Effects of posture on peripheral vascular responses to lower body positive pressure

American Journal of Physiology-Heart and Circulatory Physiology

Tahara

et al. 2014

Self Cite

Watanabe K, Ichinose M, Tahara R, Nishiyasu T. Individual differences in cardiac and vascular components of the pressor response to isometric handgrip exercise in humans. Am J Physiol Heart Circ Physiol 306: H251-H260, 2014. First published November 8, 2013 doi:10.1152/ajpheart.00699.2013.-We tested the hypotheses that, in humans, changes in cardiac output (CO) and total peripheral vascular resistance (TPR) occurring in response to isometric handgrip exercise vary considerably among individuals and that those individual differences are related to differences in muscle metaboreflex and arterial baroreflex function. Thirty-nine healthy subjects performed a 1-min isometric handgrip exercise at 50% of maximal voluntary contraction. This was followed by a 4-min postexercise muscle ischemia (PEMI) period to selectively maintain activation of the muscle metaboreflex. All subjects showed increases in arterial pressure during exercise. Interindividual coefficients of variation (CVs) for the changes in CO and TPR between rest and exercise periods (CO: 95.1% and TPR: 87.8%) were more than twofold greater than CVs for changes in mean arterial pressure (39.7%). There was a negative correlation between CO and TPR responses during exercise (r ϭ Ϫ0.751, P Ͻ 0.01), but these CO and TPR responses correlated positively with the corresponding responses during PEMI (r ϭ 0.568 and 0.512, respectively, P Ͻ 0.01). The CO response during exercise did not correlate with PEMI-induced changes in an index of cardiac parasympathetic tone and cardiac baroreflex sensitivity. These findings demonstrate that the changes in CO and TPR that occur in response to isometric handgrip exercise vary considerably among individuals and that the two responses have an inverse relationship. They also suggest that individual differences in components of the pressor response are attributable in part to variations in muscle metaboreflex-mediated cardioaccelerator and vasoconstrictor responses. cardiac output; peripheral vascular resistance; muscle metaboreflex; arterial baroreflex DURING ISOMETRIC EXERCISE, arterial blood pressure, heart rate (HR), and sympathetic nerve activity all increase in association with increases in the intensity and duration of the exercise. This pressor response is governed mainly by neural mechanisms: central command (52) as well as a feedback system operating via afferent input from exercising skeletal muscle receptors (muscle metaboreflex and mechanoreflex) (40,41,51) and from arterial and cardiopulmonary baroreceptors (arterial and cardiopulmonary baroreflexes) (51, 52). While the increase in arterial pressure during isometric exercise is a well-established response, the responses of the components mediating the pressor response, cardiac output (CO) and total peripheral vascular resistance (TPR), remain controversial. In fact, previous studies have shown that, during isometric handgrip exercise in healthy humans, the pressor response occurs via an increase in CO (16,32,[34][35][36]57), an increase in TPR (6, 17), or both of those...

Section: Subjectsmentioning

confidence: 99%

Section: Subjectsmentioning

confidence: 99%

Individual differences in cardiac and vascular components of the pressor response to isometric handgrip exercise in humans

American Journal of Physiology-Heart and Circulatory Physiology

Tahara

et al. 2014

Self Cite

“…We measured FBF using Doppler ultrasound as previously described (12,19,24). Briefly, a Doppler ultrasound system (HDI 5000; ATL Ultrasound) equipped with a hand-held transducer probe (model L12-5) with an operating frequency of 6 MHz was used to simultaneously measure two-dimensional brachial artery diameter and mean blood velocity (MBV).…”

Section: Subjectsmentioning

confidence: 99%

“…We calculated Dm for each minute as the mean Dm value from 20 consecutive beats during the previous 30 s. The cross-sectional area of the brachial artery (CSA) was estimated using the representative D m as CSA ϭ (Dm/10/2) 2 ·. MBV was continuously estimated by means of a computer program developed with the aid of LabVIEW (version 6.0; National Instruments), as described in detail elsewhere (12,24). Our system collects MBV at 100 Hz together with the analog signals representing the ECG and blood pressure waveform.…”

Section: Subjectsmentioning

confidence: 99%

Evaluation of muscle metaboreflex function through graded reduction in forearm blood flow during rhythmic handgrip exercise in humans

Delliaux

American Journal of Physiology-Heart and Circulatory Physiology

et al. 2011

Self Cite

perfusion of active skeletal muscle elicits a reflex pressor response termed the muscle metaboreflex. Our aim was to determine the muscle metaboreflex threshold and gain in humans by creating an open-loop relationship between active muscle blood flow and hemodynamic responses during a rhythmic handgrip exercise. Eleven healthy subjects performed the exercise at 5 or 15% of maximal voluntary contraction (MVC) in random order. During the exercise, forearm blood flow (FBF), which was continuously measured using Doppler ultrasound, was reduced in five steps by manipulating the inner pressure of an occlusion cuff on the upper arm. The FBF at each level was maintained for 3 min. The initial reductions in FBF elicited no hemodynamic changes, but once FBF fell below a threshold, mean arterial blood pressure (MAP) and heart rate (HR) increased and total vascular conductance (TVC) decreased in a linear manner. The threshold FBF during the 15% MVC trial was significantly higher than during the 5% MVC trial. The gain was then estimated as the slope of the relationship between the hemodynamic responses and FBFs below the threshold. The gains for the MAP and TVC responses did not differ between workloads, but the gain for the HR response was greater in the 15% MVC trial. Our findings thus indicate that increasing the workload shifts the threshold for the muscle metaboreflex to higher blood flows without changing the gain of the reflex for the MAP and TVC responses, whereas it enhances the gain for the HR response.neural cardiovascular regulation; peripheral reflexes; integrated circulatory regulation WHEN OXYGEN DELIVERY TO ACTIVE skeletal muscle is insufficient to meet the metabolic demands during dynamic exercise, metabolites (e.g., lactic acid, adenosine, potassium, diprotonated phosphate, H ϩ , and arachidonic acid products, among others) accumulate within the active muscle and stimulate group III and IV afferent neurons. These sensory neurons project to the medulla oblongata, and their activity elicits reflex increases in sympathetic nerve activity and systemic blood pressure in an effort to enhance blood flow to the ischemic muscle (1,11,14,27,29,31,41). Termed the muscle metaboreflex, this response is thought to provide important functional links between metabolism in active muscles and central hemodynamics during exercise.The function of the muscle metaboreflex during dynamic exercise has been investigated in dogs through examination of the cardiovascular responses to graded reductions of hindlimb blood flow (11,15,34,36,41). In this experimental model, hindlimb blood flow is maintained at a constant level using an occluder placed at the terminal aorta, despite the evoked systemic presser response and/or local vasodilation in the ischemic muscles. This model thus creates an open-loop relationship between active skeletal muscle blood flow and both systemic and local cardiovascular responses, which enables experimental control of the hemodynamic changes that would otherwise influence the activation level of the muscle m...

“…We evaluated SV using Doppler ultrasound (27). A Doppler ultrasound system (Echo Doppler; HDI 3500; Atl/Philips Ultrasound, Bothwell, WA), equipped with a hand-held transducer probe (operating frequency: 2 MHz), was used to measure ascending aortic blood velocity.…”

Section: Measurementsmentioning

confidence: 99%

Cardiovascular responses to forearm muscle metaboreflex activation during hypercapnia in humans

Delliaux

American Journal of Physiology-Regulatory, Integrative and Comp

et al. 2015

Self Cite

Ten healthy males participated under three experimental conditions: 1) hypercapnia (HCA, PET CO 2 : ϩ10 mmHg, by inhalation of a CO 2-enriched gas mixture); 2) muscle metaboreflex activation (MMA, by 5 min of local circulatory occlusion after 1 min of 50% maximum voluntary contraction isometric handgrip under normocapnia); and 3) HCAϩMMA. We measured mean arterial pressure (MAP), heart rate (HR), and cardiac output (CO); calculated stroke volume (SV), and total peripheral resistance (TPR); and evaluated myocardial oxygen consumption (MV O2) and cardiac work (CW) noninvasively. MAP increased in the three experimental conditions but HCAϩMMA led to the highest MAP, CO, and HR. Moreover, HCAϩMMA increased SV and was associated with the highest MV O2 and CW. HCA and MMA exhibited inhibitory interactions with MAP, HR, TPR, MV O2, and CW, increases of which were smaller during HCAϩMMA than the sum of the increases during HCA and MMA alone (MAP: ϩ28 Ϯ 2 vs. ϩ34 Ϯ 2 mmHg, P Ͻ 0.001; HR: ϩ15 Ϯ 2 vs. ϩ22 Ϯ 3 bpm, P Ͻ 0.01; TPR: ϩ1.1 Ϯ 1.4 vs. ϩ3.0 Ϯ 1.5 mmHg·l·min Ϫ1 , P Ͻ 0.05; MV O2: ϩ50.25 Ϯ 4.74 vs. ϩ59.48 Ϯ 5.37 mmHg·min Ϫ1 ·10 Ϫ2 , P Ͻ 0.01; CW: ϩ59.10 Ϯ 7.52 vs. ϩ63.67 Ϯ 7.71 ml mmHg·min Ϫ1 ·10 Ϫ4 , P Ͻ 0.05). Oppositely, HCA and MMA interactions were linearly additive for CO (ϩ2.3 Ϯ 0.4 l/min) and SV (ϩ13 Ϯ 4 ml). We showed that muscle metaboreflex and hypercapnia interact in healthy humans, reducing vasoconstriction but enhancing SV.hypercapnia; muscle metaboreflex; hypertension; stroke volume; myocardial oxygen consumption REGULATION OF ARTERIAL BLOOD pressure involves the integration of humoral, hormonal, and neurogenic components. For example, whereas hypercapnia has direct humoral vasodilatory effects (19,20), the neurally mediated central chemoreflex increases cardiovascular sympathetic nervous system activity, leading heart rate (HR), stroke volume (SV), cardiac output (CO), vascular resistance, and then blood pressure all to increase (31). During exercise, blood pressure is also regulated by muscle reflexes (2, 17). The muscle metaboreflex forms a second direct excitatory input for the neural control of cardiovascular function (21, 29, 42) that also stimulates sympathetic pathways (29,30,33) leading to increases in HR, SV, CO, vascular resistance, and then blood pressure.It is known that central chemoreflex and muscle metaboreflex signals converge to common areas in the brain (43) and exert similar excitatory effects through the cardiovascular autonomic nervous system. On the other hand, little is known about the hemodynamic effects of muscle metaboreflex activation during hypercapnia. Ponikowski (35) showed that muscle ergoreflex activation was an independent predictor of ventilation sensitivity to hypercapnia in chronic heart failure and argued for the existence of interactions between the muscle metaboreflex and hypercapnic chemoreflex. Despite the likelihood that these two reflexes interact during exercise, this topic received little direct attention before the pioneering work of Lykidis et al. (22,23),...