Oxygen uptake transients at the onset and offset of arm and leg work

The halftimes (t1/2) of the VO2 on-and off-responses have been determined on 4 moderately active subjects (1) in arm cranking (VO2 congruent to 1 1/min). (2) in leg pedaling at 4 graded submaximal (VO2 congruent to 0.8 to 2.51/min) work loads, and (3) when superimposing arm cranking on preexisting leg pedaling, both in the supine and in the upright position. In supine experiments the mean t1/2 of the VO2 on-response was longer for arm cranking than for leg pedaling (64 vs 44-49 sec) at equal VO2; however, at the same percentage of arm and leg VO2 max the respective t1/2 were similar. In sitting experiments all t1/2 of the VO2 on-response were shorter than when supine, but the t1/2 for the arms were still slightly longer than those for the legs. When arm cranking was superimposed on preexisting leg pedaling, the t1/4 for arms was reduced both in supine (from 64 to 35-38 sec) and in the sitting position (from 44 to 40 sec). The halftime of the VO2 off-response were much shorter (20-32 sec) than those of the on-response and similar in all experiments. In all conditions the O2 deficits at work onset were considerably larger than the fast component of the corresponding O2 debts during the first minutes of recovery. The difference was totally accounted for by anaerobic glycolysis occurring early during the VO2 on-response, particularly in arm exercise. It is concluded that at submaximal work loads the O2 deficit is accounted for the fast component of the O2 debt plus the O2 equivalent of the early lactate production.     

Muscle oxygenation during incremental arm and leg exercise in men and women

The purpose of this study was to compare the rates of muscle deoxygenation in the exercising muscles during incremental arm cranking and leg cycling exercise in healthy men and women. Fifteen men and 10 women completed arm cranking and leg cycling tests to exhaustion in separate sessions in a counterbalanced order. Cardiorespiratory measurements were monitored using an automated metabolic cart interfaced with an electrocardiogram. Tissue absorbency was recorded continuously at 760 nm and 850 nm during incremental exercise and 6 min of recovery, with a near infrared spectrometer interfaced with a computer. Muscle oxygenation was calculated from the tissue absorbency measurements at 30%, 45%, 60%, 75% and 90% of peak oxygen uptake (VO2) during each exercise mode and is expressed as a percentage of the maximal range observed during exercise and recovery (%Mox). Exponential regression analysis indicated significant inverse relationships (P < 0.01) between %Mox and absolute VO2 during arm cranking and leg cycling in men (multiple R = -0.96 and -0.99, respectively) and women (R = -0.94 and -0.99, respectively). No significant interaction was observed for the %Mox between the two exercise modes and between the two genders. The rate of muscle deoxygenation per litre of VO2 was 31.1% and 26.4% during arm cranking and leg cycling, respectively, in men, and 26.3% and 37.4% respectively, in women. It was concluded that the rate of decline in %Mox for a given increase in VO2 between 30% and 90% of the peak VO2 was independent of exercise mode and gender.     

Metabolic efficiency during arm and leg exercise at the same relative intensities

This study was conducted to compare gross efficiency (GE), net efficiency (NE), work efficiency (WE), and delta efficiency (DE) between arm crank and cycle exercise at the same relative intensities. Eight college-aged males underwent two experimental trials presented in a randomized counterbalanced order. During each trial subjects performed three intermittent 7-min exercise bouts separated by 10-min rest intervals on an arm or semirecumbent leg ergometer. The power outputs for the three bouts of arm crank or cycle exercise corresponded to 50, 60, and 70% of the mode-specific VO2peak. GE, NE, and WE were determined as the ratio of Kcal.min-1 equivalent of power output to Kcal.min-1 of total energy expended, energy expended above rest and energy expended above unloaded exercise, respectively. DE was determined as the ratio of the increment of Kcal.min-1 of power output above the previous lower intensity to the increment of kcal.min-1 of total energy expended above the previous lower intensity. GE and NE did not differ between arm crank and cycle exercises. However, WE was lower (P < 0.05) during arm crank than cycle exercise at 50, 60, and 70% VO2peak. DE was also lower (P < 0.05) during arm crank than cycle exercise at delta 50-60 and at delta 60-70% VO2peak. It is concluded metabolic efficiency as determined by work and delta efficiency indices was lower during arm crank compared with cycle exercise at the same relative intensities. These findings add to the understanding of the difference in metabolic efficiency between upper and lower body exercise.     

Respiratory muscle work compromises leg blood flow during maximal exercise

We hypothesized that during exercise at maximal O2 consumption (VO2max), high demand for respiratory muscle blood flow (Q) would elicit locomotor muscle vasoconstriction and compromise limb Q. Seven male cyclists (VO2max 64 +/- 6 ml.kg-1.min-1) each completed 14 exercise bouts of 2.5-min duration at VO2max on a cycle ergometer during two testing sessions. Inspiratory muscle work was either 1) reduced via a proportional-assist ventilator, 2) increased via graded resistive loads, or 3) was not manipulated (control). Arterial (brachial) and venous (femoral) blood samples, arterial blood pressure, leg Q (Qlegs; thermodilution), esophageal pressure, and O2 consumption (VO2) were measured. Within each subject and across all subjects, at constant maximal work rate, significant correlations existed (r = 0.74-0.90; P < 0.05) between work of breathing (Wb) and Qlegs (inverse), leg vascular resistance (LVR), and leg VO2 (VO2legs; inverse), and between LVR and norepinephrine spillover. Mean arterial pressure did not change with changes in Wb nor did tidal volume or minute ventilation. For a +/-50% change from control in Wb, Qlegs changed 2 l/min or 11% of control, LVR changed 13% of control, and O2 extraction did not change; thus VO2legs changed 0.4 l/min or 10% of control. Total VO2max was unchanged with loading but fell 9.3% with unloading; thus VO2legs as a percentage of total VO2max was 81% in control, increased to 89% with respiratory muscle unloading, and decreased to 71% with respiratory muscle loading. We conclude that Wb normally incurred during maximal exercise causes vasoconstriction in locomotor muscles and compromises locomotor muscle perfusion and VO2.     

Central and regional circulatory effects of adding arm exercise to leg exercise

7 young, healthy, male subjects performed exercise on bicycle ergometers in two 20 min periods with an interval of 1 h. The first 10 min of each 20 min period consisted of arm exercise (38--62% of Vo2 max for arm exercise) or leg exercise (58--78% of Vo2 max for leg exercise). During the last 10 min the subjects performed combined arm and leg exercise (71--83% of Vo2 max for this type of exercise). The following variables were measured during each type of exercise: oxygen uptake, heart rate, mean arterial blood pressure, cardiac output, leg blood flow (only during leg exercise and combined exercise), arterio-venous concentration differences for O2 and lactate at the levels of the axillary and the external iliac vessels. Superimposing a sufficiently strenuous arm exercise (oxygen uptake for arm exercise greater than 40% of oxygen uptake for combined exercise) on leg exercise caused a reduction in blood flow and oxygen uptake in the exercising legs with unchanged mean arterial blood pressure. Superimposing leg exercise on arm exercise caused a decrease in mean arterial blood pressure and an increased axillary arterio-venous oxygen difference. These findings indicate that the oxygen supply to one large group of exercising muscles may be limited by vasoconstriction or by a fall in arterial pressure, when another large group of muscles is exercising simultaneously.     

Effects of prior arm exercise on pulmonary gas exchange kinetics during high-intensity leg exercise in humans

The activation of MAPKs is controlled by the balance between MAPK kinase and MAPK phosphatase activities. The latter is mediated by a subset of phosphatases with dual specificity (VH-1 family). Here, we describe a new member of this family encoded by the puckered gene of Drosophila. Mutations in this gene lead to cytoskeletal defects that result in a failure in dorsal closure related to those associated with mutations in basket, the Drosophila JNK homolog. We show that puckered mutations result in the hyperactivation of DJNK, and that overexpression of puc mimics basket mutant phenotypes. We also show that puckered expression is itself a consequence of the activity of the JNK pathway and that during dorsal closure, JNK signaling has a dual role: to activate an effector, encoded by decapentaplegic, and an element of negative feedback regulation encoded by puckered.     

Validity of oxygen uptake measurements during exercise under moderate hyperoxia

PURPOSE: The validity of oxygen uptake in hyperoxia (FIO2 = 30%) measured by an automated system (MedGraphics, CPX/D system) was assessed during the simulation of gas exchanges during exercise with a mechanical system and during submaximal exercise by human subjects. METHODS: The simulation system reproduced a stable and accurate VO2 for 30 min (sim-test). This trial was repeated nine times in normoxia and nine times in hyperoxia. Ten subjects also performed two submaximal exercises (55% of normoxic VO2max) on a cycle ergometer at the same absolute power in normoxia and in hyperoxia (ex-test). RESULTS: There was a significant downward drift of the oxygen fraction measurement in hyperoxia (< or = 0.10% for FIO2 and FEO2) during sim-test, but VO2 measurement remained stable in the two conditions. There was also a downward drift of the oxygen fraction measurement in the two conditions (< or = 0.07% for FIO2) during ex-test. VO2 was significantly higher in hyperoxia (+4.6%), and this result was confirmed using a modified Douglas bag method. CONCLUSIONS: These findings show that the CPX/D system is stable and valid for assessing VO2 in moderate hyperoxia.     

Augmented upper body contribution to oxygen uptake during upper body exercise with concurrent leg functional electrical stimulation in persons with spinal cord injury

The purpose of this pilot study was to compare the contribution of upper body musculature to VO2 with and without concurrent leg FES (LFES). Eight subjects with spinal cord injury, lesion levels range C6-T12, performed upper body exercise (UBE) during no LFES (NOS), LFES at 40 mA (LOS), and 80 mA (HIS), at rest, 60% and 80% of VO2peak. Resting VO2 values were obtained during NOS, LOS and HIS conditions and were then subtracted from their respective whole body VO2 values to give an estimate of upper body VO2. Small and non significant increases were found in the HIS vs NOS condition at 60% VO2peak. Larger differences of 7.8% were found in the HIS vs NOS condition at 80% VO2peak (11.35+/-3.8 ml kg(-1) min(-1) to 12.24+/-4.0 ml kg(-1) min(-1)), although this too was not significant, perhaps due to the small number of subjects in this study and the consequently low statistical power to detect a significant difference. We discuss the implications for these preliminary results in the context of the existing literature on this topic.     

Prediction of maximum oxygen uptake during physical exercise on bicycle ergometer

Possibilities to predict maximum oxygen uptake (VO2max) during exercising on bicycle ergometer using the Russian Rating Perceived Exertion (RPE) was studied. Results of examination of 13 athletes demonstrate the possibility of predicting individual and group average VO2max on the basis of data from submaximum testing and the empirical formulas from the value of VO2max registered at RPE numbers 13 and 15. These VO2max values can serve as markers for assessing the dynamics of physical performance.     

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.     

Effects of arm support on shoulder and arm muscle activity during sedentary work

The aim of this study was to evaluate different arm supports by comparing the activity of shoulder and arm muscles during various work tasks, with and without the lower arm supported. Twelve female subjects, aged between 23 and 37 years, were asked to perform three types of tasks: typing, simulated assembly work (in two different positions), and pipetting. The supports used were: fixed arm support (FIX), horizontal movable arm support (HOR), and spring-loaded arm support (SLA). During the experiments, the electromyograms (EMG) of four muscles were simultaneously recorded: m. deltoideus anterior and lateralis, m. trapezius pars descendens and m. extensor carpi radialis brevis. Normalization was made against maximum isometric contraction. The mean values of the normalized EMG levels showed a reduced EMG level of the shoulder muscles when using arm supports in all the tasks, and for all muscles but the wrist extensor, compared to the EMG levels without arm supports. The horizontal movable support was more effective in reducing the EMG levels of the shoulder muscles than other arm supports, in tasks at table height. Thus, it is possible to reduce muscle activity of the shoulder region by using arm supports. Further research is needed to make biomechanical calculations to compare the EMG level of these muscles using suspension and the effects of inclination of work task.     

Decline in maximal oxygen uptake on work performance in rats during the developmental phase

Development-related changes in maximal oxygen uptake (VO2max) and work performance were examined in young sedentary rats 4-11 weeks after birth during exercise. The running speed to elicit VO2max increased from 4 to 8 weeks of age, whereas the exercise VO2max declined progressively. Therefore, the work performance during the developmental phase, when rapid growth occurs, seems to be little related to the decline in the relative VO2 max.     

Determinants of oxygen uptake. Implications for exercise testing

For exercise modalities such as cycling which recruit a substantial muscle mass, muscle oxygen uptake (VO2) is the primary determinant of pulmonary VO2. Indeed, the kinetic complexities of pulmonary VO2 associated with exercise onset and the non-steady state of heavy (> lactate threshold) and severe [> asymptote of power-time relationship for high intensity exercise (W)] exercise reproduce with close temporal and quantitative fidelity those occurring across the exercising muscles. For moderate (< lactate threshold) exercise and also rapidly incremental work tests, pulmonary (and muscle) VO2 increases as a linear function of work rate (approximately equal to 9 to 11 ml O2/W/min) in accordance with theoretical determinations of muscle efficiency (approximately equal to 30%). In contrast, for constant load exercise performed in the heavy and severe domains, a slow component of the VO2 response is manifest and pulmonary and muscle VO2 increase as a function of time as well as work rate beyond the initial transient associated with exercise onset. In these instances, muscle efficiency is reduced as the VO2 cost per unit of work becomes elevated, and in the severe domain, this VO2 slow component drives VO2 to its maximum and fatigue ensues rapidly. At pulmonary maximum oxygen uptake (VO2max) during cycling, the maximal cardiac output places a low limiting ceiling on peak muscle blood flow, O2 delivery and thus muscle VO2. However, when the exercise is designed to recruit a smaller muscle mass (e.g. leg extensors, 2 to 3kg), mass-specific muscle blood flow and VO2 at maximal exercise are 2 to 3 times higher than during conventional cycling. consequently, for any exercise which recruits more than approximately equal to 5 to 6kg of muscle at pulmonary VO2max, there exists a mitochondrial or VO2 reserve capacity within the exercising muscles which cannot be accessed due to oxygen delivery limitations. The implications of these latter findings relate to the design of exercise tests. Specifically, if the purpose of exercise testing is to evaluate the oxidative capacity of a small muscle mass (< 5 to 6kg), the testing procedure should be designed to restrict the exercise to those muscles so that a central (cardiac output, muscle O2 delivery) limitation is not invoked. It must be appreciated that exercise which recruits a greater muscle mass will not stress the maximum mass-specific muscle blood flow and VO2 but rather the integration of central (cardiorespiratory) and peripheral (muscle O2 diffusing capacity) limitations.     

Unaltered oxygen uptake kinetics at exercise onset with lower-body positive pressure in humans

The purpose of this study was to determine the influence of a reduced skeletal muscle blood flow on oxygen uptake (VO2) kinetics at the onset of cycle ergometer exercise. Seven healthy subjects performed rest-to-exercise transitions with a lower-body positive pressure (LBPP) of 45 Torr. Two work rates were selected for each subject: a moderate intensity (VO2, approximately 1.9 l min-1; delta[lactate], approximately 1 mequiv l-1) below the estimated lactate threshold and a heavy intensity (VO2, approximately 2.6 l min-1; delta[lactate], approximately 3 mequiv l-1) above this threshold. Pulmonary gas exchange variables and ventilatory (VE) responses were computed breath-by-breath from mass spectrometer and turbine volume meter signals, respectively, and mean response times (MRT) calculated. Samples of 'arterialized' venous blood were used for the determination of [lactate], pH and [K+]. While the application of 45 Torr LBPP had no effects on VO2 kinetics during moderate exercise (MRT: 33.5 +/- 1.2 s at 45 Torr vs. 32.8 +/- 1.3 s at 0 Torr; P > 0.05) or on [lactate], pH or [K+], breathing frequency (f) was increased (P < 0.05) and tidal volume (VT) reduced (P < 0.05). The addition of LBPP during heavy exercise did not alter VO2 kinetics (MRT: 35.2 +/- 1.5 s at 45 Torr vs. 34.8 +/- 1.5 s at 0 Torr; P > 0.05), or [lactate], pH or [K+]. Although both the VE (via an increased f) and CO2 output (VCO2) were significantly greater with LBPP by approximately 30 l min-1 and approximately 500 ml min-1, respectively, end-tidal CO2 partial pressure was decreasing, suggesting an additional ventilatory stimulus. These data can be interpreted to suggest that oxygen delivery is not critically dependent upon blood flow to the working muscle at exercise onset, while LBPP-induced increases in VE during suprathreshold exercise may be related to an accumulation of metabolites at the working muscle or the effects of pressure per se.     

Kinetics of oxygen uptake at the onset of exercise in boys and men

The objective of this study was to compare the O2 uptake (VO2) kinetics at the onset of heavy exercise in boys and men. Nine boys, aged 9-12 yr, and 8 men, aged 19-27 yr, performed a continuous incremental cycling task to determine peak VO2 (VO2 peak). On 2 other days, subjects performed each day four cycling tasks at 80 rpm, each consisting of 2 min of unloaded cycling followed twice by cycling at 50% VO2 peak for 3.5 min, once by cycling at 100% VO2 peak for 2 min, and once by cycling at 130% VO2 peak for 75 s. O2 deficit was not significantly different between boys and men (respectively, 50% VO2 peak task: 6.6 +/- 11.1 vs. 5.5 +/- 7.3 ml . min-1 . kg-1; 100% VO2 peak task: 28.5 +/- 8.1 vs. 31.8 +/- 6.3 ml . min-1 . kg-1; and 130% VO2 peak task: 30.1 +/- 5.7 vs. 35.8 +/- 5.3 ml . min-1 . kg-1). To assess the kinetics, phase I was excluded from analysis. Phase II VO2 kinetics could be described in all cases by a monoexponential function. ANOVA revealed no differences in time constants between boys and men (respectively, 50% VO2 peak task: 22. 8 +/- 5.1 vs. 26.4 +/- 4.1 s; 100% VO2 peak task: 28.0 +/- 6.0 vs. 28.1 +/- 4.4 s; and 130% VO2 peak task: 19.8 +/- 4.1 vs. 20.7 +/- 5. 7 s). In conclusion, O2 deficit and fast-component VO2 on-transients are similar in boys and men, even at high exercise intensities, which is in contrast to the findings of other studies employing simpler methods of analysis. The previous interpretation that children rely less on nonoxidative energy pathways at the onset of heavy exercise is not supported by our findings.     

Correlates of maximal oxygen consumption during treadmill exercise

According to the Balke treadmill protocol, 39 healthy male USAF volunteers were subjected to maximal exercise. The subjects as a group passed the anaerobic threshold by the end of exercise since average venous lactate concentrations increased from 11.2 +/- 1.6 mg% (95% confidence limits) to 93.0 +/- 8.5 mg% (95% confidence limits), and the average gas exchange ratio (R) at the end of the exercise was greater than unity (p less than 0.0005). Tests for correlations showed weak but statistically significant (p less than 0.05) relationships between change in venous lactic acid concentrations and R (r = 0.44) and maximal heart rate (r = 0.34). Maximal oxygen consumption was correlated with time of exercise (r = 0.70) and subject weight (r = 0.33). Subject age and initial plasma lactate concentrations were not significantly correlated with any other variables. Multiple linear regression yielded an equation for prediction of maximal oxygen consumption which included terms for time of exercise and subject weight. Although the multiple correlation coefficent (r = 0.75) was statistically significant (p less than 0.05), it was considered insufficient for accurate prediction of maximal oxygen consumption.     

Maximal oxygen uptake: "classical" versus "contemporary" viewpoints: a rebuttal

Bassett and Howley contend that the 1996 J. B. Wolffe lecture is erroneous because: 1) A. V. Hill did establish the existence of the "plateau phenomenon," 2) the maximum oxygen consumption (VO2max) is limited by the development of anaerobiosis in the active muscle, and 3) endurance performance is also determined by skeletal muscle anaerobiosis because the VO2max is the best predictor of athletic ability. As a result, 4) cardiovascular and not skeletal muscle factors determine endurance performance. They further contend that Hill's "scientific hunches were correct," requiring "only relatively minor refinements" in the past 70 yr. But the evidence presented in this rebuttal shows that Hill neither sought nor believed in either the "plateau phenomenon" or the concept of the individual maximum oxygen consumption. These twin concepts were created by Taylor et al. (97) in 1955 and erroneously attributed to Hill. Rather Hill believed that there was a universal human VO2max of 4 L x min(-1). His error resulted from his incorrect belief that the real VO2 unmeasurable because it includes a large "anaerobic component," rose exponentially at running speeds greater than 13.2 km x h(-1). But Hill and his colleagues were indeed the first to realize the danger that a plateau in cardiac output (CO) and hence in VO2 would pose for the heart itself. For unlike skeletal muscle, the pumping capacity of the heart is both dependent on, but also the determinant of, its own blood supply. Thus, if the CO reaches a peak causing the "plateau phenomenon," the immediate cause of that peak will have been a plateau in myocardial oxygen delivery, causing a developing myocardial ischemia. The ischemia must worsen as exercise continues beyond the supposed VO2 "plateau." To accommodate this dilemma, Hill and his colleagues proposed a governor "either in the heart muscle or in the nervous system" necessary to prevent myocardial ischemia developing during maximal exercise. This governor would cause maximal exercise to terminate before the development of a plateau in either coronary flow, CO, or VO2, or the onset of skeletal muscle anaerobiosis. Accordingly, a new physiological model is proposed in which skeletal muscle recruitment is regulated by a central "governor" specifically to prevent the development of a progressive myocardial ischemia that would precede the development of skeletal muscle anaerobiosis during maximum exercise. As a result cardiovascular function "limits" maximum exercise capacity, probably as a result of a limiting myocardial oxygen delivery. The model is compatible with all the published findings of cardiovascular function during exercise in hypobaric hypoxia, in which there is a greater likelihood that myocardial hypoxia will develop.     

H-reflex and F-wave potentials in leg and arm muscles

The systematic analyses of secondary muscle potentials of H-reflex and F-wave type were done in multicentric study. The examinations were carried out in healthy volunteers with 9 muscles analysed on the legs and 9 on the lower arms and hands. The H-reflex potential was found regularly in thigh muscles (vastus medialis 100%, biceps femoris 97%, semitendinosus 93%). Less frequently but still with high incidence it appeared in posterior lower leg muscles (soleus 93%, caput mediale gastrocnemii 73%). In anterior tibial muscle and extensor digitorum brevis it did not appear at all. Only exceptionally it was found in short peroneal muscle (3%) and occasionally, only on proximal nerve stimulation, in flexor hallucis brevis. The similar distribution pattern was found in lower arm and hand muscles with analysis on both sides. In flexor digitorum superficialis (73-70%) and flexor carpi radialis (73-57%) the percentage of H-potential muscles was the highest, in flexor carpi ulnaris (47-40%) lesser but still remarkable. Brachioradialis (37-30%) and extensor digitorum communis (27-27%) percentage decreased further. The even more distal, pronator quadratus (21-20%) and abuctor digiti minimi (17-17%) presented as muscles with low incidence of H-reflex positivity. In extensor indicis proprius (3%) the lowest H-potential incidence was found and in opponens pollicis no H-potential at all. F-waves if evaluated as "F-frequency" follow the similar distribution pattern. The lowest "F-frequency" was found on the legs in anterior tibial, short peroneal and extensor digitorum brevis muscles. In the last one more than one half of stimuli failed to evoke the F-potential. Those are the muscles in which H-potentials almost never appeared. The highest "F-frequency" was recorded in thigh, posterior lower leg muscle and flexor hallucis brevis. Some of the examinees displayed in almost all examined muscles H-potential (6 of 30), the others (9 of 30) had it in neither one or in a single muscle. It looks like as if a kind of H-reflex or F-wave individuals exist. If the H- or F-potentials distribution pattern got projected on the homunculus in quadrupedal position the following idea appears. The thigh muscles, the plantar flexors of the feet and hand and finger flexors are first of all tonic muscles mostly involved in standing or holding. The extensors of the foot/toes, respectively of hand/fingers interrupt phasically the sustained action of standing by lifting the foot/hand from the ground. The muscles with mostly tonic function produce much H-reflexes, transitional forms or at least F-wave with high "F-frequency". Is that a kind of phylogenetical remnants, better developed in the motorically less differentiated legs? Have the H-reflex muscles if compared with F-wave muscles different motor units structure? Have they different motoneurons, with different liability to produce recurrent discharges?     

Oxygen uptake kinetics during low level exercise in patients with heart failure: relation to neurohormones, peak oxygen consumption, and clinical findings

OBJECTIVE: To investigate whether oxygen uptake (VO2) kinetics during low intensity exercise are related to clinical signs, symptoms, and neurohumoral activation independently of peak oxygen consumption in chronic heart failure. DESIGN: Comparison of VO2 kinetics with peak VO2, neurohormones, and clinical signs of chronic heart failure. SETTING: Tertiary care centre. PATIENTS: 48 patients with mild to moderate chronic heart failure. INTERVENTIONS: Treadmill exercise testing with "breath by breath" gas exchange monitoring. Measurement of atrial natriuretic factor (ANF), brain natriuretic peptide (BNP), and noradrenaline. Assessment of clinical findings by questionnaire. MAIN OUTCOME MEASURES: O2 kinetics were defined as O2 deficit (time [rest to steady state] x DeltaVO2 -sigmaVO2 [rest to steady state]; normalised to body weight) and mean response time of oxygen consumption (MRT; O2 deficit/DeltaVO2). RESULTS: VO2 kinetics were weakly to moderately correlated to the peak VO2 (O2 deficit, r = -0.37, p < 0.05; MRT, r = -0.49, p < 0.001). Natriuretic peptides were more closely correlated with MRT (ANF, r = 0.58; BNP, r = 0.53, p < 0.001) than with O2 deficit (ANF, r = 0.48, p = 0.001; BNP, r = 0.37, p < 0.01) or peak VO2 (ANF, r = -0.40; BNP, r = -0.31, p < 0.05). Noradrenaline was correlated with MRT (r = 0. 33, p < 0.05) and O2 deficit (r = 0.39, p < 0.01) but not with peak VO2 (r = -0.20, NS). Symptoms of chronic heart failure were correlated with all indices of oxygen consumption (MRT, r = 0.47, p < 0.01; O2 deficit, r = 0.39, p < 0.01; peak VO2, r = -0.48, p < 0. 01). Multivariate analysis showed that the correlation of VO2 kinetics with neurohormones and symptoms of chronic heart failure was independent of peak VO2 and other variables. CONCLUSIONS: Oxygen kinetics during low intensity exercise may provide additional information over peak VO2 in patients with chronic heart failure, given the better correlation with neurohormones which represent an index of homeostasis of the cardiovascular system.     

Mechanisms facilitating oxygen delivery during exercise in patients with chronic heart failure

The aim of the study was to estimate the relative importance of the Bohr effect and redistribution of blood from the non-exercising tissues on the arterial-venous oxygen content differences across the exercising extremities and the central circulation in patients with chronic heart failure; the relationship among femoral vein, systemic and pulmonary artery oxygen partial pressure and hemoglobin saturation was determined. It has been reported that the maximal reduction in femoral vein pO2 precedes peak oxygen consumption and lactic acidosis threshold in patients with chronic heart failure and normal subjects during exercise. The increase in oxygen consumption at work rates above lactic acidosis threshold, therefore, must be accounted for by increase in blood flow in the exercising muscles and right-ward shift on the oxyhemoglobin dissociation curve. Since the total cardiac output increase is blunted in patients with chronic heart failure, diversion of blood flow from non-exercising to exercising tissues may account for some of the increase in muscle blood flow. Ten patients with chronic heart failure performed a progressively increasing leg cycle ergometer exercise test up to maximal effort while measuring ventilation and gas concentration for computation of oxygen uptake and carbon dioxide production, breath-by-breath. Blood samples were obtained, simultaneously, from systemic and pulmonary arteries and femoral vein at rest and every minute during exercise to peak oxygen consumption. At comparable levels of exercise, femoral vein pO2, hemoglobin saturation and oxygen content were lower than in the pulmonary artery. PCO2 and lactate concentration increased steeply in femoral vein and pulmonary artery blood above lactic acidosis threshold (due to lactic acid build-up and buffering), but more steeply in femoral vein blood. These increases allowed femoral vein oxyhemoglobin to dissociate without a further decrease in femoral vein pO2 (Bohr effect). The lowest femoral vein pO2 (16.6 +/- 3.9 mmHg) was measured at 66 +/- 22% of peak VO2 and before the lowest oxyhemoglobin saturation was reached. Artero-venous oxygen content difference was higher in the femoral vein than in the pulmonary artery; this difference became progressively smaller as oxygen consumption increased. "Ideal" oxygen consumption for a given cardiac output (oxygen consumption expected if all body tissues had maximized oxygen extraction) was always higher than the measured oxygen consumption; however the difference between the two was lost at peak exercise. This difference positively correlated with peak oxygen consumption and cardiac output increments at submaximal but not at maximal exercise. In conclusion, femoral vein pO2 reached its lowest value at a level of exercise at or below the lactic acidosis threshold. Further extraction of oxygen above the lactic acidosis threshold was accounted for by a right shift of the oxyhemoglobin dissociation curve. The positive correlation between increments of cardiac output vs "ideal" and measured oxygen consumption suggests a redistribution of blood flow from non-exercising to exercising regions of the body. Furthermore the positive correlation between exercise capacity and the difference between "ideal" and measured oxygen consumption suggests that patients with the poorer function have the greater capability to optimize blood flow redistribution during exercise.