Interval and continuous exercise elicit equivalent postexercise hypotension in prehypertensive men, despite differences in regulation

2011 ◽  
Vol 36 (6) ◽  
pp. 881-891 ◽  
Author(s):  
Shawn P. Lacombe ◽  
Jack M. Goodman ◽  
Carly M. Spragg ◽  
Sam Liu ◽  
Scott G. Thomas

Equicaloric bouts of interval (IE: 5 × 2:2 min at 85% and 40% maximal oxygen uptake) and steady state (SS: 21 min at 60% maximal oxygen uptake) exercise were performed by 13 older prehypertensive males on separate days, at equivalent times of day, to assess the influence of exercise mode on postexercise hypotension (PEH). Exercise conditions were compared with a control session. Cardiovascular measures were collected for 30 min prior to, and 60 min following exercise. PEH, as measured by mean postexercise systolic blood pressure (SBP) decrease (IE: –4 ± 6 mm Hg; SS: –3 ± 4 mm Hg; control: 4 ± 4 mm Hg), area under the SBP curve (IE: –240 ± 353 mm Hg·min; SS: –192 ± 244 mm Hg·min), and minimum SBP achieved (IE: –15 ± 7 mm Hg; SS: –13 ± 7 mm Hg), was equivalent after both conditions. Stroke volume was significantly reduced (IE: –14.6 ± 16.0 mL; SS: –10.1 ± 14.2 mL, control –1.7 ± 2.2 mL) and heart rate was significantly elevated (IE: 13 ± 8 beats·min–1; SS: 7.9 ± 8 beats·min–1; control: –2 ± 3 beats·min–1) postexercise after both conditions. Cardiac output and total peripheral resistance were nonsignificantly decreased and increased postexercise, respectively. Baroreflex sensitivity (BRS) was reduced following IE (p < 0.05) and heart rate variability (HRV) parameters were reduced after both conditions, with IE eliciting larger and longer reductions in some indices. The results from the current study indicate that older prehypertensive adults experience similar PEH following equicaloric bouts of IE and SS exercise despite larger alterations in HRV and BRS elicited by IE.

2019 ◽  
Vol 33 (1) ◽  
pp. 39-53 ◽  
Author(s):  
Stefan Duschek ◽  
Alexandra Hoffmann ◽  
Casandra I. Montoro ◽  
Gustavo A. Reyes del Paso

Abstract. Chronic low blood pressure (hypotension) is accompanied by symptoms such as fatigue, reduced drive, faintness, dizziness, cold limbs, and concentration difficulties. The study explored the involvement of aberrances in autonomic cardiovascular control in the origin of this condition. In 40 hypotensive and 40 normotensive subjects, impedance cardiography, electrocardiography, and continuous blood pressure recordings were performed at rest and during stress induced by mental calculation. Parameters of cardiac sympathetic control (i.e., stroke volume, cardiac output, pre-ejection period, total peripheral resistance), parasympathetic control (i.e., heart rate variability), and baroreflex function (i.e., baroreflex sensitivity) were obtained. The hypotensive group exhibited markedly lower stroke volume, heart rate, and cardiac output, as well as higher pre-ejection period and baroreflex sensitivity than the control group. Hypotension was furthermore associated with a smaller blood pressure response during stress. No group differences arose in total peripheral resistance and heart rate variability. While reduced beta-adrenergic myocardial drive seems to constitute the principal feature of the autonomic impairment that characterizes chronic hypotension, baroreflex-related mechanisms may also contribute to this state. Insufficient organ perfusion due to reduced cardiac output and deficient cardiovascular adjustment to situational requirements may be involved in the manifestation of bodily and mental symptoms.


2020 ◽  
Vol 30 (5) ◽  
pp. 433-439 ◽  
Author(s):  
Priyanka Garg ◽  
Kavita Yadav ◽  
Ashok Kumar Jaryal ◽  
Garima Kachhawa ◽  
Alka Kriplani ◽  
...  

2006 ◽  
Vol 16 (5) ◽  
pp. 412-417 ◽  
Author(s):  
Mathias Baumert ◽  
Lars Brechtel ◽  
J??rgen Lock ◽  
Mario Hermsdorf ◽  
Roland Wolff ◽  
...  

2011 ◽  
Vol 301 (4) ◽  
pp. H1540-H1550 ◽  
Author(s):  
Megan S. Johnson ◽  
Vincent G. DeMarco ◽  
Cheryl M. Heesch ◽  
Adam T. Whaley-Connell ◽  
Rebecca I. Schneider ◽  
...  

The aim of this investigation was to evaluate sex differences in baroreflex and heart rate variability (HRV) dysfunction and indexes of end-organ damage in the TG(mRen2)27 (Ren2) rat, a model of renin overexpression and tissue renin-angiotensin-aldosterone system overactivation. Blood pressure (via telemetric monitoring), blood pressure variability [BPV; SD of systolic blood pressure (SBP)], spontaneous baroreflex sensitivity, HRV [HRV Triangular Index (HRV-TI), standard deviation of the average NN interval (SDNN), low and high frequency power (LF and HF, respectively), and Poincaré plot analysis (SD1, SD2)], and cardiovascular function (pressure-volume loop analysis and proteinuria) were evaluated in male and female 10-wk-old Ren2 and Sprague Dawley rats. The severity of hypertension was greater in Ren2 males (R2-M) than in Ren2 females (R2-F). Increased BPV, suppression of baroreflex gain, decreased HRV, and associated end-organ damage manifested as cardiac dysfunction, myocardial remodeling, elevated proteinuria, and tissue oxidative stress were more pronounced in R2-M compared with R2-F. During the dark cycle, HRV-TI and SDNN were negatively correlated with SBP within R2-M and positively correlated within R2-F; within R2-M, these indexes were also negatively correlated with end-organ damage [left ventricular hypertrophy (LVH)]. Furthermore, within R2-M only, LVH was strongly correlated with indexes of HRV representing predominantly vagal (HF, SD1), but not sympathetic (LF, SD2), variability. These data demonstrated relative protection in females from autonomic dysfunction and end-organ damage associated with elevated blood pressure in the Ren2 model of hypertension.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A177-A177
Author(s):  
H Tsai ◽  
T Kuo ◽  
C Yang

Abstract Introduction Insomnia is a risk factor for hypertension and cardiovascular events, and this association is strongest for sleep-onset insomnia. However, little is known about insomnia on cardiovascular modulation, especially soon after morning awakening, the peak period of time for cardiovascular incidents. This study explored morning cardiovascular function in individuals with sleep-onset insomnia by analysing heart rate variability, blood pressure variability, and baroreflex sensitivity. Methods Sleep structure of the participants (15 good sleepers and 13 individuals with sleep-onset insomnia) was measured by laboratory polysomnography, followed by continuous recordings of the participant’s blood pressure and heart rate for 10 min in the morning. Results When compared to the good sleepers, the insomnia group showed significant reductions in total sleep time, a longer sleep-onset latency, and reduced sleep efficiency. The sleep structure, including durations of sleep stages, numbers of awakenings and arousal index did not differ between the groups. After morning awakening (averaged time: 12.33 ± 10.48 min), the shorter R-R intervals, lower total power, and lower high-frequency power of heart rate variability were observed among individuals with sleep-onset insomnia, compared with good sleepers. Elevated slopes of systolic and diastolic blood pressure, as well as lower baroreflex sensitivity, were also shown in the insomnia group. Indices of sympathetic activity, including low-frequency percentage of heart rate variability or low-frequency power of blood pressure variability, did not differ between the groups. Conclusion Weak vagal activity and blunted baroreflex sensitivity were evident among sleep-onset insomnia. These findings indicate difficulty in initiating sleep, without significant sleep fragmentation, can independently affect morning cardiovascular function. This study provides a possible link between sleep-onset insomnia and risk of cardiovascular events. Support N/A


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