Moderate Dynamic Exercise Research Articles

Arterial Baroreceptor Denervation Enhances Muscle Metaboreflex Induced Increases in Effective Arterial Elastance Without Worsening Stoke Work During Dynamic Exercise in Heart Failure

Optimal energy transfer from the left ventricle to the systemic circulation is paramount to the maintenance of workload performance during exercise. This interaction between the heart and circulation is quantified by the ventricular‐vascular coupling relationship which is the ratio of direct assessments of arterial and ventricular elastance. During exercise, increases in both arterial and ventricular elastance occur as a result of sympatho‐excitatory efferent responses brought about by activation of metabosensitive skeletal muscle afferents ‐ termed the muscle metaboreflex. In heart failure, ventricular elastance is reduced and arterial elastance is increased causing ventricular‐vascular uncoupling at rest and further sympatho‐activation elicited by the muscle metaboreflex worsens this relationship through profound systemic vasoconstriction. Recent studies have concluded that the arterial baroreflex substantially buffers vasoconstriction within peripheral vascular beds. In heart failure, the arterial baroreflex buffering capacity is significantly reduced and muscle metaboreflex induced vasoconstriction is enhanced. To what extent this shift in metaboreflex control of peripheral sympathetic tone affects ventricular‐vascular coupling is unknown. We examined the effect of sino‐aortic baroreceptor denervation (SAD) on the ventricular‐vascular relationship at rest and during moderate dynamic exercise (6.4 km/h 10% grade) in chronically instrument conscious canines before and after the induction of heart failure to determine whether loss of baroreflex buffering engendered further uncoupling of the ventricular‐vascular relationship in heart failure. Increases in effective arterial elastance (Ea), were significantly enhanced during muscle metaboreflex activation after SAD (0.5 ± 0.1 mmHg/ml to 2.0 ± 0.4 mmHg/mL). Furthermore, SAD elicited a significant increase in the ability to improve stroke work during muscle metaboreflex activation (2.7 ± 0.1 L*mmHg to 3.5 ± 0.1 L*mmHg) suggesting that even without the arterial baroreflex muscle metaboreflex activation in healthy subjects maintains ventricular‐vascular coupling. In heart failure, SAD elicited a 2‐fold increase in Ea during muscle metaboreflex activation (0.9 ± 0.2 mmHg/ml to 1.8 ± 0.2 mmHg/ml). Stroke work did not improve during muscle metaboreflex activation in heart failure with SAD. Thus, enhanced increases in Ea are likely not matched by ventricular elastance thereby exacerbating the already uncoupled ventricular‐vascular relationship. We conclude that the arterial baroreflex actively restrains increases in Ea and stroke work during muscle metaboreflex activation and SAD does not appear to significantly impact the ventricular‐vascular relationship in healthy subjects. In heart failure, the arterial baroreflex retains some degree of restraint over metaboreflex induced increases in Ea and thus is likely a mechanism which prevents worsening of the already impaired energy transfer from the left ventricle to the systemic circulation.

Effects of Aging on Cardiac Autonomic Response during Resistance Exercise at Critical Load

Background: Critical load (CL) indicates the transition from moderate dynamic exercise to intense exercise and can be useful as a parameter of exercise intolerance during resistance exercise. In this sense, this study aimed to assess and contrast the cardiac autonomic response by heart rate variability during resistance exercise at CL in elderly and young individuals. Methods: Twenty apparently healthy active men, were allocated into young group (n=10) and elderly group (n=10), who underwent: 1) one repetition maximum (1RM) test on the Leg Press at 45º; 2) constant load exercise tests (70%, 80% and 90% of 1RM and intermediate load) in order to calculate the CL; and 3) CL assessment with record of heart rate (HR) and R-R intervals (R-Ri) to heart rate variability assessment. Results: During CL, the elderly presented lower value of mean HR in relation to young group (p<0.05), and mean R-Ri, RMSSD and SD1 were higher in elderly compared to young (p<0.05). In addition, delta (exercise minus rest) mean HR, STDRR, RMSSD, RRtri, TINN, SD1, SD2 and correlation dimension were lower in elderly compared to young (p<0.05). Conclusion: Elderly presented lower response to vagal withdrawal and less complexity compared to the young people during resistance exercise at CL.

Effect of moderate dynamic exercise on QT, QTC and QTD intervals in young obese adults

Effect of moderate dynamic exercise on QT, QTC and QTD intervals in young obese adults

Regulation of oxygen saturation in retinal blood vessels in response to dynamic exercise.

To evaluate the impact of dynamic exercise on retinal vessel oxygen saturation in healthy individuals. Twenty-six healthy participants underwent moderate dynamic exercise (modified Master's two-step exercise). In all subjects, intraocular pressures (IOP), systolic and diastolic blood pressures (SBP and DBP), retinal vessel calibres and retinal arterial and venous oxygen saturation were measured at baseline, immediately following exercise and 15min postexercise. Moderate dynamic exercise increased SBP and DBP immediately postexercise (SBP: 116 (±13) mmHg to 150 (±21) mmHg; p<0.001 and DBP: 69 (±10) mmHg to 74 (±10); p<0.001), while IOP decreased by an average of 2mmHg (baseline: 13 (±3) mmHg)) immediately postexercise (11 (±2) mmHg). Oxygen saturation in retinal arteries remained unchanged (baseline=93±8%; immediately postexercise=94±9% and 15min postexercise=96±8%; p=0.069), but increased in retinal veins immediately postexercise and did not return to baseline values within 15min postexercise (baseline=54±12%; immediately postexercise=56±15%; 15min postexercise=57±12%; p=0.036). There is a mild increase in retinal venous oxygen saturation and there is a trend towards an increase in arterial saturation in otherwise healthy individuals following dynamic exercise.

Cardiovascular Benefits of Moderate Exercise Training in Marfan Syndrome: Insights From an Animal Model.

BackgroundMarfan syndrome (MF) leads to aortic root dilatation and a predisposition to aortic dissection, mitral valve prolapse, and primary and secondary cardiomyopathy. Overall, regular physical exercise is recommended for a healthy lifestyle, but dynamic sports are strongly discouraged in MF patients. Nonetheless, evidence supporting this recommendation is lacking. Therefore, we studied the role of long‐term dynamic exercise of moderate intensity on the MF cardiovascular phenotype.Methods and ResultsIn a transgenic mouse model of MF (Fbn1 C1039G/+), 4‐month‐old wild‐type and MF mice were subjected to training on a treadmill for 5 months; sedentary littermates served as controls for each group. Aortic and cardiac remodeling was assessed by echocardiography and histology. The 4‐month‐old MF mice showed aortic root dilatation, elastic lamina rupture, and tunica media fibrosis, as well as cardiac hypertrophy, left ventricular fibrosis, and intramyocardial vessel remodeling. Over the 5‐month experimental period, aortic root dilation rate was significantly greater in the sedentary MF group, compared with the wild‐type group (∆mm, 0.27±0.07 versus 0.13±0.02, respectively). Exercise significantly blunted the aortic root dilation rate in MF mice compared with sedentary MF littermates (∆mm, 0.10±0.04 versus 0.27±0.07, respectively). However, these 2 groups were indistinguishable by aortic root stiffness, tunica media fibrosis, and elastic lamina ruptures. In MF mice, exercise also produced cardiac hypertrophy regression without changes in left ventricular fibrosis.ConclusionsOur results in a transgenic mouse model of MF indicate that moderate dynamic exercise mitigates the progression of the MF cardiovascular phenotype.

Cardiac parasympathetic outflow during dynamic exercise in humans estimated from power spectral analysis of P-P interval variability.

What is the central question of this study? Should we use the high-frequency (HF) component of P-P interval as an index of cardiac parasympathetic nerve activity during moderate exercise? What is the main finding and its importance? The HF component of P-P interval variability remained even at a heart rate of 120-140 beats min(-1) and was further reduced by atropine, indicating incomplete cardiac vagal withdrawal during moderate exercise. The HF component of R-R interval is invalid as an estimate of cardiac parasympathetic outflow during moderate exercise; instead, the HF component of P-P interval variability should be used. The high-frequency (HF) component of R-R interval variability has been widely used as an indirect estimate of cardiac parasympathetic (vagal) outflow to the sino-atrial node of the heart. However, we have recently found that the variability of the R-R interval becomes much smaller during dynamic exercise than that of the P-P interval above a heart rate (HR) of ∼100 beats min(-1). We hypothesized that cardiac parasympathetic outflow during dynamic exercise with a higher intensity may be better estimated using the HF component of P-P interval variability. To test this hypothesis, the HF components of both P-P and R-R interval variability were analysed using a Wavelet transform during dynamic exercise. Twelve subjects performed ergometer exercise to increase HR from the baseline of 69 ± 3 beats min(-1) to three different levels of 100, 120 and 140 beats min(-1). We also examined the effect of atropine sulfate on the HF components in eight of the 12 subjects during exercise at an HR of 140 beats min(-1) . The HF component of P-P interval variability was significantly greater than that of R-R interval variability during exercise, especially at the HRs of 120 and 140 beats min(-1). The HF component of P-P interval variability was more reduced by atropine than that of R-R interval variability. We conclude that cardiac parasympathetic outflow to the sino-atrial node can be estimated better by the HF component of P-P interval variability during exercise and that cardiac parasympathetic nerve activity exists during moderate dynamic exercise.

Muscle sympathetic activity in resting and exercising humans with and without heart failure

The sympathetic nervous system is critical for coordinating the cardiovascular response to various types of physical exercise. In a number of disease states, including human heart failure with reduced ejection fraction (HFrEF), this regulation can be disturbed and adversely affect outcome. The purpose of this review is to describe sympathetic activity at rest and during exercise in both healthy humans and those with HFrEF and outline factors, which influence these responses. We focus predominately on studies that report direct measurements of efferent sympathetic nerve traffic to skeletal muscle (muscle sympathetic nerve activity; MSNA) using intraneural microneurographic recordings. Differences in MSNA discharge between subjects with and without HFrEF both at rest and during exercise and the influence of exercise training on the sympathetic response to exercise will be discussed. In contrast to healthy controls, MSNA increases during mild to moderate dynamic exercise in the presence of HFrEF. This increase may contribute to the exercise intolerance characteristic of HFrEF by limiting muscle blood flow and may be attenuated by exercise training. Future investigations are needed to clarify the neural afferent mechanisms that contribute to efferent sympathetic activation at rest and during exercise in HFrEF.

Divergent muscle sympathetic responses to dynamic leg exercise in heart failure and age-matched healthy subjects.

People with diminished ventricular contraction who develop heart failure have higher sympathetic nerve firing rates at rest compared with healthy individuals of a similar age and this is associated with less exercise capacity. During handgrip exercise, sympathetic nerve activity to muscle is higher in patients with heart failure but the response to leg exercise is unknown because its recording requires stillness. We measured sympathetic activity from one leg while the other leg cycled at a moderate level and observed a decrease in nerve firing rate in healthy subjects but an increase in subjects with heart failure. Because these nerves release noradrenaline, which can restrict muscle blood flow, this observation helps explain the limited exercise capacity of patients with heart failure. Lower nerve traffic during exercise was associated with greater peak oxygen uptake, suggesting that if exercise training attenuated sympathetic outflow functional capacity in heart failure would improve. The reflex fibular muscle sympathetic nerve (MSNA) response to dynamic handgrip exercise is elicited at a lower threshold in heart failure with reduced ejection fraction (HFrEF). The present aim was to test the hypothesis that the contralateral MSNA response to mild to moderate dynamic one-legged exercise is augmented in HFrEF relative to age- and sex-matched controls. Heart rate (HR), blood pressure and MSNA were recorded in 16 patients with HFrEF (left ventricular ejection fraction = 31 ± 2%; age 62 ± 3 years, mean ± SE) and 13 healthy control subjects (56 ± 2 years) before and during 2 min of upright one-legged unloaded cycling followed by 2 min at 50% of peak oxygen uptake (V̇O2,peak). Resting HR and blood pressure were similar between groups whereas MSNA burst frequency was higher (50.0 ± 2.0 vs. 42.3 ± 2.7 bursts min(-1), P = 0.03) and V̇O2,peak lower (18.0 ± 2.0 vs. 32.6 ± 2.8 ml kg(-1) min(-1), P < 0.001) in HFrEF. Exercise increased HR (P < 0.001) with no group difference (P = 0.1). MSNA burst frequency decreased during mild to moderate dynamic exercise in the healthy controls but increased in HFrEF (-5.5 ± 2.0 vs. 6.9 ± 1.8 bursts min(-1), P < 0.001). Exercise capacity correlated inversely with MSNA burst frequency at 50% V̇O2,peak (n = 29; r = -0.64; P < 0.001). At the same relative workload, one-legged dynamic exercise elicited a fall in MSNA burst frequency in healthy subjects but sympathoexcitation in HFrEF, a divergence probably reflecting between-group differences in reflexes engaged by cycling. This finding, coupled with an inverse relationship between MSNA burst frequency during loaded cycling and subjects' V̇O2,peak, is consistent with a neurogenic determinant of exercise capacity in HFrEF.

P669: Acute effects of moderate dynamic exercise on brain plasticity

P669: Acute effects of moderate dynamic exercise on brain plasticity

The history of "Exercise Is Medicine" in ancient civilizations.

In 2007, the American College of Sports Medicine, with endorsement from the American Medical Association and the Office of the Surgeon General, launched a global initiative to mobilize physicians, healthcare professionals and providers, and educators to promote exercise in their practice or activities to prevent, reduce, manage, or treat diseases that impact health and the quality of life in humans. Emerging from this initiative, termed Exercise Is Medicine, has been an extensively documented position stand by the American College of Sports Medicine that recommended healthy adults perform 150 min of moderate dynamic exercise per week. The purpose of this article is to demonstrate the foundation for this global initiative and its exercise prescription for health and disease prevention has roots that began in antiquity more than two millennia ago. Individuals and concepts to remember are that Susruta of India was the first “recorded” physician to prescribe moderate daily exercise, Hippocrates of Greece was the first “recorded” physician to provide a written exercise prescription for a patient suffering from consumption, and the global influence of Galen from Rome combined with his recommendation on the use of exercise for patients in the management of disease prevailed until the 16th century. Historically intertwined with these concepts was exercise being advocated by select physicians to minimize the health problems associated with obesity, diabetes, and inactivity.

Muscle Oxygenation, EMG, and Cardiovascular Responses for Cabin Attendants vs. Controls

The goal was to investigate the effect of acute moderate hypobaric exposure on the physiological responses to sustained contractions (local) and light to moderate dynamic exercise (systemic) for cabin attendants (CAB) and a matched control group (CON). There were 14 CAB and 13 CON who participated. The experimental protocol was designed as a 2 x 2 randomized crossover study for which subjects performed a forearm isometric test and a cycling test in normobaric (NORM) and hypobaric [HYPO; 574 mmHg approximately 8000 ft (2440 m) above sea level (ASL)] conditions. Oxygen saturation (StO2%) was measured in the extensor carpi radialis muscle at rest and during an isometric wrist extension (20% MVC). Heart rate (HR), ventilation (V(E)), and oxygen uptake (VO2) were measured at rest, during cycling exercise at intensities of 50 W and 100 W, and during recovery. Blood samples were collected and analyzed for hemoglobin concentrations. Local response: There was a significant effect of HYPO for both CAB and CON with a decrease in StO2% of 6.5% both at rest and during contraction. Systemic response: there was no general effect of HYPO on HR, VE, or VO2. No differences were found between groups in either the local or systemic response or in the blood parameters. This study shows an effect of moderate hypobaric exposure on local muscle oxygenation during rest and sustained contraction. Whether this has an impact on fatigue development during work among cabin attendants is discussed.

α1‐Adrenergic receptor control of the cerebral vasculature in humans at rest and during exercise

We tested the hypothesis that pharmacological blockade of α(1)-adrenoreceptors (by prazosin), at rest and during steady-state dynamic exercise, would impair cerebral autoregulation and result in cerebral vasodilatation in healthy humans. In 10 subjects, beat-to-beat mean arterial pressure and mean middle cerebral artery blood velocity were determined at rest and during low (Ex90) and moderate workload (Ex130) on an upright bicycle ergometer without and with prazosin. Plasma noradrenaline concentrations increased significantly from rest to Ex130 during control conditions (from 1.8 ± 0.2 to 3.2 ± 0.3 pmol (ml plasma)(-1)). In the control conditions, the transfer function gain between mean arterial pressure and mean middle cerebral artery blood velocity in the low-frequency range was decreased at Ex90 (P = 0.035) and Ex130 (P = 0.027) from rest. A significant increase in critical closing pressure (CCP) was also observed in the control conditions from rest to Ex90 to Ex130 (from 18 ± 3 to 24 ± 4 to 31 ± 4 mmHg). An average of 74 ± 2% blockade of blood pressure response was achieved with oral prazosin. Following blockade, plasma noradrenaline concentrations further increased at rest and during Ex130 from the control value (from 2.6 ± 0.3 to 4.4 ± 0.5 pmol (ml plasma)(-1)). Prazosin also resulted in an increase in low-frequency gain (P < 0.003) compared with the control conditions. Prazosin blockade abolished the increases in CCP during Ex130 and increased the cerebrovascular conductance index (P = 0.018). These data indicate that in the control conditions a strengthening of cerebral autoregulation occurred with moderate dynamic exercise that is associated with an increase in CCP as a result of the exercise-mediated augmentation of sympathetic activity. Given that α(1)-adrenergic receptor blockade attenuated the increase in dynamic cerebral autoregulation and CCP, we conclude that increases in sympathetic activity have a role in establishing cerebral vascular tone in humans.

Dynamic cardiac output regulation at rest, during exercise, and muscle metaboreflex activation: impact of congestive heart failure

We tested whether mild and moderate dynamic exercise and muscle metaboreflex activation (MMA) affect dynamic baroreflex control of heart rate (HR) and cardiac output (CO), and the influence of stroke volume (SV) fluctuations on CO regulation in normal (N) and pacing-induced heart failure (HF) dogs by employing transfer function analyses of the relationships between spontaneous changes in left ventricular systolic pressure (LVSP) and HR, LVSP and CO, HR and CO, and SV and CO at low and high frequencies (Lo-F, 0.04-0.15 Hz; Hi-F, 0.15-0.6 Hz). In N dogs, both workloads significantly decreased the gains for LVSP-HR and LVSP-CO in Hi-F, whereas only moderate exercise also reduced the LVSP-CO gain in Lo-F. MMA during mild exercise further decreased the gains for LVSP-HR in both frequencies and for LVSP-CO in Lo-F. MMA during moderate exercise further reduced LVSP-HR gain in Lo-F. Coherence for HR-CO in Hi-F was decreased by exercise and MMA, whereas that in Lo-F was sustained at a high level (>0.8) in all settings. HF significantly decreased dynamic HR and CO regulation in all situations. In HF, the coherence for HR-CO in Lo-F decreased significantly in all settings; the coherence for SV-CO in Lo-F was significantly higher. We conclude that dynamic exercise and MMA reduces dynamic baroreflex control of HR and CO, and these are substantially impaired in HF. In N conditions, HR modulation plays a major role in CO regulation. In HF, influence of HR modulation wanes, and fluctuations of SV dominate in CO variations.

The distribution of blood flow in the carotid and vertebral arteries during dynamic exercise in humans

The mechanism underlying the plateau or relative decrease in cerebral blood flow (CBF) during maximal incremental dynamic exercise remains unclear. We hypothesized that cerebral perfusion is limited during high-intensity dynamic exercise due to a redistribution of carotid artery blood flow. To identify the distribution of blood flow among the arteries supplying the head and brain, we evaluated common carotid artery (CCA), internal carotid artery (ICA), external carotid artery (ECA) and vertebral artery (VA) blood flow during dynamic exercise using Doppler ultrasound. Ten subjects performed graded cycling exercise in a semi-supine position at 40, 60 and 80% of peak oxygen uptake (VO2 peak) for 5 min at each workload. The ICA blood flow increased by 23.0 ± 4.6% (mean ± SE) from rest to exercise at 60% (VO2 peak). However, at 80% (VO2 peak), ICA blood flow returned towards near resting levels (9.6 ± 4.7% vs. rest). In contrast, ECA, CCA and VA blood flow increased proportionally with workload. The change in ICA blood flow during graded exercise was correlated with end-tidal partial pressure of CO2 (r = 0.72). The change in ICA blood flow from 60% (VO2 peak) to 80% (VO2 peak) was negatively correlated with the change in ECA blood flow (r = −0.77). Moreover, there was a significant correlation between forehead cutaneous vascular conductance and ECA blood flow during exercise (r = 0.79). These results suggest that during high-intensity dynamic exercise the plateau or decrease in ICA blood flow is partly due to a large increase in ECA blood flow, which is selectively increased to prioritize thermoregulation.

Progressive muscle metaboreflex activation gradually decreases spontaneous heart rate baroreflex sensitivity during dynamic exercise

Ischemia of active skeletal muscle elicits a pressor response termed the muscle metaboreflex. We tested the hypothesis that in normal dogs during dynamic exercise, graded muscle metaboreflex activation (MMA) would progressively attenuate spontaneous heart rate baroreflex sensitivity (SBRS). The animals were chronically instrumented to measure heart rate (HR), cardiac output (CO), mean and systolic arterial pressure (MAP and SAP), and left ventricular systolic pressures (LVSP) at rest and during mild or moderate treadmill exercise before and during progressive MMA [via graded reductions of hindlimb blood flow (HLBF)]. SBRS [slopes of the linear relationships (LRs) between HR and LVSP or SAP during spontaneous sequences of > or =3 consecutive beats when HR changed inversely vs. pressure] decreased during mild exercise from the resting values (-5.56 +/- 0.86 vs. -2.67 +/- 0.50 beats.min(-1).mmHg(-1), P <0.05), and in addition, these LRs were shifted upward. Progressive MMA gradually and linearly increased MAP, CO, and HR; linearly decreased SBRS; and shifted LRs upward and rightward to higher HR and pressures denoting baroreflex resetting. Moderate exercise caused a substantial reduction in SBRS (-1.57 +/- 0.38 beats.min(-1).mmHg(-1), P <0.05) and both an upward and rightward resetting. Gradual MMA at this higher workload also caused significant progressive increases in MAP, CO, and HR and progressive decreases in SBRS, and the LRs were shifted to higher MAP and HR. Our results demonstrate that gradual MMA during mild and moderate dynamic exercise progressively decreases SBRS. In addition, baroreflex control of HR is progressively reset to higher blood pressure and HR in proportion to the extent of MMA.

Dynamic Cardiac Output Regulation during Exercise, Muscle Metaboreflex Activation and Heart Failure

We tested whether moderate dynamic exercise (EX) and muscle metaboreflex activation (MMA) affects dynamic baroreflex control of heart rate (HR), cardiac output (CO), and the influence of stroke volume (SV) fluctuations on CO regulation in normal (N) and pacing‐induced heart failure (HF) dogs by employing transfer function analyses of the relationships between spontaneous changes in left ventricular systolic pressure (LVSP) and HR, LVSP and CO, HR and CO, and SV and CO at low and high frequencies (Lo‐F, 0–0.25 Hz; Hi‐F 0.25‐0.6 Hz). In N dogs, EX significantly decreased transfer function gains for LVSP‐HR and LVSP‐CO in Hi‐F and reduced the LVSP‐CO gain in Lo‐F. MMA further reduced LVSP‐HR gain in Lo‐F. Coherence for HR‐CO in Hi‐F was decreased by EX and MMA, whereas that in Lo‐F was sustained at high levels (&gt; 0.8) in all the settings. HF significantly reduced LVSP‐HR gain in Hi‐F. LVSP‐CO gain was decreased in both Lo‐F and Hi‐F. EX and MMA caused similar effects as observed in N conditions. In HF, the coherence for HR‐CO in Lo‐F decreased significantly in all settings, the coherence for SV‐CO in Lo‐F was significantly higher. We conclude that EX and MMA reduces dynamic baroreflex control of HR and CO and those are substantially diminished in HF. In N conditions HR modulation plays a major role in CO regulation. In HF, influence of HR modulation wanes and fluctuations of SV dominates in CO variations. NIH HL 55473

Progressive Muscle Metaboreflex Activation Gradually Decreases Spontaneous Heart Rate Baroreflex Sensitivity During Dynamic Exercise

We tested whether graded muscle metaboreflex activation (MMA) during dynamic exercise would progressively attenuate spontaneous heart rate baroreflex sensitivity (SBRS) in dogs. We measured heart rate (HR), cardiac output (CO), mean arterial and left ventricular systolic pressures (MAP, LVSP) at rest and during mild or moderate treadmill exercise before and during progressive MMA [via graded reductions of hindlimb blood flow (HLBF)]. SBRS (slopes of the linear relationships (LRs) between HR and LVSP during spontaneous sequences of ≥ 3 consecutive beats when HR changed inversely vs. pressure) decreased during mild exercise from the values at rest (−6.0 ± 1.2 vs. −3.0 ± 0.7 bpm/mmHg, P &lt; 0.05) and these LRs were shifted upwards. Progressive MMA gradually and linearly increased MAP, CO, and HR and linearly decreased SBRS and shifted LRs upward and rightward denoting baroreflex resetting. Moderate exercise caused a substantial reduction in SBRS (−1.8 ± 0.5 bpm/mmHg, P &lt; 0.05) and both an upward and rightward resetting. Gradual MMA again caused significant increases in MAP, CO and HR and progressive decreases in SBRS and LRs shifted to higher MAP and HR. Our results demonstrate that gradual MMA during mild and moderate dynamic exercise progressively decreases SBRS. In addition, baroreflex control of HR is progressively reset to higher blood pressure and HR in proportion to the extent of MMA. NIH HL 55473

Spontaneous baroreflex control of cardiac output during dynamic exercise, muscle metaboreflex activation, and heart failure

We have previously shown that spontaneous baroreflex-induced changes in heart rate (HR) do not always translate into changes in cardiac output (CO) at rest. We have also shown that heart failure (HF) decreases this linkage between changes in HR and CO. Whether dynamic exercise and muscle metaboreflex activation (via imposed reductions in hindlimb blood flow) further alter this translation in normal and HF conditions is unknown. We examined these questions using conscious, chronically instrumented dogs before and after pacing-induced HF during mild and moderate dynamic exercise with and without muscle metaboreflex activation. We measured left ventricular systolic pressure (LVSP), CO, and HR and analyzed the spontaneous HR-LVSP and CO-LVSP relationships. In normal animals, mild exercise significantly decreased HR-LVSP (-3.08 +/- 0.5 vs. -5.14 +/- 0.6 beats.min(-1).mmHg(-1); P < 0.05) and CO-LVSP (-134.74 +/- 24.5 vs. -208.6 +/- 22.2 ml.min(-1).mmHg(-1); P < 0.05). Moderate exercise further decreased both and, in addition, significantly reduced HR-CO translation (25.9 +/- 2.8% vs. 52.3 +/- 4.2%; P < 0.05). Muscle metaboreflex activation at both workloads decreased HR-LVSP, whereas it had no significant effect on CO-LVSP and the HR-CO translation. HF significantly decreased HR-LVSP, CO-LVSP, and the HR-CO translation in all situations. We conclude that spontaneous baroreflex HR responses do not always cause changes in CO during exercise. Moreover, muscle metaboreflex activation during mild and moderate dynamic exercise reduces this coupling. In addition, in HF the HR-CO translation also significantly decreases during both workloads and decreases even further with muscle metaboreflex activation.

Spontaneous baroreflex control of heart rate during exercise and muscle metaboreflex activation in heart failure

In heart failure (HF), there is a reduced baroreflex sensitivity at rest, and during dynamic exercise there is enhanced muscle metaboreflex activation (MRA). However, how the arterial baroreflex modulates HR during exercise is unknown. We tested the hypothesis that spontaneous baroreflex sensitivity (SBRS) is attenuated during exercise in HF and that MRA further depresses SBRS. In seven conscious dogs we measured heart rate (HR), cardiac output, and left ventricular systolic pressure at rest and during mild and moderate dynamic exercise, before and during MRA (via imposed reductions of hindlimb blood flow), and before and after induction of HF (by rapid ventricular pacing). SBRS was assessed by the sequences method. In control, SBRS was reduced from rest with a progressive resetting of the baroreflex stimulus-response relationship in proportion to exercise intensity and magnitude of MRA. In HF, SBRS was significantly depressed in all settings; however, the changes with exercise and MRA occurred with a pattern similar to the control state. As in control, the baroreflex stimulus-response relationship showed an intensity- and muscle metaboreflex (MMR)-dependent rightward and upward shift. The results of this study indicate that HF induces an impairment in baroreflex control of HR at rest and during exercise, although the effects of exercise and MRA on SBRS occur with a similar pattern as in control, indicating the persistence of some vagal activity.

Muscle metaboreflex attenuates spontaneous heart rate baroreflex sensitivity during dynamic exercise

Hypoperfusion of active skeletal muscle elicits a reflex pressor response termed the muscle metaboreflex. Dynamic exercise attenuates spontaneous baroreflex sensitivity (SBRS) in the control of heart rate (HR) during rapid, spontaneous changes in blood pressure (BP). Our objective was to determine whether muscle metaboreflex activation (MRA) further diminishes SBRS. Conscious dogs were chronically instrumented for measurement of HR, cardiac output, mean arterial pressure, and left ventricular systolic pressure (LVSP) at rest and during mild (3.2 km/h) or moderate (6.4 km/h at 10% grade) dynamic exercise before and after MRA (via partial reduction of hindlimb blood flow). SBRS was evaluated as the slopes of the linear relations (LRs) between HR and LVSP during spontaneous sequences of at least three consecutive beats when HR changed inversely vs. pressure (expressed as beats x min(-1) x mmHg(-1)). During mild exercise, these LRs shifted upward, with a significant decrease in SBRS (-3.0 +/- 0.4 vs. -5.2 +/- 0.4, P<0.05 vs. rest). MRA shifted LRs upward and rightward and decreased SBRS (-2.1 +/- 0.1, P<0.05 vs. mild exercise). Moderate exercise shifted LRs upward and rightward and significantly decreased SBRS (-1.2 +/- 0.1, P<0.05 vs. rest). MRA elicited further upward and rightward shifts of the LRs and reductions in SBRS (-0.9 +/- 0.1, P<0.05 vs. moderate exercise). We conclude that dynamic exercise resets the arterial baroreflex to higher BP and HR as exercise intensity increases. In addition, increases in exercise intensity, as well as MRA, attenuate SBRS.