat R-R intervals were measured during external application of graded pressures to the carotid sinuses from 40 to -65 mmHg; changes of R-R intervals were plotted against carotid pressure (systolic pressure minus neck chamber pressure). The maximum slope of the response relationship increased (P less than 0.05) from preexercise to 12 h (3.7 +/- 0.4 to 7.1 +/- 0.7 ms/mmHg) and remained significantly elevated through 24 h. The range of the R-R response was also increased from 217 +/- 24 to 274 +/- 32 ms (P less than 0.05). No significant differences were observed during the control 24-h period. An acute bout of graded exercise designed to elicit exhaustion increases the sensitivity and range of the carotid-cardiac baroreflex response for 24 h and enhances its capacity to buffer against hypotension by increasing heart rate. These results may represent an underlying mechanism that contributes to blood pressure stability after intense exercise.

1990 ◽  
Vol 68 (4) ◽  
pp. 1458-1464 ◽  
Author(s):  
V. A. Convertino ◽  
D. F. Doerr ◽  
D. L. Eckberg ◽  
J. M. Fritsch ◽  
J. Vernikos-Danellis

We studied vagally mediated carotid baroreceptor-cardiac reflexes in 11 healthy men before, during, and after 30 days of 6 degrees head-down bed rest to test the hypothesis that baroreflex malfunction contributes to orthostatic hypotension in this model of simulated microgravity. Sigmoidal baroreflex response relationships were provoked with ramped neck pressure-suction sequences comprising pressure elevations to 40 mmHg followed by serial R-wave-triggered 15-mmHg reductions to -65 mmHg. Each R-R interval was plotted as a function of systolic pressure minus the neck chamber pressure applied during the interval. Compared with control measurements, base-line R-R intervals and the minimum, maximum, range, and maximum slope of the R-R interval-carotid pressure relationships were reduced (P less than 0.05) from bed rest day 12 through recovery day 5. Baroreflex slopes were reduced more in four subjects who fainted during standing after bed rest than in six subjects who did not faint (-1.8 +/- 0.7 vs. -0.3 +/- 0.3 ms/mmHg, P less than 0.05). There was a significant linear correlation (r = 0.70, P less than 0.05) between changes of baroreflex slopes from before bed rest to bed rest day 25 and changes of systolic blood pressure during standing after bed rest. Although plasma volume declined by approximately 15% (P less than 0.05), there was no significant correlation between reductions of plasma volume and changes of baroreflex responses. There were no significant changes of before and after plasma norepinephrine or epinephrine levels before and after bed rest during supine rest or sitting.(ABSTRACT TRUNCATED AT 250 WORDS)


1989 ◽  
Vol 256 (2) ◽  
pp. R549-R553 ◽  
Author(s):  
J. M. Fritsch ◽  
R. F. Rea ◽  
D. L. Eckberg

We studied human baroreflex resetting during 25 min of drug-induced arterial pressure changes in 10 healthy volunteers. Average (+/- SE) base-line systolic pressure of 113 +/- 4 fell to 102 +/- 3 during nitroprusside infusions and rose to 135 +/- 6 mmHg during phenylephrine infusions. Average base-line R-R intervals of 932 +/- 37 shortened to 820 +/- 39 during nitroprusside infusions and lengthened to 1,251 +/- 61 ms during phenylephrine infusions. Carotid baroreceptor-cardiac reflex responses were evaluated with a complex series of neck chamber pressure changes, and R-R intervals were plotted as functions of carotid distending pressure. Baroreceptor-cardiac reflex relations shifted on both R-R interval and arterial pressure axes during drug infusions, but there was no significant change of the maximum slope or range of R-R interval responses. The position of baseline R-R intervals on the reflex relation (operational point) changed significantly. Resting R-R intervals were closer to threshold during pressure reductions and closer to saturation for baroreceptor-cardiac responses during pressure elevations. These results document short-term partial resetting of human baroreceptor-cardiac reflex responses as early as 25 min after the onset of arterial pressure changes.


2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Travis J. Saunders ◽  
Andrew Palombella ◽  
K. Ashlee McGuire ◽  
Peter M. Janiszewski ◽  
Jean-Pierre Després ◽  
...  

Objective. To examine the effect of acute and short-term (~1 week) aerobic exercise training on plasma adiponectin levels in inactive, abdominally obese men.Materials and Methods. Inactive and abdominally obese men (n=38, waist circumference ≥102 cm) recruited from Kingston, Canada were randomly allocated to perform three bouts of aerobic treadmill exercise at either low (50% VO2peak) or high (75% VO2peak) intensity during a 1-week period. Blood samples were taken before and after the first exercise session and 24–72 hours following the completion of the final exercise session.Results. Adiponectin levels were elevated immediately following an acute bout of exercise at both high and low intensities (High:5.79±0.42versus5.05±0.41 ug/mL; Low:5.24±0.44versus4.37±0.44 ug/mL,P<0.05) and remained elevated following 30 minutes of rest. In comparison to baseline, adiponectin levels were also elevated 24–72 hours following the final exercise session (High:5.47±0.48versus4.88±0.48 ug/mL; Low:5.18±0.49versus4.47±0.49 ug/mL,P<0.05).Conclusion. Both acute and short-term aerobic exercise result in a significant increase in plasma adiponectin levels in inactive, abdominally obese men independent of intensity.


2014 ◽  
Vol 6 (2) ◽  
pp. 29-34
Author(s):  
Nirmala Limbu ◽  
Ramanjan Sinha ◽  
Meenakshi Sinha ◽  
Bishnu Hari Paudel

Objective: We aimed to investigate how EEG frequency bands change in females in response to acute exercise compared to males.Methods: Consenting healthy adult females (n=15) & males (n=15) bicycled an ergometer at 50% HRmax for 20 min. EEG was recorded using 10-20 system from mid-frontal (F4 & F3), central (C4 & C3), parietal (P4 & P3), temporal (T4 & T3) & occipital (O2 & O1) regions. Exercise-induced EEG changes were compared between two sexes by Mann Whitney test. EEG power (μV2) is presented as median & interquartile range.Results: In females, as compared to males, resting right side delta, alpha, and beta activities were more in almost all recorded sites [delta: F4= 49.82 (44.23-63.56) vs. 35.5 (32.70-44.44), p < 0.001; etc], [alpha F4: 127.62 (112.89-149.03) vs. 49.36 (46.37-52.98), p < 0.001; etc], [beta F4= 18.96 (15.83-25.38)  vs. 14.77 (10.34-17.55), p < 0.05; C4= 21.16 (18.4-25.9) vs. 15.48 (9.66-19.40), p < 0.01; etc]. Similarly, females resting right theta activity was more in parietal [P4= 33.04 (25.1-42.41) vs. 22.3 (18.36-34.33), p < 0.05] & occipital [O2= 50.81 (30.64-66.8) vs. 26.85 (22.18-34.42), p < 0.001] regions than in males. They had similar picture on the left side also. The delta values of right alpha power was less in female in frontal [F4= -11.61 (-45.24 -3.64) vs. 9.48 (1.05-16.58), p < 0.01] and central [C4= -72 (-32.98-9.48) vs. 22.69 (13.03-33.05), p < 0.01] regions compared to males. Also, they had less delta values of left central alpha [C3= -8.32 (-32.65-6.1) vs. 16.5 (0.36-36.36), p < 0.01] and temporal beta [T3= -6.29 (-10.09- -1.49) vs. 1.24 (-0.84- 2.8), p < 0.001] power compared to males.Conclusion: At rest females may have high EEG powers in different bands. In response to acute exercise, they respond in reverse way as compared to males.DOI: http://dx.doi.org/10.3126/ajms.v6i2.11116Asian Journal of Medical Sciences Vol.6(2) 2015 30-35


1982 ◽  
Vol 242 (2) ◽  
pp. H185-H190 ◽  
Author(s):  
B. G. Wallin ◽  
D. L. Eckberg

We examined the role of carotid baroreceptors in the short-term modulation of sympathetic outflow to the muscle vascular bed and parasympathetic outflow to the heart in 10 healthy adults. Afferent carotid baroreceptor activity was modified with 30-mmHg neck suction or pressure applied during held expiration, and efferent sympathetic activity was measured with microelectrodes inserted percutaneously into peroneal nerve muscle fascicles. Sympathetic responses were conditioned importantly by directional changes of carotid transmural pressure: increased pressure (onset of neck suction or offset of neck pressure) inhibited (totally) sympathetic activity, and reduced pressure (offset of neck suction or onset of neck pressure) augmented sympathetic activity. Responses occurred after a latency of about 2 s and did not persist as long as changes of neck-chamber pressure. Cardiac intervals were prolonged by increased carotid transmural pressures and shortened by decreased carotid transmural pressures, but, in contrast to sympathetic responses, cardiac responses adapted only slightly during neck-chamber pressure changes. Our results suggest that in the human a common baroreceptor input is processed differently in central vagal and sympathetic networks. Muscle sympathetic responses to changing levels of afferent baroreceptor traffic are profound but transitory. They appear to be conditioned more by changes of arterial pressure than by its absolute levels.


1993 ◽  
Vol 265 (5) ◽  
pp. H1629-H1637 ◽  
Author(s):  
S. Yamaguchi ◽  
Y. Tamada ◽  
H. Miyawaki ◽  
Y. Niida ◽  
A. Fukui ◽  
...  

The diastolic and systolic pressure of one ventricle is increased by an increase in volume and/or pressure of the opposite ventricle; however, a mechanism for the ventricular interaction remains unclear. We hypothesized that the shape change of one ventricle elicited by the opposite ventricle would lead to resetting of the regional length, which may explain the ventricular interaction. We used 15 cross-circulated isovolumically contracting canine hearts in which both ventricular volumes were independently controlled. Diastolic regional segment area was calculated by multiplying circumferential and longitudinal lengths on right ventricular free wall (RVFW; n = 6), interventricular septum (IVS; n = 11), and left ventricular (LV) FW (n = 12). The regional area at relatively small volumes of both ventricles were expressed as 100%. With constant RV volume, increasing LV from 7 to 19 ml increased RV diastolic and systolic pressures by 2.7 and 5.5 mmHg, respectively. Conversely, increasing RV volume increased LV diastolic and systolic pressures by 2.3 and 7.5 mmHg, respectively. Increasing LV volume increased RVFW regional area from 121.0 to 124.6% (P < 0.01) and increased IVS regional area from 103.3 to 108.7% (P < 0.01), whereas the RV volume was held constant. Increasing RV volume also increased LVFW and IVS regional areas from 109.9 to 111.6% (P < 0.01) and from 106.8 to 108.9% (P < 0.05), respectively. Ventricular shape change elicited by ventricular interaction will increase the regional wall area, even though the volume of the chamber is unchanged. The increase in the regional area alters the position of the tissue on its resting and active length-tension relations and, thus, leads to enhancement of the chamber pressure.


Vascular ◽  
2015 ◽  
Vol 24 (3) ◽  
pp. 264-272 ◽  
Author(s):  
CL Delaney ◽  
JI Spark

Objective This study assesses the impact of treadmill-based SET alone or in combination with resistance training on systemic inflammatory response, in patients with intermittent claudication (IC). Methods Thirty-five patients with IC were randomised to 12 weeks of treadmill-only SET (Group 1) or a combination of treadmill and lower-limb resistance SET (Group 2). A panel of pro- and anti-inflammatory markers were assessed before, during and after the SET. Results Over the duration of SET, homocysteine increased within Group 1 (12.0–15.5 µmol/L, p = 0.003) but not Group 2, (13.7–14.7 µmol/) while neutrophil elastase (NE) increased within Group 2 (174.5–238.2 ng/mL, p = 0.007) but not Group 1 (300.8–312.0 ng/mL). In both groups NE increased following acute exercise at the start of the SET. Differences in cytokine expression was evident between the two groups (in Group 1, pro-inflammatory cytokines interleukin-12 and interferon-gamma decreased following an acute bout of exercise at the end of SET, where as in Group 2 pro-inflammatory cytokines interleukin-6 and 8 were seen to increase after an acute bout of exercise at the end of SET). Conclusion SET in patients with IC influences the complex immune-modulatory state of atherosclerosis through inflammatory pathways that induce both pro-inflammatory and immunosuppressive responses.


Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 333
Author(s):  
Johanna Vogel ◽  
Daniel Niederer ◽  
Georg Jung ◽  
Kerstin Troidl

Background: The vascular effects of training under blood flow restriction (BFR) in healthy persons can serve as a model for the exercise mechanism in lower extremity arterial disease (LEAD) patients. Both mechanisms are, inter alia, characterized by lower blood flow in the lower limbs. We aimed to describe and compare the underlying mechanism of exercise-induced effects of disease- and external application-BFR methods. Methods: We completed a narrative focus review after systematic literature research. We included only studies on healthy participants or those with LEAD. Both male and female adults were considered eligible. The target intervention was exercise with a reduced blood flow due to disease or external application. Results: We identified 416 publications. After the application of inclusion and exclusion criteria, 39 manuscripts were included in the vascular adaption part. Major mechanisms involving exercise-mediated benefits in treating LEAD included: inflammatory processes suppression, proinflammatory immune cells, improvement of endothelial function, remodeling of skeletal muscle, and additional vascularization (arteriogenesis). Mechanisms resulting from external BFR application included: increased release of anabolic growth factors, stimulated muscle protein synthesis, higher concentrations of heat shock proteins and nitric oxide synthase, lower levels in myostatin, and stimulation of S6K1. Conclusions: A main difference between the two comparators is the venous blood return, which is restricted in BFR but not in LEAD. Major similarities include the overall ischemic situation, the changes in microRNA (miRNA) expression, and the increased production of NOS with their associated arteriogenesis after training with BFR.


2014 ◽  
Vol 10 (2) ◽  
pp. 146-153 ◽  
Author(s):  
Terri Schneider ◽  
Stefanie De Jesus ◽  
Harry Prapavessis

Recent systematic reviews have concluded that a single session of exercise ameliorates cravings and tobacco withdrawal symptoms; however, smoking behaviour (topography) has not been adequately addressed in the literature. This study examined the effect of an acute bout of exercise on smoking topography following a temporary period of smoking abstinence. Forty-eight adult smokers (Nfemale = 34, Mage = 43.14), who had been smoking for an average of 23.90 years, were randomised to an acute (10 minutes) bout of exercise (N = 23) or passive sitting (control) group. Cigarette cravings were assessed at baseline and immediately pre and post treatment condition during a 15-hour smoking abstinence period. Smoking topography which included puff count, puff volume, puff duration, inter-puff interval, and total cigarette duration was assessed at baseline and post treatment. Although exercise reduced cravings, compared to the control group, smoking topography remained unchanged across time between groups. Furthermore, craving reduction was unrelated to any smoking topography variables. Although there is evidence that exercise can delay time to first cigarette, this study demonstrates that the change to smoking topography is negligible when participants are invited to smoke.


2015 ◽  
Vol 93 (6) ◽  
pp. 413-419 ◽  
Author(s):  
David Opitz ◽  
Edward Lenzen ◽  
Andreas Opiolka ◽  
Melanie Redmann ◽  
Martin Hellmich ◽  
...  

Chronic elevated lactate levels are associated with insulin resistance in patients with type 2 diabetes mellitus (T2DM). Furthermore, lactacidosis plays a role in limiting physical performance. Erythrocytes, which take up lactate via monocarboxylate transporter (MCT) proteins, may help transport lactate within the blood from lactate-producing to lactate-consuming organs. This study investigates whether cycling endurance training (3 times/week for 3 months) alters the basal erythrocyte content of MCT-1, and whether it affects lactate distribution kinetics in the blood of T2DM men (n = 10, years = 61 ± 9, body mass index = 31 ± 3 kg/m2) following maximal exercise (WHO step-incremental cycle ergometer test). Immunohistochemical staining indicated that basal erythrocyte contents of MCT-1 protein were up-regulated (+90%, P = 0.011) post-training. Erythrocyte and plasma lactate increased from before acute exercise (= resting values) to physical exhaustion pre- as well as post-training (pre-training: +309%, P = 0.004; +360%, P < 0.001; post-training: +318%, P = 0.008; +300%, P < 0.001), and did not significantly decrease during 5 min recovery. The lactate ratio (erythrocytes:plasma) remained unchanged after acute exercise pre-training, but was significantly increased after 5 min recovery post-training (compared with the resting value) (+22%, P = 0.022). The results suggest an increased time-delayed influx of lactate into erythrocytes following an acute bout of exercise in endurance-trained diabetic men.


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