Regional hemodynamics during postexercise hypotension. I. Splanchnic and renal circulations.

Moderate exercise elicits a relative postexercise hypotension that is caused by an increase in systemic vascular conductance. Previous studies have shown that skeletal muscle vascular conductance is increased postexercise. It is unclear whether these hemodynamic changes are limited to skeletal muscle vascular beds. The aim of this study was to determine whether the splanchnic and/or renal vascular beds also contribute to the rise in systemic vascular conductance during postexercise hypotension. A companion study aims to determine whether the cutaneous vascular bed is involved in postexercise hypotension (Wilkins BW, Minson CT, and Halliwill JR. J Appl Physiol 97: 2071-2076, 2004). Heart rate, arterial pressure, cardiac output, leg blood flow, splanchnic blood flow, and renal blood flow were measured in 13 men and 3 women before and through 120 min after a 60-min bout of exercise at 60% of peak oxygen uptake. Vascular conductances of leg, splanchnic, and renal vascular beds were calculated. One hour postexercise, mean arterial pressure was reduced (79.1 +/- 1.7 vs. 83.4 +/- 1.8 mmHg; P < 0.05), systemic vascular conductance was increased by approximately 10%, leg vascular conductance was increased by approximately 65%, whereas splanchnic (16.0 +/- 1.8 vs. 18.5 +/- 2.4 ml.min(-1).mmHg(-1); P = 0.13) and renal (20.4 +/- 3.3 vs. 17.6 +/- 2.6 ml.min(-1).mmHg(-1); P = 0.14) vascular conductances were unchanged compared with preexercise. This suggests there is neither vasoconstriction nor vasodilation in the splanchnic and renal vasculature during postexercise hypotension. Thus the splanchnic and renal vascular beds neither directly contribute to nor attenuate postexercise hypotension.     

H2-receptor-mediated vasodilation contributes to postexercise hypotension.

The early (approximately 30 min) postexercise hypotension response after a session of aerobic exercise is due in part to H1-receptor-mediated vasodilation. The purpose of this study was to determine the potential contribution of H2-receptor-mediated vasodilation to postexercise hypotension. We studied 10 healthy normotensive men and women (ages 23.7 +/- 3.4 yr) before and through 90 min after a 60-min bout of cycling at 60% peak O2 uptake on randomized control and H2-receptor antagonist days (300 mg oral ranitidine). Arterial pressure (automated auscultation), cardiac output (acetylene washin) and femoral blood flow (Doppler ultrasound) were measured. Vascular conductance was calculated as flow/mean arterial pressure. Sixty minutes postexercise on the control day, femoral (delta62.3 +/- 15.6%, where Delta is change; P < 0.01) and systemic (delta13.8 +/- 5.3%; P = 0.01) vascular conductances were increased, whereas mean arterial pressure was reduced (Delta-6.7 +/- 1.1 mmHg; P < 0.01). Conversely, 60 min postexercise with ranitidine, femoral (delta9.4 +/- 9.2%; P = 0.34) and systemic (delta-2.8 +/- 4.8%; P = 0.35) vascular conductances were not elevated and mean arterial pressure was not reduced (delta-2.2 +/- 1.3 mmHg; P = 0.12). Furthermore, postexercise femoral and systemic vascular conductances were lower (P < 0.05) and mean arterial pressure was higher (P = 0.01) on the ranitidine day compared with control. Ingestion of ranitidine markedly reduces vasodilation after exercise and blunts postexercise hypotension, suggesting H2-receptor-mediated vasodilation contributes to postexercise hypotension.     

Regional hemodynamics during postexercise hypotension. II. Cutaneous circulation.

After an acute bout of exercise, there is an unexplained elevation in systemic vascular conductance that is not completely offset by an increase in cardiac output, resulting in a postexercise hypotension. The contributions of the splanchnic and renal circulations are examined in a companion paper (Pricher MP, Holowatz LA, Williams JT, Lockwood JM, and Halliwill JR. J Appl Physiol 97: 2065-2070, 2004). The purpose of this study was to determine the contribution of the cutaneous circulation in postexercise hypotension under thermoneutral conditions (approximately 23 degrees C). Arterial blood pressure was measured via an automated sphygmomanometer, internal temperature was measured via an ingestible pill, and skin temperature was measured with eight thermocouples. Red blood cell flux (laser-Doppler flowmetry) was monitored at four skin sites (chest, forearm, thigh, and leg), and cutaneous vascular conductance (CVC) was calculated (red blood cell flux/mean arterial pressure) and scaled as percent maximal CVC (local heating to 43 degrees C). Ten subjects [6 men and 4 women; age 23 +/- 1 yr; peak O(2) uptake (Vo(2 peak)) 45.8 +/- 2.0 ml.kg(-1).min(-1)] volunteered for this study. After supine rest (30 min), subjects exercised on a bicycle ergometer for 1 h at 60% of their Vo(2 peak) and were then positioned supine for 90 min. Exercise elicited a postexercise hypotension reaching a nadir at 46.0 +/- 4.5 min postexercise (77 +/- 1 vs. 82 +/- 2 mmHg preexercise; P < 0.05). Internal temperature increased (38.0 +/- 0.1 vs. 36.7 +/- 0.1 degrees C preexercise; P < 0.05), remaining elevated at 90 min postexercise (36.9 +/- 0.1 degrees C vs. preexercise; P < 0.05). CVC at all four skin sites was elevated by the exercise bout (P < 0.05), returning to preexercise values within 50 min postexercise (P > 0.05). Therefore, although transient changes in CVC occur postexercise, they do not appear to play an obligatory role in mediating postexercise hypotension under thermoneutral conditions.     

Is postexercise hypotension related to excess postexercise oxygen consumption through changes in leg blood flow?

After a single bout of aerobic exercise, oxygen consumption remains elevated above preexercise levels [excess postexercise oxygen consumption (EPOC)]. Similarly, skeletal muscle blood flow remains elevated for an extended period of time. This results in a postexercise hypotension. The purpose of this study was to explore the possibility of a causal link between EPOC, postexercise hypotension, and postexercise elevations in skeletal muscle blood flow by comparing the magnitude and duration of these postexercise phenomena. Sixteen healthy, normotensive, moderately active subjects (7 men and 9 woman, age 20-31 yr) were studied before and through 135 min after a 60-min bout of upright cycling at 60% of peak oxygen consumption. Resting and recovery VO2 were measured with a custom-built dilution hood and mass spectrometer-based metabolic system. Mean arterial pressure was measured via an automated blood pressure cuff, and femoral blood flow was measured using ultrasound. During the first hour postexercise, VO2 was increased by 11 +/- 2%, leg blood flow was increased by 51 +/- 18%, leg vascular conductance was increased by 56 +/- 19%, and mean arterial pressure was decreased by 2.2 +/- 1.0 mmHg (all P <0.05 vs. preexercise). At the end of the protocol, VO2 remained elevated by 4 +/- 2% (P <0.05), whereas leg blood flow, leg vascular conductance, and mean arterial pressure returned to preexercise levels (all P >0.7 vs. preexercise). Taken together, these data demonstrate that EPOC and the elevations in skeletal muscle blood flow underlying postexercise hypotension do not share a common time course. This suggests that there is no causal link between these two postexercise phenomena.     

Influence of endurance exercise training status and gender on postexercise hypotension.

In sedentary individuals, postexercise hypotension after a single bout of aerobic exercise is due to a peripheral vasodilation. Endurance exercise training has the potential to modify this response and perhaps reduce the degree of postexercise hypotension. We tested the hypothesis that endurance exercise-trained men and women would have blunted postexercise hypotension compared with sedentary subjects but that the mechanism of hypotension would be similar (i.e., vasodilation). We studied 16 endurance-trained and 16 sedentary men and women. Arterial pressure, cardiac output, and total peripheral resistance were determined before and after a single 60-min bout of exercise at 60% peak oxygen consumption. All groups exhibited a similar degree of postexercise hypotension (approximately 4-5 mmHg; P < 0.05 vs. preexercise). In sedentary men and women, hypotension was the result of vasodilation (Deltaresistance: -8.9 +/- 2.2%). In endurance-trained women, hypotension was also the result of vasodilation (-8.1 +/- 4.1%). However, in endurance-trained men, hypotension was the result of a reduced cardiac output (-5.2 +/- 2.4%; P < 0.05 vs. all others) and vasodilation was absent (-0.7 +/- 3.3%; P < 0.05 vs. all others). Thus we conclude the magnitude of postexercise hypotension is similar in sedentary and endurance-trained men and women but that endurance-trained men and women achieve this fall in pressure via different mechanisms.     

Reductions in blood pressure after acute exercise by hypertensive rats

Postexercise reductions in blood pressure at rest have been reported for hypertensive subjects. To determine whether post-exercise hypotension would occur in spontaneously hypertensive rats and to test the hypothesis that any reductions would result because of decreases in regional vascular resistances, hypertensive rats (n = 19) were instrumented with indwelling arterial catheters and Doppler probes to measure regional blood flows from the iliac, superior mesenteric, and renal arteries. Data were collected from animals who performed a 20- and a 40-min treadmill test at between 60 and 70% of their maximum O2 uptake. When the animals ran for 20 min, there was a pre- to postexercise drop in mean arterial pressure (MAP) from 158 +/- 3.6 to 150 +/- 3.6 mmHg (P less than 0.05), which was recorded 30 min after the exercise had ceased. The pre- to postexercise reduction in MAP after 40 min of treadmill running was from 154 +/- 3.1 to 138 +/- 3.0 mmHg (P less than 0.05) as recorded 30 min postexercise. Postexercise heart rate was significantly lower after the 40-min exercise bout, from a preexercise mean of 351 +/- 3 beats/min to 324 +/- 5 beats/min 30 min after the treadmill had stopped. Surprisingly, marked pre- to postexercise reductions in regional vascular resistance were not observed in either the iliac, superior mesenteric, or renal vascular beds. These data demonstrated the existence of postexercise hypotension in genetic hypertensive rats and suggested that reductions in cardiac output were the primary hemodynamic mechanism for this finding.     

Effect of systemic nitric oxide synthase inhibition on postexercise hypotension in humans.

An acute bout of aerobic exercise results in a reduced blood pressure that lasts several hours. Animal studies suggest this response is mediated by increased production of nitric oxide. We tested the extent to which systemic nitric oxide synthase inhibition [N(G)-monomethyl-L-arginine (L-NMMA)] can reverse the drop in blood pressure that occurs after exercise in humans. Eight healthy subjects underwent parallel experiments on 2 separate days. The order of the experiments was randomized between sham (60 min of seated upright rest) and exercise (60 min of upright cycling at 60% peak aerobic capacity). After both sham and exercise, subjects received, in sequence, systemic alpha-adrenergic blockade (phentolamine) and L-NMMA. Phentolamine was given first to isolate the contribution of nitric oxide to postexercise hypotension by preventing reflex changes in sympathetic tone that result from systemic nitric oxide synthase inhibition and to control for alterations in resting sympathetic activity after exercise. During each condition, systemic and regional hemodynamics were measured. Throughout the study, arterial pressure and vascular resistances remained lower postexercise vs. postsham despite nitric oxide synthase inhibition (e.g., mean arterial pressure after L-NMMA was 108.0+/-2.4 mmHg postsham vs. 102.1+/-3.3 mmHg postexercise; P<0.05). Thus it does not appear that postexercise hypotension is dependent on increased production of nitric oxide in humans.     

H1 and H2 receptors mediate postexercise hyperemia in sedentary and endurance exercise-trained men and women.

In sedentary individuals, H(1) receptors mediate the early portion of postexercise skeletal muscle hyperemia, whereas H(2) receptors mediate the later portion. It is not known whether postexercise hyperemia also presents in endurance-trained individuals. We hypothesized that the postexercise skeletal muscle hyperemia would also exist in endurance-trained individuals and that combined blockade of H(1) and H(2) receptors would abolish the long-lasting postexercise hyperemia in trained and sedentary individuals. We studied 28 sedentary and endurance trained men and women before and through 90 min after a 60-min bout of cycling at 60% peak O(2) uptake on control and combined H(1)- and H(2)-receptor antagonist days (fexofenadine and ranitidine). We measured arterial pressure (brachial auscultation) and femoral blood flow (Doppler ultrasound). On the control day, femoral vascular conductance (calculated as flow/pressure) was elevated in all groups 60 min after exercise (sedentary men: Delta86 +/- 35%, trained men, Delta65 +/- 18%; sedentary women, Delta61 +/- 19%, trained women: Delta59 +/- 23%, where Delta is change; all P < 0.05 vs. preexercise). In contrast, on the histamine antagonist day, femoral vascular conductance was not elevated in any of the groups after exercise (sedentary men: Delta21 +/- 17%, trained men: Delta9 +/- 5%, sedentary women: Delta19 +/- 4%, trained women: Delta11 +/- 11%; all P > 0.16 vs. preexercise; all P < 0.05 vs. control day). These data suggest postexercise skeletal muscle hyperemia exists in endurance trained men and women. Furthermore, histaminergic mechanisms produce the long-lasting hyperemia in sedentary and endurance-trained individuals.     

Cardiopulmonary baroreflex is reset during dynamic exercise.

The purpose of this study was to examine the hypothesis that the operating point of the cardiopulmonary baroreflex resets to the higher cardiac filling pressure of exercise associated with the increased cardiac filling volumes. Eight men (age 26 +/- 1 yr; height 180 +/- 3 cm; weight 86 +/- 6 kg; means +/- SE) participated in the present study. Lower body negative pressure (LBNP) was applied at 8 and 16 Torr to decrease central venous pressure (CVP) at rest and during steady-state leg cycling at 50% peak oxygen uptake (104 +/- 20 W). Subsequently, two discrete infusions of 25% human serum albumin solution were administered until CVP was increased by 1.8 +/- 0.6 and 2.4 +/- 0.4 mmHg at rest and 2.9 +/- 0.9 and 4.6 +/- 0.9 mmHg during exercise. During all protocols, heart rate, arterial blood pressure, and CVP were recorded continuously. At each stage of LBNP or albumin infusion, forearm blood flow and cardiac output were measured. During exercise, forearm vascular conductance increased from 7.5 +/- 0.5 to 8.7 +/- 0.6 U (P = 0.024) and total systemic vascular conductance from 7.2 +/- 0.2 to 13.5 +/- 0.9 l.min(-1).mmHg(-1) (P < 0.001). However, there was no significant difference in the responses of both forearm vascular conductance and total systemic vascular conductance to LBNP and the infusion of albumin between rest and exercise. These data indicate that the cardiopulmonary baroreflex had been reset during exercise to the new operating point associated with the exercise-induced change in cardiac filling volume.     

Low-dose estrogen therapy does not change postexercise hypotension, sympathetic nerve activity reduction, and vasodilation in healthy postmenopausal women

The aim of this study was to determine whether estrogen therapy enhances postexercise muscle sympathetic nerve activity (MSNA) decrease and vasodilation, resulting in a greater postexercise hypotension. Eighteen postmenopausal women received oral estrogen therapy (ET; n=9, 1 mg/day) or placebo (n=9) for 6 mo. They then participated in one 45-min exercise session (cycle ergometer at 50% of oxygen uptake peak) and one 45-min control session (seated rest) in random order. Blood pressure (BP, oscillometry), heart rate (HR), MSNA (microneurography), forearm blood flow (FBF, plethysmography), and forearm vascular resistance (FVR) were measured 60 min later. FVR was calculated. Data were analyzed using a two-way ANOVA. Although postexercise physiological responses were unaltered, HR was significantly lower in the ET group than in the placebo group (59+/-2 vs. 71+/-2 beats/min, P<0.01). In both groups, exercise produced significant decreases in systolic BP (145+/-3 vs. 154+/-3 mmHg, P=0.01), diastolic BP (71+/-3 vs. 75+/-2 mmHg, P=0.04), mean BP (89+/-2 vs. 93+/-2 mmHg, P=0.02), MSNA (29+/-2 vs. 35+/-1 bursts/min, P<0.01), and FVR (33+/-4 vs. 55+/-10 units, P=0.01), whereas it increased FBF (2.7+/-0.4 vs. 1.6+/-0.2 ml x min(-1) x 100 ml(-1), P=0.02) and did not change HR (64+/-2 vs. 65+/-2 beats/min, P=0.3). Although ET did not change postexercise BP, HR, MSNA, FBF, or FVR responses, it reduced absolute HR values at baseline and after exercise.     

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.     

Effects of the menstrual cycle and sex on postexercise hemodynamics

Factors associated with the menstrual cycle, such as the endogenous hormones estrogen and progesterone, have dramatic effects on cardiovascular regulation. It is unknown how this affects postexercise hemodynamics. Therefore, we examined the effects of the menstrual cycle and sex on postexercise hemodynamics. We studied 14 normally menstruating women [24.0 (4.2) yr; SD] and 14 men [22.5 (3.5) yr] before and through 90 min after cycling at 60% .VO2(peak) for 60 min. Women were studied during their early follicular, ovulatory, and mid-luteal phases; men were studied once. In men and women during all phases studied, mean arterial pressure was decreased after exercise throughout 60 min (P < 0.001) postexercise and returned to preexercise values at 90 min (P = 0.089) postexercise. Systemic vascular conductance was increased following exercise in both sexes throughout 60 min (P = 0.005) postexercise and tended to be elevated at 90 min postexercise (P = 0.052), and femoral vascular conductance was increased following exercise throughout 90 min (P < 0.001) postexercise. Menstrual phase and sex had no effect on the percent reduction in arterial pressure (P = 0.360), the percent rise in systemic vascular conductance (P = 0.573), and the percent rise in femoral vascular conductance (P = 0.828) from before to after exercise, nor did the pattern of these responses differ across recovery with phase or sex. This suggests that postexercise hemodynamics are largely unaffected by sex or factors associated with the menstrual cycle.     

Cutaneous active vasodilation in humans during passive heating postexercise.

The hypothesis that exercise causes an increase in the postexercise esophageal temperature threshold for onset of cutaneous vasodilation through an alteration of active vasodilator activity was tested in nine subjects. Increases in forearm skin blood flow and arterial blood pressure were measured and used to calculate cutaneous vascular conductance at two superficial forearm sites: one with intact alpha-adrenergic vasoconstrictor activity (untreated) and one infused with bretylium tosylate (bretylium treated). Subjects remained seated resting for 15 min (no-exercise) or performed 15 min of treadmill running at either 55, 70, or 85% of peak oxygen consumption followed by 20 min of seated recovery. A liquid-conditioned suit was used to increase mean skin temperature ( approximately 4.0 degrees C/h), while local forearm temperature was clamped at 34 degrees C, until cutaneous vasodilation. No differences in the postexercise threshold for cutaneous vasodilation between untreated and bretylium-treated sites were observed for either the no-exercise or exercise trials. Exercise resulted in an increase in the postexercise threshold for cutaneous vasodilation of 0.19 +/- 0.01, 0.39 +/- 0.02, and 0.53 +/- 0.02 degrees C above those of the no-exercise resting values for the untreated site (P < 0.05). Similarly, there was an increase of 0.20 +/- 0.01, 0.37 +/- 0.02, and 0.53 +/- 0.02 degrees C for the treated site for the 55, 70, and 85% exercise trials, respectively (P < 0.05). It is concluded that reflex activity associated with the postexercise increase in the onset threshold for cutaneous vasodilation is more likely mediated through an alteration of active vasodilator activity rather than through adrenergic vasoconstrictor activity.     

Effects of muscle metaboreceptor stimulation on cutaneous blood flow from glabrous and nonglabrous skin in mildly heated humans.

Given differences in sympathetic innervation to glabrous and nonglabrous skin, we tested the hypothesis that muscle metaboreceptor regulation of cutaneous vascular conductance (CVC) differs between these skin regions. Subjects (n = 21) performed isometric handgrip exercise (IHG; 50% maximal voluntary contraction for 60 s), followed by 2 min of postexercise ischemia. Throughout IHG and postexercise ischemia, CVC was measured from glabrous (palm) and nonglabrous (forearm and chest) regions contralateral to the exercising arm. These procedures were conducted after the subjects had been exposed to an ambient temperature of 35 degrees C and a relative humidity of 50% for 60 min. These thermal conditions were intended to cause slight increases in cutaneous blood flow via sympathetic withdrawal. Esophageal, sublingual, and mean skin temperatures did not change markedly during IHG or postexercise ischemia. During IHG, forearm CVC did not change, chest CVC increased slightly, and palm CVC decreased substantially (from 100 to 34.8 +/- 3.5%; P = 0.001). During muscle metaboreceptor stimulation due to postexercise ischemia, CVC from nonglabrous regions returned to preexercise baselines, whereas CVC at the palm remained below preexercise baseline (68.2 +/- 4.2%; P = 0.001 relative to preexercise baseline). These results indicate that in mildly heated humans muscle metaboreflex stimulation is capable of modulating CVC in glabrous, but not in nonglabrous, skin.     

Evidence for a rapid vasodilatory contribution to immediate hyperemia in rest-to-mild and mild-to-moderate forearm exercise transitions in humans.

Controversy exists regarding the contribution of a rapid vasodilatory mechanism(s) to immediate exercise hyperemia. Previous in vivo investigations have exclusively examined rest-to-exercise (R-E) transitions where both the muscle pump and early vasodilator mechanisms may be activated. To isolate vasodilatory onset, the present study investigated the onset of exercise hyperemia in an exercise-to-exercise (E-E) transition, where no further increase in muscle pump contribution would occur. Eleven subjects lay supine and performed a step increase from rest to 3 min of mild (10% maximal voluntary contraction), rhythmic, dynamic forearm handgrip exercise, followed by a further step to moderate exercise (20% maximal voluntary contraction) in each of arm above (condition A) or below (condition B) heart level. Beat-by-beat measures of brachial arterial blood flow (Doppler ultrasound) and blood pressure (arterial tonometry) were performed. We observed an immediate increase in forearm vascular conductance in E-E transitions, and the magnitude of this increase matched that of the R-E transitions within each of the arm positions (condition A: E-E, 52.8 +/- 10.7 vs. R-E, 60.3 +/- 11.7 ml.min(-1).100 mmHg(-1), P = 0.66; condition B: E-E, 43.2 +/- 12.8 vs. R-E, 33.9 +/- 8.2 ml.min(-1).100 mmHg(-1), P = 0.52). Furthermore, changes in forearm vascular conductance were identical between R-E and E-E transitions over the first nine contraction-relaxation cycles in condition A. The immediate and identical increase in forearm vascular conductance in R-E and E-E transitions within arm positions provides strong evidence that rapid vasodilation contributes to immediate exercise hyperemia in humans. Specific vasodilatory mechanisms responsible remain to be determined.     

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.     

Muscle metaboreflex modulates the arterial baroreflex dynamic effects on peripheral vascular conductance in humans

We aimed to investigate the interaction between the arterial baroreflex and muscle metaboreflex [as reflected by alterations in the dynamic responses shown by leg blood flow (LBF: by the ultrasound Doppler method), leg vascular conductance (LVC), mean arterial blood pressure (MAP), and heart rate (HR)] in humans. In 12 healthy subjects (10 men and 2 women), who performed sustained 1-min handgrip exercise at 50% maximal voluntary contraction followed immediately by an imposed postexercise muscle ischemia (PEMI), 5-s periods of neck pressure (NP; 50 mmHg) or neck suction (NS; -60 mmHg) were used to evaluate carotid baroreflex function both at rest (Con) and during PEMI. First, the decreases in LVC and LBF and the augmentation of MAP elicited by NP were all greater during PEMI than in Con (DeltaLVC, -1.2 +/- 0.2 vs. -1.9 +/- 0.2 ml.min(-1).mmHg(-1); DeltaLBF, -97.3 +/- 11.2 vs. -177.0 +/- 21.8 ml/min; DeltaMAP, 6.7 +/- 1.2 vs. 11.5 +/- 1.4 mmHg, Con vs. PEMI; each P < 0.05). Second, in Con, NS significantly increased both LVC and LBF (DeltaLVC, 0.9 +/- 0.2 ml.min(-1).mmHg(-1); DeltaLBF, 46.6 +/- 9.8 ml/min; significant change from baseline: each P < 0.05), and, whereas during PEMI no significant increases in LVC and LBF occurred during NS itself (DeltaLVC, 0.2 +/- 0.1 ml.min(-1).mmHg(-1); DeltaLBF, 10.8 +/- 9.6 ml/min; each P > 0.05), a decrease was evident in each parameters at 5 s after the cessation of NS. Third, during PEMI, the decrease in MAP elicited by NS was smaller (DeltaMAP, -8.4 +/- 1.0 vs. -5.8 +/- 0.4 mmHg, Con vs. PEMI; P < 0.05), and it recovered to its initial level more quickly after NS (vs. Con). Finally, however, the HR responses to NS and NP were not different between PEMI and Con. These results suggest that during muscle metaboreflex activation in humans, the arterial baroreflex dynamic effect on peripheral vascular conductance is modulated, as exemplified by 1) an augmentation of the NP-induced LVC decrease, and 2) a loss of the NS-induced LVC increase.     

Does nitric oxide contribute to the basal vasodilation of pregnancy in conscious rabbits?

Pregnancy produces marked systemic vasodilation, but the mechanism is unknown. Experiments were performed in conscious rabbits to test the hypotheses that increased nitric oxide (NO) production contributes to the increased vascular conductance, but that the contribution varies among vascular beds. Rabbits were instrumented with aortic and vena caval catheters and ultrasonic flow probes implanted around the ascending aorta, superior mesenteric artery, terminal aorta, and/or a femoral artery. Hemodynamic responses to intravenous injection of N(omega)-nitro-L-arginine (L-NA; 20 mg/kg or increasing doses of 2, 5, 10, 15, and 20 mg/kg) were determined in rabbits first before pregnancy (NP) and then at the end of gestation (P). L-NA produced similar increases in arterial pressure between groups, but the following responses were larger (P < 0.05) when the rabbits were pregnant: 1) decreases in total peripheral conductance [-3.7 +/- 0.3 (NP), -5.0 +/- 0.5 (P) ml x min(-1) x mmHg(-1)], 2) decreases in mesenteric conductance [-0.47 +/- 0.05 (NP), -0.63 +/- 0.07 (P) ml x min(-1) x mmHg(-1)], 3) decreases in terminal aortic conductance [-0.43 +/- 0.05 (NP), -0.95 +/- 0.19 ml x min(-1) x mmHg(-1) (P)], and 4) decreases in heart rate [-41 +/- 4 (NP), -62 +/- 5 beats/min (P)]. Nevertheless, total peripheral and terminal aortic conductances remained elevated in the pregnant rabbits (P < 0.05) after L-NA. Furthermore, decreases in cardiac output and femoral conductance were not different between the reproductive states. We conclude that the contribution of NO to vascular tone increases during pregnancy, but only in some vascular beds. Moreover, the data support a role for NO in the pregnancy-induced increase in basal heart rate. Finally, unknown factors in addition to NO must also underlie the basal vasodilation observed during pregnancy.     

Gender differences in cardiovascular regulation during recovery from exercise.

Are women more susceptible to acute postexercise orthostatic hypotension compared with men? We hypothesized that decreases in arterial pressure during recovery from dynamic exercise are greater in women compared with men. We studied 8 men and 11 women during inactive and active recovery from cycling exercise. Heart rate, stroke volume (SV), cardiac output, mean arterial pressure (MAP), and total peripheral resistance (TPR) were measured during and after 3 min of exercise at 60% of calculated maximum heart rate. At 1 min after exercise, MAP decreased less (P < 0.05) during inactive recovery in men (-18 +/- 2 mmHg) compared with women (-30 +/- 2 mmHg). This difference was due to greater decreases in SV and less increase in TPR during inactive recovery from exercise in women compared with men. These differences persisted for 5 min after exercise. MAP decreased less during active recovery in men compared with women. These findings suggest that women may have increased risk of postexercise orthostatic hypotension and that active recovery from exercise may reduce this risk.     

Skeletal muscle collagen content in humans after high-force eccentric contractions.

The purpose of this study was to investigate the effects of high-force eccentric muscle contractions on collagen remodeling and on circulating levels of matrix metalloproteinases (MMP) and tissue inhibitors of metalloproteinases (TIMP) in humans. Nine volunteers [5 men and 4 women, mean age 23 (SD 4) yr] each performed a bout of 100 maximum voluntary eccentric contractions of the knee extensors. Muscle biopsies were taken before exercise and on days 4 and 22 afterward. Image analysis of stained tissue sections was used to quantify endomysial collagen staining intensity. Maximum voluntary contractile isometric force was recorded preexercise and on days 1, 2, 3, 4, 8, 11, and 14 postexercise. Venipuncture blood samples were also drawn on these days for measurement of serum creatine kinase activity and concentrations of MMP-9, TIMP-1, TIMP-2, and the MMP-2/TIMP-2 complex. Maximum voluntary contractile force declined by 39 +/- 23% (mean +/- SD) on day 2 postexercise and recovered thereafter. Serum creatine kinase activity peaked on day 4 postexercise (P < 0.01). Collagen type IV staining intensity increased significantly on day 22 postexercise to 126 +/- 29% (mean +/- SD) of preexercise values (P < 0.05). Serum MMP-9 levels increased on day 8 postexercise (P < 0.01), and serum TIMP-1 was also significantly elevated on days 1, 2, 3, 4, and 14 postexercise (P < 0.05). These results suggest that a single bout of eccentric muscle contractions results in remodeling of endomysial type IV collagen, possibly via the MMP pathway.