Single Bout Of Dynamic Exercise Research Articles

Skeletal Muscle Hyperemia: A Potential Bridge Between Post-exercise Hypotension and Glucose Regulation.

For both healthy individuals and patients with type 2 diabetes (T2D), the hemodynamic response to regular physical activity is important for regulating blood glucose, protecting vascular function, and reducing the risk of cardiovascular disease. In addition to these benefits of regular physical activity, evidence suggests even a single bout of dynamic exercise promotes increased insulin-mediated glucose uptake and insulin sensitivity during the acute recovery period. Importantly, post-exercise hypotension (PEH), which is defined as a sustained reduction in arterial pressure following a single bout of exercise, appears to be blunted in those with T2D compared to their non-diabetic counterparts. In this short review, we describe research that suggests the sustained post-exercise vasodilation often observed in PEH may sub-serve glycemic regulation following exercise in both healthy individuals and those with T2D. Furthermore, we discuss the interplay of enhanced perfusion, both macrovascular and microvascular, and glucose flux following exercise. Finally, we propose future research directions to enhance our understanding of the relationship between post-exercise hemodynamics and glucose regulation in healthy individuals and in those with T2D.

Effects of acute interval handgrip exercise on cognitive performance

Previous studies have reported that even a single bout of dynamic exercise improves cognitive performance. However, the acute effect of the interval handgrip (HG) exercise protocol, which is effective in reducing resting blood pressure, on cognitive performance is poorly understood. Cognitive performance was assessed in 17 young healthy subjects before and after a resting control (e.g., time control) and the interval HG exercise (Exercise), which consisted of four trials of 2-min HG exercise at 25% of maximum voluntary contraction with 3-min recovery in between each trial. Mean arterial blood pressure (MAP) and middle cerebral artery blood velocity (MCA V) were measured continuously throughout the experiment. Memory recognition and executive function were assessed using memory recognition and Go/No-Go tasks, respectively. During interval HG exercise, MAP and mean MCA V increased from the resting baseline condition (both P < 0.049) and returned to the resting baseline levels during recovery after the interval HG exercise (both P=1.000). The reaction time and performance accuracy of the memory recognition task did not change in either the time control condition or Exercise condition (P=0.514 and P=0.414 respectively). However, the changes in reaction time of Go/No-Go task from the baseline in Exercise condition was significantly shorter than that in time-control condition (P=0.004) without affecting performance accuracy (P=0.482). The results of the present study show that an acute interval HG exercise could improve the processing speed in executive function despite no post-exercise improvement in hemodynamic parameters in young healthy subjects. These findings suggest that the interval HG exercise is a useful exercise mode that can be expected to have a positive effect on the processing speed in executive function regardless of cardiovascular adaptation to exercise.

The influence of water ingestion on postexercise hypotension and standing haemodynamics

In young healthy adults, postexercise hypotension (PEH) occurs after a single bout of dynamic exercise due to peripheral vasodilation. Gravitational stress may further aggravate the magnitude of PEH, thus predisposing to orthostatic intolerance. As water drinking activates sympathetic vasoconstriction, it might offset PEH via enhanced α-adrenergic vascular responsiveness. We hypothesized that water ingestion before exercise would decrease the magnitude of PEH and improve the haemodynamic reaction to active standing postmaximal exercise. In a randomized fashion, 17 healthy adults (nine men; eight women, 21·2±1·6years) ingested 50 and 500ml of water before completing resting, cycle ergometer and recovery protocols on two separate days. After exercise, measurements [arterial blood pressure (BP), heart rate and spectral heart rate variability (HRV)] were taken in the seated position followed by 5min of active standing. Compared to that seen post-50ml of water, the 500ml volume elicited an overall increase in BP (P<0·05). Nevertheless, the magnitude of PEH was not different after either volume of water. There was an overall bradycardic effect of water, and this was accompanied by increased high-frequency power (P<0·05). Finally, no BP, heart rate or HRV differences were found between conditions in response to active standing. These data suggest that, despite being well preserved after maximal exercise, the water pressor response does not affect the magnitude of PEH. They also indicate that drinking 500ml of water does not impact the BP, heart rate or HRV response to 5min of active standing during recovery postmaximal exercise.

A single bout of dynamic exercise by healthy adults enhances the generation of monocyte-derived-dendritic cells

The ex vivo generation of monocyte-derived-dendritic cells (mo-DCs) has facilitated the use of DCs in immunotherapy research. However, low blood monocyte numbers frequently limit the manufacture of sufficient numbers of mo-DCs for subsequent experimental and clinical procedures. Because exercise mobilizes monocytes to the blood, we tested if acute dynamic exercise by healthy adults would augment the generation of mo-DCs without compromising their differentiation or function. We compared mo-DC generation from before- and after-exercise blood over 8-days of culture. Function was assessed by FITC-dextran uptake and the stimulation of autologous cytomegalovirus (pp65)-specific-T-cells. Supporting the hypothesis, we found a near fourfold increase in number of mo-DCs generated after-exercise. Furthermore, relative FITC-dextran uptake, differentiation rate, and stimulation of pp65-specific-T-cells did not differ between before- and after-exercise mo-DCs. We conclude that exercise enhances the ex vivo generation of mo-DCs without compromising their function, and so may overcome some limitations associated with manufacturing these cells for immunotherapy.

Exercise Increases intrinsic and synaptic excitability of NTS second‐order baroreceptive neurons in SHRs (686.21)

A single bout of dynamic exercise lowers blood pressure in hypertensive subjects, named post‐exercise hypotension (PEH). We previously showed that exercise reduced GABA release in the NTS. Within the NTS, the balance of excitatory and inhibitory synaptic transmissions is integrated into the intrinsic excitability of baroreceptive neurons to shape baroreflex output from the NTS to downstream synapses. Here, I tested the hypothesis that a single exercise bout increases intrinsic excitability and excitatory synaptic inputs in NTS 2nd‐order baroreceptive neurons. Resting membrane potential (Rem), spiking response to depolarization, inwardly‐rectified K currents (Kir), spontaneous excitatory postsynaptic currents (sEPSCs), and miniature EPSCs were recorded in anatomically identified 2nd‐order baroreceptive neurons in a brainstem slice. Neurons from the PEH group (n=10) had a slightly depolarized Rem and significantly higher spiking activity (p&lt;0.05) at Rem. When the neurons were current‐clamped at ‐60 mV there was no significant difference in spiking activity or spiking response to depolarization between sham and PEH. In addition, Kir currents were smaller in neurons from the PEH group. Neurons from the PEH group (n=7) also had higher sEPSC and mEPSC frequencies (p&lt;0.05). Data suggest that increased intrinsic and synaptic excitability of NTS 2nd‐order baroreceptive neurons may contribute to the PEH.

The 894G&gt;T endothelial nitric oxide synthase genetic polymorphism affects hemodynamic responses to mental stress performed before and after exercise

Nitric oxide is the primary mediator of vasodilation during mental stress. Since genetic polymorphisms in the nitric oxide synthase (eNOS) gene seem to impair the production of NO, this study aimed to evaluate the effect of an exercise bout on hemodynamic responses to mental stress in subjects with the 894G>T polymorphism of eNOS. Subjects without (wild-type group; n = 16) or with (polymorphic-type group; n = 19) the 894G>T polymorphism underwent a mental stress challenge before and after a maximal cardiopulmonary exercise test. Blood pressure was measured by auscultation and forearm blood flow by venous occlusion plethysmography. The groups were similar regarding anthropometric, metabolic, resting blood pressure and exercise variables. Before exercise, systolic blood pressure response during mental stress was higher in the polymorphic-type group (∆wild-type: 8.0 ± 2.0% vs. ∆polymorphic-type: 12.5 ± 1.8%, P = 0.01), while the increase in forearm vascular conductance was similar between the groups (∆wild-type 90.8 ± 26.4% vs. ∆polymorphic-type: 86.3 ± 24.1%, P = 0.44). After exercise, the systolic blood pressure at baseline and during mental stress was lower than before exercise in the whole group (P < 0.05), but the pressure response during mental stress was still higher in the polymorphic-type group (∆wild-type: 5.8 ± 1.5% vs. ∆polymorphic-type: 10.2 ± 1.4%, P = 0.01). The increase in forearm vascular conductance was inhibited only in the polymorphic-type group (∆before exercise 86.3 ± 24.1% vs. ∆after exercise: 41.5 ± 12.6%, P = 0.04). In conclusion, these results suggest the 894G>T eNOS polymorphism is associated with altered hemodynamic responses to mental stress both before and after a single bout of dynamic exercise with potential clinical implications.

Reduced expression of FXYD domain containing ion transport regulator 5 (FXYD5) in hypertension

l-nitroarginine methyl ester (L-NAME, 40 mg/kg, i.p.) significantly inhibited post exercise hypotension (25±11 and 5±3mm Hg, respectively; P<0.05). In addition, the superoxide anion generation was decreased, while the plasma nitrite production and serine phosphorylation of endothelial nitric oxide synthase were significantly elevated in spontaneously hypertensive rats at 30 min after the termination of exercise. Taken together, these data demonstrate that the increased phosphorylation of endothelial nitric oxide synthase plays a crucial role in the reduction of arterial pressure following a single bout of dynamic exercise in spontaneously hypertensive rats.

The influence of thermal factors on post‐exercise haemodynamics in endurance exercise‐trained men

The influence of thermal factors on post‐exercise haemodynamics in endurance exercise‐trained men

Endothelial nitric oxide synthase activation contributes to post-exercise hypotension in spontaneously hypertensive rats

We investigated the role that endothelial nitric oxide synthase plays in post-exercise hypotension in spontaneously hypertensive rats. To accomplish this, rats were subjected to a single bout of dynamic exercise on a treadmill at 15 m/min for 20 min. l-Nitroarginine methyl ester ( l-NAME, 40 mg/kg, i.p.) significantly inhibited post-exercise hypotension (25 ± 11 and 5 ± 3 mm Hg, respectively; P < 0.05). In addition, the superoxide anion generation was decreased, while the plasma nitrite production and serine phosphorylation of endothelial nitric oxide synthase were significantly elevated in spontaneously hypertensive rats at 30 min after the termination of exercise. Taken together, these data demonstrate that the increased phosphorylation of endothelial nitric oxide synthase plays a crucial role in the reduction of arterial pressure following a single bout of dynamic exercise in spontaneously hypertensive rats.

Neurokinin‐1 receptor expressing neurons in the nucleus of the solitary tract are required for full expression of post‐exercise hypotension in spontaneously hypertensive rats

A single bout of exercise decreases blood pressure (post‐exercise hypotension; PEH) in both hypertensive humans and spontaneously hypertensive rats (SHR). Our recent studies suggest that in SHR, PEH may be dependent in part on activation of neurokinin‐1 receptors (NK1‐R) in the nucleus of the solitary tract (NTS). The current experiments were performed to test the hypothesis that selective elimination of NK1‐R expressing neurons in the NTS would attenuate PEH in SHR. The NK1‐R targeted neurotoxin, stable substance‐P saporin (SSP‐SAP) was microinjected into the NTS to ablate NK1‐R neurons in adult male SHR implanted with telemetry transmitters to measure blood pressure (BP) and heart rate. SSP‐SAP induced a transient (5 day) increase in BP after ablation relative to control (blank saporin; p&lt;0.01) rats. Blood pressure variability, assessed as the standard deviation of daily systolic BP, increased by the second week after NK1‐R neuron ablation (p&lt;0.05). Two weeks after NK1‐R neuron ablation, rats were subjected to a single bout of dynamic exercise or sham exercise. SSP‐SAP significantly blunted PEH (p&lt;0.005, 2‐way RM ANOVA). For example, by 120 min post‐exercise blood pressure was decreased by −15.2 ± 2 mmHg in control (n=4) versus 0.5 ± 2.7 mmHg in SSP‐SAP (n=6) treated rats. We conclude that ablation of NTS NK1‐R expressing neurons increases blood pressure variability and attenuates PEH in SHR. (Support: HL‐67183)

Forebrain regions associated with postexercise differences in autonomic and cardiovascular function during baroreceptor unloading

The cortical regions representing peripheral autonomic reactions in humans are poorly understood. This study examined whether changes in forebrain activity were associated with the altered physiological responses to lower body negative pressure (LBNP) following a single bout of dynamic exercise (POST-EX). We hypothesized that, compared with the nonexercised condition (NO-EX), POST-EX would elicit greater reductions in stroke volume (SV) and larger increases in heart rate (HR) and muscle sympathetic nerve activity (MSNA) during LBNP (5, 15, and 35 mmHg). Forebrain neural activity (n = 11) was measured using blood oxygen level-dependent (BOLD) functional magnetic resonance imaging. HR, SV, arterial blood pressure (ABP), and MSNA were collected separately. Compared with NO-EX, baseline ABP was reduced, whereas HR and total vascular conductance (TVC) were elevated in POST-EX (P < 0.05). In both conditions, 5 mmHg LBNP did not elicit a change (from baseline) in any physiological parameter. Compared with NO-EX, 35 mmHg LBNP-mediated decreases in SV and TVC produced greater increases in HR and MSNA during POST-EX (P < 0.05). The right posterior insula and dorsal anterior cingulate cortex demonstrated a larger decrease in BOLD at 5 mmHg LBNP but greater BOLD increase at 15 and 35 mmHg LBNP POST-EX vs. NO-EX (P < 0.005). Conversely, the thalamus and ventral medial prefrontal cortex displayed the opposite BOLD activity pattern (i.e., larger increase at 5 mmHg LBNP but greater decrease at 15 and 35 mmHg LBNP POST-EX vs. NO-EX). Our findings suggest that discrete forebrain regions may be involved with the generation of baroreflex-mediated sympathetic and cardiovascular responses elicited by moderate LBNP.

Mechanism behind Augmentation in Baroreflex Sensitivity after Acute Exercise in Spontaneously Hypertensive Rats

A single bout of dynamic exercise increases baroreflex sensitivity (BRS) in spontaneously hypertensive rats (SHR). We examined whether change in hemodynamics (increases in blood pressure and heart rate) associated with dynamic exercise contribute to the post-exercise modulation of BRS. SHR aged 12 weeks were chronically instrumented with a carotid artery catheter and jugular vein catheter. They were then allocated to three groups submitted to 40 min of 1) running on a treadmill at 12 m/min (Run), 2) concomitant infusion of isoproterenol and a relatively high dose of phenylephrine (Iso+Phe(high)), or 3) concomitant infusion of isoproterenol and a relatively low dose of phenylephrine (Iso+Phe(low)). Arterial pressure and heart rate were continuously recorded throughout the experiments. BRS estimated by heart rate responses to phenylephrine injection and systolic blood pressure-low frequency power amplitude (SBP-LFamp) evaluated by power spectral analysis of SBP, a marker of sympathetic activity, were examined before and after running (Run group), or administration of drugs (Iso+Phe(high) or Iso+Phe(low) groups). BRS increased significantly from 1.4 to 1.9 bpm/mmHg after running, but not after administration of Iso+Phe(high) or Iso+Phe(low). Blood pressure and SBP-LFamp significantly decreased in each of the Run, Iso+Phe(high) and Iso+Phe(low) groups. These results suggest that hemodynamic change alone does not contribute to post-exercise modulation of BRS, while hemodynamic change or sympathetic activation during exercise contributes to post-exercise hypotension associated with a reduction of sympathetic activity.

Acute exercise increases the ventricular arrhythmia threshold via the intrinsic adenosine receptor system in conscious hypertensive rats

Coronary artery occlusion-induced tachyarrhythmias that culminate in ventricular fibrillation are the leading cause of death in developed countries. The intrinsic adenosine receptor system protects the heart from an ischemic insult. Thus the increased functional demands made on the heart during exercise may produce protective adaptations mediated by endogenous adenosine. Therefore, we tested the hypothesis that a single bout of dynamic exercise increases the ventricular arrhythmia threshold (VAT) induced by coronary artery occlusion in conscious hypertensive rats via the intrinsic adenosine receptor system. To test this hypothesis, we recorded the VAT before and on an alternate day after a single bout of dynamic treadmill exercise (12 m/min, 10% grade for 40 min). A single bout of dynamic exercise significantly reduced postexercise arterial pressure (Delta-24 +/- 4 mmHg) and increased VAT (Delta+1.95 +/- 0.31 min). Adenosine receptor blockade with the nonselective adenosine receptor antagonists theophylline or aminophylline (10 mg/kg) attenuated the cardioprotective effects of a single bout of dynamic exercise. Results suggest that strategies that increase myocardial ATP requirements leading to adenosine production provide protection against coronary artery occlusion.

Previous exercise attenuates muscle sympathetic activity and increases blood flow during acute euglycemic hyperinsulinemia

Insulin infusion causes muscle vasodilation, despite the increase in sympathetic nerve activity. In contrast, a single bout of exercise decreases sympathetic activity and increases muscle blood flow during the postexercise period. We tested the hypothesis that muscle sympathetic activity would be lower and muscle vasodilation would be higher during hyperinsulinemia performed after a single bout of dynamic exercise. Twenty-one healthy young men randomly underwent two hyperinsulinemic euglycemic clamps performed after 45 min of seated rest (control) or bicycle exercise (50% of peak oxygen uptake). Muscle sympathetic nerve activity (MSNA, microneurography), forearm blood flow (FBF, plethysmography), blood pressure (BP, oscillometric method), and heart rate (HR, ECG) were measured at baseline (90 min after exercise or seated rest) and during hyperinsulinemic euglycemic clamps. Baseline glucose and insulin concentrations were similar in the exercise and control sessions. Insulin sensitivity was unchanged by previous exercise. During the clamp, insulin levels increased similarly in both sessions. As expected, insulin infusion increased MSNA, FBF, BP, and HR in both sessions (23 +/- 1 vs. 36 +/- 2 bursts/min, 1.8 +/- 0.1 vs. 2.2 +/- 0.2 ml.min(-1).100 ml(-1), 89 +/- 2 vs. 92 +/- 2 mmHg, and 58 +/- 1 vs. 62 +/- 1 beats/min, respectively, P < 0.05). BP and HR were similar between sessions. However, MSNA was significantly lower (27 +/- 2 vs. 31 +/- 2 bursts/min), and FBF was significantly higher (2.2 +/- 0.2 vs. 1.8 +/- 0.1 ml.min(-1).100 ml(-1), P < 0.05) in the exercise session compared with the control session. In conclusion, in healthy men, a prolonged bout of dynamic exercise decreases MSNA and increases FBF. These effects persist during acute hyperinsulinemia performed after exercise.

Hemodynamic of Post-Dynamic Submaximal Exercise in Obese Women with and without Type 2 Diabetes

1459 PURPOSE: Post-exercise hypotension (PEH) is the decrease in resting systolic blood pressure (SBP) after an acute bout of exercise. PEH has been attributed to decreases in vascular resistance and cardiac output in hypertensives but hemodynamic responses may differ in other clinical populations. To evaluate the hemodynamic contributors to the hypotensive effect of a single bout of dynamic exercise in obese women (30.1–43.4 kg/m2, 45–59 years) with (n = 8) and without (n = 9) type 2 diabetes (T2D). METHODS: We evaluated SBP, total peripheral resistance (TPR), stroke volume (SV), heart rate (HR), and cardiac output at pre-exercise and at 10, 20, and 30 min after 20 min of treadmill exercise at 65% of VO2 max. Hemodynamic variables were measured using beat-to-beat finger plethysmography (Portapres) in the supine position. Data were analyzed using an ANOVA with repeated measures (pre-exercise, 10, 20, and 30 min post-exercise). RESULTS: SBP was significantly (p<.05) reduced from pre-exercise at 10–30 min into recovery in the obese group but not in the T2D group. SBP changes from pre-exercise to 30 min post-exercise were significantly (p<.05) greater in the obese group (− 9 ± 10 mm Hg) compared to the T2D group (3 ± 11 mm Hg). Both groups demonstrated a similar change in TPR during recovery with a reduction at 10 min followed by a significant (p<.05) increase at 30 min post-exercise. SV was significantly (p<.05) reduced from pre-exercise at 10–30 min post-exercise in both groups without significance between groups. HR was significantly (p<.05) increased from pre-exercise at 10 and 20 min but not at 30 min post-exercise in both groups. Cardiac output changed significantly (p<.05) from pre-exercise values to the lowest level at 30 min post-exercise in the obese (− 0.7 ± 0.7 L/min) and T2D (− 0.5 ± 0.9 L/min) (p = .09 for group × condition interaction). CONCLUSIONS: These findings indicate that PEH during 30 min after submaximal exercise is observed in obese women without T2D but not in obese women with T2D. PEH in obese women without T2D is mediated primarily by a reduction in cardiac output due to a large decrease in SV. The higher SBP at 30 min post-exercise in T2D women was primarily due to lower decrease in cardiac output, since the increase in TPR was similar in both groups. Sponsored by NY State Diabetes Bridge Grant

Postexercise hypotension in conscious SHR is attenuated by blockade of substance P receptors in NTS.

In hypertensive subjects, a single bout of dynamic exercise results in an immediate lowering of blood pressure back toward normal. This postexercise hypotension (PEH) also occurs in the spontaneously hypertensive rat (SHR). In both humans and SHRs, PEH features a decrease in sympathetic nerve discharge, suggesting the involvement of central nervous system pathways. Given that substance P is released in the nucleus tractus solitarius (NTS) by activation of baroreceptor and skeletal muscle afferent fibers during muscle contraction, we hypothesized that substance P acting at neurokinin-1 (NK-1) receptors in the NTS might contribute to PEH. We tested the hypothesis by determining, in conscious SHRs, whether NTS microinjections of the NK-1 receptor antagonist SR-140333 before exercise attenuated PEH. The antagonist, in a dose (60 pmol) that blocked substance P- and spared D,L-homocysteic acid-induced depressor responses, significantly attenuated the PEH by 37%, whereas it had no effect on blood pressure during exercise. Vehicle microinjection had no effect. The antagonist also had no effect on heart rate responses during both exercise and the PEH period. The data suggest that a substance P (NK-1) receptor mechanism in the NTS contributes to PEH.

Postexercise alpha-adrenergic receptor hyporesponsiveness in hypertensive rats is due to nitric oxide.

We tested the hypothesis that a single bout of dynamic exercise produces a postexercise hypotension (PEH) and alpha(1)-adrenergic receptor hyporesponsiveness in spontaneously hypertensive rats (SHR). The postexercise alpha(1)-adrenergic receptor hyporesponsiveness is due to an enhanced buffering of vasoconstriction by nitric oxide. Male (n = 8) and female (n = 5) SHR were instrumented with a Doppler ultrasonic flow probe around the femoral artery. Distal to the flow probe, a microrenathane catheter was inserted into a branch of the femoral artery for the infusion of the alpha(1)-adrenergic receptor agonist phenylephrine (PE). A microrenathane catheter was inserted into the descending aorta via the left common carotid artery for measurements of arterial pressure (AP) and heart rate. Dose-response curves to PE (3.8 x 10(-3) - 1.98 x 10(-2)microg/kHz) were generated before and after a single bout of dynamic exercise. Postexercise AP was reduced in male (13 +/- 3 mmHg) and female SHR (18 +/- 7 mmHg). Postexercise vasoconstrictor responses to PE were reduced in males due to an enhanced influence of nitric oxide. However, in females, postexercise vasoconstrictor responses to PE were not altered. Results suggest that nitric oxide- mediated alpha(1)-adrenergic receptor hyporesponsiveness contributes to PEH in male but not female SHR.

Acute exercise reduces the response to colon distension in T(5) spinal rats.

Individuals with spinal cord injuries above thoracic level 6 (T(6)) experience life-threatening bouts of hypertension, termed autonomic dysreflexia (AD). AD is mediated by peripheral alpha-adrenergic receptor supersensitivity as well as a reorganization of spinal pathways controlling sympathetic preganglionic neurons. A single bout of dynamic exercise may be a safe therapeutic approach to reduce the severity of AD because mild-to-moderate dynamic exercise reduces postexercise alpha-adrenergic receptor responsiveness, lowers postexercise sympathetic nerve activity, and reduces the postexercise response to stress. Therefore, this study was designed to test the hypothesis that mild-to-moderate dynamic exercise attenuates the postexercise response to colon distension (mechanism to elicit AD). To test this hypothesis, six male Wistar rats (406 +/- 23 g), 5 wk post-T(5) spinal cord transection, were instrumented with an arterial catheter. After recovery, the response to graded colon distension (10, 30, 50, and 80 mmHg, in random order) was determined before and after a single bout of mild-to-moderate dynamic exercise (9-12 m/min, 0% grade for 40 min). After exercise, the pressor response to graded colon distension was significantly attenuated (preexercise change: 2 +/- 1, 9 +/- 1, 14 +/- 1, and 24 +/- 2 vs. postexercise change: 2 +/- 1, 2 +/- 1, 9 +/- 1, and 12 +/- 3 mmHg). Thus acute exercise is a safe, therapeutic approach to reduce the severity of AD in paraplegic subjects.

Central blockade of vasopressin V(1) receptors attenuates postexercise hypotension.

We tested the hypothesis that central arginine vasopressin (AVP) mediates postexercise reductions in arterial pressure (AP) and heart rate (HR). To test this hypothesis, nine spontaneously hypertensive rats (SHR) were instrumented with a 22-gauge stainless steel guide cannula in the right lateral cerebral ventricle and with a carotid arterial catheter. After the rats recovered, AP and HR were assessed before and after a single bout of dynamic exercise with the central administration of vehicle or the selective AVP V(1)-receptor antagonist d(CH(3))(5) Tyr(Me)-AVP (AVP-X). AP and HR were significantly decreased below preexercise values with central administration of vehicle [P < 0.05, change (Delta)-21 +/- 4 mmHg and Delta-20 +/- 6 beats/min, respectively]. In sharp contrast, after exercise with central administration of AVP-X, both AP (Delta+8 +/- 5 mmHg) and HR (Delta+24 +/- 9 beats/min) were not significantly different from preexercise values (P > 0.05). Furthermore, AVP-X at rest did not significantly alter AP (181 +/- 11 vs. 178 +/- 11 mmHg, P > 0.05) or HR (328 +/- 24 vs. 331 +/- 22 beats/min, P > 0.05). Thus central blockade of AVP V(1) receptors prevented postexercise reductions in AP and HR. These data suggest that AVP, acting within the central nervous system, mediates postexercise reductions in AP and HR in the SHR.

POST-EXERCISE ELEVATIONS IN SYMPATHETIC NERVE ACTIVITY AND BAROREFLEX FUNCTION IN NORMOTENSIVE RABBITS

We tested the hypothesis that a single bout of dynamic exercise reduces post-exercise arterial pressure, heart rate, and renal sympathetic nerve activity and attenuates the arterial baroreflex control of heart rate and renal sympathetic nerve activity in normotensive New Zealand White rabbits. Animals were chronically instrumented with right jugular venous and left femoral arterial catheters, and electrodes around the renal sympathetic nerve. Arterial pressure, heart rate, and renal sympathetic nerve activity were recorded for two hours pre-exercise and two hours after a single bout of treadmill exercise (post-exercise). Post-exercise heart rate, arterial pressure, and renal sympathetic nerve activity were elevated above pre-exercise values (71±3 bpm, 13±1 mmHg, and 80±21%, respectively). These data demonstrate that normotensive rabbits do not exhibit post-exercise hypotension, due in part to elevations in sympathetic nerve activity. In addition, arterial baroreflex regulation of heart rate and renal sympathetic nerve activity were determined pre- and post-exercise. Exercise shifted the baroreflex function curve for heart rate and renal sympathetic nerve activity upward and to the right without a change in gain. These data suggest that post-exercise elevations in sympathetic nerve activity are due, in part, to an elevation of the operating point of the arterial baroreflex to a higher pressure. These responses in normotensive rabbits contrast sharply with the responses in hypertensive individuals and animals. Understanding the mechanisms contributing to the differences between hypertensive and normotensive subjects may lead to measures designed to lower arterial pressure in hypertensive individuals.