The influence of straining maneuvers on the pressor response during isometric exercise

Experiments were performed to determine to what extent increments in esophageal and abdominal pressure would have on arterial blood pressure during fatiguing isometric exercise. Arterial blood pressure was measured during handgrip and leg isometric exercise performed with both a free and occluded circulation to active muscles. Handgrip contractions were exerted at 33 and 70% MVC (maximum voluntary contraction) by 4 volunteers in a sitting position and calf muscle contractions at 50 and 70% MVC with the subjects in a kneeling position. Esophageal pressure measured at the peak of inspirations did not change during either handgrip or leg contractions but peak expiratory pressures increased progressively during both handgrip and leg contractions as fatigue occurred. These increments were independent of the tensions of the isometric contractions exerted. Intra-abdominal pressures measured at the peak of either inspiration or expiration did not change during inspiration with handgrip contractions but increased during expiration. During leg exercise, intraabdominal pressures increased during both inspiration and expiration, reaching peak levels at fatigue. The arterial blood pressure also reached peak levels at fatigue, independent of circulatory occlusion and tension exerted, averaging 18.5-20 kPa (140-150 mm Hg) for both handgrip and leg contractions. While blood pressure returned to resting levels following exercise with a free circulation, it declined by only 2.7-3.8 kPa after leg and handgrip exercise, respectively, during circulatory occlusion. These results indicate that straining maneuvers contribute 3.5 to 7.8 kPa to the change in blood pressure depending on body position.     

The effects of athletic training and muscle contractile character on the pressor response to isometric exercise of the human triceps surae

In this study, the influence of athletic training status and the contractile character of the active muscle on the magnitude of the pressor response (PR) to voluntary and electrically evoked isometric plantar flexion was investigated. Subjects were 10 sprint-trained athletes (sprint) (100-m, 200-m and 400-m) [mean (SD) age, 21 (2) years], 14 endurance trained athletes (distance) [22 (2) years] and 8 untrained men (control) [23 (3) years]. Twitch time to peak tension (TPT) in the sprint group [108 (7) ms] was significantly less (P<0.001) than that of the distance group [124 (10) ms]. During voluntary contraction, the mean change in systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (fc) was not significantly different between groups. During electrically evoked contractions, mean changes in SBP, DBP and fc were not significantly different between the sprint, distance and control groups. However, division of the sprint group into 400-m (sprint I) and 100/200-m athletes (sprint II) showed that an increase in DBP of 1.6 kPa (12 mm Hg) in sprint I was significantly less (P<0.05) than the 2.5 kPa (19 mm Hg) increase observed for both the distance and control groups. Prediction of the DBP response from our previously published relationship between TPT and DBP showed close agreement in all subject groups except sprint I; in these subjects the observed DBP response was only 55% of that predicted. Attenuation of the PR in the involuntary experiment suggests that some aspect of sprint training, but not endurance training, modifies the muscle afferent input to the PR in man.     

The pressor response to involuntary isometric exercise of young and elderly human muscle with reference to muscle contractile characteristics

Changes in heart rate (f_c) and blood pressure (BP) were observed in eight healthy young men aged [mean (SD)] 20(l) years and ten healthy elderly men aged 65 (5) years, during electrically evoked contractions of the ankle plantar flexors and elbow flexors which were sustained for 2 min. There was no significant difference in the f_c response to evoked contraction of the ankle plantar flexors or elbow flexors between young and elderly subjects. During contraction of the elbow flexors, elderly subjects produced an unexpectedly large rise in systolic BP which was significantly greater than that of the young subjects. The exaggerated response seen in the elderly group may be due to a more rigid arterial tree which is thought to occur with advancing age. Electrically evoked contraction of the slower contracting elderly ankle plantar flexors resulted in a significantly diminished diastolic BP response when compared with that of the young subjects. In contrast, during electrically evoked contraction of the elbow flexors, which showed a similar twitch time course in young and elderly subjects, the diastolic BP response was not significantly different between groups. This may reflect differences in the peripheral reflex input to the pressor response in elderly arm and leg muscles which, in turn, may be influenced by relative fast twitch fibre area.     

The pressor response to voluntary and electrically evoked isometric contractions in man

Blood pressure and heart rate changes during sustained isometric exercise were studied in 11 healthy male volunteers. The responses were measured during voluntary and involuntary contractions of the biceps brachii at 30% of maximal voluntary contraction (MVC), and the triceps surae at 30% and 50% MVC. Involuntary contractions were evoked by percutaneous electrical stimulation of the muscle. Measurements of the time to peak tension of maximal twitch showed the biceps brachii (67.0 +/- 7.9 ms) muscle to be rapidly contracting, and the triceps surae (118.0 +/- 10.5 ms) to be slow contracting. The systolic and diastolic blood pressures increased linearly throughout the contractions, and systolic blood pressure increased more rapidly than diastolic. There was no significant difference in response to stimulated or voluntary contractions, nor was there any significant difference between the responses to contractions of the calf or arm muscles at the same relative tension. In contrast the heart rate rose to a higher level (P less than 0.01) in the biceps brachii than the triceps surae at given % MVC, and during voluntary compared with the electrically evoked contractions in the two muscle groups. It was concluded that the arterial blood pressure response to isometric contractions, unlike heart rate, is primarily due to a reflex arising within the active muscles (cf. Hultman and Sj?holm 1982) which is associated with relative tension but independent of contraction time and muscle mass.     

The combined effect of the cold pressor test and isometric exercise on heart rate and blood pressure

The purpose of this study was to determine if the cold pressor test during isometric knee extension [15% of maximal voluntary contraction (MVC)] could have an additive effect on cardiovascular responses. Systolic and diastolic blood pressures, heart rate and pressure rate product were measured in eight healthy male subjects. The subjects performed the cold pressor tests and isometric leg extensions singly and in combination. The increases of systolic and diastolic blood pressure during isometric exercise were of almost the same magnitude as those during the cold pressor test. The responses of arterial blood pressure, and heart rate to a combination of the cold pressor test and isometric knee extension were greater than for each test separately. It is suggested that this additional effect of cold immersion of one hand during isometric exercise may have been due to vasoconstriction effects in the contralateral unstressed limb. In summary, the circulatory effects of the local application of cold during static exercise at 15% MVC were additive.     

Carotid baroreflex pressor responses at rest and during exercise: cardiac output vs. regional vasoconstriction

The arterial baroreflex mediates changes in arterial pressure via reflex changes in cardiac output (CO) and regional vascular conductance, and the relative roles may change between rest and exercise and across workloads. Therefore, we quantified the contribution of CO and regional vascular conductances to carotid baroreflex-mediated increases in mean arterial pressure (MAP) at rest and during mild to heavy treadmill exercise (3.2 kph; 6.4 kph, 10% grade; and 8 kph, 15% grade). Dogs (n = 8) were chronically instrumented to measure changes in MAP, CO, hindlimb vascular conductance, and renal vascular conductance in response to bilateral carotid occlusion (BCO). At rest and at each workload, BCO caused similar increases in MAP (average 35 +/- 2 mmHg). In response to BCO, neither at rest nor at any workload were there significant increases in CO; therefore, the pressor response occurred via peripheral vasoconstriction. At rest, 10.7 +/- 1.4% of the rise in MAP was due to vasoconstriction in the hindlimb, whereas 4.0 +/- 0.7% was due to renal vasoconstriction. Linear regression analysis revealed that, with increasing workloads, relative contributions of the hindlimb increased and those of the kidney decreased. At the highest workload, the decrease in hindlimb vascular conductance contributed 24.3 +/- 3.4% to the pressor response, whereas the renal contribution decreased to only 1.6 +/- 0.3%. We conclude that the pressor response during BCO was mediated solely by peripheral vasoconstriction. As workload increases, a progressively larger fraction of the pressor response is mediated via vasoconstriction in active skeletal muscle and the contribution of vasoconstriction in inactive beds (e.g., renal) becomes progressively smaller.     

Cardiovascular response to hand-grip isometric exercise in healthy men. Noninvasive study

Noninvasive polygraphic tracings obtained at rest and during isometric hand-grip exercise were analysed in 67 healthy subjects. The purpose of the study was to determine the response of noninvasive polygraphic parameters to isometric exercise. During the third minute of sustained squeezing of a balloon dynamometer (30% of maximal voluntary contraction) a significant increase occurred in heart rate (+16.8 +/- 10.7 beats/min) an increase in both systolic and diastolic blood pressure (+3.4 +/- 1.6 kPa and 2.6 +/- 1.7 kPa respectively), increase in apexcardiographic index 100.a/D (+14.5 +/- 15.0% "D" amplitude), decrease of diastolic amplitude time index square root 2-c/(2-0) X (a/D) (-20.1 +/- 26.5), shortening of pulse transmission time (-0.006 +/- 0.005 s) and prolongation of cardiac cycle length corrected for left ventricular ejection time (+0.011 +/- 0.010 s) discussed. All these changes were statistically significant.     

Endogenous endothelin attenuates the pressor response to acute environmental stress via the ETA receptor

Clinical studies have documented an abrupt rise in plasma endothelin-1 (ET-1) coincident with an increase in mean arterial pressure (MAP) during the response to acute stress. We therefore examined the ET(A) and ET(B) receptor-dependent effects of ET-1 on the pressor response to acute environmental stress in ET-1-dependent hypertension. Stress was induced by administration of air jet pulses (3 min) in ET(B) receptor-deficient (ET(B) sl/sl) rats fed normal salt (NS; 0.8% NaCl), high salt (HS; 8% NaCl), and HS plus the ET(A) receptor antagonist ABT-627 (5 mg.kg(-1).day(-1)) on successive weeks. MAP was chronically monitored by telemetry. Total pressor response (area under the curve) was significantly reduced in ET(B) sl/sl rats maintained on a HS vs. NS diet [-6.8 mmHg (SD 18.7) vs. 29.3 mmHg (SD 8.1) x 3 min, P < 0.05]. Conversely, the total pressor response was augmented in both wild-type [34.2 mmHg (SD 29.2) x 3 min, P < 0.05 vs. NS] and ET(B) sl/sl rats [49.1 mmHg (SD 11.8) x 3 min, P < 0.05 vs. NS] by ABT-627. Blockade of ET(B) receptors in Sprague-Dawley rats caused an increase in basal MAP that was enhanced by HS and lowered by mixed ET(A)/ET(B) receptor antagonism; none of these treatments, however, had any effect on the pressor response. These data demonstrate that increasing endogenous ET-1 suppresses the pressor response to acute stress through ET(A) receptor activation in a genetic model of ET-1-dependent hypertension. These results are consistent with reports that ET-1 can attenuate sympathetically mediated responses.     

Carotid distensibility, baroreflex sensitivity, and orthostatic stress.

In this study, we tested the hypothesis that carotid arteries undergo rapid changes in distensibility on moving from the supine to head-up tilt (HUT) postures and, subsequently, that this change in carotid distensibility (cDa) might be associated with concurrent reductions in cardiovagal baroreflex sensitivity (BRS). Thus the effect of posture on carotid vascular mechanics and cardiovagal BRS with consideration for altered central hemodynamics (i.e., stroke volume; Doppler ultrasound) was examined. Carotid pulse pressure (cPP; Millar transducer) and contralateral B-mode ultrasound images were assessed at the carotid artery during supine and 60 degrees HUT postures. From these measures, cDa was calculated at 5-mmHg pressure increments experienced during the cardiac cycle (n = 6). cPP (n = 9) was not different in the two postures. A smaller stroke volume being ejected into a smaller carotid artery in HUT explained the maintenance of cPP in HUT. Also, compared with supine, cDa was reset to a lower level in HUT (main effect of posture; P < 0.05). Cardiovagal BRS (sequence method) was diminished in HUT vs. supine (P < 0.05). A positive correlation was observed between the tilt-induced changes in maximal cDa (in early systole) and cardiovagal BRS (r2 = 0.75; P < 0.05), but there was little predictive relationship between changes in cPP, systolic vessel dimensions, or average cDa and the corresponding change in BRS. The present results indicate that HUT elicits rapid changes in carotid artery mechanics and further suggest that reductions in the maximal cDa measured in early systole contribute to reduced cardiovagal BRS with HUT.     

Gadolinium attenuates exercise pressor reflex in cats

The exercise pressor reflex, which arises from the contraction-induced stimulation of group III and IV muscle afferents, is widely believed to be evoked by metabolic stimuli signaling a mismatch between blood/oxygen demand and supply in the working muscles. Nevertheless, mechanical stimuli may also play a role in evoking the exercise pressor reflex. To determine this role, we examined the effect of gadolinium, which blocks mechanosensitive channels, on the exercise pressor reflex in both decerebrate and alpha-chloralose-anesthetized cats. We found that gadolinium (10 mM; 1 ml) injected into the femoral artery significantly attenuated the reflex pressor responses to static contraction of the triceps surae muscles and to stretch of the calcaneal (Achilles) tendon. In contrast, gadolinium had no effect on the reflex pressor response to femoral arterial injection of capsaicin (5 microg). In addition, gadolinium significantly attenuated the responses of group III muscle afferents, many of which are mechanically sensitive, to both static contraction and to tendon stretch. Gadolinium, however, had no effect on the responses of group IV muscle afferents, many of which are metabolically sensitive, to either static contraction or to capsaicin injection. We conclude that mechanical stimuli arising in contracting skeletal muscles contribute to the elicitation of the exercise pressor reflex.     

Changes in isometric function following rhythmic exercise

Seven male subjects exercised for 1, 3, 10 and 20 min on a cycle ergometer at 20, 60 and 80% VO2max, and then held to fatigue a sustained contraction of the quadriceps at 40% maximal voluntary contraction in order to determine what influence various levels of dynamic exercise would have on isometric function of the same group of muscles. Muscle temperature was measured before and within 15 s of the completion of the cycling to determine whether changes in muscle temperature might influence the subsequent isometric performance. Isometric endurance was shorter as the severity of the cycling increased beyond 20% VO2max, and as the duration of cycling increased up to 10 min. There were discrete linear relationships between muscle temperature and isometric endurance associated with cycling at 60% and 80% VO2max. There was a direct inverse relationship between quadriceps strength after cycling and muscle temperature, yet a significant reduction in strength occurred only after cycling at 80% VO2max. These results suggest that the encroachment on endurance and strength are controlled by different mechanisms. The heart rates during the isometric contractions were dependent on the preceding rhythmic exercise and decreased after exercise at 60 or 80% VO2max. In contrast, the blood pressure always increased during the isometric contractions, reaching similar values at the point of fatigue, regardless of the severity of the previous rhythmic exercise. These data provide additional evidence that separate mechanisms control changes in heart rate and blood pressure.     

ETa-receptor blockade, but not ACE inhibition, blunts retinal vessel response during isometric exercise

Angiotensin II and endothelin-1 are potent vasoconstrictors that appear to play a role in retinal blood flow regulation. In the present study, we investigated the possible role of the angiotensin and the endothelin system in the regulation of retinal vessel diameters during isometric exercise in healthy humans. The study design was randomized, double-masked, placebo-controlled, and three-way cross over. Twelve healthy subjects performed squatting exercises for 6 min during infusion of either an angiotensin-converting enzyme inhibitor (enalapril), an ET(A)-receptor antagonist (BQ-123), or placebo. Retinal vessel diameters were measured continuously with the Zeiss retinal vessel analyzer. Systemic hemodynamics were assessed noninvasively, and intraocular pressure was measured with applanation tonometry. Squatting induced a significant increase in blood pressure and pulse rate, which was paralleled by a vasoconstriction in retinal arteries and veins. Intraocular pressure was only slightly increased during the squatting periods. BQ-123 significantly blunted the exercise-induced decrease in venous (P < 0.01) and arterial (P < 0.02, ANOVA) vessel diameters but had no effect on basal retinal diameters. By contrast, enalapril did neither influence vessel diameter at baseline conditions nor in response to isometric exercise. The data of the present study indicate that retinal vasoconstriction during isometric exercise is modified by ET(A)-receptor blockade, whereas it is not altered by angiotensin-converting enzyme inhibition. Hence, the present data indicate that endothelin-1, but not angiotensin II, is involved in retinal blood flow regulation during isometric exercise.     

Reduction in extracellular muscle volume increases heart rate and blood pressure response to isometric exercise

To investigate the effect of local dehydration on heart rate and blood pressure during static exercise, six healthy male subjects performed exercise of the calf muscles with different extracellular volumes of the working muscles. Exercise consisted of 5 min of static calf muscle contractions at about 10% of maximal voluntary contraction. The body position during exercise was identical in all tests, i.e. supine with the knee joint 90 degrees flexed. During a 25-min pre-exercise period three different protocols were employed to manipulate the calf volume. In test A the subjects rested in the exercise position; in test B the body position was the same as in A but calf volumes were increased by venous congestion [cuffs inflated to 10.67 kPa (80 mmHg)]; in test C the calf volumes were decreased by lifting the calves about 40 cm above heart level with the subjects supine. To clamp the changed calf volumes in tests B and C, cuffs were inflated to 300 mmHg 5 min before the onset of exercise. This occlusion was maintained for 1 min after the termination of exercise. Compared to tests A and B, the reduced volume of test C led to significant increases in heart rate and blood pressure during exercise. Oxygen uptake did not exceed resting levels in tests B and C until the cuffs were deflated, indicating that only calf muscles contributed to the neurogenic peripheral drive. It is concluded that extracellular muscle volume plays a significant role in adjusting heart rate and blood pressure during static exercise.     

WISE 2005: stroke volume changes contribute to the pressor response during ischemic handgrip exercise in women.

The mechanism of the pressor response to small muscle mass (e.g., forearm) exercise and during metaboreflex activation may include elevations in cardiac output (Q) or total peripheral resistance (TPR). Increases in Q must be supported by reductions in visceral venous volume to sustain venous return as heart rate (HR) increases. Therefore, this study tested the hypothesis that increases in Q, supported by reductions in splanchnic volume (portal vein constriction), explain the pressor response during handgrip exercise and metaboreflex activation. Seventeen healthy women performed 2 min of static ischemic handgrip exercise and 2 min of postexercise circulatory occlusion (PECO) while HR, stroke volume and superficial femoral artery flow (Doppler), blood pressure (Finometer), portal vein diameter (ultrasound imaging), and muscle sympathetic nerve activity (MSNA; microneurography) were measured followed by the calculation of Q, TPR, and leg vascular resistance (LVR). Compared with baseline, mean arterial blood pressure (MAP) (P < 0.001) and Q (P < 0.001) both increased in each minute of exercise accompanied by a approximately 5% reduction in portal vein diameter (P < 0.05). MAP remained elevated during PECO, whereas Q decreased below exercise levels. MSNA was elevated above baseline during the second minute of exercise and through the PECO period (P < 0.05). Neither TPR nor LVR was changed from baseline during exercise and PECO. The data indicate that the majority of the blood pressure response to isometric handgrip exercise in women was due to mobilization of central blood volume and elevated stroke volume and Q rather than elevations in TVR or LVR resistance.     

Muscle fiber type-specific response of Hsp70 expression in human quadriceps following acute isometric exercise.

To investigate the time course of fiber type-specific heat shock protein 70 (Hsp70) expression in human skeletal muscle after acute exercise, 10 untrained male volunteers performed single-legged isometric knee extensor exercise at 60% of their maximal voluntary contraction (MVC) with a 50% duty cycle (5-s contraction and 5-s relaxation) for 30 min. Muscle biopsies were collected from the vastus lateralis before (Pre) exercise in the rested control leg (C) and immediately after exercise (Post) in the exercised leg (E) only and on recovery days 1 (R1), 2 (R2), 3 (R3), and 6 (R6) from both legs. As demonstrated by Western blot analysis, whole muscle Hsp70 content was unchanged (P > 0.05) immediately after exercise (Pre vs. Post), was increased (P < 0.05) by approximately 43% at R1, and remained elevated throughout the entire recovery period in E only. Hsp70 expression was also assessed in individual muscle fiber types I, IIA, and IIAX/IIX by immunohistochemistry. There were no fiber type differences (P > 0.05) in basal Hsp70 expression. Immediately after exercise, Hsp70 expression was increased (P < 0.05) in type I fibers by approximately 87% but was unchanged (P > 0.05) in type II fibers (Pre vs. Post). At R1 and throughout recovery, Hsp70 content in E was increased above basal levels (P < 0.05) in all fiber types, but Hsp70 expression was always highest (P < 0.05) in type I fibers. Hsp70 content in C was not different from Pre at any time throughout recovery. Glycogen depletion was observed at Post in all type II, but not type I, fibers, suggesting that the fiber type differences in exercise-induced Hsp70 expression were not related to glycogen availability. These results demonstrate that the time course of exercise-induced Hsp70 expression in human skeletal muscle is fiber type specific.     

Arterial distensibility: acute changes following dynamic exercise in normal subjects

The time course of acute changes in large artery distensibility immediately and for 60 min following maximum treadmill exercise in normal subjects was characterized by simultaneously measuring upper and lower limb pulse wave velocity (PWV). A new oscillometric technique was used, which has proven to be sensitive to changes in distensibility induced by acute changes in vascular tone independently of blood pressure. The observed changes in PWV are attributable to changes in vascular tone corresponding to recovery from a systemic net constrictor response and a local net dilator response to exercise with persisting postexercise vasodilatation. They are inadequately explained by associated changes in blood pressure and cannot be attributed to changes in heart rate or viscosity. Modeled as a system of n coupled linear differential equations, the minimum (and adequate) order required to reproduce these patterns was n = 1 for the upper and n = 2 for the exercising lower limb. The economy of the solution suggests entrainment among the multiple interactive mechanisms governing vasomotor control.     

Effect of isometric exercise on catecholamines in the coronary circulation.

Arterial and coronary sinus blood levels of catecholamines, adenosine 3', 5'-cyclic monophosphate (c-AMP) and lactate were measured during isometric exercise in fourteen patients. In no patient did lactate production occur. Mean resting total catecholamine levels both arterial (0.53 +/- 0.07 ng/ml; 2.94 +/- 0.38 nmol/l) and coronary sinus (0.4 +/- 0.08 ng/ml; 2.22 +/- 0.44 nmol/l), did not change significantly on exercise. Coronary sinus c-AMP levels fell on exercise from 11.5 +/- 0.8 nmol/l (resting) to 9.9 +/- 0.8 nmol/l (exercise) (P less than 0.01) with an arterial-coronary sinus difference of 1.2 nmol/l (P less than 0.01) on exercise. Our findings suggest that isometric exercise does not normally result in excessive cardiac symphathetic activity.     

Subfornical organ-angiotensin II pressor system takes part in pressor response of emotional circuit

It has been proved that there are the subfornical organ (SFO)-nucleus paraventricularis (NPV)-rostral ventrolateral medulla (RVL) angiotension II (AngII) pressor system and the central amygdaloid nucleus (AC)-lateral hypothalamus/perifornical region (LH/PF) emotional pressor system in the brain. Because the LH/PF contains abundant AngII ergic neurons projecting to the SFO, the purpose of the present study was to examine whether the (SFO-NPV-RVL) AngII pressor system takes part in the AC-pressor response via AngII ergic neurons in the LH/PF. The results showed that (1) L-glutamate microinjection into the AC or LH/PF induced pressor responses. (2) Both the AC- and LH/PF-pressor responses could be reversed by preinjection of [Sar(1), Thr(8)]-angiotensin II (an antagonist of AngII) into either the SFO, NPV or RVL. Taken together with our previous findings that the projections of the CRF-ergic and SP-ergic neurons in the AC could activate the LH/PF, the above findings prove that: besides several known mechanisms of the brain AngII inducing pressor response, the (SFO-NPV-RVL) AngII pressor system also takes part in the AC-emotional pressor response via AngII ergic projections from the LH/PF to the SFO, which may be the neurophysiological basis of the brain AngII playing an important role in developing hypertension of the SHRs.     

VR-1 receptor blockade attenuates the pressor response to capsaicin but has no effect on the pressor response to contraction in cats

Vanilloid type 1 (VR-1) receptors are stimulated by capsaicin and hydrogen ions, the latter being a by-product of muscular contraction. We tested the hypothesis that activation of VR-1 receptors during static contraction contributes to the exercise pressor reflex. We established a dose of iodoresinaferatoxin (IRTX), a VR-1 receptor antagonist, that blocked the pressor response to capsaicin injected into the arterial supply of muscle. Specifically, in eight decerebrated cats, we compared pressor responses to capsaicin (10 mug) injected into the right popliteal artery, which was subsequently injected with IRTX (100 mug), with those to capsaicin injected into the left popliteal artery, which was not injected with IRTX. The pressor response to capsaicin injected into the right popliteal artery averaged 49 +/- 9 mmHg before IRTX and 9 +/- 2 mmHg after IRTX (P < 0.05). In contrast, the pressor response to capsaicin injected into the left popliteal artery averaged 46 +/- 10 mmHg before and 43 +/- 6 mmHg after (P > 0.05). We next determined whether VR-1 receptors mediated the pressor response to contraction of the triceps surae. During contraction without circulatory occlusion, the pressor response before IRTX (100 mug) averaged 26 +/- 3 mmHg, whereas it averaged 22 +/- 3 mmHg (P > 0.05) after IRTX (n = 8). In addition, during contraction with occlusion, the pressor responses averaged 35 +/- 3 mmHg before IRTX injection and 49 +/- 7 mmHg after IRTX injection (n = 7). We conclude that VR-1 receptors play little role in evoking the exercise pressor reflex.