Biomedical subjects

J K Shoemaker

Publications and source records attributed to J K Shoemaker.

At least 37 records · Page 2Linked to original sources

PubMed1999

Blood flow dynamics in heart failure.

BACKGROUND: Exercise intolerance in heart failure (HF) may be due to inadequate vasodilation, augmented vasoconstriction, and/or altered muscle metabolic responses that lead to fatigue. METHODS AND RESULTS: Vascular and metabolic responses to rhythmic forearm exercise were tested in 9 HF patients and 9 control subjects (CTL) during 2 protocols designed to examine the effect of HF on the time course of oxygen delivery versus uptake (protocol 1) and on vasoconstriction during exercise with 50 mm Hg pressure about the forearm to evoke a metaboreflex (protocol 2). In protocol 1, venous lactate and H+ were greater at 4 minutes of exercise in HF versus CTL (P<0.05) despite similar blood flow and oxygen uptake responses. In protocol 2, mean arterial pressure increased similarly in each group during ischemic exercise. In CTL, forearm blood flow and vascular conductance were similar at the end of ischemic and ambient exercise. In HF, forearm blood flow and vascular conductance were reduced during ischemic exercise compared with the ambient trial. CONCLUSIONS: Intrinsic differences in skeletal muscle metabolism, not vasodilatory dynamics, must account for the augmented glycolytic metabolic responses to moderate-intensity exercise in class II and III HF. The inability to increase forearm vascular conductance during ischemic handgrip exercise, despite a normal pressor response, suggests that enhanced vasoconstriction of strenuously exercising skeletal muscle contributes to exertional fatigue in HF.

Adult↗

PubMed1999

Prostaglandin inhibition causes an increase in reactive hyperaemia after ischaemic exercise in human forearm.

The hypothesis that prostaglandins contribute to the reactive hyperaemia after 5 min of ischaemia or 5 min of ischaemic exercise was investigated in six men by inhibiting prostaglandin production with ibuprofen (1800 mg) and indomethacin (225 mg) over 24 h before testing. Blood flow was measured continuously in the baseline and after ischaemia by combined pulsed and echo Doppler as the product of velocity and cross-sectional area. After 5 min of ischaemia, there were no differences in blood flow between placebo and the two drug conditions, except at 5 and 10 s when flow with indomethacin was greater than both placebo and ibuprofen. After 5 min of ischaemic exercise, blood flow was significantly greater as a consequence of increased vascular conductance in each of ibuprofen and indomethacin than placebo from 5 until 90 s of recovery. We conclude that prostaglandin inhibition had little or no effect on reactive hyperaemia after 5 min of circulatory occlusion alone, but that blood flow after ischaemic exercise was elevated due to increased vascular conductance when prostaglandin synthesis was inhibited.

Adult↗

PubMed1999

Adaptation of blood flow during the rest to work transition in humans.

Beat-by-beat measurements show that limb blood flow rises rapidly and in a biphasic manner at the onset of rhythmic exercise in humans. In this review the time course of change in limb flow with the onset of exercise is described and the mechanisms that may or may not contribute to its regulation are discussed. The pumping action of contracting skeletal muscle appears to form an important regulator of increasing flow with the first contraction. However, evidence from human studies suggests that vasodilation begins with the first contraction. Whether this early dilation is regulated by neural recruitment of motor fibers and/or muscle contraction per se is discussed, but the mechanism(s) remains unclear. Finally, the contribution of endothelial-derived relaxation factors to the exponential increase in flow at the exercise onset is examined. Based on studies in humans with intra-arterial infusion of blocking drugs, neither acetylcholine, nitric oxide, nor prostaglandins appear to be essential for a normal dynamic flow response on going from rest to exercise. Overall, evidence from human studies supports the hypothesis that the rate of increase in blood flow during rhythmic voluntary exercise is closely coupled to motor unit recruitment with dilation beginning at the first contraction.

Adaptation, Physiological↗

PubMed1999

Upright posture reduces forearm blood flow early in exercise.

The hypothesis that upright posture could modulate forearm blood flow (FBF) early in exercise was tested in six subjects. Both single (2-s duration) and repeated (1-s work/2-s rest cadence for 12 contractions) handgrip contractions (12 kg) were performed in the supine and 70 degrees head-up tilt (HUT) positions. The arm was maintained at heart level to diminish myogenic effects. Baseline brachial artery diameters were assessed at rest in each position. Brachial artery mean blood velocity (MBV; Doppler) and mean arterial pressure (MAP) (Finapres) were measured continuously to calculate FBF and vascular conductance. MAP was not changed with posture. Antecubital venous pressure (Pv) was reduced in HUT (4.55 +/- 1.3 mmHg) compared with supine (11.3 +/- 1.9 mmHg) (P < 0.01). For the repeated contractions, total excess FBF (TEF) was reduced in the HUT position compared with supine (P < 0.02). With the single contractions, peak FBF, peak vascular conductance, and TEF during 30 s after release of the contraction were reduced in the HUT position compared with supine (P < 0.01). Sympathetic blockade augmented the FBF response to a single contraction in HUT (P < 0.05) and tended to increase this response while supine (P = 0.08). However, sympathetic blockade did not attenuate the effect of HUT on peak FBF and TEF after the single contractions. Raising the arm above heart level while supine, to diminish Pv, resulted in FBF dynamics that were similar to those observed during HUT. Alternatively, lowering the arm while in HUT to restore Pv to supine levels restored the peak FBF and vascular conductance responses, but not TEF response, after a single contraction. It was concluded that upright posture diminishes the hyperemic response early in exercise. The data demonstrate that sympathetic constriction restrains the hyperemic response to a single contraction but does not modulate the postural reduction in postcontraction hyperemia. Therefore, the attenuated blood flow response in the HUT posture was largely related to factors associated with diminished venous pressures and not sympathetic vasoconstriction.

Adult↗

PubMed1999

Contributions of MSNA and stroke volume to orthostatic intolerance following bed rest.

We examined whether the altered orthostatic tolerance following 14 days of head-down tilt bed rest (HDBR) was related to inadequate sympathetic outflow or to excessive reductions in cardiac output during a 10- to 15-min head-up tilt (HUT) test. Heart rate, blood pressure (BP, Finapres), muscle sympathetic nerve activity (MSNA, microneurography), and stroke volume blood velocity (SVV, Doppler ultrasound) were assessed during supine 30 degrees (5 min) and 60 degrees (5-10 min) HUT positions in 15 individuals who successfully completed the pre-HDBR test without evidence of orthostatic intolerance. Subjects were classified as being orthostatically tolerant (OT, n = 9) or intolerant (OI, n = 6) following the post-HDBR test. MSNA, BP, and SVV during supine and HUT postures were not altered in the OT group. Hypotension during 60 degrees HUT in the post-bed rest test for the OI group (P < 0.05) was associated with a blunted increase in MSNA (P < 0.05). SVV was reduced following HDBR in the OI group (main effect of HDBR, P < 0.02). The data support the hypothesis that bed rest-induced orthostatic intolerance is related to an inadequate increase in sympathetic discharge that cannot compensate for a greater postural reduction in stroke volume.

Adolescent↗

PubMed1999

Are we a gift shop? A perspective on grade inflation.

Grade inflation is a phenomenon that has been written about extensively since the mid 1970s. It is theorized that it made its initial appearance as an adjustment to the rigorous educational standards that were imposed in the post-Sputnik era. Some authors speculate that grade inflation as we know it is an outcome of student demands for high grades combined with faculty willingness to capitulate to them. Others believe the problem is related to lack of faculty knowledge about evaluation methods, or the quest for positive student evaluations in support of promotion, tenure, and merit decisions. Of particular concern is the lack of published studies of grade inflation in nursing education. The purpose of this article is to describe what we know about grade inflation-its history, causative factors, and implications for nursing.

Assertiveness↗

PubMed1998

Relationships between fluid and electrolyte hormones and plasma volume during exercise with training and detraining.

PURPOSE: The purpose of this study was to investigate the relationship between training-induced alterations in plasma volume (PV) and changes in fluid and electrolyte regulatory hormones during prolonged exercise. METHODS: Seven male subjects (VO2peak 49.2 +/- 2.4 mL.kg-1.min-1, X +/- SE) performed a cycling test before (C) and after (T) 6 d of training and after 6 d of detraining (DT). Training was conducted for 2 h.d-1 at 68% VO2peak at a room temperature between 26-28 degrees C. The 60-min exercise challenge included 20 min at 50%, 65%, and 75% VO2peak workloads. RESULTS: Training resulted in a calculated 13.8 +/- 1.6% PV expansion (P < 0.05) which recovered to C levels with DT (1.8 +/- 2.3%, P > 0.05). Compared with that at C, training resulted in a reduction of aldosterone (ALDO) concentration at all exercise intensities (P < 0.05) which normalized to C levels with DT. With T, epinephrine (EPI) concentrations were reduced at the highest power output only (365 +/- 51 vs 113 +/- 22 pg.mL-1; P < 0.05) and returned to C levels with DT. Arginine vasopressin (AVP) concentrations were also reduced at the highest workload only (20.2 +/- 3.2 pg.mL-1 vs 10.4 +/- 0.7 pg.mL-1; P < 0.05) and remained depressed after DT (11.8 +/- 1.3 pg.mL-1; P < 0.05). Atrial natriuretic factor (ANF) and norepinephrine (NOREPI) were not affected by T or DT. CONCLUSIONS: The results suggest that concentrations of ALDO, and to a lesser extent EPI, during exercise are related to PV levels, whereas ANF and NOREPI concentrations are not. AVP concentrations are related to other adaptive factors, the effects of which persist for a longer time course than do PV changes.

Adult↗

PubMed1998

Vasodilation contributes to the rapid hyperemia with rhythmic contractions in humans.

The hypothesis that the rapid increases in blood flow at the exercise onset are exclusively due to the mechanical effects of the muscle pump was tested in six volunteers during dynamic handgrip exercise. While supine, each subject completed a series of eight different exercise tests in which brachial artery blood pressure (BP) was altered by 25-30 mmHg (1 mmHg = 133.3 Pa) by positioning the arm above or below the heart. Two different weights, corresponding to 4.9 and 9.7% of maximal voluntary isometric contraction, were raised and lowered at two different contraction rate schedules (1s:1s and 2s:2s work-rest) each with a 50% duty cycle. Beat-by-beat measures of mean blood velocity (MBV) (pulsed Doppler) were obtained at rest and for 5 min following step increases in work rate with emphasis on the first 24 s. MBV was increased 50-100% above rest following the first contraction in both arm positions (p < 0.05). The increase in MBV from rest was greater in the below position compared with above, and this effect was observed following the first and subsequent contractions (p < 0.05). However, the positional effect on the increase in MBV could not be explained entirely by the approximately 40% greater BP in this position. Also, the greater workload resulted in greater increases in MBV as early as the first contraction, compared with the light workload (p < 0.05) despite similar reductions in forearm volume following single contractions. MBV was greater with faster contraction rate tests by 8 s of exercise. It was concluded that microvascular vasodilation must act in concert with a reduction in venous pressure to increase forearm blood flow within the initial 2-4 s of exercise.

Adult↗

PubMed1998

Sympathetic discharge and vascular resistance after bed rest.

The effect of -6 degrees head-down-tilt bed rest (HDBR) for 14 days on supine sympathetic discharge and cardiovascular hemodynamics at rest was assessed. Mean arterial pressure, heart rate (n = 25), muscle sympathetic nerve activity (MSNA; n = 16) burst frequency, and forearm blood flow (n = 14) were measured, and forearm vascular resistance (FVR) was calculated. Stroke distance, our index of stroke volume, was derived from measurements of aortic mean blood velocity (Doppler) and R-R interval (n = 7). With these data, an index of total peripheral resistance was determined. Heart rate at rest was greater in the post (71 +/- 2 beats/min)- compared with the pre-HDBR test (66 +/- 2 beats/min; P < 0.003), but mean arterial pressure was unchanged. Aortic stroke distance during post-HDBR (15.5 +/- 1.1 cm/beat) was reduced from pre-HDBR levels (20.0 +/- 1.5 cm/beat) (P < 0.03). Also, MSNA burst frequency was reduced in the post (16.7 +/- 2.8 beats/min)- compared with the pre (25.2 +/- 2.6 beats/min)-HDBR condition (P < 0.01). Bed rest did not alter forearm blood flow, FVR, or total peripheral resistance. Thus reductions in MSNA with HDBR were not associated with a decrease in FVR.

Adaptation, Physiological↗

PubMed1998

Head-down-tilt bed rest alters forearm vasodilator and vasoconstrictor responses.

To test the hypothesis that head-down-tilt bed rest (HDBR) for 14 days alters vascular reactivity to vasodilatory and vasoconstrictor stimuli, the reactive hyperemic forearm blood flow (RHBF, measured by venous occlusion plethysmography) and mean arterial pressure (MAP, measured by Finapres) responses after 10 min of circulatory arrest were measured in a control trial (n = 20) and when sympathetic discharge was increased by a cold pressor test (RHBF + cold pressor test; n = 10). Vascular conductance (VC) was calculated (VC = RHBF/MAP). In the control trial, peak RHBF at 5 s after circulatory arrest (34.1 +/- 2.5 vs. 48.9 +/- 4.3 ml . 100 ml-1 . min-1) and VC (0.34 +/- 0.02 vs. 0.53 +/- 0.05 ml . 100 ml-1 . min-1 . mmHg-1) were reduced in the post- compared with the pre-HDBR tests (P < 0. 05). Total excess RHBF over 3 min was diminished in the post- compared with the pre-HDBR trial (84.8 vs. 117 ml/100 ml, P < 0.002). The ability of the cold pressor test to lower forearm blood flow was less in the post- than in the pre-HDBR test (P < 0.05), despite similar increases in MAP. These data suggest that regulation of vascular dilation and the interaction between dilatory and constrictor influences were altered with bed rest.

Adult↗

PubMed1998

Alveolar oxygen uptake and femoral artery blood flow dynamics in upright and supine leg exercise in humans.

We tested the hypothesis that the slower increase in alveolar oxygen uptake (VO2) at the onset of supine, compared with upright, exercise would be accompanied by a slower rate of increase in leg blood flow (LBF). Seven healthy subjects performed transitions from rest to 40-W knee extension exercise in the upright and supine positions. LBF was measured continuously with pulsed and echo Doppler methods, and VO2 was measured breath by breath at the mouth. At rest, a smaller diameter of the femoral artery in the supine position (P < 0. 05) was compensated by a greater mean blood flow velocity (MBV) (P < 0.05) so that LBF was not different in the two positions. At the end of 6 min of exercise, femoral artery diameter was larger in the upright position and there were no differences in VO2, MBV, or LBF between upright and supine positions. The rates of increase of VO2 and LBF in the transition between rest and 40 W exercise, as evaluated by the mean response time (time to 63% of the increase), were slower in the supine [VO2 = 39.7 +/- 3.8 (SE) s, LBF = 27.6 +/- 3.9 s] than in the upright positions (VO2 = 29.3 +/- 3.0 s, LBF = 17.3 +/- 4.0 s; P < 0.05). These data support our hypothesis that slower increases in alveolar VO2 at the onset of exercise in the supine position are accompanied by a slower increase in LBF.

Adult↗

PubMed1998

Maintained exercise pressor response in heart failure.

The impact of forearm blood flow limitation on muscle reflex (metaboreflex) activation during exercise was examined in 10 heart failure (HF) (NYHA class III and IV) and 9 control (Ctl) subjects. Rhythmic handgrip contractions (25% maximal voluntary contraction, 30 contractions/min) were performed over 5 min under conditions of ambient pressure or with +50 mmHg positive pressure about the exercising forearm. Mean arterial blood pressure (MAP) and venous effluent hemoglobin (Hb) O2 saturation, lactate and H+ concentrations ([La] and [H+], respectively) were measured at baseline and during exercise. For ambient contractions, the increase (Delta) in MAP by end exercise (DeltaMAP; i.e., the exercise pressor response) was the same in both groups (10.1 +/- 1.2 vs. 7.33 +/- 1.3 mmHg, HF vs. Ctl, respectively) despite larger Delta[La] and Delta[H+] for the HF group (P < 0.05). With ischemic exercise, the DeltaMAP for HF (21.7 +/- 2.7 mmHg) exceeded that of Ctl subjects (12.2 +/- 2.8 mmHg) (P < 0.0001). Also, for HF, Delta[La] (2.94 +/- 0.4 mmol) and Delta[H+] (24.8 +/- 2.7 nmol) in the ischemic trial were greater than in Ctl (1.63 +/- 0.4 mmol and 15.3 +/- 2.8 nmol; [La] and [H+], respectively) (P < 0.02). Hb O2 saturation was reduced in Ctl from approximately 43% in the ambient trial to approximately 27% with ischemia (P < 0.0001). O2 extraction was maximized under ambient exercise conditions for HF but not for Ctl. Despite progressive increases in blood perfusion pressure over the course of ischemic exercise, no improvement in Hb O2 saturation or muscle metabolism was observed in either group. These data suggest that muscle reflex activation of the pressor response is intact in HF subjects but the resulting improvement in perfusion pressure does not appear to enhance muscle oxidative metabolism or muscle blood flow, possibly because of associated increases in sympathetic vasoconstriction of active skeletal muscle.

Adult↗

PubMed1998

Effects of acetylcholine and nitric oxide on forearm blood flow at rest and after a single muscle contraction.

We tested the hypothesis that ACh or nitric oxide (NO) might be involved in the vasodilation that accompanies a single contraction of the forearm. Eight adults (3 women and 5 men) completed single 1-s-duration contractions of the forearm to raise and lower a weight equivalent to approximately 20% maximal voluntary contraction through a distance of 5 cm. In a second protocol, each subject had a cuff, placed completely about the forearm, inflated to 120 mmHg for a 1-s period, then released as a simulation of the mechanical effect of muscle contraction. Three conditions were studied, always in this order: 1) control, with intra-arterial infusion of saline; 2) after muscarinic blockade with atropine; and 3) after NO synthase inhibition with NG-monomethyl-L-arginine (L-NMMA) plus atropine. Forearm blood flow (FBF), measured by combined pulsed and echo Doppler ultrasound, was reduced at rest with L-NMMA-atropine compared with the other two conditions. After the single contraction, there were no effects of atropine, but L-NMMA reduced the peak FBF and the total postcontraction hyperemia. After the single cuff inflation, atropine had no effects, whereas L-NMMA caused changes similar to those seen after contraction, reducing the peak FBF and the total hyperemia. The observation that L-NMMA reduced FBF in response to both cuff inflation and a brief contraction indicates that NO from the vascular endothelium might modulate the basal level of vascular tone and the mechanical component of the hyperemia with exercise. It is unlikely that ACh and NO from the endothelium are involved in the dilator response to a single muscle contraction.

Acetylcholine↗

PubMed1997

Time course of brachial artery diameter responses to rhythmic handgrip exercise in humans.

OBJECTIVE: Whether the dimensions of conduit arteries contribute to the time course of change in blood flow during voluntary rhythmic exercise, and the mechanisms governing such a response in humans, are not known. METHODS: The time course of change in the vascular and blood flow dynamics in the brachial artery during the transition between rest and 5 min of rhythmic handgrip exercise was assessed in humans using continuous measures of brachial artery mean blood velocity (MBV; pulsed Doppler), diameter (echo Doppler) and mean arterial pressure (Finapres). The exercise cadence was 1s/1s (Fast) and 1s/2s (Slow) work/rest schedules while supine with the arm positioned above or below the heart. RESULTS: Brachial artery diameter of the active arm was reduced 5% at approximately 10 s following the onset of exercise performed above the heart (P < 0.05), irrespective of work rate, and returned to rest levels by 30 s with no concurrent changes in arterial pressure. By 2 min of the Fast contraction rate exercise, brachial artery diameter of the active arm was greater than rest (P < 0.05) irrespective of arm position. Brachial artery dimensions in the contralateral inactive arm were not altered during exercise (P > 0.05). Compared with rest, MBV and forearm blood flow at 5 s of exercise were increased in the active arm but were reduced transiently in the inactive limb (P < 0.05). CONCLUSIONS: Conduit artery responses to exercise were dependent upon the work rate and arm position. The delayed dilation in the heavier exercise, independent of arm position, suggests that stimuli related to the metabolic activity of the distal active skeletal muscle may influence the dimensions of the conduit artery.

Adult↗

PubMed1997

Failure of manual massage to alter limb blood flow: measures by Doppler ultrasound.

The ability of manual massage to alter muscle blood flow through three types of massage treatments in a small (forearm) and a large (quadriceps) muscle mass was tested in 10 healthy individuals. A certified massage therapist administered effleurage, petrissage, and tapotement treatments to the forearm flexors (small muscle mass) and quadriceps (large muscle mass) muscle groups in a counterbalanced manner. Limb blood flow was determined from mean blood velocity (MBV) (pulsed Doppler) and vessel diameter (echo Doppler). MBV values were obtained from the continuous data sets prior to treatment, and at 5, 10, and 20 s and 5 min following the onset of massage. Arterial diameters were measured immediately prior to and following the massage treatments; these values were not different and were averaged for the blood flow calculations. The MBV (e.g., 5.77 +/- 0.4 and 9.73 +/- 0.7 cm.s-1) and blood flows (39.1 +/- 6.4 and 371 +/- 30 ml.min-1) for brachial and femoral arteries, respectively, were not altered by any of the massage treatments in either the forearm or quadriceps muscle groups (P > 0.05). Mild voluntary handgrip (approximately 35% maximal voluntary isometric contraction) and knee extension (15 cm) contractions resulted in peak blood velocities (15.2 +/- 1.2 and 28.1 +/- 3.1 cm.s-1) and blood flow (126 +/- 19 and 1087 +/- 144 ml.min-1) for brachial and femoral arteries, respectively, which were significantly elevated from rest (P < 0.05). The results indicate that manual massage does not elevate muscle blood flow irrespective of massage type or the muscle mass receiving the treatment. Further, the results indicate that if an elevated muscle blood flow is the desired therapeutic effect, then light exercise would be beneficial whereas massage would not.

Adult↗

PubMed1997

Contributions of acetylcholine and nitric oxide to forearm blood flow at exercise onset and recovery.

The contributions of acetylcholine and/or nitric oxide (NO) to the rapid changes in human forearm blood flow (FBF) at the onset and recovery from mild exercise were studied in eight subjects. Rhythmic handgrip contractions were performed during brachial artery infusions of saline (2 ml/min; control), atropine (0.2 mg over 3 min), to block acetylcholine binding to muscarinic receptors, or atropine + NG-monomethyl-L-arginine (L-NMMA; 4 mg/min for 4 min), to additionally inhibit NO synthase. Brachial artery mean blood velocity (MBV; pulsed Doppler ultrasound) and diameter (echo Doppler) were measured continuously, and FBF was calculated. Atropine reduced acetylcholine-induced increases in FBF by approximately 71% (P < 0.05). FBF at rest was reduced by atropine and further reduced with atropine + L-NMMA. Both drug conditions reduced FBF during exercise by approximately 10% compared with control, with no difference between drug treatments. Brachial artery diameter was unchanged from rest by exercise, recovery, and drug treatments. Neither drug treatment altered the rate or magnitude of the increase in FBF above rest. Peak FBF after exercise was reduced by atropine and atropine + L-NMMA. Total FBF during 5 min of recovery was reduced with atropine + L-NMMA compared with control and atropine. The results suggest that 1) acetylcholine and NO mechanisms additively contribute to FBF levels at rest, 2) a cholinergic mechanism adjusts the absolute FBF levels during exercise, 3) neither acetylcholine nor NO is essential to observe the normal time course or magnitude of the exercise response, and 4) NO contributes to the FBF response during recovery from exercise.

Acetylcholine↗

PubMed1997

Augmented sympathetic tone alters muscle metabolism with exercise: lack of evidence for functional sympatholysis.

It is unclear whether sympathetic tone opposes dilator influences in exercising skeletal muscle. We examined high levels of sympathetic tone, evoked by lower body negative pressure (LBNP, -60 mmHg) on intramuscular pH and phosphocreatine (PCr) levels (31P-nuclear magnetic resonance spectroscopy) during graded rhythmic handgrip (30 contractions/min; approximately 17, 34, 52 and 69% maximal voluntary contraction). Exercise was performed with LBNP and without LBNP (Control). At the end of exercise, LBNP caused lower levels of muscle pH (6.59 +/- 0.09) compared with Control (6.78 +/- 0.05; P < 0.05). PCr recovery, an index of mitochondrial respiration, was less during the recovery phase of the LBNP trial. Exercise mean arterial pressure was not altered by LBNP. The protocols were repeated with measurements of forearm blood flow velocity and deep venous samples (active forearm) of hemoglobin (Hb) saturation, pH, and lactate. With LBNP, mean blood velocity was reduced at rest, during exercise, and during recovery compared with Control (P < 0.05). Also, venous Hb saturation and pH levels during exercise and recovery were lower with LBNP and lactate was higher compared with Control (P < 0.05). We conclude that LBNP enhanced sympathetic tone and reduced oxygen transport. At high workloads, there was a greater reliance on nonoxidative metabolism. In other words, sympatholysis did not occur.

Adult↗

PubMed1997

Alveolar oxygen uptake and blood flow dynamics in knee extension ergometry.

The relationship was studied between the increase in oxygen uptake (VO2) measured breath-by-breath at the mouth, and the increase in femoral artery blood flow measured continuously with pulsed and echo Doppler methods. Five men exercised at 50 W on a knee extension ergometer in both the supine and the upright posture. The kinetics of the responses were determined by curve fitting to obtain the mean response time (MRT = 63% of the time required to achieve steady state). In the upright position, the increase in blood flow (MRT = 12.4 +/- 9.4 s, mean +/- SD) was faster than the increase in VO2 (29.6 +/- 9.3 s). Likewise in the supine position, blood flow increased more rapidly (25.1 +/- 9.7 s vs. 36.7 +/- 9.6 s). It should be noted that the increase in blood flow appeared to be faster than VO2, yet when blood flow adapted more slowly in the supine posture, it had an impact on the adaptation of VO2. This suggests that blood flow might have important effects on metabolism at the onset of submaximal exercise.

Blood Flow Velocity↗