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Maximal Exercise (maximal + exercise)
Selected AbstractsCerebral Metabolism is Influenced by Muscle Ischaemia During Exercise in HumansEXPERIMENTAL PHYSIOLOGY, Issue 2 2003Mads K. Dalsgaard Maximal exercise reduces the cerebral metabolic ratio (O2/(glucose + 1/2lactate)) to < 4 from a resting value close to 6, and only part of this decrease is explained by the ,intent' to exercise. This study evaluated whether sensory stimulation of brain by muscle ischaemia would reduce the cerebral metabolic ratio. In 10 healthy human subjects the cerebral arterial-venous differences (a-v differences) for O2, glucose and lactate were assessed before, during and after three bouts of 10 min cycling with equal workload: (1) control exercise at light intensity, (2) exercise that elicited a high rating of perceived exertion due to a 100 mmHg thigh cuff, and (3) exercise followed by 5 min of post-exercise muscle ischaemia that increased blood pressure by , 20%. Control exercise did not significantly affect the a-v differences. However, during the recovery from exercise with thigh cuffs the cerebral metabolic ratio decreased from a resting value of 5.4 ± 0.2 to 4.0 ± 0.4 (mean ±s.e.m.. P < 0.05) as a discrete lactate efflux from the brain at rest shifted to a slight uptake. Also, following post-exercise muscle ischaemia, the cerebral metabolic ratio decreased to 4.5 ± 0.3 (P < 0.05). The results support the hypothesis that during exercise, cerebral metabolism is influenced both by the mental effort to exercise and by sensory input from skeletal muscles. [source] Pharmacokinetics of detomidine administered to horses at rest and after maximal exerciseEQUINE VETERINARY JOURNAL, Issue 5 2009J. A. E. HUBBELL Summary Reason for performing study: Increased doses of detomidine are required to produce sedation in horses after maximal exercise compared to calm or resting horses. Objectives: To determine if the pharmacokinetics of detomidine in Thoroughbred horses are different when the drug is given during recuperation from a brief period of maximal exercise compared to administration at rest. Methods: Six Thoroughbred horses were preconditioned by exercising them on a treadmill. Each horse ran a simulated race at a treadmill speed that caused it to exercise at 120% of its maximal oxygen consumption. One minute after the end of exercise, horses were treated with detomidine. Each horse was treated with the same dose of detomidine on a second occasion a minimum of 14 days later while standing in a stocks. Samples of heparinised blood were obtained at various time points on both occasions. Plasma detomidine concentrations were determined by liquid chromatographymass spectrometry. The plasma concentration vs. time data were analysed by nonlinear regression analysis. Results: Median back-extrapolated time zero plasma concentration was significantly lower and median plasma half-life and median mean residence time were significantly longer when detomidine was administered after exercise compared to administration at rest. Median volume of distribution was significantly higher after exercise but median plasma clearance was not different between the 2 administrations. Conclusions and potential relevance: Detomidine i.v. is more widely distributed when administered to horses immediately after exercise compared to administration at rest resulting in lower peak plasma concentrations and a slower rate of elimination. The dose requirement to produce an equivalent effect may be higher in horses after exercise than in resting horses and less frequent subsequent doses may be required to produce a sustained effect. [source] Implications of different degrees of arytenoid cartilage abduction on equine upper airway characteristicsEQUINE VETERINARY JOURNAL, Issue 7 2008V. RAKESH Summary Reason for performing study: The necessary degree of arytenoid cartilage abduction (ACA) to restore airway patency at maximal exercise has not been determined. Objectives: Use computational fluid dynamics modelling to measure the effects of different degrees of ACA on upper airway characteristics of horses during exercise. Hypothesis: Maximal ACA by laryngoplasty is necessary to restore normal peak airflow and pressure in Thoroughbred racehorses with laryngeal hemiplegia. Methods: The upper airway was modeled with the left arytenoid in 3 different positions: maximal abduction; 88% cross-sectional area of the rima glottis; and 75% cross-sectional area of the rima glottis. The right arytenoid cartilage was maximally abducted. Two models were assumed: Model 1: no compensation of airway pressures; and Model 2: airway pressure compensation occurs to maintain peak airflow. The cross-sectional pressure and velocity distributions for turbulent flow were studied at peak flow and at different positions along the airway. Results: Model 1: In the absence of a change in driving pressure, 12 and 25% reductions in cross-sectional area of the larynx resulted in 4.11 and 5.65% reductions in peak airflow and 3.68 and 5.64% in tidal volume, respectively, with mild changes in wall pressure. Model 2: To maintain peak flow, a 6.27% increase in driving tracheal pressure was required to compensate for a cross-sectional reduction of 12% and a 13.63% increase in driving tracheal pressure was needed for a cross-sectional area reduction of 25%. This increase in negative driving pressure resulted in regions with low intraluminal and wall pressures, depending on the degree of airway diameter reduction. Conclusion: Assuming no increase in driving pressure, the decrease in left ACA reduced airflow and tidal volume. With increasing driving pressure, a decrease in left ACA changed the wall pressure profile, subjecting the submaximally abducted arytenoid cartilage and adjacent areas to airway collapse. Clinical relevance: The surgical target of ACA resulting in 88% of maximal cross-sectional area seems to be appropriate. [source] Nitric oxide synthase inhibition in Thoroughbred horses augments O2 extraction at rest and submaximal exercise, but not during short-term maximal exerciseEQUINE VETERINARY JOURNAL, Issue S36 2006M. MANOHAR Summary Reason for performing study: Work is required to establish the role of endogenous nitric oxide (NO) in metabolism of resting and exercising horses. Objectives: To examine the effects of NO synthase inhibition on O2 extraction and anaerobic metabolism at rest, and during submaximal and maximal exertion. Methods: Placebo and NO synthase inhibition (with N,-nitro-L-arginine methyl ester [l -NAME] administered at 20 mg/kg bwt i.v.) studies were performed in random order, 7 days apart on 7 healthy, exercise-trained Thoroughbred horses at rest and during incremental exercise leading to 120 sec of maximal exertion at 14 m/sec on a 3.5% uphill grade. Results: At rest, NO synthase inhibition significantly augmented the arterial to mixed-venous blood O2 content gradient and O2 extraction as mixed-venous blood O2 tension and saturation decreased significantly. While NO synthase inhibition did not affect arterial blood-gas tensions in exercising horses, the exercise-induced increment in haemoglobin concentration and arterial O2 content was attenuated. In the l -NAME study, during submaximal exercise, mixed-venous blood O2 tension and haemoglobin-O2 saturation decreased to a greater extent causing O2 extraction to increase significantly. During maximal exertion, arterial hypoxaemia, desaturation of haemoglobin and hypercapnia of a similar magnitude developed in both treatments. Also, the changes in mixed-venous blood O2 tension and haemoglobin-O2 saturation, arterial to mixed-venous blood O2 content gradient, O2 extraction and markers of anaerobic metabolism (lactate and ammonia production, and metabolic acidosis) were not different from those in the placebo study. Conclusion: Endogenous NO production augments O2 extraction at rest and during submaximal exertion, but not the during short-term maximal exercise. Also, NO synthase inhibition does not affect anaerobic metabolism at rest or during exertion. Potential relevance: It is unlikely that endogenous NO release modifies aerobic or anaerobic metabolism in horses performing short-term maximal exertion. [source] Abnormal vascular reactivity at rest and exercise in obese boysEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 2 2009L. Karpoff Abstract Background, Obese children exhibit vascular disorders at rest depending on their pubertal status, degree of obesity, and level of insulin resistance. However, data regarding their vascular function during exercise remain scarce. The aims of the present study were to evaluate vascular morphology and function at rest, and lower limb blood flow during exercise, in prepubertal boys with mild-to-moderate obesity and in lean controls. Materials and methods, Twelve moderately obese prepubertal boys [Body Mass Index (BMI: 23·9 ± 2·6 kg m,2)] and thirteen controls (BMI:17·4 ± 1·8 kg m,2), matched for age (mean age: 11·6 ± 0·6 years) were recruited. We measured carotid intima-media thickness (IMT) and wall compliance and incremental elastic modulus, resting brachial flow-mediated dilation (FMD) and nitrate-dependent dilation (NDD), lower limb blood flow during local knee-extensor incremental and maximal exercise, body fat content (DEXA), blood pressure, blood lipids, insulin and glucose. Results, Compared to lean controls, obese boys had greater IMT (0·47 ± 0·06 vs. 0·42 ± 0·03 mm, P < 0·05) but lower FMD (4·6 ± 2·8 vs. 8·8 ± 3·2%, P < 0·01) in spite of similar maximal shear rate, without NDD differences. Lower limb blood flow (mL min,1·100 g,1) increased significantly from rest to maximal exercise in both groups, although obese children reached lower values than lean counterparts whatever the exercise intensity. Conclusions, Mild-to-moderate obesity in prepubertal boys without insulin resistance is associated with impaired endothelial function and blunted muscle perfusion response to local dynamic exercise without alteration of vascular smooth muscle reactivity. [source] Endothelial markers in chronic heart failure: training normalizes exercise-induced vWF releaseEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 9 2004L. W. E. Sabelis Abstract Background, Chronic heart failure (CHF) is characterized by endothelial dysfunction. Vascular endothelium is important for control of haemostasis and vasoregulation. The aim of the present study was to investigate plasma levels of several endothelial markers and the exercise-induced changes on these plasma levels in CHF patients. Subsequently, the effect of a 6-month training programme on these markers is described. Materials and methods, Twenty-nine male CHF patients (NYHA II/III, age 60 ± 8 year, body mass index 26·7 ± 2·3 kg m,2, left ventricular ejection fraction 26·3,7·2%; mean ± SD) participated. Patients were randomly assigned to a training or control group. Training (26 weeks; combined strength and endurance exercises) was four sessions/week: two sessions supervised and two sessions at home. Before and after intervention, anthropometry, endothelial markers (haemostasis and vasoregulation), maximal workload and peak oxygen uptake were assessed. Results, Physical training positively affected maximal workload. Plasma levels of endothelial markers were not affected by physical training and not related to exercise tolerance. After training, stimulated (maximal exercise) plasma von Willebrand Factor (vWF) release was present, whereas at baseline this release was absent. Conclusion, Physical training led to normalization of the stimulated plasma vWF release. Plasma levels of other endothelial markers were not affected by physical training either at rest or under stimulated (maximal exercise) conditions. [source] Sex influence on myocardial function with exercise in adolescentsAMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 5 2010Thomas Rowland Objectives: Ventricular systolic functional response to exercise has been reported to be superior in adult men compared to women. This study explored myocardial responses to maximal upright progressive exercise in late pubertal males and females. Methods: Doppler echocardiographic techniques were utilized to estimate myocardial function response to a bout of progressive cycle exercise. Results: Systolic functional capacity, as indicated by ejection rate (12.5 ± 2.8 and 13.1 ± 1.0 [×10,2] ml s,1 cm,2 for boys and girls, respectively) and peak aortic velocity (208 ± 45 and 196 ± 12 cm s,1, respectively) at maximal exercise, did not differ between the two groups. Similarly, peak values as well as increases in transmitral pressure gradient (mitral E flow velocity), ventricular relaxation (tissue Doppler imaging E,), and left ventricular filling pressure (E/E, ratio) as estimates of diastolic function were similar in males and females. Conclusions: This study failed to reveal qualitative or quantitative differences between adolescent boys and girls in ventricular systolic or diastolic functional responses to maximal cycle exercise. Am. J. Hum. Biol. 22:680,682, 2010. © 2010 Wiley-Liss, Inc. [source] Oxygen cost of ventilation during incremental exercise to VO2 maxRESPIROLOGY, Issue 2 2006Chantal A. VELLA Objective: Evidence of significant oxygen requirements for ventilation during exercise (exercise hyperpnoea) prompted the investigation into whether the oxygen cost of ventilation affects the presence of a whole-body VO2 plateau at maximal exercise. The purposes of this study were to: (i) use isocapnic hyperpnoea trials to determine the oxygen cost of ventilation (VO2VENT) across a range of ventilation (VE); (ii) determine the mean VO2VENT at maximal exercise expressed as a percentage of whole-body VO2 max; and (iii) determine if a plateau in VO2 is more evident when the VO2VENT is subtracted from whole-body VO2 at maximal exercise. Methods: A total of 21 subjects performed a VO2 max test on the cycle ergometer to determine the range of VE for each subject. From the initial VO2 max test, nine VE values across the range of VE were selected for each subject and the oxygen cost of each was measured. Results: The mean maximal VO2VENT equalled 8.8 ± 3.3% of VO2 max and ranged from 5.0% to 17.6%. VO2VENT increased exponentially with increasing VE, but there was considerable subject variability in the oxygen cost per litre of VE as VE increased. Subtracting the VO2VENT from whole-body VO2 at maximal exercise increased the detection of a plateau in VO2 at VO2 max. Conclusions: The data of the present study indicate that the VO2VENT is a significant portion of VO2 max and may be a limiting factor of maximal exercise performance in some subjects. [source] Influence of body fat distribution on oxygen uptake and pulmonary performance in morbidly obese females during exerciseRESPIROLOGY, Issue 1 2001Jing Li Objective: The aim of this study was to determine the effects of fat distribution on aerobic and ventilatory response to exercise testing in morbidly obese (MO) females. Methodology: The study population consisted of 164 MO females, 55% (n = 90) with upper body or abdominal adiposity (UBD), as defined by waist,hip circumference ratio (WHR) , 0.80, and 45% (n = 74) with lower body fat distribution (LBD) (WHR < 0.80). An incremental exercise testing on cycle ergometer was performed to determine the effect of exercise on oxygen consumption (V·O2), carbon dioxide production (V·CO2), minute ventilation (V·E), tidal volume ( T), respiratory rate (fb) and heart rate (HR). Results: Upper body adiposity individuals had significantly higher O2 and V·CO2 than LBD subjects (P < 0.05) from 0 watt (W) of pedalling up to their anaerobic threshold (AT) and maximal exercise. E was significantly higher in UBD subjects compared with LBD subjects, from 20 W during exercise up to AT and peak work levels (P < 0.05). Upper body adiposity group also had a significantly higher fb than the LBD group at rest, after each workload and at AT and peak exercise work rates (P < 0.05). T was lower in UBD subjects at free pedalling and up to AT and peak workload with significant difference at 60 and 80 W (P < 0.05). The anaerobic threshold, expressed as work rate, was significantly lower in the UBD subjects (P < 0.05) and peak workload achieved did not differ significantly between the two groups. Conclusions: Upper body adiposity subjects had higher oxygen requirement, more rapid and shallow breathing, higher ventilatory demand, but lower anaerobic threshold than the LBD individuals during progressive exercise. It suggests that the cardiopulmonary endurance to exercise in MO patients with upper body fat distribution is lower than in those with lower body fat distribution. [source] The response to paired motor cortical stimuli is abolished at a spinal level during human muscle fatigueTHE JOURNAL OF PHYSIOLOGY, Issue 23 2009Chris J. McNeil During maximal exercise, supraspinal fatigue contributes significantly to the decline in muscle performance but little is known about intracortical inhibition during such contractions. Long-interval inhibition is produced by a conditioning motor cortical stimulus delivered via transcranial magnetic stimulation (TMS) 50,200 ms prior to a second test stimulus. We aimed to delineate changes in this inhibition during a sustained maximal voluntary contraction (MVC). Eight subjects performed a 2 min MVC of elbow flexors. Single test and paired (conditioning,test interval of 100 ms) stimuli were delivered via TMS over the motor cortex every 7,8 s throughout the effort and during intermittent MVCs in the recovery period. To determine the role of spinal mechanisms, the protocol was repeated but the TMS test stimulus was replaced by cervicomedullary stimulation which activates the corticospinal tract. TMS motor evoked potentials (MEPs) and cervicomedullary motor evoked potentials (CMEPs) were recorded from biceps brachii. Unconditioned MEPs increased progressively with fatigue, whereas CMEPs increased initially but returned to the control value in the final 40 s of contraction. In contrast, both conditioned MEPs and CMEPs decreased rapidly with fatigue and were virtually abolished within 30 s. In recovery, unconditioned responses required <30 s but conditioned MEPs and CMEPs required ,90 s to return to control levels. Thus, long-interval inhibition increased markedly as fatigue progressed. Contrary to expectations, subcortically evoked CMEPs were inhibited as much as MEPs. This new phenomenon was also observed in the first dorsal interosseous muscle. Tested with a high intensity conditioning stimulus during a fatiguing maximal effort, long-interval inhibition of MEPs was increased primarily by spinal rather than motor cortical mechanisms. The spinal mechanisms exposed here may contribute to the development of central fatigue in human muscles. [source] During hypoxic exercise some vasoconstriction is needed to match O2 delivery with O2 demand at the microcirculatory levelTHE JOURNAL OF PHYSIOLOGY, Issue 1 2008Carsten Lundby To test the hypothesis that the increased sympathetic tonus elicited by chronic hypoxia is needed to match O2 delivery with O2 demand at the microvascular level eight male subjects were investigated at 4559 m altitude during maximal exercise with and without infusion of ATP (80 ,g (kg body mass),1 min,1) into the right femoral artery. Compared to sea level peak leg vascular conductance was reduced by 39% at altitude. However, the infusion of ATP at altitude did not alter femoral vein blood flow (7.6 ± 1.0 versus 7.9 ± 1.0 l min,1) and femoral arterial oxygen delivery (1.2 ± 0.2 versus 1.3 ± 0.2 l min,1; control and ATP, respectively). Despite the fact that with ATP mean arterial blood pressure decreased (106.9 ± 14.2 versus 83.3 ± 16.0 mmHg, P < 0.05), peak cardiac output remained unchanged. Arterial oxygen extraction fraction was reduced from 85.9 ± 5.3 to 72.0 ± 10.2% (P < 0.05), and the corresponding venous O2 content was increased from 25.5 ± 10.0 to 46.3 ± 18.5 ml l,1 (control and ATP, respectively, P < 0.05). With ATP, leg arterial,venous O2 difference was decreased (P < 0.05) from 139.3 ± 9.0 to 116.9 ± 8.4,1 and leg was 20% lower compared to the control trial (1.1 ± 0.2 versus 0.9 ± 0.1 l min,1) (P= 0.069). In summary, at altitude, some degree of vasoconstriction is needed to match O2 delivery with O2 demand. Peak cardiac output at altitude is not limited by excessive mean arterial pressure. Exercising leg is not limited by restricted vasodilatation in the altitude-acclimatized human. [source] Protective effects of long term dietary restriction on swimming exercise-induced oxidative stress in the liver, heart and kidney of ratCELL BIOCHEMISTRY AND FUNCTION, Issue 2 2007Cenk Aydin Abstract In this study, we evaluated the hypothesis that long term dietary restriction would have beneficial effects on the oxidative stress and antioxidant enzyme systems in liver, heart and kidney in adult male rats undergoing different intensities of swimming exercise. Sixty male, Sprague,Dawley rats were assigned as either dietary restricted on every other week day (DR) or fed ad libitum (AL) groups, and each group was further subdivided into sedentary, endurance swimming exercise training (submaximal exercise) and exhaustive swimming exercise (maximal exercise) groups. Animals in the submaximal exercise group swam 5 days/week for 8 weeks, while maximal exercise was performed as an acute bout of exercise. In parallel with the increase in the intensity of the exercise, the degree of lipid peroxidation and protein oxidation were increased in both the DR and AL groups; however the rate of increase was lower in the DR group. Reduced glutathione (GSH), glutathione peroxidase (GSH-Px) and glutathione reductase (GR) enzyme activities were lower in the DR group than in the AL group. In parallel with the increase in exercise intensity, GSH and GR enzyme activities decreased, whereas an increase was observed in GSH-Px enzyme activity. In conclusion, the comparison between the DR and AL groups with the three swimming exercise conditions shows that the DR group is greatly protected against different swimming exercise-induced oxidative stress compared with the AL group. Copyright © 2005 John Wiley & Sons, Ltd. [source] Prefrontal cortex oxygenation during incremental exercise in chronic fatigue syndromeCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 6 2008J. Patrick Neary Summary This study examined the effects of maximal incremental exercise on cerebral oxygenation in chronic fatigue syndrome (CFS) subjects. Furthermore, we tested the hypothesis that CFS subjects have a reduced oxygen delivery to the brain during exercise. Six female CFS and eight control (CON) subjects (similar in height, weight, body mass index and physical activity level) performed an incremental cycle ergometer test to exhaustion, while changes in cerebral oxy-haemoglobin (HbO2), deoxy-haemoglobin (HHb), total blood volume (tHb = HbO2 + HHb) and O2 saturation [tissue oxygenation index (TOI), %)] was monitored in the left prefrontal lobe using a near-infrared spectrophotometer. Heart rate (HR) and rating of perceived exertion (RPE) were recorded at each workload throughout the test. Predicted VO2peak in CFS (1331 ± 377 ml) subjects was significantly (P , 0·05) lower than the CON group (1990 ± 332 ml), and CFS subjects achieved volitional exhaustion significantly faster (CFS: 351 ± 224 s; CON: 715 ± 176 s) at a lower power output (CFS: 100 ± 39 W; CON: 163 ± 34 W). CFS subjects also exhibited a significantly lower maximum HR (CFS: 154 ± 13 bpm; CON: 186 ± 11 bpm) and consistently reported a higher RPE at the same absolute workload when compared with CON subjects. Prefrontal cortex HbO2, HHb and tHb were significantly lower at maximal exercise in CFS versus CON, as was TOI during exercise and recovery. The CFS subjects exhibited significant exercise intolerance and reduced prefrontal oxygenation and tHb response when compared with CON subjects. These data suggest that the altered cerebral oxygenation and blood volume may contribute to the reduced exercise load in CFS, and supports the contention that CFS, in part, is mediated centrally. [source] | |||||||||||||