Baroreflex function in endurance- and static exercise-trained men

Smith, Michael L.; Graitzer, H. M.; Hudson, Donna L.; Raven, Peter B.

doi:10.1152/jappl.1988.64.2.585

Cited by 51 publications

(39 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In addition, there may be a ceiling for maximal vagal activity and vagal effects on the heart may be greatest in young adult humans and may not be able to be enhanced. Both cross-sectional (Smith et al, 1988) and longitudinal data (Kingwell et al, 1992) suggest that cardiac vagal baroreflex control is not enhanced by endurance training in young individuals. In contrast, our prior work showed that baroreflex gain is preserved in older active individuals and this was achieved primarily through enhanced neural control (Hunt et al, 2001).…”

Section: Discussionmentioning

confidence: 98%

Effects of fitness and age on the response to vagotonic atropine

Lee¹,

Picard²,

Beske³

et al. 2008

Autonomic Neuroscience

View full text Add to dashboard Cite

Previous work indicates compromised cardiac vagal control plays a prominent role in reducing arterial baroreflex gain with age, however older fit individuals display cardiovagal baroreflex responses similar to young individuals. The purpose of this study was to test the hypothesis that chronic aerobic exercise mitigates against age-related declines in cardiac parasympathetic receptor function. In forty-four young and old (fit and unfit) individuals, we used the parasympathomimetic responses to low doses of atropine to probe cardiac cholinergic receptor responses. Data was collected before and after eight doses of atropine sulfate from 0.4 to 7.2 ug/kg. Chronotropic responses were assessed from average RR intervals and heart rate variabilities were derived in time and frequency domains. All subjects exhibited bradycardia with at least one dose of atropine and peak bradycardia occurred at a similar dose in each group. However, changes in heart rate variability did not consistently track the chronotropic responses within subjects (r-square from 0.90 down to 0). As expected, basal RR interval was longer in the fit groups and was unaffected by age. However, the degree of RR interval lengthening with parasympathomimetic atropine was unaffected by physical fitness and was significantly less in all older subjects. These data indicate there are certain prepotent age-related declines in the cardiac parasympathetic system that cannot be prevented by regular physical activity. Keywordsatropine; vagal; heart rate variability; muscarinic receptor Our previous work indicates a decline in cardiac parasympathetic neural control compromises baroreflex gain with age (Kaushal et al., 2002) and this decline can be offset by regular physical activity (Hunt et al., 2001). This suggests a reduced cardiac vagal control accompanying physiologic aging may result essentially from progressive deconditioning (Goldsmith et al., 1997). Greater resting cardiac vagal tone is a distinguishing characteristic of physically fit individuals (Ekblom et al., 1973;Frick et al., 1967;Shi et al., 1995;Smith et al., 1989) and a vagally mediated resting bradycardia is observed in younger as well as older humans after exercise training (Stratton et al., 1994). Moreover, our prior work shows that older fit individuals can display baroreflex-mediated cardiac vagal control similar to young individuals (Hunt et al., 2001). In these individuals, baroreflex responses are maintained despite age-related Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Atropine sulfate is routinely used to probe the cardiac parasympathe...

show abstract

Section: Discussionmentioning

confidence: 98%

Effects of fitness and age on the response to vagotonic atropine

Lee¹,

Picard²,

Beske³

et al. 2008

Autonomic Neuroscience

View full text Add to dashboard Cite

show abstract

“…Regarding this finding, Levine and colleagues (Levine et al 1991;Levine, 1993) suggested that endurance training induced cardiac remodelling; greater ventricular diastolic chamber compliance and distensibility on the steeper part of the Frank-Starling cardiac function curve may be a mechanical, non-autonomic cause of orthostatic intolerance. In addition, an attenuation of arterial baroreflex function is a contributory factor for the increased predisposition to orthostatic hypotension in endurance-trained individuals (Raven et al 1984;Smith et al 1988;Stevens et al 1992;Ogoh et al 2003). Likewise, Cooper & Hainsworth (2002) demonstrated that patients with posturally related syncope fail to enhance carotid baroreflex sensitivity during orthostatic stress.…”

Section: Discussionmentioning

confidence: 99%

“…The systemic cardiovascular regulatory system is exquisitely adapted for maintaining an adequate cerebral circulation to prevent syncope (Raven et al 1984;Smith et al 1988;Stevens et al 1992;Cooper & Hainsworth, 2001, 2002Ogoh et al 2003), but the contribution of the systemic cardiovascular regulatory system to orthostatic tolerance is unknown. Another considerable physiological factor that determines orthostatic tolerance is cerebral blood flow (CBF) or its regulation, because CBF is reduced immediately after orthostatic stimulation, e.g.…”

Section: Introductionmentioning

confidence: 99%

Blood flow in internal carotid and vertebral arteries during graded lower body negative pressure in humans

Ogoh

Sato

Okazaki

et al. 2015

Experimental Physiology

View full text Add to dashboard Cite

New Findings r What is the central question of this study?Recently, the heterogeneity of the cerebral arterial circulation has been argued. Orthostatic tolerance may be associated with an orthostatic stress-induced change in blood flow in vertebral arteries rather than in internal carotid arteries, because vertebral arteries supply blood to the medulla oblongata, which is the location of important cardiac, vasomotor and respiratory control centres. r What is the main finding and its importance?The effect of graded orthostatic stress on vertebral artery blood flow is different from that on internal carotid artery blood flow. This response allows for the possibility that orthostatic tolerance may be associated with haemodynamic changes in posterior rather than anterior cerebral blood flow.Recently, the heterogeneity of the cerebral arterial circulation has been argued, but the characteristics of vertebral artery (VA) and internal carotid artery (ICA) blood flow during graded orthostatic stress remain unknown. We hypothesized that the change in blood flow in VA is not similar to that in ICA blood flow during graded orthostatic stress. We measured blood flows in both ICA and VA during graded lower body negative pressure (LBNP; −20, −35 and −50 mmHg) by using two colour-coded ultrasound systems. The effect of graded orthostatic stress on the VA blood flow was different from that on the ICA blood flow (LBNP × artery, P = 0.006). The change in ICA blood flow was associated with the level of LBNP (r = 0.287, P = 0.029), and a reduction in ICA blood flow from pre-LBNP was observed during −50 mmHg LBNP (from 411 ± 35 to 311 ± 40 ml min −1 , P = 0.044) without symptoms of presyncope. In contrast, VA blood flow was unchanged during graded LBNP compared with the baseline (P = 0.597) relative to the reduction in ICA blood flow and thus there was no relationship between VA blood flow and the level of LBNP (r = 0.167, P = 0.219). These findings suggest that the change in ICA blood flow is due to the level of LBNP during graded orthostatic stress, but the change in VA blood flow is different from that in ICA blood flow across the different levels of LBNP. These findings provide the possibility that posterior cerebral blood flow decreases only during severe orthostatic stress and is therefore more likely to be linked with orthostatic tolerance.

show abstract

“…In the normal condition, EX increases cardiac vagal tone and reduces sympathetic outflow at rest (8,12,21). On the other hand, variable changes in arterial baroreflex sensitivity (BRS) have been reported to be reduced (32,43,49,51) in subjects after a course of EX. Few data exist on the role of EX in the modulation of neurohumoral function in CHF.…”

mentioning

confidence: 99%

Exercise training enhances baroreflex sensitivity by an angiotensin II-dependent mechanism in chronic heart failure

Mousa

Liu

Cornish

et al. 2008

Journal of Applied Physiology

View full text Add to dashboard Cite

Exercise training (EX) has become an important modality capable of enhancing the quality of life and survival of patients with chronic heart failure (CHF). Although 4 wk of EX in animals with CHF evoked a reduction in renal sympathetic nerve activity and ANG II plasma levels and an enhancement in baroreflex sensitivity at rest (Liu JL, Irvine S, Reid IA, Patel KP, Zucker IH, Circulation 102: 1854-1862, 2000; Liu JL, Kulakofsky J, Zucker IH, J Appl Physiol 92: 2403-2408, 2002), it is unclear whether these phenomena are causally related. CHF was induced in rabbits by ventricular pacing (360-380 beats/min) for 3 wk. CHF rabbits were EX for 4 wk at 15-18 m/min, 6 days/wk, 30-40 min/day. Three groups of rabbits were studied: CHF (with no EX), CHF-EX, and CHF-EX + ANG II infusion [in which ANG II levels were kept at or near levels observed in CHF (non-EX) rabbits by subcutaneous osmotic minipump infusion]. EX prevented the increase in plasma ANG II levels shown in CHF rabbits. CHF and CHF-EX + ANG II infusion rabbits had significantly depressed baroreflex sensitivity slopes (P < 0.01 for sodium nitroprusside and P < 0.001 for phenylephrine) and higher baseline renal sympathetic nerve activities than CHF-EX animals. EX downregulated mRNA and protein expression of ANG II type 1 receptors in the rostral ventrolateral medulla in CHF rabbits. This was prevented by ANG II infusion. These data are consistent with the view that the reduction in sympathetic nerve activity and the improvement in baroreflex function in CHF after EX are due to the concomitant reduction in ANG II and angiotensin receptors in the central nervous system.

show abstract

Baroreflex function in endurance- and static exercise-trained men

Cited by 51 publications

References 0 publications

Effects of fitness and age on the response to vagotonic atropine

Effects of fitness and age on the response to vagotonic atropine

Blood flow in internal carotid and vertebral arteries during graded lower body negative pressure in humans

Exercise training enhances baroreflex sensitivity by an angiotensin II-dependent mechanism in chronic heart failure

Contact Info

Product

Resources

About