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ABSTRACT: We investigated the hypothesis that acute pharmacological inhibition of neuronal nitric oxide (NO) synthase(nNOS)would augment sympathetic vasoconstriction in resting and contracting skeletal muscle. Sprague-Dawley rats (n=13) were anesthetized and instrumented with an indwelling brachial artery catheter, femoral artery flow probe and lumbar sympathetic chain stimulating electrodes. Triceps surae muscles were stimulated to contract at 60% of maximal contractile force (MCF). in Series 1 (n=9), the percentage change of femoral vascular conductance (%FVC) in response to sympathetic stimulations delivered at 2 and 5Hz was determined at rest and during muscle contraction before and after selective nNOS blockade with S-methyl-L-thiocitrulline (SMTC, 0.6mg.kg-1, IV) and subsequent non-selective NOS blockade with L-NAME (5mg.kg-1, IV). In Series 2 (n=4), L-NAME was injected first, followed by SMTC to determine if the effect of L-NAME on constrictor response was influenced by selective nNOS inhibition. Sympathetic stimulation decreased FVC at rest (2Hz: -25±7%FVC; 5Hz: -44±8%FVC) and during contraction (2Hz: -7±3%FVC; 5Hz: -19±5%FVC). The decrease in FVC in response to sympathetic stimulation was greater in the presence of SMTC at rest (2Hz: -32±6%FVC; 5Hz: -49±8%FVC) and during contraction (2Hz: -21±4%FVC; 5Hz: -28±4%FVC). L NAME further increased (p<0.05) sympathetic vasoconstriction at rest (2Hz; -47±4%FVC; 5Hz: -60±6%FVC) and during contraction (2Hz: -33±3%FVC; 5Hz: -40±6%FVC). The effect of L-NAME was not altered by the order of nNOS inhibition. These data demonstrate that NO derived from nNOS and eNOS contribute to the inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle.
Journal of Applied Physiology 05/2013; · 3.75 Impact Factor
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ABSTRACT: We hypothesized that acute superoxide (O2(-)) scavenging would attenuate sympathetic vasoconstrictor responsiveness by augmenting nitric oxide (NO)- mediated inhibition of sympathetic vasoconstriction in exercise trained rats. Sprague-Dawley rats were randomly assigned to sedentary time-control (S; n=7), mild-(M: 20m⋅min(-1) 5grade; n=7) or heavy-intensity (H: 40m⋅min(-1) 5grade; n=7) exercise training (ET) groups and trained 5 days⋅week-1 for 4 weeks with matched training volume. Following ET, rats were anesthetised and instrumented for lumbar sympathetic chain stimulation and measurement of femoral vascular conductance (FVC). in resting skeletal muscle, the percentage change of FVC in response to continuous (2Hz) and patterned (20 and 40Hz) sympathetic stimulation was determined during control conditions, O2(-) scavenging (TIRON, 1 g⋅kg(-1)⋅h(-1) IV) and combined O2(-) scavenging + NO synthase blockade (L-NAME, 5mg⋅kg(-1) IV). ET augmented the vasoconstrictor response to sympathetic stimulation in a training intensity-dependent manner (p<0.05) (S: 2Hz: -26.0±7.1%; 20Hz: -26.9±7.3%; 40Hz: -27.7±7.0%; M: 2Hz: -37.4±8.3%; 20Hz: -35.9±7.4%; 40Hz: -38.2±9.4%; H: 2Hz: -46.9±7.8%; 20Hz: -48.5±7.2%; 40Hz: -51.2±7.3%). O2(-) scavenging did not alter (p>0.05) the vasoconstrictor response in S rats (S: 2Hz: -23.9±7.6%; 20Hz: -26.1±9.1%; 40Hz: -27.5±7.2%) whereas, the response in ET rats was diminished (M: 2Hz: -26.3±5.1%; 20Hz: -28.7±5.3%; 40Hz: -28.5±5.6%; H: 2Hz: -35.5±10.3%; 20Hz: -38.6±6.8%; 40Hz: -43.9±5.9%, p<0.05). TIRON + L-NAME increased vasoconstrictor responsiveness (p<0.05) in ET rats (M: 2Hz: -47.7±9.8%; 20Hz: -41.2±7.2%; 40Hz: -50.5±7.9%; H: 2Hz: -55.8±7.6%; 20Hz: -55.7±7.8%; 40Hz: -58.7±6.2%) whereas, in S rats the response was unchanged (2Hz: -29.4±8.7%; 20Hz: -30.0±7.4%; 40Hz: -35.2±10.3%; p>0.05). These data indicate that the augmented sympathetic vasoconstrictor responsiveness in ET rats was related to increased oxidative stress and altered NO-mediated inhibition of vasoconstriction.
Journal of Applied Physiology 04/2013; · 3.75 Impact Factor
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ABSTRACT: We tested the hypothesis that short-term mild- (M) and heavy-intensity (H) exercise training (ET) would enhance sympatholysis through a nitric oxide (NO)-dependent mechanism. Sprague-dawley rats (n=36) were randomly assigned to a sedentary (S), or M (20m·min(-1) 5% grade) or H (40m·min(-1) 5% grade) intensity exercise trained groups. Rats assigned to M and H groups trained 5d·week(-1) for 4 weeks with the volume of training matched between groups. Rats were anesthetised and instrumented for stimulation of the lumbar sympathetic chain and the measurement of arterial blood pressure and femoral artery blood flow. The triceps surae muscle group was stimulated to contract rhythmically at 30% and 60% of maximal contractile force (MCF). The percent change of femoral vascular conductance (%FVC) in response to sympathetic stimulation delivered at 2 and 5Hz was determined at rest and during contraction at 30% and 60% MCF. The vascular response to sympathetic stimulation was reduced as a function of MCF in all rats (p<0.05). At 30% MCF, the magnitude of sympatholysis (%FVC rest - contraction, Δ%FVC) was greater in H compared to M and S (2Hz: S: 9±5, M: 11±8, H: 18±7; 5Hz: S: 6±6, M: 12±9, H: 18±7 Δ%FVC, p<0.05) and was greater in H and M compared to S at 60% MCF (2Hz: S: 15±5; M: 25±3; H: 36±6; 5Hz: S: 22±6; M: 33±9; H: 39±9 Δ%FVC, p<0.05). NOS blockade did not alter the magnitude of sympatholysis in S during contraction at 30 or 60% MCF. In contrast, NOS inhibition diminished sympatholysis in H at 30% MCF and M and H at 60% MCF (p<0.05). The present findings indicate that short-term exercise training augments sympatholysis in a training intensity dependent manner and through an NO dependent mechanism.
The Journal of Physiology 01/2013; · 4.72 Impact Factor
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ABSTRACT: We tested the hypotheses that 4 wk of exercise training would diminish the magnitude of vasoconstriction in response to sympathetic nerve stimulation and augment endothelium-dependent vasodilation (EDD) in resting skeletal muscle in a training intensity-dependent manner. Sprague-Dawley rats were randomly assigned to sedentary time-control (S), mild- (M; 20 m/min, 5% grade), or heavy-intensity (H; 40 m/min, 5% grade) treadmill exercise groups. Animals trained 5 days/wk for 4 wk with training volume matched between groups. Rats were anesthetized and instrumented for study 24 h after the last training session. Arterial pressure and femoral artery blood flow were measured, and femoral vascular conductance (FVC) was calculated. Lumbar sympathetic chain stimulation was delivered continuously at 2 Hz and in patterns at 20 and 40 Hz. EDD was assessed by the vascular response to intra-arterial bolus injections of ACh. The response (% change FVC) to sympathetic stimulation increased (P < 0.05) in a training intensity-dependent manner at 2 Hz (S: -20.2 ± 9.8%, M: -34.0 ± 6.7%, and H: -44.9 ± 2.0%), 20 Hz (S: -22.0 ± 10.6%, M: -31.2 ± 8.4%, and H: -42.8 ± 5.9%), and 40 Hz (S: H -24.5 ± 8.5%, M: -35.1 ± 8.9%, H: -44.9 ± 6.5%). The magnitude of EDD also increased in a training intensity-dependent manner (P < 0.05). These data demonstrate that short-term exercise training augments the magnitude of vasoconstriction in response to sympathetic stimulation and EDD in resting skeletal muscle in a training intensity-dependent manner.
AJP Regulatory Integrative and Comparative Physiology 06/2012; 303(3):R332-9. · 3.34 Impact Factor
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ABSTRACT: We tested the hypothesis that adrenergic and nonadrenergic receptor responsiveness and protein expression would be altered with advancing age. Young (n = 6; 22 ± 1 mo; mean ± SE) and old (n = 6; 118 ± 9 mo) beagles were instrumented with flow probes and an indwelling catheter for continuous measurement of external iliac blood flow and arterial blood pressure. Vascular conductance (VC) was calculated as hindlimb blood flow/mean arterial pressure. Selective agonists for α-1, α-2, neuropeptide-Y (NPY), and purinergic (P2X) receptors were infused at rest and during treadmill running at moderate (2.5 mph) and heavy (4 mph with 2.5% grade) exercise intensities. Feed arteries were dissected from gracilis muscles, and α-1D, α-1B, α-2A, P2X-4, P2X-1, and NPY-Y1 receptor protein expression was determined. Phenylephrine produced similar decreases (P > 0.05) in VC in young and old beagles at rest (young: -62 ± 5%; old: -59 ± 5%) and during moderate (young: -67 ± 5%; old: -62 ± 4%) and heavy (young: -54 ± 4%; old: -49 ± 3%) exercise. Clonidine caused similar (P > 0.05) decreases in VC in old compared with young dogs at rest (young: -59 ± 8%; old: -70 ± 6%) and during moderate (young: -52 ± 6%; old: -47 ± 5%)- and heavy (young: -42 ± 5%; old: -43 ± 5%)-intensity exercise. NPY infusion resulted in a similar decline in VC in young and old beagles at rest (young: -40 ± 7%; old: -39 ± 9%) and during moderate (young: -47 ± 6%; old: -40 ± 6%)- and heavy (young: -40 ± 3%; old: -38 ± 4%)-intensity exercise. α-β-Methylene-ATP also produced similar decreases in VC in young and old beagles at rest (young: -36 ± 6%; old: -40 ± 8%) and during exercise at moderate (young: -42 ± 5%; old: -40 ± 9%) and heavy (young: -47 ± 5%; old: -42 ± 8%) intensities. α-1B receptor protein expression was elevated (P < 0.05) in old compared with young dogs, whereas there were no age-related differences in α-1D or α-2A receptor expression and nonadrenergic P2X-4, P2X-1, and NPY-Y1 receptor expression. The present findings indicate that postsynaptic adrenergic and nonadrenergic receptor responsiveness was not altered by advancing age. Moreover, the expression of adrenergic and nonadrenergic receptors in skeletal-muscle feed arteries was largely unaffected by aging.
Journal of Applied Physiology 12/2011; 112(5):841-8. · 3.75 Impact Factor
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ABSTRACT: Non-interval and interval training progressions were used to determine (i) the mean rate at which treadmill speed could be incremented daily using a non-interval training progression to train rats to run continuously at different intensities and (ii) the number of training days required for rats to run continuously at different exercise intensities with non-interval- and interval-based training progressions to establish methods of progressive overload for rodent exercise training studies. Rats were randomly assigned to mild-intensity (n = 5, 20 m·min(-1), 5% grade), moderate-intensity (n = 5, 30 m·min(-1), 5% grade), and heavy-intensity non-interval groups (n = 5, 40 m·min(-1), 5% grade) or a heavy-intensity interval (n = 5, 40 m·min(-1), 5% grade) group and ran 5 days·week(-1) for 6 weeks. Non-interval training involved a daily increase of treadmill speed, whereas interval training involved a daily increase of interval time, until the animal could run continuously at a prescribed intensity. In mild-, moderate-, and heavy-intensity non-interval-trained rats, treadmill speed was increased by 0.6 ± 0.7 m·min(-1)·day(-1), 0.6 ± 0.2 m·min(-1)·day(-1), and 0.8 ± 0.1 m·min(-1)·day(-1), respectively. Target training intensity and duration were obtained following 0.4 ± 0.5 days, 17 ± 3 days, and 23 ± 3 training days (p < 0.05) in mild-, moderate-, and heavy-intensity groups, respectively. In contrast, interval-trained rodents required 11 ± 1 training days. These data demonstrate that rodents will tolerate an increase in treadmill speed of ∼0.7 ± 0.1 m·min(-1)·day(-1) and that this progression enables rats to run continuously at moderate and heavy intensities with 3-4 weeks of progressive overload. Interval training significantly reduces the number of training days required to attain a target intensity.
Applied Physiology Nutrition and Metabolism 10/2011; 36(5):723-9. · 2.13 Impact Factor
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ABSTRACT: The relationship between the adjustment of muscle deoxygenation (Δ[HHb]) and phase II V(O(2p)) during moderate-intensity exercise was examined before (Mod 1) and after (Mod 2) a bout of heavy-intensity "priming" exercise. Moderate intensity V(O(2p)) and Δ[HHb] kinetics were determined in 18 young males (26 ± 3 yr). V(O(2p)) was measured breath-by-breath. Changes in Δ[HHb] of the vastus lateralis muscle were measured by near-infrared spectroscopy. V(O(2p)) and Δ[HHb] response profiles were fit using a monoexponential model, and scaled to a relative % of the response (0-100%). The Δ[HHb]/Vo(2) ratio for each individual (reflecting the local matching of O(2) delivery to O(2) utilization) was calculated as the average Δ[HHb]/Vo(2) response from 20 s to 120 s during the exercise on-transient. Phase II τV(O(2p)) was reduced in Mod 2 compared with Mod 1 (P < 0.05). The effective τ'Δ[HHb] remained the same in Mod 1 and Mod 2 (P > 0.05). During Mod 1, there was an "overshoot" in the Δ[HHb]/Vo(2) ratio (1.08; P < 0.05) that was not present during Mod 2 (1.01; P > 0.05). There was a positive correlation between the reduction in the Δ[HHb]/Vo(2) ratio and the smaller τV(O(2p)) from Mod 1 to Mod 2 (r = 0.78; P < 0.05). This study showed that a smaller τV(O(2p)) during a moderate bout of exercise subsequent to a heavy-intensity priming exercise was associated with improved microvascular O(2) delivery during the on-transient of exercise, as suggested by a smaller Δ[HHb]/Vo(2) ratio.
Journal of Applied Physiology 08/2011; 111(5):1410-5. · 3.75 Impact Factor
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ABSTRACT: The ventricular response to passive heat stress has predominantly been studied in the supine position. It is presently unclear how acute changes in venous return influence ventricular function during heat stress. To address this question, left ventricular (LV) systolic and diastolic function were studied in 17 healthy men (24.3 ± 4.0 yr; mean ± SD), using two-dimensional transthoracic echocardiography with Doppler ultrasound, during tilt-table positioning (supine, 30° head-up tilt, and 30° head-down tilt), under normothermic and passive heat stress (core temperature 0.8 ± 0.1°C above baseline) conditions. The supine heat stress LV volumetric and functional response was consistent with previous reports. Combining head-up tilt with heat stress reduced end-diastolic (25.2 ± 4.1%) and end-systolic (65.4 ± 10.5%) volume from baseline, whereas heart rate (37.7 ± 2.0%), ejection fraction (9.4 ± 2.4%), and LV elastance (37.7 ± 3.6%) increased, and stroke volume (-28.6 ± 9.4%) and early diastolic inflow (-17.5 ± 6.5%) and annular tissue (-35.6 ± 7.0%) velocities were reduced. Combining head-down tilt with heat stress restored end-diastolic volume, whereas LV elastance (16.8 ± 3.2%), ejection fraction (7.2 ± 2.1%), and systolic annular tissue velocities (22.4 ± 5.0%) remained elevated above baseline, and end-systolic volume was reduced (-15.3 ± 3.9%). Stroke volume and the early and late diastolic inflow and annular tissue velocities were unchanged from baseline. This investigation extends previous work by demonstrating increased LV systolic function with heat stress, under varied levels of venous return, and highlights the preload dependency of early diastolic function during passive heat stress.
AJP Heart and Circulatory Physiology 05/2011; 301(2):H599-608. · 3.71 Impact Factor
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ABSTRACT: The adjustments of pulmonary oxygen uptake V O2p limb blood flow (LBF) and muscle deoxygenation (ΔHHb) were examined during transitions to moderate-intensity, knee-extension exercise in seven older (OA; 71 ± 7 year) and seven young (YA; 26 ± 3 year) men. YA and OA performed repeated step transitions from an active baseline (3 W; 100 g) to a similar relative intensity of ~80% estimated lactate threshold (θ(L)), and YA also performed the same absolute work rate as the OA (24 W, 800 g). Breath-by-breath V O2p femoral artery LBF (Doppler ultrasound) and muscle HHb (near-infrared spectroscopy) were measured. Phase 2V O2p LBF, and ΔHHb data were fit with a mono-exponential model. τ V O2p was greater in OA (58 ± 21 s) than YA(80%) (31 ± 9 s) and YA(24W) (29 ± 11 s). The increase in LBF per increase in V O2p was not different between groups (5.3-5.8 L min(-1)/L min(-1)); however, the τLBF was greater in OA (44 ± 19 s) than YA(24W) (18 ± 7 s). The overall adjustment in ΔHHb (τ'ΔHHb) was not different between OA and YA, but was faster than τ V O2p in OA. This faster τ'ΔHHb than τ V O2p resulted in an "overshoot" of the normalized ΔHHb/Δ V O2p response relative to the steady state level that was significantly greater in OA compared with YA suggesting that the adjustment of microvascular blood flow is slowed in OA thereby requiring a greater reliance on O(2) extraction during the transition to exercise.
Arbeitsphysiologie 11/2010; 110(4):739-51. · 2.15 Impact Factor
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ABSTRACT: We examined biventricular function during passive heat stress in endurance trained (ET) and untrained (UT) men to evaluate whether aerobic fitness alters the volumetric response. Body temperature was elevated ~0.8°C above baseline in 20 healthy men (10 ET, 64.4 ± 3.0 ml·kg(-1)·min(-1); and 10 UT, 46.3 ± 6.2 ml·kg(-1)·min(-1)) by circulating warm water (50°C) throughout a tube-lined suit. Cardiac magnetic resonance imaging was used to measure biventricular volumes, function, filling velocities, volumetric flow rates, and left ventricular (LV) twist and circumferential strain at baseline (BL) and after 45 min of heat stress. In both groups, passive heat stress reduced biventricular end-diastolic (ET, -19.5 ± 24.0 ml; UT, -25.1 ± 23.8 ml) and end-systolic (ET, -15.9 ± 8.8 ml; UT, -17.6 ± 7.9 ml) volumes and left atrial volume (ET, -19.2 ± 11.6 ml; UT, -15.0 ± 12.7 ml) and significantly increased heart rate (ET, 29.3 ± 9.0 beats/min; UT, 31.7 ± 10.4 beats/min) and cardiac output (ET, 3.8 ± 2.2 l/min; UT, 3.2 ± 1.4 l/min) similarly, while biventricular stroke volume was unchanged. There were no between-group differences in any parameter. Heat stress increased (P < 0.05), as a percentage of baseline values, biventricular ejection fraction (ET, 3.4 ± 5.3%; UT, 4.4 ± 3.7%), annular systolic tissue velocities (ET, 32.5 ± 34.9%; UT, 44.0 ± 38.1%), and peak LV twist (ET, 51.6 ± 59.7%; UT, 59.7 ± 54.2%) and untwisting rates (ET, 45.5 ± 42.3%; UT, 51.8 ± 55.0%) similarly in both groups. Early LV diastolic tissue and blood velocities, volumetric flow rates, and strain rates (diastole) were unchanged with heat stress in both groups. The present findings indicate that aerobic fitness does not influence the biventricular response to passive heat stress.
Journal of Applied Physiology 11/2010; 109(5):1545-51. · 3.75 Impact Factor
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ABSTRACT: Left ventricular (LV) systolic function increases with passive heat stress (HS); however, less is known about diastolic function. Eight healthy subjects (24.0 +/- 2.0 yr of age) underwent whole body passive heating approximately 1 degrees C above baseline (BL). Cardiac magnetic resonance imaging was used to measure biventricular volumes, function, filling velocities, volumetric flow rates, and LV twist and strain at BL and after 45 min of HS. Passive heating reduced left atrial volume (-17.6 +/- 11.7 ml, P < 0.05), right and LV end-diastolic volumes (-22.7 +/- 11.0 and -25.7 +/- 24.9 ml, respectively; P < 0.05), and LV stroke volume (-6.7 +/- 6.8 ml, P < 0.05) from BL. LV ejection fraction (EF), end-systolic elastance, septal and lateral mitral annular systolic velocities, circumferential strain, and peak LV twist increased with HS (P < 0.05). Right ventricular stroke volume, EF, and systolic tissue velocities were unchanged with HS (P > 0.05). Early LV diastolic tissue and blood velocities and strain rates were maintained with HS, whereas untwisting rate increased significantly from 166.4 +/- 46.9 to 268.7 +/- 76.8 degrees /s (P < 0.05). The major novel finding of this study was that, secondary to an increase in peak LV twist and untwisting rate, early diastolic blood and tissue velocities and strain rates are maintained despite a reduction in filling pressure.
AJP Heart and Circulatory Physiology 03/2010; 298(3):H930-7. · 3.71 Impact Factor
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ABSTRACT: Although obesity significantly reduces end-expiratory lung volume (EELV), the relationship between EELV and detailed measures of fat distribution has not been studied in obese men and women. To investigate, EELV and chest wall fat distribution (ie, rib cage, anterior subcutaneous abdominal fat, posterior subcutaneous fat, and visceral fat) were measured in lean men and women (ie, < 25% body fat) and obese men and women (ie, > 30% body fat).
All subjects underwent pulmonary function testing, hydrostatic weighing, and MRI scans. Data were analyzed for the men and women separately by independent t test, and the relationships between variables were determined by regression analysis.
All body composition measurements were significantly different among the lean and obese men and women (p < 0.001). However, with only a few exceptions, fat distribution was similar among the lean and obese men and women (p > 0.05). The mean EELV was significantly lower in the obese men (39 +/- 6% vs 46 +/- 4% total lung capacity [TLC], respectively; p < 0.0005) and women (40 +/- 4% vs 53 +/- 4% TLC, respectively; p < 0.0001) compared with lean control subjects. Many estimates of body fat were significantly correlated with EELV for both men and women.
In both men and women, the decrease in EELV with obesity appears to be related to the cumulative effect of increased chest wall fat rather than to any specific regional chest wall fat distribution. Also, with only a few exceptions, relative fat distribution is markedly similar between lean and obese subjects.
Chest 10/2008; 134(4):704-11. · 5.25 Impact Factor
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ABSTRACT: At the onset of exercise, an increase in muscle and pulmonary O2 consumption is met by increases in muscle O2 delivery and muscle O2 extraction. Thus, the study of pulmonary O2 uptake kinetics reflects the integrated response between the convective and diffusive O2 delivery systems and the muscle metabolic machinery (i.e., mitochondrial enzyme activation and provision of acetyl groups to the tricarboxcylic acid cycle) to increase muscle O2 consumption. Pulmonary O2 uptake kinetics are slowed in older adults compared with young adults and previous studies suggest that the slower O2 uptake kinetics may be the result of an age-associated decline in the ability of older adults to increase O2 delivery to active muscles. However, an inherent limitation to understanding the control of and limitations to pulmonary O2 uptake kinetics is that it is methodologically difficult to examine the adaptation of muscle perfusion and O2 delivery and muscle O2 utilization in the muscle microcirculation of active muscles in the dynamically exercising human. In this review, we provide an overview of the effect of ageing on pulmonary O2 uptake kinetics (reflecting the activation of muscle O2 consumption) during the transition to moderate-intensity exercise. Age-related changes in O2 delivery systems and muscle oxidative capacity are examined as potential limitations to pulmonary O2 uptake kinetics. We then review recent studies from our laboratory that have investigated the control of pulmonary O2 uptake kinetics at the level of the muscle microcirculation by examining the adaptation of muscle O2 delivery and muscle O2 utilization using near-infrared spectroscopy during the transition to exercise in healthy young and older adults.
Applied Physiology Nutrition and Metabolism 01/2008; 32(6):1251-62. · 2.13 Impact Factor
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Experimental Physiology 10/2007; 92(5):971. · 3.21 Impact Factor
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ABSTRACT: The effect of prior exercise on pulmonary O(2) uptake (Vo(2)(p)), leg blood flow (LBF), and muscle deoxygenation at the onset of heavy-intensity alternate-leg knee-extension (KE) exercise was examined. Seven subjects [27 (5) yr; mean (SD)] performed step transitions (n = 3; 8 min) from passive KE following no warm-up (HVY 1) and heavy-intensity (Delta50%, 8 min; HVY 2) KE exercise. Vo(2)(p) was measured breath-by-breath; LBF was measured by Doppler ultrasound at the femoral artery; and oxy (O(2)Hb)-, deoxy (HHb)-, and total (Hb(tot)) hemoglobin/myoglobin of the vastus lateralis muscle were measured continuously by near-infrared spectroscopy (NIRS; Hamamatsu NIRO-300). Phase 2 Vo(2)(p), LBF, and HHb data were fit with a monoexponential model. The time delay (TD) from exercise onset to an increase in HHb was also determined and an HHb effective time constant (HHb - MRT = TD + tau) was calculated. Prior heavy-intensity exercise resulted in a speeding (P < 0.05) of phase 2 Vo(2)(p) kinetics [HVY 1: 42 s (6); HVY 2: 37 s (8)], with no change in the phase 2 amplitude [HVY 1: 1.43 l/min (0.21); HVY 2: 1.48 l/min (0.21)] or amplitude of the Vo(2)(p) slow component [HVY 1: 0.18 l/min (0.08); HVY 2: 0.18 l/min (0.09)]. O(2)Hb and Hb(tot) were elevated throughout the on-transient following prior heavy-intensity exercise. The tauLBF [HVY 1: 39 s (7); HVY 2: 47 s (21); P = 0.48] and HHb-MRT [HVY 1: 23 s (4); HVY 2: 21 s (7); P = 0.63] were unaffected by prior exercise. However, the increase in HHb [HVY 1: 21 microM (10); HVY 2: 25 microM (10); P < 0.001] and the HHb-to-Vo(2)(p) ratio [(HHb/Vo(2)(p)) HVY 1: 14 microM x l(-1) x min(-1) (6); HVY 2: 17 microM x l(-1) x min(-1) (5); P < 0.05] were greater following prior heavy-intensity exercise. These results suggest that the speeding of phase 2 tauVo(2)(p) was the result of both elevated local O(2) availability and greater O(2) extraction evidenced by the greater HHb amplitude and HHb/Vo(2)(p) ratio following prior heavy-intensity exercise.
Journal of Applied Physiology 09/2007; 103(3):771-8. · 3.75 Impact Factor
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ABSTRACT: Our laboratory has previously reported a decline in sympathetic nervous system restraint of skeletal muscle blood flow during prolonged mild-intensity exercise. This decline may be explained by a decrease in alpha(1)- and alpha(2)-adrenergic receptor responsiveness over time. Thus the purpose of the present study was to investigate the effect of exercise duration on alpha(1)- and alpha(2)-adrenergic receptor responsiveness during prolonged constant-load exercise. Mongrel dogs (n = 6) were instrumented chronically with transit-time flow probes on the external iliac arteries and an indwelling catheter in a branch of the femoral artery. On separate days, flow-adjusted doses of selective alpha(1)- (phenylephrine) alpha(2)-adrenergic-receptor (clonidine) agonists, and tyramine (to evoke endogenous norepinephrine release) were infused following 5, 30 and 50 min of mild-intensity treadmill exercise (3 miles/h), with hindlimb blood flow (HBF) and mean arterial pressure (MAP) monitored continuously. Vascular conductance (VC) was calculated as HBF/MAP. While the dogs ran on the treadmill at 3 miles/h, infusion of phenylephrine resulted in similar decreases in VC after 5 [73% (SD 10)], 30 [76% (SD 9)], and 50 [73% (SD 10)] min of exercise. Infusion of the alpha(2)-agonist clonidine also produced similar decreases in VC after 5 [58% (SD 10)], 30 [58% (SD 11)], and 50 [53% (SD 12)] min of exercise. Infusion of tyramine resulted in similar decreases in VC after 5 [55% (SD 15)], 30 [51% (SD 10)], and 50 [50% (SD 7)] min of exercise. These results demonstrate that alpha(1)- and alpha(2)-adrenergic receptor responsiveness to infusion of selective alpha(1)- and alpha(2)-adrenergic-receptor agonists and endogenous norepinephrine release (tyramine) does not decline during prolonged mild-intensity exercise. Thus a decrease in alpha-adrenergic receptor responsiveness over time does not appear to be responsible for the decrease in sympathetic restraint of muscle blood flow during prolonged exercise.
AJP Heart and Circulatory Physiology 02/2007; 292(1):H392-8. · 3.71 Impact Factor
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ABSTRACT: Eight men were exposed to progressive isocapnic hypoxia for 10 min to test the hypothesis that (i) cerebral and muscle tissue would follow similar deoxygenation profiles during an acute hypoxic ventilatory response (AHVR) test; and (ii) strong cerebrovascular responsiveness to hypoxia would be related to attenuated cerebral deoxygenation. End-tidal O(2) concentration was reduced from normoxia (approximately 102 mmHg) to approximately 45 mmHg while arterial oxygen saturation (SpO2 %) declined from 98+/-1% to 77+/-7% (P<0.001). Near-infrared spectroscopy (NIRS)-derived local cerebral tissue (frontal lobe) deoxyhemoglobin increased 5.55+/-2.22 microM, while oxyhemoglobin and tissue oxygenation index decreased 2.57+/-1.99 microM and 6.2+/-3.4%, respectively (all P<0.001). In muscle (m. vastus lateralis) the NIRS changes from the initial normoxic level were non-significant. Cerebral blood velocity (V(mean), transcranial Doppler) in the middle cerebral artery increased from 53.4+/-10.4 to 60.6+/-11.6 cms(-1) (P<0.001). In relation to the decline in SpO2 % the mean rate of increase of V(mean) and AHVR were 0.33+/-0.19 cms(-1)%(-1) and 0.52+/-0.20l min(-1)%(-1), respectively. We conclude that cerebral, but not muscle, tissue shows changes reflecting a greater deoxygenation during acute hypoxia. However, the changes in NIRS parameters were not related to cerebrovascular responsiveness or ventilatory chemosensitivity during graded hypoxia.
Respiratory Physiology & Neurobiology 02/2007; 155(1):71-81. · 2.24 Impact Factor
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ABSTRACT: Sympathetic nerves fire in bursts followed by brief periods of quiescence. Periods of quiescence may be a valuable part of coding for different neurotransmitters. We compared adrenergic- and non-adrenergic-mediated vasoconstriction with repeating burst patterns versus constant frequency stimulation. Seventeen rats were killed, and the femoral arteries dissected out and mounted in organ tissue baths at 37 degrees C and pH 7.4. Field stimulation was applied to artery rings from five rats at constant frequencies of 2-6 Hz for 144 impulses. In 12 rats, artery rings were stimulated with two burst pattern protocols consisting of repeating pairs, triplets, quadruplets or sextuplets performed using either 8 or 30 Hz as the instantaneous frequency for a total of 144 impulses. All protocols were repeated with the P2 purinergic antagonist pyridoxal-phosphate-6-azophenyl-2'4'-disulphonic acid (PPADs; 0.42 m) or the alpha(1)-antagonist prazosin (1.59 microM). Tension was decreased by the addition of the P2 antagonist PPADs (P < 0.05). Prazosin abolished tension at all constant frequencies (P < 0.05). P2 and alpha(1)-antagonism decreased tension with 8 and 30 Hz burst pattern field stimulation. However, the magnitude of decrease in tension with prazosin was less with burst patterns compared to the same average constant frequencies (P < 0.05). It appears that P2X receptors and alpha(1)-receptors in the femoral artery are sensitive to frequency and patterns of electrical stimulation.
Experimental Physiology 12/2006; 91(6):1051-8. · 3.21 Impact Factor
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ABSTRACT: Sympathetic nervous system restraint of skeletal muscle blood flow during dynamic exercise has been well documented. However, whether sympathetic restraint of muscle blood flow persists and is constant throughout prolonged exercise has not been established. We hypothesized that both alpha1- and alpha2-adrenergic receptors would restrain skeletal muscle blood flow throughout prolonged constant-load exercise and that the restraint would increase as a function of exercise duration. Mongrel dogs were instrumented chronically with transit-time flow probes on the external iliac arteries and an indwelling catheter in a branch of the femoral artery. Flow-adjusted doses of selective alpha1- (prazosin) and alpha2-adrenergic receptor (rauwolscine) antagonists were infused after 5, 30, and 50 min of treadmill exercise at 3 and 6 miles/h. During mild-intensity exercise (3 miles/h), prazosin infusion resulted in a greater (P < 0.05) increase in vascular conductance (VC) after 5 [42% (SD 6)], compared with 30 [28% (SD 6)] and 50 [28% (SD 8)] min of running. In contrast, prazosin resulted in a similar increase in VC after 5 [29% (SD 10)], 30 [24% (SD 9)], and 50 [22% (SD 9)] min of moderate-intensity (6 miles/h) exercise. Rauwolscine infusion resulted in a greater (P < 0.05) increase in VC after 5 [39% (SD 14)] compared with 30 [26% (SD 9)] and 50 [22% (SD 4)] min of exercise at 3 miles/h. Rauwolscine infusion produced a similar increase in VC after 5 [19% (SD 3)], 30 [15% (SD 6)], and 50 [16% (SD 2)] min of exercise at 6 miles/h. These results suggest that the ability of alpha1- and alpha2-adrenergic receptors to produce vasoconstriction and restrain blood flow to active muscles may be influenced by both the intensity and duration of exercise.
Journal of Applied Physiology 06/2006; 100(5):1563-8. · 3.75 Impact Factor
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ABSTRACT: The purpose was to examine the adaptation of pulmonary O(2) uptake (Vo(2p)) and deoxygenation of the vastus lateralis muscle at the onset of heavy-intensity, constant-load cycling exercise in young (Y; 24 +/- 4 yr; mean +/- SD; n = 5) and older (O; 68 +/- 3 yr; n = 6) adults. Subjects performed repeated transitions on 4 separate days from 20 W to a work rate corresponding to heavy-intensity exercise. Vo(2p) was measured breath by breath. The concentration changes in oxyhemoglobin, deoxyhemoglobin (HHb), and total hemoglobin/myoglobin were determined by near-infrared spectroscopy (Hamamatsu NIRO-300). Vo(2p) data were filtered, interpolated to 1 s, and averaged to 5-s bins. HHb-near-infrared spectroscopy data were filtered and averaged to 5-s bins. A monoexponential model was used to fit Vo(2p) [phase 2, time constant (tau) of Vo(2p)] and HHb [following the time delay (TD) from exercise onset to the start of an increase in HHb] data. The tauVo(2p) was slower (P < 0.001) in O (49 +/- 8 s) than Y (29 +/- 4 s). The HHb TD was similar in O (8 +/- 3 s) and Y (7 +/- 1 s); however, the tau HHb following TD was faster (P < 0.05) in O (8 +/- 2 s) than Y (14 +/- 2 s). The slower Vo(2p) kinetics and faster muscle deoxygenation in O compared with Y during heavy-intensity exercise imply that the kinetics of muscle perfusion are slowed relatively more than those of Vo(2p) in O. This suggests that the slowed Vo(2p) kinetics in O may be a consequence of a slower adaptation of local muscle blood flow relative to that in Y.
Journal of Applied Physiology 06/2005; 98(5):1697-704. · 3.75 Impact Factor
