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Biomedical subjects

Urs A Leuenberger

Publications and source records attributed to Urs A Leuenberger.

At least 19 recordsLinked to original sources
PubMed2006

Vasoconstriction seen in coronary bypass grafts during handgrip in humans.

In animal studies, sympathetically mediated coronary vasoconstriction has been demonstrated during exercise. Human studies examining coronary artery dynamics during exercise are technically difficult to perform. Recently, noninvasive transthoracic Duplex ultrasound studies demonstrated that 1) patients with left internal mammary artery (LIMA) grafts to the left anterior descending artery can be imaged and 2) the LIMA blood flow patterns are similar to those seen in normal coronary arteries. Accordingly, subjects with LIMA to the left anterior descending artery were studied during handgrip protocols as blood flow velocity in the LIMA was determined. Beat-by-beat analysis of changes in diastolic coronary blood flow velocity (CBV) was performed in six male clinically stable volunteers (60 +/- 2 yr) during two handgrip protocols. Arterial blood pressure (BP) and heart rate (HR) were also measured, and an index of coronary vascular resistance (CVR) was calculated as diastolic BP/CBV. Fatiguing handgrip performed at [40% of maximal voluntary contraction (MVC)] followed by circulatory arrest did not evoke an increase in CVR (P = not significant). In protocol 2, short bouts of handgrip (15 s) led to increases in CVR (18 +/- 3% at 50% MVC and 20 +/- 8% at 70% MVC). BP was also increased during handgrip. Our results reveal that in conscious humans, coronary vasoconstriction occurs within 15 s of onset of static handgrip at intensities at or greater than 50% MVC. These responses are likely to be due to sympathetic vasoconstriction of the coronary circulation.

Blood Pressure↗
PubMed2006

Aldosterone impairs baroreflex sensitivity in healthy adults.

Animal studies suggest that acute and chronic aldosterone administration impairs baroreceptor/baroreflex responses. We tested the hypothesis that aldosterone impairs baroreflex control of cardiac period [cardiovagal baroreflex sensitivity (BRS)] and muscle sympathetic nerve activity (MSNA, sympathetic BRS) in humans. Twenty-six young (25 +/- 1 yr old, mean +/- SE) adults were examined in this study. BRS was determined by using the modified Oxford technique (bolus infusion of nitroprusside, followed 60 s later by bolus infusion of phenylephrine) in triplicate before (Pre) and 30-min after (Post) beginning aldosterone (experimental, 12 pmol.kg(-1).min(-1); n = 10 subjects) or saline infusion (control; n = 10). BRS was quantified from the R-R interval-systolic blood pressure (BP) (cardiovagal BRS) and MSNA-diastolic BP (sympathetic BRS) relations. Aldosterone infusion increased serum aldosterone levels approximately fourfold (P < 0.05) and decreased (P < 0.05) cardiovagal (19.0 +/- 2.3 vs. 15.6 +/- 1.7 ms/mmHg Pre and Post, respectively) and sympathetic BRS [-4.4 +/- 0.4 vs. -3.0 +/- 0.4 arbitrary units (AU).beat(-1).mmHg(-1)]. In contrast, neither cardiovagal (19.3 +/- 3.3 vs. 20.2 +/- 3.3 ms/mmHg) nor sympathetic BRS (-3.8 +/- 0.5 vs. -3.6 +/- 0.5 AU.beat(-1).mmHg(-1)) were altered (Pre vs. Post) in the control group. BP, heart rate, and MSNA at rest were similar in experimental and control subjects before and after the intervention. Additionally, neural and cardiovascular responses to a cold pressor test and isometric handgrip to fatigue were unaffected by aldosterone infusion (n = 6 subjects). These data provide direct experimental support for the concept that aldosterone impairs baroreflex function (cardiovagal and sympathetic BRS) in humans. Therefore, aldosterone may be an important determinant/modulator of baroreflex function in humans.

Adaptation, Physiological↗
PubMed2006

Effect of repetitive hypoxic apnoeas on baroreflex function in humans.

Baroreflex function is impaired in patients with obstructive sleep apnoea. We tested the hypothesis that short-term exposure to repetitive hypoxic apnoeas (RHA) produces prolonged impairment in baroreflex function. Baroreflex function was determined using the modified Oxford technique in 14 subjects (26 +/- 1 years). Baroreflex sensitivity (BRS) was quantified from the R-R interval-systolic blood pressure (BP; cardiovagal BRS), heart rate-systolic BP (HR BRS) and muscle sympathetic nerve activity (MSNA)-diastolic BP (sympathetic BRS) relations. RHA involved subjects performing repetitive end-expiratory apnoeas (20 s) every minute for 30 min during intermittent hypoxia to accentuate oxygen desaturation. After RHA, BP and MSNA at rest were elevated. BRS was measured approximately 7 (Post 1), approximately 30 (Post 2) and approximately 50 min (Post 3) after RHA to provide insight into the temporal pattern of responses. Cardiovagal BRS (16.8 +/- 1.3, 16.5 +/- 1.6, 17.6 +/- 2.0 and 17.4 +/- 1.5 ms mmHg(-1) for Pre, Post 1, Post 2 and Post 3, respectively), HR BRS (-1.1 +/- 0.1, -1.1 +/- 0.1, -1.3 +/- 0.1 and -1.4 +/- 0.1 beats min(-1) mmHg(-1)) and sympathetic BRS (-4.5 +/- 0.6, -4.4 +/- 0.7, -3.7 +/- 0.5 and -4.7 +/- 1.0 arbitrary units (au) beat(-1) mmHg(-1)) were unchanged by RHA. In contrast, the operating points of the baroreflexes were shifted rightward (to higher levels of BP) and upward (to higher levels of heart rate and MSNA) after RHA (P < 0.05). Time control studies performed in five additional subjects showed no change in any of the measured variables over time. Collectively, these data indicate that short-term exposure to RHA shifts ('resets') the baroreflex stimulus-response curve to higher levels of BP without influencing BRS for extended periods of time.

Adolescent↗
PubMed2006

Renal vasoconstrictor responses to static exercise during orthostatic stress in humans: effects of the muscle mechano- and the baroreflexes.

Renal circulatory adjustments to stress contribute to blood pressure and volume regulation. Both handgrip (HG) and disengagement of baroreflexes with lower body negative pressure (LBNP) can engage the sympathetic nervous system (SNS). However, the effect of simultaneous HG and LBNP on the renal circulation in humans is not known. Eighteen young healthy volunteers were studied. Beat-to-beat changes in renal blood flow velocity (RBV; Duplex Ultrasound), mean arterial pressure (MAP; Finapres) and heart rate (ECG) were monitored during (a) 15 s HG at 30% maximum voluntary contraction (MVC); (b) LBNP at -10 and -30 mmHg (each level for 5 min); and (c) 15 s HG (at 30% MVC) during LBNP at both levels. Renal vascular resistance index (RVR units) was calculated by dividing MAP by RBV. The increases in RVR during HG alone (12 +/- 6%) were not different from the responses noted during combined HG and LBNP (17 +/- 6% at -10 mmHg and 25 +/- 8% at -30 mmHg). These results suggest occlusion occurs between a neural circuit engaged during 15 s of HG (central command and/or the muscle mechanoreflex) and a circuit activated by LBNP. In additional experiments (n = 6), similar non-algebraic summation of RVR was seen during 15 s involuntary biceps contractions (engages only muscle reflexes) and LBNP. With respect to RVR, neural occlusion occurs between baroreflexes and the muscle mechanoreflex. Muscle mechanoreflex mediated renal vasoconstriction during short bouts of HG is not influenced by baroreflex disengagement.

Adult↗
PubMed2006

Influence of sex and active muscle mass on renal vascular responses during static exercise.

During exercise, reflex renal vasoconstriction helps maintain blood pressure and redistributes blood flow to the contracting muscle. Sex and muscle mass have been shown to influence certain cardiovascular responses to exercise. Whether sex and/or muscle mass influence renal vasoconstrictor responses to exercise is unknown. We studied healthy men (n = 10) and women (n = 10) matched for age and body mass index during handgrip (HG, small muscle mass) and quadriceps contraction (QC, large muscle mass) as beat-to-beat changes in renal blood flow velocity (RBV; duplex ultrasound), mean arterial pressure (MAP; Finapres), and heart rate (ECG) were monitored. Renal vascular resistance (RVR) index was calculated as MAP / RBV. Responses to HG vs. QC were compared in 13 subjects. We found that 1) RVR responses to short (15-s) bouts and fatiguing HG were similar in men and women (change in RVR during 15-s HG at 70% of maximum voluntary contraction = 23 +/- 4 and 31 +/- 4% in men and women, respectively, P = not significant); 2) post-HG circulatory responses were similar in men and women; and 3) HG and QC were similar during short (15-s) bouts (change in RVR during HG at 50% of maximum voluntary contraction = 19 +/- 3 and 18 +/- 5% for arm and leg, respectively, P = not significant). Our findings suggest that muscle reflex-mediated renal vasoconstriction is similar in men and women during static exercise. Moreover, muscle mass does not contribute to the magnitude of the reflex renal vasoconstrictor response seen with muscle contraction.

Adaptation, Physiological↗
PubMed2005

Effects of intermittent hypoxia on sympathetic activity and blood pressure in humans.

Sympathetic nerve activity and arterial pressure are frequently elevated in patients with obstructive sleep apnea (OSA). The mechanisms responsible for chronic sympathetic activation and hypertension in OSA are unknown. To determine whether repetitive apneas raise sympathetic nerve activity and/or arterial pressure, awake and healthy young subjects performed voluntary end-expiratory apneas for 20 s per min for 30 min (room air apneas). To accentuate intermittent hypoxia, in a separate group of subjects, hypoxic gas (inspired O2 10%) was added to the inspiratory port for 20 s before each apnea (hypoxic apneas). Mean arterial pressure (MAP) and muscle sympathetic nerve activity (MSNA, peroneal microneurography) were determined before and up to 30 min following the repetitive apneas. Following 30 hypoxic apneas (O2 saturation nadir 83.1+/-1.2%), MSNA increased from 17.4+/-2.7 to 23.4+/-2.5 bursts/min and from 164+/-28 to 240+/-35 arbitrary units respectively (P<0.01 for both; n=10) and remained elevated while MAP increased transiently from 80.5+/-3.7 to 83.1+/-3.9 mm Hg (P<0.05; n=11). In contrast, in the subjects who performed repetitive apneas during room air exposure (O2 saturation nadir 95.1+/-0.8%), MAP and MSNA did not change (n=8). End-tidal CO2 post-apnea, an index of apnea-induced hypercapnia, was similar in the 2 groups. In a separate control group, no effect of time on MAP or MSNA was noted (n=7). Thus, repetitive hypoxic apneas result in sustained sympathetic activation and a transient elevation of blood pressure. These effects appear to be due to intermittent hypoxia and may play a role in the sympathetic activation and hypertension in OSA.

Adult↗
PubMed2005

Renal vascular response to static handgrip exercise: sympathetic vs. autoregulatory control.

Static exercise causes activation of the sympathetic nervous system, which results in increased blood pressure (BP) and renal vascular resistance (RVR). The question arises as to whether renal vasoconstriction that occurs during static exercise is due to sympathetic activation and/or related to a pressure-dependent renal autoregulatory mechanism. To address this issue, we monitored renal blood flow velocity (RBV) responses to two different handgrip (HG) exercise paradigms in 7 kidney transplant recipients (RTX) and 11 age-matched healthy control subjects. Transplanted kidneys are functionally denervated. Beat-by-beat analyses of changes in RBV (observed via duplex ultrasound), BP, and heart rate were performed during HG exercise in all subjects. An index of RVR was calculated as BP/RBV. In protocol 1, fatiguing HG exercise (40% of maximum voluntary contraction) led to significant increases in RVR in both groups. However, at the end of exercise, RVR was more than fourfold higher in control subjects than in the RTX group (88 vs. 20% increase over baseline; interaction, P < 0.001). In protocol 2, short bouts of HG exercise (15 s) led to significant increases in RVR at higher workloads (50 and 70% of maximum voluntary contraction) in the control subjects (P < 0.001). RVR did not increase in the RTX group. In conclusion, we observed grossly attenuated renal vasoconstrictor responses to exercise in RTX subjects, in whom transplanted kidneys were considered functionally denervated. Our results suggest that renal vasoconstrictor responses to exercise in conscious humans are mainly dependent on activation of a neural mechanism.

Adult↗
PubMed2005

Heterogeneous vasodilator responses of human limbs: influence of age and habitual endurance training.

Forearm endothelium-dependent vasodilation is impaired with age in sedentary, but not endurance-trained, men. The purpose of this investigation was to determine whether these age- and physical activity-related differences in endothelium-dependent vasodilation also occur in the leg. Brachial and common femoral arterial blood flow were measured with Doppler ultrasound during increasing doses of acetylcholine (1, 4, and 16 microg.100 ml limb tissue(-1).min(-1)), substance P (8, 31, and 125 pg.100 ml limb tissue(-1).min(-1)), and sodium nitroprusside (0.063, 0.25, and 1 microg.100 ml limb tissue(-1).min(-1)) in 23 healthy men (8 younger sedentary, 8 older sedentary, and 7 older endurance trained). Increases in forearm blood flow to the highest dose of acetylcholine and sodium nitroprusside were smaller (P < 0.05) in older sedentary (841 +/- 142%, 428 +/- 74%) compared with younger sedentary (1,519 +/- 256%, 925 +/- 163%) subjects. Similarly, increases in forearm blood flow to sodium nitroprusside (1 microg.100 ml limb tissue(-1).min(-1)) were smaller (P < 0.05) in older endurance-trained (505 +/- 110%) compared with younger sedentary (925 +/- 163%) subjects. In contrast, no differences in leg blood flow responses to intra-arterial infusions of acetylcholine, substance P, or sodium nitroprusside were noted between subject groups. These results demonstrate that 1) acetylcholine- and sodium nitroprusside-induced vasodilation are attenuated in the forearm vasculature and preserved in the leg vasculature of older sedentary subjects and 2) sodium nitroprusside-induced vasodilation remains attenuated in the forearm vasculature of healthy older endurance-trained men but preserved in the leg vasculature of these men.

Acetylcholine↗
PubMed2004

Renal blood flow in heart failure patients during exercise.

During exercise, reflex renal vasoconstriction maintains blood pressure and helps in redistributing blood flow to the contracting muscle. Exercise intolerance in heart failure (HF) is thought to involve diminished perfusion in active muscle. We studied the temporal relationship between static handgrip (HG) and renal blood flow velocity (RBV; duplex ultrasound) in 10 HF and in 9 matched controls during 3 muscle contraction paradigms. Fatiguing HG (protocol 1) at 40% of maximum voluntary contraction led to a greater reduction in RBV in HF compared with controls (group main effect: P <0.05). The reduction in RBV early in HG tended to be more prominent during the early phases of protocol 1. Similar RBV was observed in the two groups during post-HG circulatory arrest (isolating muscle metaboreflex). Short bouts (15 s) of HG at graded intensities (protocol 2; engages muscle mechanoreflex and/or central command) led to greater reductions in RBV in HF than controls (P <0.03). Protocol 3, voluntary and involuntary biceps contraction (eliminates central command), led to similar increases in renal vasoconstriction in HF (n=4). Greater reductions in RBV were found in HF than in controls during the early phases of exercise. This effect was not likely due to a metaboreflex or central command. Thus our data suggest that muscle mechanoreflex activity is enhanced in HF and serves to vigorously vasoconstrict the kidney. We believe this compensatory mechanism helps preserve blood flow to exercising muscle in HF.

Blood Flow Velocity↗
PubMed2004

Effect of aging on renal blood flow velocity during static exercise.

During exercise, activation of the sympathetic nervous system causes reflex renal vasoconstriction. The effects of aging on this reflex are poorly understood. This study evaluated the effects of age on renal vasoconstrictor responses to handgrip. Seven older (65 +/- 9 yr) and nine younger (25 +/- 2 yr) subjects were studied. Beat-by-beat analyses of changes in renal blood flow velocity (RBV; duplex ultrasound) were performed during two handgrip paradigms. Arterial blood pressure (BP) and heart rate were also measured, and an index of renal vascular resistance (RVR) was calculated (BP/RBV). In protocol 1, fatiguing handgrip [40% of maximal voluntary contraction (MVC)] caused a greater increase in RVR in the older subjects (old 90% +/- 15 increase, young 52% +/- 4 increase; P = 0.03). During posthandgrip circulatory arrest (isolates muscle metaboreflex), the increases in RVR were only approximately 1/2 of the increase seen at end grip. In protocol 2, 15-s bouts of handgrip at graded intensities led to increases in RVR in both subject groups. This effect was not seen until 50% MVC workload (P < 0.05). RVR responses occurred early and were greater in older than in younger subjects at 50% MVC (32 +/- 6% vs. 16 +/- 5%; P = 0.02) and 70% MVC (39 +/- 11% vs. 24 +/- 8%; P = 0.02). Static exercise-induced renal vasoconstriction is enhanced with aging. Because the characteristics of this response suggest a predominant role for mechanoreceptor engagement, we hypothesize that mechanoreceptor responses are augmented with aging.

Adult↗
PubMed2004

Different vasodilator responses of human arms and legs.

Forearm vascular responses to intra-arterial infusions of endothelium-dependent and -independent vasodilators have been thoroughly characterized in humans. While the forearm is a well-established experimental model for studying human vascular function, it is of limited consequence to systemic cardiovascular control owing to its small muscle mass and blood flow requirements. In the present study we determined whether these responses could be generalized to the leg. Based upon blood pressure differences between the leg and arm during upright posture, we hypothesized that the responsiveness to endothelium-dependent vasodilators would be greater in the forearm than the leg. Brachial and femoral artery blood flow (Q, ultrasound Doppler) at rest and during intra-arterial infusions of endothelium-dependent (acetylcholine and substance P) and -independent (sodium nitroprusside) vasodilators were measured in eight healthy men (22-27 years old). Resting blood flows in the forearm before infusion of acetylcholine, substance P or sodium nitroprusside were 25 +/- 4, 30 +/- 7 and 29 +/- 5 ml min(-1), respectively, and in the leg were 370 +/- 32, 409 +/- 62 and 330 +/- 30 ml min(-1), respectively. At the highest infusion rate of acetylcholine (16 microg (100 ml tissue)(-1) min(-1)) there was a greater (P < 0.05) increase in Q to the forearm (1864 +/- 476%) than to the leg (569 +/- 86%). Similarly, at the highest infusion rate of substance P (125 pg (100 ml tissue)(-1) min(-1)) there was a greater (P < 0.05) increase in Q to the forearm (911 +/- 286%) than to the leg (243 +/- 58%). The responses to sodium nitroprusside (1 microg (100 ml tissue)(-1) min(-1)) were also greater (P < 0.05) in the forearm (925 +/- 164%) than in the leg (326 +/- 65%). These data indicate that vascular responses to both endothelium-dependent and -independent vasodilator agents are blunted in the leg compared to the forearm.

Acetylcholine↗
PubMed2004

Leg blood flow and VO2 during peak cycle exercise in younger and older women.

PURPOSE: To test the hypothesis that leg blood flow and leg O2 extraction during peak exercise are reduced with age in healthy normally active women. METHODS: Thirteen younger (20-27 yr) and 12 older (60-71 yr) nonendurance trained women performed graded upright leg cycling to maximum exertion (VO2peak), while leg blood flow (femoral vein thermodilution), cardiac output (acetylene rebreathing), mean arterial pressure (MAP, radial artery), and blood O2 contents were measured. RESULTS: Peak leg VO2 was 32% lower in the older versus younger women (0.81 +/- 0.06 vs 1.18 +/- 0.10 L x min(-1)) and was correlated with peak systemic VO2 (1.33 +/- 0.1 vs 1.78 +/- 0.1 L x min(-1)) in both groups. Peak leg blood flow and estimated leg vascular conductance were 29% and 38% lower, respectively, in the older women (both P < 0.001). Peak leg blood flow and peak estimated cardiac output were correlated in the older (r2 = 0.51, P = 0.02), but not younger (r2 = 0.10, P = 0.35), group. Estimates of peak systemic and leg arterial-venous O2 difference did not differ between groups (both P > 0.28). CONCLUSIONS: Reduced leg blood flow is a major contributor to the reduced peak systemic VO2 observed in older nonendurance trained women. Diminished leg blood flow during peak exercise in older women, in turn, is due to both central (reduced cardiac output) and peripheral (reduced leg vascular conductance) limitations.

Adult↗
PubMed2003

Control of skin sympathetic nerve activity during intermittent static handgrip exercise.

BACKGROUND: Exercise activates the sympathetic nervous system as a function of the type and intensity of exercise and of the target organ studied. Although central command and activity of metabolically sensitive afferents from exercising muscle are the principal determinants of sympathetic outflow directed to skeletal muscle, the mechanisms that govern sympathetic outflow directed to skin are less clear. METHODS AND RESULTS: We measured skin sympathetic nerve activity (SSNA) during intermittent static handgrip (SHG; at 45% of maximal voluntary contraction; four 5-second contractions per minute for 3 minutes), during unrestricted forearm perfusion (control), during stimulation of forearm mechanoreceptors with venous congestion, and during ischemia produced by forearm circulatory arrest. Under all 3 conditions, SSNA increased within 1 to 2 seconds of the onset of handgrip. During ischemia but not during venous congestion, SSNA increased more compared with control (P<0.05) and remained elevated when forearm ischemia was maintained after handgrip exercise (posthandgrip circulatory arrest). In addition, simulated handgrip and intermittent forearm compression produced by a pneumatic cuff also evoked brief increases of SSNA. CONCLUSIONS: In addition to central neural factors, afferent input from exercising muscle plays an important role in modulating sympathetic outflow directed to skin.

Adult↗
PubMed2003

Impaired leg vasodilation during dynamic exercise in healthy older women.

The purpose of the present study was to test the hypothesis that leg blood flow responses during leg cycle ergometry are reduced with age in healthy non-estrogen-replaced women. Thirteen younger (20-27 yr) and thirteen older (61-71 yr) normotensive, non-endurance-trained women performed both graded and constant-load bouts of leg cycling at the same absolute exercise intensities. Leg blood flow (femoral vein thermodilution), mean arterial pressure (MAP; radial artery), mean femoral venous pressure, cardiac output (acetylene rebreathing), and blood O2 contents were measured. Leg blood flow responses at light workloads (20-40 W) were similar in younger and older women. However, at moderate workloads (50-60 W), leg blood flow responses were significantly attenuated in older women. MAP was 20-25 mmHg higher (P < 0.01) in the older women across all work intensities, and calculated leg vascular conductance (leg blood flow/estimated leg perfusion pressure) was lower (P < 0.05). Exercise-induced increases in leg arteriovenous O2 difference and O2 extraction were identical between groups (P > 0.6). Leg O2 uptake was tightly correlated with leg blood flow across all workloads in both subject groups (r2 = 0.80). These results suggest the ability of healthy older women to undergo limb vasodilation in response to submaximal exercise is impaired and that the legs are a potentially important contributor to the augmented systemic vascular resistance seen during dynamic exercise in older women.

Adult↗
PubMed2003

Augmented leg vasoconstriction in dynamically exercising older men during acute sympathetic stimulation.

Vasoconstrictor responsiveness to acute sympathetic stimulation declines with advancing age in resting skeletal muscle. The purpose of the present study was to determine if age-related reductions in sympathetic vasoconstrictor responsiveness also occur in exercising skeletal muscle. Thirteen younger (20-30 years) and seven older (62-74 years) healthy non-endurance-trained men performed cycle ergometer exercise at ~60 % of peak oxygen uptake while leg blood flow (femoral vein thermodilution), mean arterial blood pressure (radial artery catheter), and plasma adrenaline and noradrenaline concentrations were measured. After steady state was reached (i.e. ~4 min), acute sympathetic stimulation was achieved by immersing a hand in ice water for 2-4 min (cold pressor test, CPT). CPT tended to cause a larger increase in mean arterial blood pressure in older men (older (O): 16 +/- 3 mmHg; younger (Y): 10 +/- 2 mmHg) during exercise, but increases in arterial noradrenaline were similar (O: 2.56 +/- 0.96 nM; Y: 1.98 +/- 0.40 nM). However, the older men demonstrated a larger percentage reduction in exercising leg vascular conductance (leg blood flow/mean arterial pressure) during CPT compared to younger men (O: -13.6 +/- 3.1 %; Y: -1.5 +/- 4.3 %; P = 0.04). Leg blood flow tended to increase in the younger men, but not in the older men (P = 0.10). These results suggest, in contrast to what has been observed in resting skeletal muscle, that vasoconstrictor responsiveness to sympathetic stimulation is not reduced, but may be augmented in exercising muscle of healthy older humans. This could reflect a reduced ability of local substances (e.g. nitric oxide) to impair vasoconstriction in response to sympathetic stimulation during exercise in older humans.

Adult↗
PubMed2003

Renal vascular responses to static handgrip: role of muscle mechanoreflex.

During exercise, the sympathetic nervous system is activated, which causes vasoconstriction. The autonomic mechanisms responsible for this vasoconstriction vary based on the particular tissue being studied. Attempts to examine reflex control of the human renal circulation have been difficult because of technical limitations. In this report, the Doppler technique was used to examine renal flow velocity during four muscle contraction paradigms in conscious humans. Flow velocity was divided by mean arterial blood pressure to yield an index of renal vascular resistance (RVR). Fatiguing static handgrip (40% of maximal voluntary contraction) increased RVR by 76%. During posthandgrip circulatory arrest, RVR remained above baseline (2.1 +/- 0.2 vs. 2.8 +/- 0.2 arbitrary units; P < 0.017) but was only 40% of the end-grip RVR value. Voluntary biceps contraction increased RVR within 10 s of initiation of contraction. This effect was not associated with an increase in blood pressure. Finally, involuntary biceps contraction also raised RVR. We conclude that muscle contraction evokes renal vasoconstriction in conscious humans. The characteristic of this response is consistent with a primary role for mechanically sensitive afferents. This statement is based on the small posthandgrip circulatory arrest response and the vasoconstriction that was observed with involuntary biceps contraction.

Adolescent↗
PubMed2003

Leg blood flow during submaximal cycle ergometry is not reduced in healthy older normally active men.

The purpose of the present study was to test the hypothesis that leg blood flow responses during submaximal cycle ergometry are reduced with age in healthy normally active men. Eleven younger (20-25 yr) and eight older (62-73 yr) normotensive, nonendurance-trained men performed both graded and constant-load bouts of leg cycling at the same absolute and relative [% of peak O(2) consumption (Vo(2 peak))] exercise intensities while leg blood flow (femoral vein thermodilution), mean arterial pressure (MAP; radial artery), cardiac output (acetylene rebreathing), blood O(2) content, and plasma catecholamines were measured. Leg blood flow responses at the same absolute submaximal power outputs (20-100 W) and at a fixed systemic O(2) demand (1.1 l/min) did not differ between groups (P = 0.14-0.19), despite lower absolute levels of cardiac output in the older men (P < 0.05). MAP at the same absolute power outputs was 8-12 mmHg higher (P < 0.05) in the older men, but calculated leg vascular conductance responses (leg blood flow/MAP) were identical in the two groups (P > 0.9). At the same relative intensity (60% Vo(2 peak)), leg norepinephrine spillover rates were approximately twofold higher in the older men (P = 0.38). Exercise-induced increases in leg arterial-venous O(2) difference were identical between groups (P > 0.9) because both arterial and venous O(2) contents were lower in the older vs. younger men. These results suggest that the ability to augment active limb blood flow and O(2) extraction during submaximal large muscle mass exercise is not impaired but is well preserved with age in healthy men who are normally active.

Absorptiometry, Photon↗