Spatial variation of aortic wall oxygen diffusion coefficient from transient polarographic measurements

Polarographic current transients following a voltage step (turn-on transient) were measured with bare cathodes (25 μm diameter) and shallowly recessed oxygen microelectrodes (<5μm diameter). Except for the initial part of the current transient, the experimental measurements were in excellent agreement with simple models in the literature, which predict an inverse relationship with . Turn-on transients were measured in aqueous solutions with known physical properties, and in aortic wall tissue from three different species (n=6 rabbits, n=3 dogs, and n=1 miniature pig). Oxygen diffusion coefficients (D) were determinedin vitro by comparing time constants measured by the same microelectrode in saline and in strips of aortic wall tissue at 37°C. On the inner side (endothelium and intima) of the aorta, D averaged (±S.E.) 7.0 (±0.8)×10⁻⁶ cm²/s in 6 rabbits, 6.4 (±1.0)×10⁻⁶ cm²/s in 3 dogs, and was 4.6×10⁻⁶ cm²/s in the pig. On the adventitial side, D was 9.5×10⁻⁶ cm²/s in 1 rabbit, 11.4 (±1.2)×10⁻⁶ cm²/s in 3 dogs, and 8.1×10⁻⁶ cm²/s in the pig. For every aortic strip on which D was measured from both sides, D for the inner wall was always lower, overall by a little more than one third (p<0.001). The lower D on the endothelial side may limit oxygen transport to the vascular wall and play a role in atherogenesis.     

A Model of NO/O<Subscript>2</Subscript> Transport in Capillary-perfused Tissue Containing an Arteriole and Venule Pair

The goal of this study was to investigate the complex co-transport of nitric oxide (NO) and oxygen (O₂) in a paired arteriole–venule, surrounded by capillary-perfused tissue using a computer model. Blood flow was assumed to be steady in the arteriolar and venular lumens and to obey Darcy’s law in the tissue. NO consumption rate was assumed to be constant in the core of the arteriolar and venular lumen and to decrease linearly to the endothelium. Average NO consumption rate by capillary blood in a unit tissue volume was assumed proportional to the blood flux across the volume. Our results predict that: (1) the capillary bed, which connects the arteriole and venule, facilitates the release of O₂ from the vessel pair to the surrounding tissue; (2) decreasing the distance between arteriole and venule can result in a higher NO concentration in the venular wall than in the arteriolar wall; (3) in the absence of capillaries in the surrounding tissue, diffusion of NO from venule to arteriole contributes little to NO concentration in the arteriolar wall; and (4) when capillaries are added to the simulation, a significant increase of NO in the arteriolar wall is observed.     

Transmural Oxygen Tension Gradients in Rat Cerebral Cortex Arterioles

Modified needle oxygen microelectrodes and vital microscopy were used to measure transmural oxygen tension gradients (PO₂) in pial arterioles with lumen diameters of 20–90  μm. A relationship between the magnitude of the transmural PO₂ gradient and arteriole wall tone was found: in control conditions, PO₂ gradients were 1.17 ± 0.06 mmHg/μm (n  = 40), while in conditions of arteriolar wall dilation the transmural PO₂ gradient decreased to 0.68 ± 0.04 mmHg/μm (p  <  0.001, n  = 38). These data provide the first measurements of transmural PO₂ gradients in pial arterioles of different calibers at different levels of vascular tone and have fundamental importance for assessing the role of arterial microvessels in tissue oxygen supply processes. The results obtained here provide evidence that oxygen consumption by the vessel wall is within the range characteristic of enveloping tissues and that oxygen consumption by the endothelial cell layer probably has no significant effect on the magnitude of the transmural PO₂ gradient. Translated from Rossiiskii Fiziologicheskii Zhurnal imeni I. M. Sechenova, Vol. 94, No. 4, pp. 394–405, April, 2008.     

<Emphasis Type="Italic">In Vitro</Emphasis> Characterization of a Compliant Biodegradable Scaffold with a Novel Bioreactor System

The influence of scaffold compliance on blood vessel tissue engineering remains unclear and compliance mismatch issues are important to an in vivo tissue-engineering approach. We have designed and constructed a modular bioreactor system that is capable of imparting pulsatile fluid flow while simultaneously measuring vessel distension with fluid pressure changes in real time. The setup uses a pneumatic PID control system to generate variable fluid pressure profiles via LabVIEW and an LED micrometer to monitor vessel distension to an accuracy of ±2 μm. The bioreactor was used to measure the compliance of elastomeric poly(1,8-octanediol citrate) (POC) scaffolds over physiologically relevant pressure ranges. The compliance of POC scaffolds could be adjusted by changing polymerization conditions resulting in scaffolds with compliance values that ranged from 3.8 ± 0.2 to 15.6 ± 4.6%/mmHg × 10⁻², depending on the distension pressures applied. Furthermore, scaffolds that were incubated in phosphate-buffered saline for 4 weeks exhibited a linear increase in compliance (2.6 ± 0.9 to 7.7 ± 1.2%/mmHg × 10⁻²) and were able to withstand normal physiological blood pressure without bursting. The ability to tailor scaffold compliance and easily measure vessel compliance in real time in vitro will improve our understanding of the role of scaffold compliance on vascular cell processes.     

Cardiac function and arteriovenous oxygen difference during exercise in obese adults

The purpose of this study was to assess cardiac function and arteriovenous oxygen difference (a-vO₂ difference) at rest and during exercise in young, normal-weight (n = 20), and obese (n = 12) men and women who were matched for age and fitness level. Participants were assessed for body composition, peak oxygen consumption (VO_2peak), and cardiac variables (thoracic bioimpedance)—cardiac index (CI), cardiac output (Q), stroke volume (SV), heart rate (HR), and ejection fraction (EF)—at rest and during cycling exercise at 65% of VO_2peak. Differences between groups were assessed with multivariate ANOVA and mixed-model ANOVA with repeated measures controlling for sex. Absolute VO_2peak and VO_2peak relative to fat-free mass (FFM) were similar between normal-weight and obese groups (Mean ± SEE 2.7 ± 0.2 vs. 3.3 ± 0.3 l min⁻¹, p = 0.084 and 52.4 ± 1.5 vs. 50.9 ± 2.3 ml kg FFM⁻¹ min⁻¹, p = 0.583, respectively). In the obese group, resting Q and SV were higher (6.7 ± 0.4 vs. 4.9 ± 0.1 l min⁻¹, p < 0.001 and 86.8 ± 4.3 vs. 65.8 ± 1.9 ml min⁻¹, p < 0.001, respectively) and EF lower (56.4 ± 2.2 vs. 65.5 ± 2.2%, p = 0.003, respectively) when compared with the normal-weight group. During submaximal exercise, the obese group demonstrated higher mean CI (8.8 ± 0.3 vs. 7.7 ± 0.2 l min⁻¹ m⁻², p = 0.007, respectively), Q (19.2 ± 0.9 vs. 13.1 ± 0.3 l min⁻¹, p < 0.001, respectively), and SV (123.0 ± 5.6 vs. 88.9 ± 4.1 ml min⁻¹, p < 0.001, respectively) and a lower a-vO₂ difference (10.4 ± 1.0 vs. 14.0 ± 0.7 ml l00 ml⁻¹, p = 0.002, respectively) compared with controls. Our study suggests that the ability to extract oxygen during exercise may be impaired in obese individuals.     

The role of muscle pump in the development of cardiovascular drift

This study examined the role of muscle pump in the development of cardiovascular drift (CV_drift) during cycling. Twelve healthy males (23.4 ± 0.5 years, mean ± SE) exercised for 90 min with 40 and 80 pedal revolutions per minute (rpm) at the same oxygen consumption, in two separate days. CV_drift was developed in both conditions as indicated by the drop in stroke volume (SV) and the rise in heart rate (HR) from the 20th min onwards (ΔSV = −16.2 ± 2.0 and −17.1 ± 1.0 ml beat⁻¹; ΔHR = 18.3 ± 2.0 and 17.5 ± 3.0 beats min⁻¹ for 40 and 80 rpm, respectively, P < 0.05) but without difference between conditions. Mean cardiac output (CO₂ rebreathing) was 14.7 ± 0.3 l min⁻¹ and 15.0 ± 0.3 l min⁻¹, and mean arterial pressure was 100.0 ± 1.0 mmHg and 96.7 ± 0.8 mmHg for 40 and 80 rpm, respectively, without significant changes over time, and without difference between conditions. Electromyographic activity (iEMG) was lower throughout exercise with 80 rpm (35.6 ± 1.2% and 11.0 ± 1.0% for 40 and 80 rpm, respectively). Similarly, total hemoglobin, determined with near-infrared spectroscopy (NIRS) was 58.0 ± 0.8 (AU) for 40 rpm and 53.0 ± 1.4 (arbitrary units) for 80 rpm, from 30th min onwards (P < 0.05), an indication of lower leg blood volume during the faster pedal rate condition. Thermal status (rectal and mean skin temperature), blood and plasma volume changes, blood lactate concentration, muscle oxygenation (NIRS signal) and the rate of perceived exertion were similar in the two trials. It seems that muscle pump is not an important factor for the development of CV_drift during cycling, at least under the present experimental conditions.     

Effect of exercise on glutamine metabolism in macrophages of trained rats

This study investigated the effect of exercise on glutamine metabolism in macrophages of trained rats. Rats were divided into three groups: sedentary (SED); moderately trained (MOD) rats that were swim trained 1 h/day, 5 days/week for 6 weeks; and exhaustively trained (EXT) rats that were similarly trained as MOD for 5 weeks and, in the 6th week, trained in three 1-h sessions/day with 150 min of rest between sessions. The animals swam with a load equivalent to 5.5% of their body weight and were killed 1 h after the last exercise session. Cells were collected, and glutamine metabolism in macrophage and function were assayed. Exercise increased phagocytosis in MOD when compared to SED (34.48 ± 1.79 vs 15.21 ± 2.91%, P < 0.05); however, H₂O₂ production was higher in MOD (75.40 ± 3.48 nmol h × 10⁵ cell⁻¹) and EXT (79.20 ± 1.18 nmol h × 10⁵ cell⁻¹) in relation to SED (32.60 ± 2.51 nmol h × 10⁵ cell⁻¹, P < 0.05). Glutamine consumption increased in MOD and EXT (26.53 ± 3.62 and 19.82 ± 2.62 nmol h × 10⁵ cell⁻¹, respectively) relative to SED (6.72 ± 0.57 nmol h × 10⁵ cell⁻¹, P < 0.05). Aspartate increased in EXT (9.72 ± 1.14 nmol h × 10⁵ cell⁻¹) as compared to SED (1.10 ± 0.19 nmol h × 10⁵ cell⁻¹, P < 0.05). Glutamine decarboxylation was increased in MOD (12.10 ± 0.27 nmol h × 10⁵ cell⁻¹) and EXT (16.40 ± 2.17 nmol h × 10⁵ cell⁻¹) relative to SED (1.10 ± 0.06 nmol h × 10⁵ cell⁻¹, P < 0.05). This study suggests an increase in macrophage function post-exercise, which was supported by enhanced glutamine consumption and metabolism, and highlights the importance for glutamine after exercise.     

Maximal voluntary hyperpnoea increases blood lactate concentration during exercise

Ventilatory work during heavy endurance exercise has not been thought to influence systemic lactate concentration. We evaluated the effect of maximal isocapnic volitional hyperpnoea upon arterialised venous blood lactate concentration ([lac⁻]_B) during leg cycling exercise at maximum lactate steady state (MLSS). Seven healthy males performed a lactate minimum test to estimate MLSS, which was then resolved using separate 30 min constant power tests (MLSS=207±8 W, mean ± SEM). Thereafter, a 30 min control trial at MLSS was performed. In a further experimental trial, the control trial was mimicked except that from 20 to 28 min maximal isocapnic volitional hyperpnoea was superimposed on exercise. Over 20–28 min minute ventilation, oxygen uptake, and heart rate during the control and experimental trials were 87.3±2.4 and 168.3±7.0 l min⁻¹ (P<0.01), the latter being comparable to that achieved in the maximal phase of the lactate minimum test (171.9±6.8 l min⁻¹), 3.46±0.20 and 3.83 ± 0.20 l min⁻¹ (P<0.01), and 158.5±2.7 and 166.8±2.7 beats min⁻¹ (P<0.05), respectively. From 20 to 30 min of the experimental trial [lac⁻]_B increased from 3.7±0.2 to 4.7±0.3 mmol l⁻¹ (P<0.05). The partial pressure of carbon dioxide in arterialised venous blood increased approximately 3 mmHg during volitional hyperpnoea, which may have attenuated the [lac⁻]_B increase. These results show that, during heavy exercise, respiratory muscle work may affect [lac⁻]_B. We speculate that the changes observed were related to the altered lactate turnover in respiratory muscles, locomotor muscles, or both.     

Mechanically versus electro-magnetically braked cycle ergometer: performance and energy cost of the Wingate Anaerobic Test

Performance and metabolic profiles of the Wingate Anaerobic Test (WAnT) were compared between a mechanically resisted (ME) and an electro-magnetically braked (EE) cycle ergometer. Fifteen healthy subjects (24.0±3.5 years, 180.5±6.1 cm, 75.4±11.9 kg) performed a WAnT on ME, and EE 3 days apart. Performance was measured as peak power (PP), minimum power (MP), mean power (AP), time to PP (TTPP), fatigue rate (FR), and maximum cadence (RPM_MAX). Lactic (W _LAC) and alactic (W _PCR) anaerobic energy were calculated from net lactate appearance and the fast component of post-exercise oxygen uptake. Aerobic metabolism (W _AER) was calculated from oxygen uptake during the WAnT. Total energy cost (W _TOT) was calculated as the sum of W _LAC, W _PCR, and W _AER. There was no difference between ME and EE in PP (873±159 vs. 931±193 W) or AP (633±89 vs. 630±89 W). In the EE condition TTPP (2.3±0.7 vs. 4.3±0.7 s) was longer (P<0.001), MP (464±78 vs. 388±57 W) was lower (P<0.001), FR (15.2±5.2 vs. 20.5±6.8%) was higher (P<0.005), and RPM_MAX (168±18 vs. 128±15 rpm) was slower (P<0.001). There was no difference in W _TOT (1,331±182 vs. 1,373±120 J kg⁻¹), W _AER (292±76 vs. 309±72 J kg⁻¹), W _PCR (495±153 vs. 515±111 J kg⁻¹) or W _LAC (545±132 vs. 549±141 J kg⁻¹) between ME and EE devices. The EE produces distinctly different performance measures but valid metabolic WAnT results that may be used to evaluate anaerobic fitness.     

<Emphasis Type="Italic">V</Emphasis>O<Subscript>2</Subscript>max during successive maximal efforts

The concept of VO₂max has been a defining paradigm in exercise physiology for >75 years. Within the last decade, this concept has been both challenged and defended. The purpose of this study was to test the concept of VO₂max by comparing VO₂ during a second exercise bout following a preliminary maximal effort exercise bout. The study had two parts. In Study #1, physically active non-athletes performed incremental cycle exercise. After 1-min recovery, a second bout was performed at a higher power output. In Study #2, competitive runners performed incremental treadmill exercise and, after 3-min recovery, a second bout at a higher speed. In Study #1 the highest VO₂ (bout 1 vs. bout 2) was not significantly different (3.95 ± 0.75 vs. 4.06 ± 0.75 l min⁻¹). Maximal heart rate was not different (179 ± 14 vs. 180 ± 13 bpm) although maximal V _E was higher in the second bout (141 ± 36 vs. 151 ± 34 l min⁻¹). In Study #2 the highest VO₂ (bout 1 vs. bout 2) was not significantly different (4.09 ± 0.97 vs. 4.03 ± 1.16 l min⁻¹), nor was maximal heart rate (184 + 6 vs. 181 ± 10 bpm) or maximal V _E (126 ± 29 vs. 126 ± 34 l min⁻¹). The results support the concept that the highest VO₂ during a maximal incremental exercise bout is unlikely to change during a subsequent exercise bout, despite higher muscular power output. As such, the results support the “classical” view of VO₂max.     

Computationally Managed Bradycardia Improved Cardiac Energetics While Restoring Normal Hemodynamics in Heart Failure

In acute heart failure, systemic arterial pressure (AP), cardiac output (CO), and left atrial pressure (P _LA) have to be controlled within acceptable ranges. Under this condition, cardiac energetic efficiency should also be improved. Theoretically, if heart rate (HR) is reduced while AP, CO, and P _LA are maintained by preserving the functional slope of left ventricular (LV) Starling’s curve (S _L) with precisely increased LV end-systolic elastance (E _es), it is possible to improve cardiac energetic efficiency and reduce LV oxygen consumption per minute (MVO ₂). We investigated whether this hemodynamics can be accomplished in acute heart failure using an automated hemodynamic regulator that we developed previously. In seven anesthetized dogs with acute heart failure (CO < 70 mL min⁻¹ kg⁻¹, P _LA > 15 mmHg), the regulator simultaneously controlled S _L with dobutamine, systemic vascular resistance with nitroprusside and stressed blood volume with dextran or furosemide, thereby controlling AP, CO, and P _LA. Normal hemodynamics were restored and maintained (CO; 88 ± 3 mL min⁻¹ kg⁻¹, P _LA; 10.9 ± 0.4 mmHg), even when zatebradine significantly reduced HR (−27 ± 3%). Following HR reduction, E _es increased (+34 ± 14%), LV mechanical efficiency (stroke work/oxygen consumption) increased (+22 ± 6%), and MVO ₂ decreased (−17 ± 4%) significantly. In conclusion, in a canine acute heart failure model, computationally managed bradycardia improved cardiac energetic efficiency while restoring normal hemodynamic conditions.     

Towards Using Photo-Plethysmogram Amplitude to Measure Blood Pressure During Sleep

There is considerable interest in non-intrusive and reliable continuous ambulatory blood pressure measurement systems. Pulse amplitude is the peak to trough amplitude of the photo-plethysmogram signal. We compared pulse amplitude with a currently popular parameter, the pulse arrival time (PAT), for estimating continuous systolic blood pressure (SBP). Overnight sleep data from 18 young, healthy subjects (14 M 4 F, age 24 ± 5 years, BMI 23.8 ± 4.0 kg/m²) was analyzed. We found that pulse amplitude was more effective than PAT for estimating SBP during sleep. Mean coherence between pulse amplitude and SBP was significantly stronger than that for PAT [p < 0.001, 95% CI: 0.21–0.25 (finger), 0.11–0.14 (wrist)]. Correlation between pulse amplitude and SBP was significantly stronger than that for PAT [p < 0.001, 95% CI: 0.46–0.53 (finger), 0.13–0.20 (wrist)]. SBP estimation errors were significantly lower using pulse amplitude [p < 0.001, 95% CI: −1.55 to −1.29 mmHg (finger), −0.53 to −0.36 mmHg (wrist)]. We also found that while pulse amplitude was closely related to SBP, the relationship weakened during and around REM sleep (ANOVA of REM, transitional Wake-REM and transitional REM-Sleep versus other sleep states: F = 24.7, p < 0.001). These results suggest that pulse amplitude is potentially a more suitable measure than pulse arrival time for estimating continuous blood pressure.     

Skin microvascular reactivity in trained adolescents

Whilst endothelial dysfunction is associated with a sedentary lifestyle, enhanced endothelial function has been documented in the skin of trained individuals. The purpose of this study was to investigate whether highly trained adolescent males possess enhanced skin microvascular endothelial function compared to their untrained peers. Seventeen highly and predominantly soccer trained boys ( [(V)\dot]\textO_2 \textpeak \dot{V}{\text{O}}_{{2\,{\text{peak}}}} : 55 ± 6 mL kg⁻¹ min⁻¹) and nine age- and maturation-matched untrained controls ( [(V)\dot]\textO_2 \textpeak \dot{V}{\text{O}}_{{2\,{\text{peak}}}} : 43 ± 5 mL kg⁻¹ min⁻¹) aged 13–15 years had skin microvascular endothelial function assessed using laser Doppler flowmetry. Baseline and maximal thermally stimulated skin blood flow (SkBF) responses were higher in forearms of trained subjects compared to untrained participants [baseline SkBF: 11 ± 4 vs. 9 ± 3 perfusion units (PU), p < 0.05; SkBF_max: 282 ± 120 vs. 204 ± 68 PU, p < 0.05]. Similarly, cutaneous vascular conductance (CVC) during local heating was superior in the forearm skin of trained versus untrained individuals (CVC_max: 3 ± 1 vs. 2 ± 1 PU mmHg⁻¹, p < 0.05). Peak hyperaemia following arterial occlusion and area under the reactive hyperaemia curve were also greater in forearm skin of the trained group (peak hyperaemia: 51 ± 21 vs. 35 ± 15 PU, p < 0.05; area under curve: 1596 ± 739 vs. 962 ± 796 PUs, p < 0.05). These results suggest that chronic exercise training in adolescents is associated with enhanced microvascular endothelial vasodilation in non-glabrous skin.     

Prediction of <Emphasis Type="Italic">V</Emphasis>O<Subscript>2max</Subscript> with daily step counts for Japanese adult women

The purpose of the study was to develop a new non-exercise VO_2max prediction model using a physical activity (PA) variable determined by pedometer-determined step counts (SC, steps day⁻¹) in Japanese women aged 20–69 years old. Eighty-seven and 102 subjects were used to develop the prediction model, and to validate the new model, respectively. VO_2max was measured using a maximal incremental test on a bicycle ergometer. SC was significantly related to VO_2max (partial correlation coefficient r = 0.40, P < 0.001) after adjusting for BMI (kg m⁻²) and age (years). When the new prediction equation developed by multiple regression to estimate VO_2max from age, BMI, and SC (R = 0.71, SEE = 5.3 ml kg⁻¹ min⁻¹, P < 0.001) was applied to the Validation group, predicted VO_2max correlated well with measured VO_2max (r = 0.81, P < 0.001), suggesting that SC is a useful PA variable for non-exercise prediction of VO_2max in Japanese women.     

Mechanics of porcine coronary arteriesex vivo employing impedance planimetry: A new intravascular technique

Our objective was to evaluate methodological aspects of impedance planimetry, a new balloon catheter-based technique, for the investigation of coronary artery mechanical wall properties. We used a four ring-electrode electrical impedance measuring system that was located inside a balloon. Two of the electrodes were used for excitation and connected to a generator producing a constant alternating current of 250 mA at 5 kHz. The other two electrodes for detection were placed midway between the excitation electrodes. The balloon was distended with electrically conducting fluid through an infusion channel. The vessel cross-sectional area (CSA) was measured according to the field gradient principle by measuring the impedance of the fluid inside the balloon. Impedance planimetry was applied in the three major branches of the coronary arteries of seven extracted porcine hearts to assess luminal CSAs in response to internal pressurization. The biomechanical wall properties were evaluated by computing the strain [(r−r ₀)·r ₀ ⁻¹, wherer is the vessels inner radius computed as (CSA · π⁻¹)^? andr ₀ is the radius of the vessel at a minimal distension pressure], the tension [(r·dP), wheredP is the transmural pressure difference], and the pressure elastic modulus (ΔP·r·Δr ⁻¹). We found thatin vitro testing demonstrated that impedance planimetry was accurate and reproducible. The technique has controllable sources of crror. Measurements were performed with consecutively increasing pressures in the range 1–25 kPa (8–188 mmHg, 0.01–0.25 atm). The CSAs increased nonlinearly and were significantly larger in the left anterior descendent coronary artery (LAD) (1 kPa, mean 5.0 mm²; 25 kPa, mean 21.8 mm²) than in both the left circumflex (Cx) (4.5–16.0 mm²) and the right coronary artery (RCA) (2.8–15.6 mm²) (analysis of variance,P<0.001 for both). The circumferential wall tension-strain relation showed exponential behavior. For a given strain, tension values for LAD were significantly lower than those of Cx (P<0.01). The pressure elastic modulus-strain relation also was exponential, and values for Cx were significantly lower than values for LAD (P<0.001) and RCA (P<0.05). Impedance planimetry was applied to the study of coronary artery biomechanicsex vivo. The LAD had the largest CSA, and the Cx was the least compliant. Methodological aspects of anin vivo introduction of the method require additional evaluation.     

Effects of spinal anesthesia on resting metabolic rate and quadriceps mechanomyography

Previous work by our group has shown by mechanomyography (MMG) that resting muscle is mechanically active. Ten patients having spinal anesthesia for surgery, which paralyses muscle below the waist, were studied to help determine whether resting-muscle mechanical activity plays a significant role in resting metabolism, and to further determine if the phenomenon is neurally mediated. Resting metabolic rate (RMR) by indirect calorimetry, and mid-anterior thigh MMG by accelerometer, were recorded before and during spinal anesthesia. Spinal anesthesia produced a 25% decrease in oxygen uptake (mean ± standard deviation: pre-spinal 228 ± 76; during spinal 171 ± 67 ml min⁻¹; P < 0.001) and 37% decrease in mean absolute MMG signal amplitude (pre-spinal-anesthetic 10.6 ± 3.9; during spinal: 6.7 ± 3.5 mm s⁻²; P < 0.001). Decreased oxygen uptake in individuals correlated with decreased resting-muscle mechanical activity (R = 0.624; P = 0.05). Paralysis of muscle below the waist reduced RMR and resting-muscle mechanical activity.     

BK<Subscript>Ca</Subscript> and K<Subscript>V</Subscript> channels limit conducted vasomotor responses in rat mesenteric terminal arterioles

Intracellular Ca²⁺ signals underlying conducted vasoconstriction to local application of a brief depolarizing KCl stimulus was investigated in rat mesenteric terminal arterioles (<40 μm). Using a computer model of an arteriole segment comprised of coupled endothelial cells (EC) and vascular smooth muscle cells (VSMC) simulations of both membrane potential and intracellular [Ca²⁺] were performed. The “characteristic” length constant, λ, was approximated using a modified cable equation in both experiments and simulations. We hypothesized that K⁺ conductance in the arteriolar wall limit the electrotonic spread of a local depolarization along arterioles by current dissipation across the VSMC plasma membrane. Thus, we anticipated an increased λ by inhibition of voltage-activated K⁺ channels. Application of the BK_Ca channel blocker iberiotoxin (100 nM) onto mesenteric arterioles in vitro and inhibition of BK_Ca channel current in silico increased λ by 34% and 32%, respectively. Similarly, inhibition of K_V channels in vitro (4-aminopyridine, 1 mM) or in silico increased λ by 41% and 21%, respectively. Immunofluorescence microscopy demonstrated expression of BK_Ca, Kv1.5, Kv2.1, but not Kv1.2, in VSMCs of rat mesenteric terminal arterioles. Our results demonstrate that inhibition of voltage-activated K⁺ channels enhance vascular-conducted responses to local depolarization in terminal arterioles by increasing the membrane resistance of VSMCs. These data contribute to our understanding of how differential expression patterns of voltage-activated K⁺ channels may influence conducted vasoconstriction in small arteriolar networks. This finding is potentially relevant to understanding the compromised microcirculatory blood flow in systemic vascular diseases such as diabetes mellitus and hypertension.     

Plasma vasopressin,renin activity,and aldosterone responses to maximal exercise in active college females

Summary The effect of maximal treadmill exercise on plasma concentrations of vasopressin (AVP); renin activity (PRA); and aldosterone (ALDO) was studied in nine female college basketball players before and after a 5-month basketball season. Pre-season plasma AVP increased (p<0.05) from a pre-exercise concentration of 3.8±0.5 to 15.8±4.8 pg · ml⁻¹ following exercise. Post-season, the pre-exercise plasma AVP level averaged 1.5±0.5 pg · ml⁻¹ and increased to 16.7±5.9 pg · ml⁻¹ after the exercise test. PRA increased (p<0.05) from a pre-exercise value of 1.6±0.6 to 6.8±1.7 ngAI · ml⁻¹ · hr⁻¹ 5 min after the end of exercise during the pre-season test. In the post-season, the pre-exercise PRA was comparable (2.4±0.6 ngAI · ml⁻¹ · hr⁻¹), as was the elevation found after maximal exercise (8.3±1.9 ngAI · ml⁻¹ · hr⁻¹). Pre-season plasma ALDO increased (p<0.05) from 102.9±30.8 pg · ml⁻¹ in the pre-exercise period to 453.8±54.8 pg · ml⁻¹ after the exercise test. In the post-season the values were 108.9±19.4 and 365.9±64.4 pg · ml⁻¹, respectively. Thus, maximal exercise in females produced significant increases in plasma AVP, renin activity, and ALDO that are comparable to those reported previously for male subjects. Moreover, this response is remarkably reproducible as demonstrated by the results of the two tests performed 5 months apart.     

The oxygen consumption with unloaded walking and load carriage using two different backpack designs

The purpose of this study was to assess the energy expenditure associated with load carriage using both a traditional rucksack and a new rucksack design, the AARN rucksack, which incorporates front balance pockets. Nine volunteers walked at 3 km h⁻¹ at various uphill and downhill gradients on a treadmill without a load and carrying a load of 25.6 kg in each of the rucksacks. The oxygen consumption associated with both of the loading conditions was significantly (P < 0.001) higher than that associated with unloaded walking at all downhill gradients tested, although there was no significant difference between the two loading conditions. During the uphill gradients the oxygen consumption associated with the AARN pack was significantly (P < 0.05) lower than that associated with the traditional pack at the 0%, 5%, 10% and 20% gradients. The mean (%) differences at these gradients, expressed in ml · kg⁻¹ · min⁻¹ were 1.18 (9%), 1.45 (8%), 1.76 (8%) and 1.88 (6%), respectively. On average for the whole protocol, the oxygen consumption associated with the AARN rucksack was 5% lower than that associated with the traditional rucksack [mean (SD) 17.28 (7.46) ml · kg⁻¹ · min⁻¹ for the AARN pack and 18.20 (7.84) ml · kg⁻¹ · min⁻¹ for the traditional pack]. The findings of the present study suggest that a load carriage system that allows the load to be distributed between the back and font of the trunk is more appropriate for carrying relatively heavy loads than a system that loads the back only. Accepted: 22 November 1999     

The effect of exercise on postprandial lipidemia in type 2 diabetic patients

To elucidate if postprandial exercise can reduce the exaggerated lipidemia seen in type 2 diabetic patients after a high-fat meal. Two mornings eight type 2 diabetic patients (males) (58 ± 1.2 years, BMI 28.0 ± 0.9 kg m⁻²) and seven non-diabetic controls ate a high-fat breakfast (680 kcal m⁻², 84% fat). On one morning, 90 min later subjects cycled 60 min at 57% . Biopsies from quadriceps muscle and abdominal subcutaneous adipose tissue were sampled after exercise or equivalent period of rest and arterialized blood for 615 min. Postprandial increases in serum total-triglyceride (TG) (incremental AUC: 1,702 ± 576 vs. 341 ± 117 mmol l⁻¹ 600 min), chylomicron-TG (incremental AUC: 1,331 ± 495 vs. 184 ± 55 mmol l⁻¹ 600 min) and VLDL-TG as well as in insulin (incremental AUC: 33,946 ± 7,414 vs. 13,670 ± 3,250 pmol l⁻¹ 600 min), C-peptide and glucose were higher in diabetic patients than in non-diabetic controls (P < 0.05). In diabetic patients these variables were reduced (P < 0.05) by exercise (total-TG incremental AUC being 1,110 ± 444, chylomicron-TG incremental AUC 1,043 ± 474 mmol l⁻¹ 600 min and insulin incremental AUC 18,668 ± 4,412 pmol l⁻¹ 600 min). Lipoprotein lipase activity in muscle (11.0 ± 2.0 vs. 24.1 ± 3.4 mU g per wet weight, P < 0.05) and post-heparin plasma at 615 min were lower in diabetic patients than in non-diabetic controls, but did not differ in adipose tissue and did not change with exercise. In diabetic patients, 210 min after exercise oxygen uptake (P < 0.05) and fat oxidation (P < 0.1) were still higher than on non-exercise days. In type 2 diabetic patients, after a high-fat meal exercise reduces the plasma concentrations of triglyceride contained in both chylomicrons and VLDL as well as insulin secretion. This suggests protection against progression of atherosclerosis and diabetes.