Metabolic responses to light arm and leg exercise when sitting

Seven male subjects performed progressive exercises with a light work load on an upper limb or bicycle ergometer in the sitting position. At any comparable work load above zero, arm exercise induced higher oxygen uptake, ventilation, heart rate, oxygen pulse, respiratory rate and tidal volume than leg exercise. At similar levels of VO2 above 0.45 1 X min-1, heart rate and ventilation were higher during arm exercise. A close linear relationship between carbon dioxide output and oxygen uptake was observed during both arm and leg exercises, the slope for arm work being steeper. The ventilatory equivalent for VCO2 (VE/VCO2) gradually decreased during both types of exercise. The ventilatory equivalent for VO2(VE/VO2) remained constant (arm) while it rose (leg) to a peak at 9.8 W and then gradually decreased. Ventilation in relation to tidal volume had a linear relationship with leg exercise, but became curvilinear with arm exercise after tidal volume exceeded 1100 ml. The observed differences in response between arm and leg exercises at a given work load appear to be influenced by differences in sympathetic outflow due to the greater level of static contraction of the relatively small muscle groups required by arm exercise.     

Maximal oxygen uptake is not limited by a central nervous system governor.

We tested the hypothesis that the work of the heart was not a limiting factor in the attainment of maximal oxygen uptake (VO2 max). We measured cardiac output (Q) and blood pressures (BP) during exercise at two different rates of maximal work to estimate the work of the heart through calculation of the rate-pressure product, as a part of the ongoing discussion regarding factors limiting VO2 max. Eight well-trained men (age 24.4 +/- 2.8 yr, weight 81.3 +/- 7.8 kg, and VO2 max 59.1 +/- 2.0 ml x min(-1) x kg(-1)) performed two maximal combined arm and leg exercises, differing 10% in watts, with average duration of time to exhaustion of 4 min 50 s and 3 min 40 s, respectively. There were no differences between work rates in measured VO2 max, maximal Q, and peak heart rate between work rates (0.02 l/min, 0.3 l/min, and 0.8 beats/min, respectively), but the systolic, diastolic, and calculated mean BP were significantly higher (19, 5, and 10 mmHg, respectively) in the higher than in the lower maximal work rate. The products of heart rate times systolic or mean BP and Q times systolic or mean BP were significantly higher (3,715, 1,780, 569, and 1,780, respectively) during the higher than the lower work rate. Differences in these four products indicate a higher mechanical work of the heart on higher than lower maximal work rate. Therefore, this study does not support the theory, which states that the work of the heart, and consequently VO2 max, during maximal exercise is hindered by a command from the central nervous system aiming at protecting the heart from being ischemic.     

Sex-related differences in free plasma catecholamines in individuals of similar performance ability during graded ergometric exercise

Sex-related differences of catecholamine responses were evaluated in nine healthy women and six age-matched men at rest and during incremental treadmill exercise. Heart rate, oxygen uptake (VO2), glucose and lactate blood levels as well as the free plasma catecholamines, noradrenaline and adrenaline, were determined. No significant differences were observed for these parameters between the two groups at rest. The females had relative VO2max and maximal running velocities similar to the males, which points to a comparable dynamic performance ability. However, at identical work loads, noradrenaline, adrenaline and glucose levels were significantly higher in women than in men. Lactate, heart rate and relative VO2 showed a similar tendency at submaximal exercise levels, indicating higher strain at identical stress levels in women. The reason for the higher sympathetic activity in women at identical work loads may be their relatively smaller skeletal muscle mass in relation to the loads during this test.     

Linear and nonlinear characteristics of oxygen uptake kinetics during heavy exercise.

We assessed the linearity of oxygen uptake (VO2) kinetics for several work intensities in four trained cyclists. VO2 was measured breath by breath during transitions from 33 W (baseline) to work rates requiring 38, 54, 85, and 100% of maximal aerobic capacity (VO2max). Each subject repeated each work rate four times over 8 test days. In every case, three phases (phases 1, 2, and 3) of the VO2 response could be identified. VO2 during phase 2 was fit by one of two models: model 1, a double exponential where both terms begin together close to the start of phase 2, and model 2, a double exponential where each of the exponential terms begins independently with separate time delays. VO2 rose linearly for the two lower work rates (slope 11 ml.min-1 W-1) but increased to a greater asymptote for the two heavier work rates. In all four subjects, for the two lighter work rates the double-exponential regression reduced to a single value for the time constant (average across subjects 16.1 +/- 7.7 s), indicating a truly monoexponential response. In addition, one of the responses to the heaviest work rate was monoexponential. For the remaining seven biexponential responses to the two heaviest work rates, model 2 produced a significantly better fit to the responses (P less than 0.05), with a mean time delay for the slow component of 105 +/- 46 s.(ABSTRACT TRUNCATED AT 250 WORDS)     

Energetics of ventricular contraction as traced in the pressure-volume diagram

The pressure-volume (P-V) relationship of the canine left ventricle can reasonably be simulated by a time-varying elastance model. In this model the total mechanical energy generated by a contraction can be determined theoretically from the change in the elastance. Applying this theory to the actual left ventricle, we have found that the area in the P-V diagram circumscribed by the end-systolic P-V relation line, the end-diastolic P-V relation curve, and the systolic segment of the P-V trajectory is equivalent to the total mechanical energy generated by ventricular contraction. We call this area the systolic P-V area (PVA). We have studied experimentally the correlation between the PVA and myocardial oxygen consumption (VO2) in the canine left ventricle. VO2 was linearly correlated with PVA regardless of the contraction mode and loading conditions in a given left ventricle. The VO2-PVA relation parallel shifted upward with positive inotropic agents. This shift comprised a significant increase in VO2 component for the unloaded contraction. We therefore consider that further analyses of the VO2-PVA relationship will greatly promote our understanding of cardiac energetics.     

Metabolic and cardiovascular adjustment to arm training

Maximal and submaximal metabolic and cardiovascular measures and work capacity were studied in control (n = 7) and experimental (n = 9) subjects (S's) during arm work prior to and following 10 wk of interval arm training. These measures were oxygen uptake (VO2), minute ventilation (VE), heart rate (HR), respiratory exchange ratio (R), cardiac output (Q), stroke volume (SV), and arteriovenous oxygen difference ((a--v)O2 diff). In addition, maximal oxygen uptake (VO2max) was measured in both groups during treadmill running. Experimental S's showed significant increases (P less than 0.01) in peak VO2 (438 ml.min-1), max VE (17.7 l.min-1), max (a--v)O2 diff (20.8 ml.l-1), and work time (9.2 min) during arm ergometry, while maximum values of Q, SV, HR, and R remained unchanged. In addition, submaximal heart rates were significantly lower during arm ergometry after training. VO2max during treadmill running remained essentially unchanged. No changes in metabolic and physiological measures were noted for the controls after the 10-wk training period. The results support the concept of training specificity for VO2max, and indicate that the improvement in peak VO2 in arm ergometry reflects enhanced oxygen utilization due to an expanded (a--v)O2 diff.     

Relation between the change of slope of heart rate and second lactic and ventilatory thresholds in muscular exercise with large load]

The time-course of heart rate, blood lactate, and ventilatory gas exchange was studied during an incremental exercise test on cycloergometer in order to ascertain whether heart rate deflection occurred at the same load as the second lactate S[La]2) and ventilatory (SV2) thresholds. Twelve moderately trained subjects, 22 to 30 years old, participated in the study. The initial power setting was 30 W for 3 min with successive increases of 30 W every min except at the end of the test where the increase was reduced to 20 and 10 W.min-1. Ventilatory flow (VE), oxygen uptake (VO2), carbon dioxide production (VCO2, ventilatory equivalents of O2 (EO2 = VE/VO2) and CO2 (ECO2 = VE/VCO2), and heart rate (HR) were determined during the last 20 s of every min. Venous blood samples were drawn at the end of each stage of effort and analyzed enzymatically for lactate concentration ([La]). The HR deflection, S[La]2, and SV2 were represented graphically by two investigators using a double blind procedure. Following the method proposed by Conconi et al. 1982, the deflection in HR was considered to begin at the point beyond which the increase in work intensity exceeded the increase in HR and the linearity of the work rate/HR relationship was lost. S[La]2 corresponded to the second breaking point of the lactate time-course curve (onset of blood lactate accumulation) and SV2 was identified at the second breaking point in the increase in VE and ventilatory equivalent for O2 uptake accompanied by a concomitant increase in ventilatory equivalent for CO2 output. We observed that the deflection point in HR was present only in 7 subjects. The work load, VO2, HR, and [La] levels at which heart rate departed from linearity did not differ significantly from those determined with S[La]2 ans SV2. The VO2 and HR values at HR deflection point were significantly correlated with those measured at S[La]2 and SV2. It is concluded that deflection in heart rate does not always occur, and when it does, it coincides with the second lactate and ventilatory gas exchange thresholds. It can thus be used for the determination of optimal intensity for individualized aerobic training.     

Left ventricular chamber stiffness at rest as a determinant of exercise capacity in heart failure subjects with decreased ejection fraction.

Impaired exercise tolerance, determined by peak oxygen consumption (VO2 peak), is predictive of mortality and the necessity for cardiac transplantation in patients with chronic heart failure (HF). However, the role of left ventricular (LV) diastolic function at rest, reflected by chamber stiffness assessed echocardiographically, as a determinant of exercise tolerance is unknown. Increased LV chamber stiffness and limitation of VO2 peak are known correlates of HF. Yet, the relationship between chamber stiffness and VO2 peak in subjects with HF has not been fully determined. Forty-one patients with HF New York Heart Association [(NYHA) class 2.4 +/- 0.8, mean +/- SD] had echocardiographic studies and VO2 peak measurements. Transmitral Doppler E waves were analyzed using a previously validated method to determine k, the LV chamber stiffness parameter. Multiple linear regression analysis of VO(2 peak) variance indicated that LV chamber stiffness k (r2 = 0.55) and NYHA classification (r2 = 0.43) were its best independent predictors and when taken together account for 59% of the variability in VO2 peak. We conclude that diastolic function at rest, as manifested by chamber stiffness, is a major determinant of maximal exercise capacity in HF.     

Metabolic and cardiovascular adjustment to work in air and water at 18, 25, and 33 degrees C.

By use of successive increments of discontinuous work with an arm-leg cycle ergometer the VO2, Q, SV, and HR were studied in six male subjects at rest and during exercise in air and in water at 18, 25, and 33 degrees C. The Q values obtained by CO2 rebreathing were reproducible. VO2 was linearly related to work with the plots for air and 33 degrees C water being similar. However, during work in 25 and 18 degrees C water, the VO2 averaged 9.0% (150 ml) and 25.3% (400 ml) higher, respectively, than values observed in 33 degrees C water, with the largest differences observed in leaner subjects. The plot of HR-VO2 was linear and almost identical during work in air and 33 degrees C water, but shifted significantly to the right in cooler water. VO2 averaged 250-700 ml higher in cold water compared to air and 33 degrees C water at a given mean heart rate. The Q vs. VO2 line was similar during work in air and in water with no effect of water or temperature. At similar levels of VO2, SV was significantly larger (P less than 0.05) in 25 and 18 degrees C water than in air or 33 degrees C water. Consequently, the reduction in heart rate during work in cold water was entirely compensated for by a proportionate increase in the SV of the heart. Q was therefore maintained at similar levels of energy expenditure in air and in 18, 25, and 30 degrees C water.     

Angiotensin-converting enzyme ID polymorphism and fitness phenotype in the HERITAGE Family Study.

It has been suggested that genetic variation in the angiotensin-converting enzyme (ACE) gene is associated with physical performance. We studied the association between the ACE insertion (I)/deletion (D) polymorphism and several fitness phenotypes measured before and after 20 wk of a standardized endurance training program in sedentary Caucasian (n = 476) and black (n = 248) subjects. Phenotypes measured were oxygen uptake (VO(2)), work rate, heart rate, minute ventilation, tidal volume, and blood lactate levels during maximal and submaximal [50 W and at 60 and 80% of maximal VO(2) (VO(2 max))] exercise and stroke volume and cardiac output during submaximal exercise (50 W and at 60% VO(2 max)). The ACE ID polymorphism was typed with the three-primer PCR method. Out of 216 association tests performed on 54 phenotypes in 4 groups of participants, only 11 showed significant (P values from 0.042 to 0. 0001) associations with the ACE ID polymorphism. In contrast to previous claims, in Caucasian offspring, the DD homozygotes showed a 14-38% greater increase with training in VO(2 max), VO(2) at 80% of VO(2 max), and all work rate phenotypes and a 36% greater decrease in heart rate at 50 W than did the II homozygotes. No associations were evident in Caucasian parents or black parents or offspring. Thus these data do not support the hypothesis that the ACE ID polymorphism plays a major role in cardiorespiratory endurance.     

Gas exchange responses to ramp exercise

In the present study, the system of oxygen uptake (VO2) during ramp function exercise protocol can be studied to provide information about the physiological mechanisms underlying the process. The values of maximal oxygen uptake (VO2max) and gas exchange threshold (GET) were reproducibly obtained using ramp test protocol. On the other hand, the determination of VO2/work rate should be restrict to below the exercise intensity of the GET. Therefore, ramp exercise test might be usage for determination of VO2max, GET and/or VO2/work rate (i.e., work efficiency). The data obtained in this study concerning the mean response time (MRT) suggests that the ramp test is not a linear, first-order system. Therefore, the ramp exercise test protocol is recommended for the determination of VO2max, GET and work efficiency, but not for MRT.     

The effect of long-term aerobic exercise on maximal oxygen consumption,left ventricular function and serum lipids in elderly women

The purpose of this study was to investigate the changes of maximal oxygen consumption, left ventricular function and serum lipids after 36 weeks of aerobic exercise in elderly women without the influence of drugs. Eight elderly women were studied by M-mode and Doppler echocardiography to assess left ventricular size, mass and function. Maximal oxygen consumption (VO(2)max) was determined for each subject by administering a treadmill exercise test. The training intensity was decided by heart rate reserve. Subjects performed exercise for 40 minutes a day, 3 days a week at 50-60% of the heart rate reserve during the 36 weeks. Exercise capacity was assessed by VO(2)max with a graded exercise test of the treadmill. Weight and % body fat decreased after training. Cardiorespiratory function improved because of the increase in VO(2)max and VO(2)max normalized for body weight after training. Systolic blood pressure significantly decreased. There are no significant difference in all left ventricular's parameters (end-diastolic dimension, end-systolic dimension, end-diastolic volume, end-systolic volume, stroke volume, cardiac output, ejection fraction, fractional shortening) after 36 weeks. Exercise training did not induce left ventricular (LV) enlargement as evidence of an absence of increase in left ventricular end-diastolic volume. The total cholesterol level and triglyceride level decreased after training. High density lipoprotein-cholesterol significantly increased and low density lipoprotein-cholesterol significantly decreased, atherogenic index (AI) significantly decreased and apolipoprotein A-I increased and apolipoprotein B decreased after training. In conclusion, although there was no significant change in left ventricular function, aerobic training showed a positive influence on body composition, maximal oxygen consumption and serum lipids.     

Ramp work tests with three different beta-blockers in normal human subjects

The effects of beta-blockade on the responses of oxygen uptake (VO2), heart rate (HR) and blood lactate (La-) were examined during ramp cycle ergometer tests (50 W.min-1 ramp slope) in 8 healthy male volunteers. Each subject took placebo, or one of four different doses of three different beta-blockers (propranolol, metoprolol or oxprenolol) 2 h prior to each test for a total of 15 exercise tests. VO2 was measured breath-by-breath, HR was sampled once per breath, and La- was obtained every minute. Linear regression analysis was applied to VO2 and HR data to obtain the kinetic parameter total lag time (TLT) and a slope value. La- was analyzed by a continuous exponential model with the lactate slope index (LSI) being derived from the individual response curves. Submaximal exercise HR was significantly depressed at the baseline as well as during the ramp tests by beta-blockade. TLT for HR was significantly affected by beta-blockade, with a dose dependent shift from a placebo value of 16 to 26 s with placebo to a value of -40 to -60 s at the highest dose. Slope of HR was significantly depressed relative to placebo. VO2 kinetics assessed by TLT were not significantly affected by beta-blockade. This slope of the VO2 vs work rate relationship was significantly less than placebo only at the highest dose of beta-blocker. The LSI was not significantly affected by beta-blockade. In contrast with the clear impairment of HR response to exercise during beta-blockade, both the VO2 and La- responses appear to be relatively unaffected by beta-blockade during ramp exercise tests.(ABSTRACT TRUNCATED AT 250 WORDS)     

A framework for biomechanics simulations using four-chamber cardiac models

Computational cardiac models have been extensively used to study different cardiac biomechanics; specifically, finite-element analysis has been one of the tools used to study the internal stresses and strains in the cardiac wall during the cardiac cycle. Cubic-Hermite finite element meshes have been used for simulating cardiac biomechanics due to their convergence characteristics and their ability to capture smooth geometries compactly–fewer elements are needed to build the cardiac geometry–compared to linear tetrahedral meshes. Such meshes have previously been used only with simple ventricular geometries with non-physiological boundary conditions due to challenges associated with creating cubic-Hermite meshes of the complex heart geometry. However, it is critical to accurately capture the different geometric characteristics of the heart and apply physiologically equivalent boundary conditions to replicate the in vivo heart motion. In this work, we created a four-chamber cardiac model utilizing cubic-Hermite elements and simulated a full cardiac cycle by coupling the 3D finite element model with a lumped circulation model. The myocardial fiber-orientations were interpolated within the mesh using the Log-Euclidean method to overcome the singularity associated with interpolation of orthogonal matrices. Physiologically equivalent rigid body constraints were applied to the nodes along the valve plane and the accuracy of the resulting simulations were validated using open source clinical data. We then simulated a complete cardiac cycle of a healthy heart and a heart with acute myocardial infarction. We compared the pumping functionality of the heart for both cases by calculating the ventricular work. We observed a 20% reduction in acute work done by the heart immediately after myocardial infarction. The myocardial wall displacements obtained from the four-chamber model are comparable to actual patient data, without requiring complicated non-physiological boundary conditions usually required in truncated ventricular heart models.     

Specification of the mouse cardiac conduction system in the absence of Endothelin signaling

Coordinated contraction of the heart is essential for survival and is regulated by the cardiac conduction system. Contraction of ventricular myocytes is controlled by the terminal part of the conduction system known as the Purkinje fiber network. Lineage analyses in chickens and mice have established that the Purkinje fibers of the peripheral ventricular conduction system arise from working myocytes during cardiac development. It has been proposed, based primarily on gain-of-function studies, that Endothelin signaling is responsible for myocyte-to-Purkinje fiber transdifferentiation during avian heart development. However, the role of Endothelin signaling in mammalian conduction system development is less clear, and the development of the cardiac conduction system in mice lacking Endothelin signaling has not been previously addressed. Here, we assessed the specification of the cardiac conduction system in mouse embryos lacking all Endothelin signaling. We found that mouse embryos that were homozygous null for both ednra and ednrb, the genes encoding the two Endothelin receptors in mice, were born at predicted Mendelian frequency and had normal specification of the cardiac conduction system and apparently normal electrocardiograms with normal QRS intervals. In addition, we found that ednra expression within the heart was restricted to the myocardium while ednrb expression in the heart was restricted to the endocardium and coronary endothelium. By establishing that ednra and ednrb are expressed in distinct compartments within the developing mammalian heart and that Endothelin signaling is dispensable for specification and function of the cardiac conduction system, this work has important implications for our understanding of mammalian cardiac development.     

Effects of short-term training using powercranks on cardiovascular fitness and cycling efficiency

Powercranks use a specially designed clutch to promote independent pedal work by each leg during cycling. We examined the effects of 6 wk of training on cyclists using Powercranks (n=6) or normal cranks (n=6) on maximal oxygen consumption (VO2max) and anaerobic threshold (AT) during a graded exercise test (GXT), and heart rate (HR), oxygen consumption (VO2), respiratory exchange ration (RER), and gross efficiency (GE) during a 1-hour submaximal ride at a constant load. Subjects trained at 70% of VO2max for 1 h.d(-1), 3 d.wk(-1), for 6 weeks. The GXT and 1-hour submaximal ride were performed using normal cranks pretraining and posttraining. The 1-hour submaximal ride was performed at an intensity equal to approximately 69% of pretraining VO2max with VO2, RER, GE, and HR determined at 15-minute intervals during the ride. No differences were observed between or within groups for VO2max or AT during the GXT. The Powercranks group had significantly higher GE values than the normal cranks group (23.6 +/- 1.3% versus 21.3 +/- 1.7%, and 23.9 +/- 1.4% versus 21.0 +/- 1.9% at 45 and 60 min, respectively), and significantly lower HR at 30, 45, and 60 minutes and VO2 at 45 and 60 minutes during the 1-hour submaximal ride posttraining. It appears that 6 weeks of training with Powercranks induced physiological adaptations that reduced energy expenditure during a 1-hour submaximal ride.     

The Astrand-Ryhming nomogram revisited

Relationships among O2 uptake (VO2), heart rate, and work rate during constant-load submaximal cycle ergometry and ramp-forced exercise to exhaustion have been studied in core groups of trained (n = 15) and untrained (n = 10), 20- to 29-yr-old males. A signal aim was to improve on the accuracy of the 1954 Astrand-Ryhming (A-R) nomogram predicting maximum aerobic power from heart rate elevation at submaximum work rates. A new nomogram has been developed based on a linear relationship, established in experimental groups, between VO2 and delta HR, the latter being defined as the elevation of exercise heart rate above that reached during zero-load pedaling at 90 rpm. The delta HR variable used in a nomogram linking it and submaximum VO2 (either derived by calculation from the concomitant steady-state work rate or measured directly from respiratory gas analysis) successfully differentiated maximum aerobic power of trained from untrained subjects in core groups whose different abilities could not otherwise be distinguished by the A-R nomogram itself. In a validation group of trained (n = 5), untrained (n = 5), and moderately trained (n = 4) 20- to 29-yr-old males, the correlation measured between VO2max values and those predicted from the new nomogram was significantly better (r = 0.98) (P less than 0.05) than predictions made from the A-R nomogram (r = 0.80).     

Heart energetic efficiency in O2-exposed rats studied in isolated working heart.

Death in normobaric hyperoxia was related in the past to pulmonary insufficiency of the edematous lung. However, high arterial O2 tension on final collapse led to the suggestion that the heart and not the lung is the first organ that fails. We measured aortic flow, coronary flow, left ventricular pressure, affluent and effluent PO2, PCO2, and pH in the working heart excised from control and normobaric O2-exposed rats (51-63 h). The oxygen consumption (VO2) of experimental hearts was not different from control, but mechanical power output (PVAP) (calculated from pressure-volume area) was reduced as a function of O2 exposure time. Myocardial contractility indexes, maximal elastance and maximal time derivative of pressure, increased as a function of O2 exposure time, being below control values after 50 h and above control values after 60 h. The individual slopes for the regression of VO2 vs. PVAP rose as a function of exposure time from values below control after 50 h exposure to values above control after 60 h. Energetic efficiency (PVAP/VO2) decreased as a function of O2 exposure time and points to possible heart failure in the intact animal. After 50 h O2 exposure the heart was energetically more efficient than the control. Possible changes in the heart are discussed.     

Errors in predicting maximal oxygen consumption in pregnant women.

This study was designed to determine the accuracy of estimated values of maximal heart rate (HRmax) and oxygen consumption (VO2) during pregnancy. We measured HR and maximal VO2 (VO2max) at rest and during cycle (CE) and treadmill exercise (TE) tests with rapidly increasing exercise intensities during gestation and after delivery. Pregnancy was found to affect the linear relationship of HR and %VO2max so that the intercept increases with advancing gestation and the slope decreases. Estimated maximal HR (HRmax, est), 220 - age (yr) x beats/min, overestimated measured HRmax by 8% (CE) and 5% (TE). For VO2max estimated by Astrand's nomogram (VO2max, est1) and by linear extrapolation of submaximal values of HR and VO2 to HRmax, est (VO2max, est2), individual errors were large (SD 17-28%). Mean VO2max, est1 overestimated measured VO2max by 20% during CE but not during TE (-2%) and elicited the erroneous impression that VO2max decreases during CE in pregnancy. Mean VO2max, est2 values were not significantly different from measured VO2max values. This apparent accuracy resulted from two opposing errors: 1) HRmax, est overestimated HRmax, and 2) above 70% VO2max the slope of the HR-%VO2max relationship was significantly reduced. Therefore neither method to estimate VO2max can replace the measurement of VO2max.     

A proposed test for determining physical working capacity at the oxygen consumption threshold (PWCVO2)

The purpose of this study was 3-fold: (a) to determine if the mathematical model used to estimate the electromyographic fatigue threshold (EMGFT) and physical working capacity at the heart rate threshold (PWCHRT) could be applied to VO2 measurements, (b) to propose a new fatigue threshold called the physical working capacity at the oxygen consumption threshold (PWCVO2), and (c) to compare the power output at the PWCVO2 to those of the EMGFT, PWCHRT, and ventilatory threshold (VT). Fifteen adult volunteers (mean age +/- SD = 22 +/- 2 years) performed a maximal cycle ergometer test to determine VO2peak and VT as well as 4 8-minute submaximal work bouts for the determination of PWCHRT, EMGFT, and PWCVO2. A 1-way repeated measures analysis of variance (ANOVA) with Tukey post hoc comparison indicated that PWCHRT (84 +/- 36) was significantly (p < 0.05) less than EMGFT (126 +/- 51), but there were no differences for PWCVO2 (111 +/- 44) and VT (111 +/- 60) versus PWCHRT or EMGFT. The results of this study indicated that (a) the mathematical model used to determine the PWCHRT and EMGFT was applicable to the measurement of VO2 and could be used to estimate the PWCVO2 during cycle ergometry, (b) there was a difference in the mean power outputs that corresponded to the fatigue thresholds determined from EMG and heart rate measurements, and (c) the PWCVO2 test may provide a useful submaximal technique for estimating the VT.