Exercise O2 Uptake Research Articles

Somatotype Components, Aerobic Fitness and Grip Strength in Kuwaiti Males and Females

Introduction and Objective: We investigated the association of endo-, meso- and ecto-morphic components of somatotype with aerobic power, mid-trunk flexibility and grip strength. Methods: Healthy male (n = 226) and female (n = 86) subjects, aged 9 - 55 years, sedentary (n = 154) or participating in sports (n = 158) were studied. Anthro-pometrics (height, weight, 8 skin folds, arm and calf circumferences, elbow and knee diameters), maximal exercise O2 uptake, mid trunk flexibility, right and left grip strength were measured. Results: Sedentary adult females were endomorphic with mesomorph tendency, and had low aerobic power (27.8 ± 0.6 ml/Kg·min) and low (48.7 ± 1 Kg) grip strength. Sedentary males (young and adults) and Sports adult males were mesomorph with endomorphic tendency. Sports junior males were balanced mesomorph. Aerobic power was 54.1 ± 0.9 ml/Kg·min in sports young males, 53.8 ± 0.9 ml/Kg·min in sports adult males, 41.2 ± 4.3 ml/Kg·min in sedentary young males, and 39.5 ± 1 ml/Kg·min in sedentary adult males. Grip strength was 89.9 ± 1.7 Kg in sports adult males, 86.7 ± 2 Kg in sedentary adult males, 75.6 ± 2.2 Kg in sports junior males and 52 ± 9.1 Kg in young sedentary males. Step-wise multiple regression analysis of somatotype components on aerobic power revealed dominant negative contribution (P 2 = 0.57, 57%), and small but significant positive contributions of mesomorphy (0.6%) and ectomorphy (0.6%): Aerobic power = [56.1 - 4.3 (endomorphy) + (mesomorphy) + 1.4 (ectomorphy)] ± 9.1 SEE. Height and somatotype components accounted for 69% of the variance (R2) in grip strength; height had greatest contribution (60%): Grip Strength = [1.7 (Height) - 6.5 (ectomorphy) - 3.4 (endomorphy) - 2 (mesomorphy) - 200] ± 12.9 SEE. Measured variables accounted for <2% of flexibility variance. Conclusion: Endomorphy contributes greatly and negatively to variance in aerobic power. Body height was the anthropometric variable with the greatest positive association with the variance in grip strength. Flexibility appears to be unrelated to somatotype components.

Pre-discharge Bedside Exercise Gas Exchange Measurements Predict 30 Day Heart Failure Patient Readmissions

Thirty day hospital readmissions for heart failure (HF) are associated with high morbidity, mortality and costs. Based on evidence relating a growing array of submaximum exercise gas exchange (Gx) measurements to outcomes in HF we hypothesized that submaximum Gx testing at the time of discharge would be an effective tool to identify which patients have high risk of readmission. Patients hospitalized for acute decompensated HF (N=50, mean age 65±14; 78% male) from 3 participating centers who met inclusion criteria (age> 18, NYHA II-IV chronic HF, and capable of exercise) provided informed consent were enrolled in the study. Subjects performed submax exercise on the day of hospital discharge. Heart and respiratory rate, Gx and O2 saturation were monitored continuously during a 6 min protocol consisting of 2 min of rest, 3 min of step exercise and 1 minute of recovery. A 6- parameter multi-metric Shape Score consisting of resting and exercise delta ETCO2, VE slope and O2 uptake efficiency slope (OUES), pulmonary capacitance (GxCap), and end exercise SaO2 were computed. RER, HR, VO2, and O2 pulse were also assessed during rest and exercise. The overall readmission (RA) rate for those Shape tested was 11 of 50 or 22%. Comparing those HF patients who were RA within 30 days vs. those who were not readmitted (NRA), volitional effort, based on peak RER, was equivalent between groups (0.94±.07 and 0.94±.10, respectively, p=.99). Patients with RA had higher Shape Scores than the NRA group (2.4±1.0 vs. 1.1±1.1, p< .005). Individual gas exchange parameters known to prognosticate in patients with chronic HF also tended to be more impaired in the RA group (Table, i.e. lower achieved VO2, higher VE/VCO2 slope, lower OUES). In this pilot study, exercise Gx using a simple, 6 min. bedside step protocol prior to discharge offers an objective means to predict likelihood for 30 day readmission in patients hospitalized with ADHF. A multi-metric Shape Gx score that integrates sub-maximum exercise Gx parameters outperforms individual Gx variables in predicting hospital readmission. While larger, definitive studies are required, bedside measurement of Gx in HF patients may represent an inexpensive, non-invasive practical clinical tool to track functional status and to effectively indentify HF patients at risk for readmission.Table 1Gas exchange variables at the time of dischargeStudy groupShape Multivariate Composite ScoreVO2 peakVE/VCO2 slopeGxCAP peakOUESΔETCO2End exercise SaO230 day readmitN= 112.4±1.0p=.0029.4±1.5p=.02441.6±16.7NS363±208NS1.12±.34p=0.06-1.0±3.8NS91±5NSNo 30 day readmitN=391.1±1.111.1±2.835.4±10.4432±1631.42±.51-.44±3.093±4 Open table in a new tab

Metabolic Cost of Rope Training

Rope training, consisting of vigorously undulating a rope with the upper body, has become a popular cardiovascular training choice in fitness centers and athletic performance enhancement facilities. Despite widespread use and growing popularity, little is known about the metabolic demands of rope training. Therefore, the purpose of this study was to quantify the cardiovascular and metabolic cost from an acute 10-minute bout of rope training. Eleven physically active participants used a 15.2-m rope anchored by a post, resulting in the participant holding 7.6 m of rope in each hand. The 10-minute protocol consisted of 15 seconds of vertical double-arm waves followed by 45 seconds of rest for 10 total repetitions. The metabolic cost was estimated from heart rate, lactate, resting O2 uptake, exercise O2 uptake, and excess postexercise O2 consumption measurements. The average heart rate for the workout was 163 ± 11 b·min with peak (Equation is included in full-text article.) of 35.4 ± 5.4 mL·kg(-1)·min(-1), and peak METs were 10.1 ± 1.6. Total energy expenditure was 467.3 ± 161.0 kJ. When expressed per unit of time, EE was 41.3 ± 14.1 kJ·min(-1). The results of this study suggest an acute 10-minute bout of rope training in a vigorous-intensity workout, resulting in high heart rates and energy expenditure, which meet previously established thresholds known to increase cardiorespiratory fitness.

Influence of intermittent hypoxia interval training on exercise-dependent erythrocyte NOS activation and blood pressure in diabetic patients

NOS-activation in erythrocytes (eryNOS) is impaired in patients suffering from type 2 diabetes. We investigated the effect of physical exercise on eryNOS activation and whether 6 week hypoxia interval training may alter this process. Male patients with diabetes mellitus type 2 (NIDDM, n= 12; age, 61.3± 8.4years; BMI, 29.8± 3.7kg/m(2)) underwent physical exercise training before and after 6week hypoxia interval training. Training was conducted 4 times per week for 90min at 15.4-12.7 Vol% of inspired oxygen. Vital parameters were recorded. Before hypoxia intervention, eryNOS phosphorylation at serine(1177) decreased significantly during exercise (basal 17.4± 12.0 compared with exercise 8.4± 9.2 arbitrary grey values (arGV); P< 0.05). After 6 weeks of hypoxia intervention, eryNOS-pSer(1177) (2.2± 2.5 arGV) was significantly lower at baseline. Ergometry showed an increase (7.6± 3.0 arGV; P< 0.05) followed by a decrease to almost baseline levels after 30min (3.8± 1.5 arGV). Maximal exercise capacity and O(2)-uptake ([Formula: see text] max) increased significantly. The effects were independent from exercise-induced elevation of blood pressure. Exercise-dependent eryNOS phosphorylation at serine(1177) was increased similar to that described for the endothelium in diabetic patients. EryNOS dysregulation was partially restored after intermittent hypoxia training.

Aerobic, Anaerobic, and Excess Postexercise Oxygen Consumption Energy Expenditure of Muscular Endurance and Strength: 1-Set of Bench Press to Muscular Fatigue

We use a new approach to the estimation of energy expenditure for resistance training involving nonsteady state measures of work (weight × displacement), exercise O2 uptake, blood lactate, and recovery O2 uptake; all lifts were performed to muscular failure. Our intent was to estimate and compare absolute and relative aerobic and anaerobic exercise energy expenditure and recovery energy expenditure. Single-set bench press lifts of ∼ 37, ∼ 46, and ∼ 56% (muscular endurance-type exercise) along with 70, 80, and 90% (strength-type exercise) of a 1 repetition maximum were performed. Collectively, the muscular endurance lifts resulted in larger total energy expenditure (60.2 ± 14.5 kJ) as compared with the strength lifts (43.2 ± 12.5 kJ) (p = 0.001). Overall work also was greater for muscular endurance (462 ± 131 J) as opposed to strength (253 ± 93 J) (p = 0.001); overall work and energy expenditure were related (r = 0.87, p = 0.001). Anaerobic exercise and recovery energy expenditure were significantly larger for all strength lifts as compared with aerobic exercise energy expenditure (p < 0.001). For the muscular endurance lifts, anaerobic energy expenditure was larger than recovery energy expenditure (p < 0.001) that in turn was larger than aerobic exercise energy expenditure (p < 0.001). We conclude that for a single set of resistance training to fatigue, the anaerobic and recovery energy expenditure contributions can be significantly larger than aerobic energy expenditure during the exercise. To our surprise, recovery energy expenditure was similar both within strength and muscular-endurance protocols and between protocols; moreover, recovery energy expenditure had little to no relationship with aerobic and anaerobic exercise energy expenditure or work.

Integrated autonomic control of bronchial blood flow and third generation airway dimensions during exercise

Neural mechanisms controlling 3rd generation airway blood flow and dimensions were studied in 8 sheep trained to run on a treadmill during moderate exercise O2 uptake 20 ml.kg−1.min−1 for 2 min, 10 min recovery. We measured rapid changes in bronchial blood flow and conductance (Qbr, Cbr), circumference (Circbr) and wall thickness (Thbr), using pulsed‐Doppler flowmetry, transit‐time sonomicrometry, and single crystal sonomicrometry, respectively. At exercise onset Pa rose to 111% (P&lt; 0.05) of resting and HR from 85 b/min to 164 b/min (P&lt; 0.001) before returning in recovery at 5 min. Qbr fell immediately to 91% and to 90% at 1.5 min (P&lt; 0.05), and early in recovery to 84% (P&lt; 0.05) before returning to pre‐exercise levels. Cbr followed a similar pattern (P&lt; 0.05). Circbr fell immediately to 96% (P&lt; 0.001) where it remained for the duration of exercise, and Thbr increased and was sustained during exercise before returning to control levels in recovery. Cholinoceptor block by i.v. methscopolamine bromide modified these responses. Pa rose to 109% of resting (P&lt; 0.01), and HR rose from 120 b/min to 168 b/min (P&lt; 0.001). A minor Qbr and Cbr fall was not significant, and only an immediate transient fall in Circbr was evident (P&lt; 0.01). Thus raised vagal activity dominates the exercise‐induced bronchovascular and airway wall constriction in 3rd generation airways during and after exercise.Funding: Hunter Medical Research Institute

Improvement of alveolar-capillary membrane diffusing capacity with exercise training in chronic heart failure.

Chronic heart failure (CHF) may impair lung gas diffusion, an effect that contributes to exercise limitation. We investigated whether diffusion improvement is a mechanism whereby physical training increases aerobic efficiency in CHF. Patients with CHF (n = 16) were trained (40 min of stationary cycling, 4 times/wk) for 8 wk; similar sedentary patients (n = 15) were used as controls. Training increased lung diffusion (DlCO, +25%), alveolar-capillary conductance (DM, +15%), pulmonary capillary blood volume (VC, +10%), peak exercise O2 uptake (peak VO2, +13%), and VO2 at anaerobic threshold (AT, +20%) and decreased the slope of exercise ventilation to CO2 output (VE/VCO2, -14%). It also improved the flow-mediated brachial artery dilation (BAD, from 4.8 +/- 0.4 to 8.2 +/- 0.4%). These changes were significant compared with baseline and controls. Hemodynamics were obtained in the last 10 patients in each group. Training did not affect hemodynamics at rest and enhanced the increase of cardiac output (+226 vs. +187%) and stroke volume (+59 vs. +49%) and the decrease of pulmonary arteriolar resistance (-28 vs. -13%) at peak exercise. Hemodynamics were unchanged in controls after 8 wk. Increases in DlCO and DM correlated with increases in peak VO2 (r = 0.58, P = 0.019 and r = 0.51, P = 0.04, respectively) and in BAD (r = 0.57, P < 0.021 and r = 0.50, P = 0.04, respectively). After detraining (8 wk), DlCO, DM, VC, peak VO2, VO2 at AT, VE/VCO2 slope, cardiac output, stroke volume, pulmonary arteriolar resistance at peak exercise, and BAD reverted to levels similar to baseline and to levels similar to controls. Results document, for the first time, that training improves DlCO in CHF, and this effect may contribute to enhancement of exercise performance.

Reduced exercise capacity in untreated adults with primary growth hormone resistance (Laron syndrome).

Primary IGF-I deficiency (Laron syndrome, LS) may decrease exercise capacity as a result of a lack of an IGF-I effect on heart, peripheral muscle or lung structure and/or function. Eight patients (six females) who had never received treatment with IGF-I, with mean age of 36 +/- 10 (SD) years (range 21-48), weight 47 +/- 9 kg (31-61), height 126 +/- 12 cm (112-140) and body mass index of 29 +/- 4 kg/m2 (24-34), and 12 age-matched controls, underwent lung function tests and incremental cycling to the limit of tolerance (CPX, MedGraphics). Predicted values for the patients were derived from adult equations based on height. In LS patients, lung function was near normal; vital capacity was 84 +/- 11% of expected (66-103). Peak exercise O2-uptake and the anaerobic threshold were reduced, 57 +/- 20% of predicted and 33 +/- 9% of predicted peak (P = 0.005 vs. controls), despite normal mean exercise breathing reserve. All parameters were normal in the controls. Exercise capacity in untreated adults with LS is significantly reduced. The limitation for most patients was not ventilatory but resulted either from low cardiac output and/or from dysfunction of the peripheral muscles. However, the relative contribution of each of these elements and/or the role of poor fitness needs further study.

Enhanced brain natriuretic peptide response to peak exercise in heart transplant recipients.

We investigated the atrial (ANP) and brain natriuretic peptides (BNP), catecholamines, heart rate, and blood pressure responses to graded upright maximal cycling exercise of eight matched healthy subjects and cardiac-denervated heart transplant recipients (HTR). Baseline heart rate and diastolic blood pressure, together with ANP (15.2 +/- 3.7 vs. 4.4 +/- 0.8 pmol/l; P < 0.01) and BNP (14.3 +/- 2. 6 vs. 7.4 +/- 0.6 pmol/l; P < 0.01), were elevated in HTR, but catecholamine levels were similar in both groups. Peak exercise O2 uptake and heart rate were lower in HTR. Exercise-induced maximal ANP increase was similar in both groups (167 +/- 34 vs. 216 +/- 47%). Enhanced BNP increase was significant only in HTR (37 +/- 8 vs. 16 +/- 8%; P < 0.05). Similar norepinephrine but lower peak epinephrine levels were observed in HTR. ANP and heart rate changes from rest to 75% peak exercise were negatively correlated (r = -0.76, P < 0.05), and BNP increase was correlated with left ventricular mass index (r = 0.83, P < 0.01) after heart transplantation. Although ANP increase was not exaggerated, these data support the idea that the chronotropic limitation secondary to sinus node denervation might stimulate ANP release during early exercise in HTR. Furthermore, the BNP response to maximal exercise, which is related to the left ventricular mass index of HTR, is enhanced after heart transplantation.

Re-interpreting anaerobic metabolism: an argument for the application of both anaerobic glycolysis and excess post-exercise oxygen comsumption (EPOC) as independent sources of energy expenditure.

Due to current technical difficulties and changing cellular conditions, the measurement of anaerobic and recovery energy expenditure remains elusive. During rest and low-intensity steady-state exercise, indirect calorimetric measurements successfully represent energy expenditure. The same steady-state O2 uptake methods are often used to describe the O2 deficit and excess post-oxygen consumption (EPOC): 1 l O2 = 5 kcal = 20.9 kJ. However, an O2 deficit plus exercise O2 uptake measurement ignores energy expenditure during recovery, and an exercise O2 uptake plus EPOC measurement misrepresents anaerobic energy expenditure. An alternative solution has not yet been proposed. Anaerobic glycolysis and mitochondrial respiration are construed here as a symbiotic union of metabolic pathways, each contributing independently to energy expenditure and heat production. Care must be taken when using O2 uptake alone to quantify energy expenditure because various high-intensity exercise models reveal that O2 uptake can lag behind estimated energy demands or exceed them. The independent bioenergetics behind anaerobic glycolysis and mitochondrial respiration can acknowledge these discrepancies. Anaerobic glycolysis is an additive component to an exercise O2 uptake measurement. Moreover, it is the assumptions behind steady-state O2 uptake that do not permit proper interpretation of energy expenditure during EPOC; 1 l O2 not = 20.9 kJ. Using both the O2 deficit and a modified EPOC for interpretation, rather than one or the other, leads to a better method of quantifying energy expenditure for higher intensity exercise and recovery.

Despite an Excellent Effect on Left Ventricular Performance, Carvedilol Fails to Improve the Pulmonary Function and Peak Exercise O2 Uptake in Chronic Heart Failure. Any Link?

Despite an Excellent Effect on Left Ventricular Performance, Carvedilol Fails to Improve the Pulmonary Function and Peak Exercise O2 Uptake in Chronic Heart Failure. Any Link?

Despite an excellent effect on left ventricular performance, carvedilol fails to improve the pulmonary function and peak exercise O2uptake in chronic heart failure. Any link?

Despite an excellent effect on left ventricular performance, carvedilol fails to improve the pulmonary function and peak exercise O2uptake in chronic heart failure. Any link?

Chronic exercise enhances in vivo and in vitro cytotoxic mechanisms of natural immunity in mice.

This study investigated the influence of 9 wk of chronic exercise on natural cytotoxicity in male C3H mice. Both in vivo cytotoxicity (pulmonary vasculature) and in vitro cytotoxicity (spleen) were determined for voluntary (wheel running; n = 30) and forced (treadmill running, 15 m/min, 30 min/day; n = 30) exercise protocols. A sedentary control group (n = 30) and a treadmill control group (5 m/min, 5 min/day; n = 30) were also included. After 9 wk of chronic exercise, submaximal exercise O2 uptake was reduced in the wheel-running group relative to that in sedentary or treadmill-trained mice. Maximal citrate synthase activity of soleus muscle was higher in treadmill-trained group compared with that in sedentary or wheel-running mice. Chronic exercise consistently reduced percent retention of CIRAS 3 tumor cells in the lungs of treadmill- (15.3 +/- 1.4) and wheel- (17.9 +/- 1.4) trained mice below that of sedentary (29.5 +/- 2.7) and treadmill control (25.8 +/- 1.8) groups (P < 0.001). Injection of anti-asialo GM1 (ASGM1) antibody increased tumor cell retention in the lungs for all groups but did not alter the differences between activity conditions. In vitro cytotoxicity was enhanced in treadmill- and wheel-trained mice relative to that in sedentary controls but was not elevated in the treadmill control group. Anti-ASGM1 injection eliminated in vitro cytotoxicity for all groups. Chronic exercise slightly increased the frequency of ASGM1-positive splenocytes in treadmill-trained mice only. These results indicate that chronic exercise enhances natural cytotoxic mechanisms in vivo and in vitro and that this enhancement is present for both forced and voluntary exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Strenuous prolonged exercise elevates resting metabolic rate and causes reduced mechanical efficiency

Resting O2 consumption, net mechanical efficiency during cycling exercise and excess postexercise O2 consumption (EPOC) was measured in 15 army cadets after 3 or 4 days of continuous simulated combat exercises (estimated energy demand: 40 MJ day-1), no organized sleep and virtually no food intake (stress experiment). They exercised for 30 minutes at a work load corresponding to about 50% of maximal O2 uptake. An identical test using the same absolute work load was repeated when the cadets were completely recovered from the combat course (control experiment). Resting O2 consumption increased by 15% from 279 +/- 7 ml min-1 (control) to 320 +/- 8 ml min-1 (stress, P less than 0.001). Mechanical efficiency decreased from 24.6 +/- 0.4% (control) to 20.9 +/- 0.2% (stress, P less than 0.001). EPOC1h increased from 0.58 +/- 0.41 l (control) to 2.24 +/- 0.2% (stress, P less than 0.05). Glucose infusion during exercise (0.20 g kg-1 body weight) had no effect on mechanical efficiency or EPOC. About 1/5 of the increase in exercise O2 uptake can be explained by a substrate shift from carbohydrates to fat, as evidenced by a reduction in R-value during exercise from 0.90 +/- 0.012 (control) to 0.80 +/- 0.010 (stress). Hence, after severe physical stress combined with sleep deprivation and food restriction, O2 uptake is increased both at rest and during submaximal exercise.

Ozone inhalation effects in females varying widely in lung size: comparison with males

It has been suggested that lung size accounts for observed gender differences in responsiveness to the same total inhaled dose of O3. To test the hypothesis that lung size is a determinant of magnitude of response within a gender, two groups of 14 healthy young adult females differing significantly in forced vital capacity [FVC; i.e., small-lung group mean = 3.74 liters (range 3.2-4.0) and large-lung group mean = 5.11 liters (range 4.5-6.2] were exposed for 1 h to filtered air (FA) and to 0.18 and 0.30 ppm O3. On each occasion, subjects exercised continuously on a cycle ergometer at a work rate that elicited a mean minute ventilation of approximately 47 l/min. For the small-lung group [mean total lung capacity (TLC) = 4.52 liters] exercise O2 uptake was 67% of maximal O2 uptake (VO2max), and that for the large-lung group (TLC 6.37 liters) was 61% of VO2max. Statistical analysis revealed significant decrements for both groups in FVC, forced expiratory volume in 1 s (FEV1.0), and forced expiratory flow rate in the middle half of FVC on exposure to 0.18 and 0.30 ppm O3. Exercise respiratory frequency increased, and tidal volume decreased significantly in both groups in response to 0.18 and 0.30 ppm O3 exposure. On exposure to 0.30 ppm O3, the number of individual subjective symptoms reported and their severity were significantly greater for both groups than those reported for the FA and 0.18 ppm O3 exposures. Both groups evidenced similar percent changes in pulmonary function and exercise ventilation response, and in subjective symptom response.(ABSTRACT TRUNCATED AT 250 WORDS)

Maximal exercise responses of tetraplegics and paraplegics.

Eight tetraplegic and 13 paraplegic subjects performed a continuous progressive loading exercise test to exhaustion on a wheelchair ergometer. Their cardiorespiratory responses at maximal O2 uptake were analyzed after initially grouping subjects according to the international system for classification of wheelchair athletes. Analysis of variance provided a basis for regrouping the subjects into tetraplegic (T), high-lesion paraplegic (HLP), and low-lesion paraplegic (LLP) groups and indicated significant differences (P less than 0.05) in maximal power output (24, 47, and 80 W) and O2 uptake (0.97, 1.62, and 2.42 l/min) for T, HLP, and LLP, respectively. T had a significantly lower maximal heart rate (110) compared with the paraplegic values (175 and 190), whereas the HLP, in contrast to the LLP, had a lower maximum ventilation (66 vs. 101 l/min) and a lower O2 pulse (9.3 vs. 12.7 ml/beat). The ventilatory equivalent for O2 was similar in all groups to values for able-bodied subjects in maximal arm crank ergometry, however, suggesting a lack of any respiratory limit to maximal O2 delivery. No differences were noted in respiratory exchange ratio or net efficiency between the groups. In addition to limitations of functional muscle mass, the data suggested that the reduced cardiac capacity of T and HLP may also be linked to their lower maximal exercise capacity and O2 uptake.

Determinants of gas exchange kinetics during exercise in the dog.

Following exercise onset, CO2 output (VCO2) and O2 uptake (VO2) increase exponentially, but with appreciably different time constants. To determine the sensitivity of the time courses of these variables to altered ventilatory kinetics, rhythmic exercise was induced abruptly in anesthetized dogs by bilateral stimulation of the peripheral ends of the cut sciatic and femoral nerves. This increased the metabolic rate by 83 +/- 25 (SD) %. The dogs were ventilated with a constant-volume pump, the frequency of which was changed exponentially from the start of the exercise up to the ventilation that returned arterial CO2 and O2 pressure (PCO2 and PO2) in the steady state to resting levels. The time constant (tau) of the increase in ventilation (VE) was varied among trials. VCO2, VO2, end-tidal PCO2 and PO2, and arterial PCO2 were measured breath by breath. tauVO2 was constant at approximately 18 s regardless of alterations in tauVE. In contrast, tauVCO2 was strongly dependent on tauVE, apparently due to the larger body stores for CO2; the transitions were isocapnic when tau VE was approximately 40 s. We conclude that ventilatory dynamics can markedly influence the dynamics of CO2 exchange during exercise, but has no appreciable effect on O2 uptake dynamics.

Efficiency of anaerobic work.

This study was undertaken to compare the efficiency of aerobic and anaerobic work. Nine subjects worked at approximately 100% VO2 max for 2 min while inspiring gas mixtures with O2 fractions ranging from 0.13 to 0.21. Exercise O2 uptake, recovery O2 uptake, and blood lactate concentration were measured. Steady level O2 uptake was measured in normoxia at submaximal loads of about 30, 50, and 70% of VO2 max. Fast recovery O2 uptake did not change as PIO2 was varied. Exercise O2 uptake and blood lactate concentrations were linearly related to PIO2. The ratio of the slopes of these lines provided an empirical expression of the O2 equivalent of blood lactate. This ratio was constant, suggesting that it is not less efficient to use ATP synthesized anaerobically. Energy input from lactate was calculated using this factor. Efficiency decreased as power output increased even at the submaximal work rates. This may result from either 1) a decrease in muscle efficiency, 2) an increase in metabolism that is not directly related to the external work, or 3) some combination of 1 and 2.

Effects of physicial conditioning on changes in exercise and recovery O2 uptake and efficiency during constant-load ergometer exercise

The purpose of this study was to determine the effects of a physical conditioning program on (1) changes in exercise O2 uptake, O2 deficit, steady-state O2, and recovery O2 uptake during the performance of constant-load bicycle exercise, and (2) to quantify changes in work efficiency as revealed by the ratio of changes in O2 deficit to changes in recovery V̇O2. For the experimental group (N = 33) after training, there was an average increase of 388 ml for 10 minutes of exercise O2 uptake, and a corresponding decrease of 310 ml O2 during 15 minutes of recovery; steady-state O2 uptake remained unchanged. These results indicated that the relationship between O2 deficit and recovery O2 uptake was essentially 1:1 and is consistent with previous results for light exercise and subsequent recovery. The O2 income/O2 recovery ratio increased 4.6 percent from 2.680 to 2.803 after training, thus showing that the O2 transport mechanisms became more effective as a result of the training. For the control group (N = 33), there were no significant changes from pre-test to post-test in any of the parameters measured. Correlations between body weight and total oxygen consumed during exercise were r = .36 and r = .42 for the experimental and control groups, respectively, indicating that there was little relationship between these variables when work output was kept constant.