Acceleration of VO2 kinetics in heavy submaximal exercise by hyperoxia and prior high-intensity exercise

MacDonald, Maureen, Preben K. Pedersen, and Richard L. Hughson. Acceleration ofO₂ kinetics in heavysubmaximal exercise by hyperoxia and prior high-intensity exercise.J. Appl. Physiol. 83(4):1318-1325, 1997.We examined the hypothesis thatO₂ uptake (O₂) wouldchange more rapidly at the onset of step work rate transitions inexercise with hyperoxic gas breathing and after prior high-intensityexercise. The kinetics ofO₂ were determined from themean response time (MRT; time to 63% of total change inO₂) andcalculations of O₂ deficit andslow component during normoxic and hyperoxic gas breathing in one groupof seven subjects during exercise below and above ventilatory threshold(VT) and in another group of seven subjects during exercise above VTwith and without prior high-intensity exercise. In exercise transitions below VT, hyperoxic gas breathing did not affect the kinetic response of O₂ at theonset or end of exercise. At work rates above VT, hyperoxic gasbreathing accelerated both the on- and off-transient MRT, reduced theO₂ deficit, and decreased theO₂ slow component fromminute 3 to minute6 of exercise, compared with normoxia. Prior exerciseabove VT accelerated the on-transient MRT and reduced theO₂ slow component fromminute 3 to minute6 of exercise in a second bout of exercise with bothnormoxic and hyperoxic gas breathing. However, the summatedO₂ deficit in the second normoxicand hyperoxic steps was not different from that of the first steps inthe same gas condition. Faster on-transient responses in exerciseabove, but not below, VT with hyperoxia and, to a lesser degree, afterprior high-intensity exercise above VT support the theory of anO₂ transport limitation at theonset of exercise for workloads >VT.

     

Pulmonary and leg VO2 during submaximal exercise: implications for muscular efficiency.

Insights into muscle energetics during exercise (e.g., muscular efficiency) are often inferred from measurements of pulmonary gas exchange. This procedure presupposes that changes of pulmonary O2 (VO2) associated with increases of external work reflect accurately the increased muscle VO2. The present investigation addressed this issue directly by making simultaneous determinations of pulmonary and leg VO2 over a range of work rates calculated to elicit 20-90% of maximum VO2 on the basis of prior incremental (25 or 30 W/min) cycle ergometry. VO2 for both legs was calculated as the product of twice one-leg blood flow (constant-infusion thermodilution) and arteriovenous O2 content difference across the leg. Measurements were made 3-5 min after each work rate imposition to avoid incorporation of the VO2 slow component above the lactate threshold. For all 17 subjects, the slope of pulmonary VO2 (9.9 +/- 0.2 ml O2.W-1.min-1) was not different (P greater than 0.05) from that for leg VO2 (9.2 +/- 0.6 ml O2.W-1.min-1). Estimation of "delta" efficiency (i.e., delta work accomplished divided by delta energy expended, calculated from slope of VO2 vs. work rate and a caloric equivalent for O2 of 4.985 cal/ml) using pulmonary VO2 measurements (29.1 +/- 0.6%) was likewise not significantly different (P greater than 0.05) from that made using leg VO2 measurements (33.7 +/- 2.4%). These data suggest that the net VO2 cost of metabolic "support" processes outside the exercising legs changes little over a relatively broad range of exercise intensities. Thus, under the conditions of this investigation, changes of VO2 measured from expired gas reflected closely those occurring within the exercising legs.     

Slower Adaptation of VO2 to steady state of submaximal exercise with beta-blockade

The kinetics of oxygen uptake (VO2) were assessed in 17 normal subjects with beta-blockade and placebo. beta-blockade was achieved with either 50 mg oral metoprolol or 40 mg oral propranolol, each twice per day. Tests were conducted on the cycle ergometer at work rates approximating 80% of the work rate at ventilatory anaerobic threshold. Work rate was initiated as a square wave starting from prior rest. Data obtained 48 h, 1 week, and 4 weeks after starting drug or placebo were pooled to increase the number of points for regression analysis of kinetic parameters. While there were no differences in the plateau values for VO2 with and without beta-blockade, the rate of adaptation to steady state was significantly slower with beta-blockade than with placebo (P less than 0.05). This resulted in an increase of oxygen deficit by approximately 200 ml O2. Cardiac output measured by CO2 rebreathing was significantly reduced by beta-blockade (metoprolol by 4.1%, propranolol by 12.2%, both P less than 0.05). Blood lactate concentration was unaffected by beta-blockade. It was concluded that the influence of beta-blockade on the oxygen transport system was responsible for the significantly slower increase of VO2 to steady state in submaximal exercise.     

Relation of heart rate to percent VO2 peak during submaximal exercise in the heat.

We tested the hypothesis that elevation in heart rate (HR) during submaximal exercise in the heat is related, in part, to increased percentage of maximal O(2) uptake (%Vo(2 max)) utilized due to reduced maximal O(2) uptake (Vo(2 max)) measured after exercise under the same thermal conditions. Peak O(2) uptake (Vo(2 peak)), O(2) uptake, and HR during submaximal exercise were measured in 22 male and female runners under four environmental conditions designed to manipulate HR during submaximal exercise and Vo(2 peak). The conditions involved walking for 20 min at approximately 33% of control Vo(2 max) in 25, 35, 40, and 45 degrees C followed immediately by measurement of Vo(2 peak) in the same thermal environment. Vo(2 peak) decreased progressively (3.77 +/- 0.19, 3.61 +/- 0.18, 3.44 +/- 0.17, and 3.13 +/- 0.16 l/min) and HR at the end of the submaximal exercise increased progressively (107 +/- 2, 112 +/- 2, 120 +/- 2, and 137 +/- 2 beats/min) with increasing ambient temperature (T(a)). HR and %Vo(2 peak) increased in an identical fashion with increasing T(a). We conclude that elevation in HR during submaximal exercise in the heat is related, in part, to the increase in %Vo(2 peak) utilized, which is caused by reduced Vo(2 peak) measured during exercise in the heat. At high T(a), the dissociation of HR from %Vo(2 peak) measured after sustained submaximal exercise is less than if Vo(2 max) is assumed to be unchanged during exercise in the heat.     

Influence of respiratory muscle work on VO(2) and leg blood flow during submaximal exercise.

The work of breathing (W(b)) normally incurred during maximal exercise not only requires substantial cardiac output and O(2) consumption (VO(2)) but also causes vasoconstriction in locomotor muscles and compromises leg blood flow (Q(leg)). We wondered whether the W(b) normally incurred during submaximal exercise would also reduce Q(leg). Therefore, we investigated the effects of changing the W(b) on Q(leg) via thermodilution in 10 healthy trained male cyclists [maximal VO(2) (VO(2 max)) = 59 +/- 9 ml. kg(-1). min(-1)] during repeated bouts of cycle exercise at work rates corresponding to 50 and 75% of VO(2 max). Inspiratory muscle work was 1) reduced 40 +/- 6% via a proportional-assist ventilator, 2) not manipulated (control), or 3) increased 61 +/- 8% by addition of inspiratory resistive loads. Increasing the W(b) during submaximal exercise caused VO(2) to increase; decreasing the W(b) was associated with lower VO(2) (DeltaVO(2) = 0.12 and 0.21 l/min at 50 and 75% of VO(2 max), respectively, for approximately 100% change in W(b)). There were no significant changes in leg vascular resistance (LVR), norepinephrine spillover, arterial pressure, or Q(leg) when W(b) was reduced or increased. Why are LVR, norepinephrine spillover, and Q(leg) influenced by the W(b) at maximal but not submaximal exercise? We postulate that at submaximal work rates and ventilation rates the normal W(b) required makes insufficient demands for VO(2) and cardiac output to require any cardiovascular adjustment and is too small to activate sympathetic vasoconstrictor efferent output. Furthermore, even a 50-70% increase in W(b) during submaximal exercise, as might be encountered in conditions where ventilation rates and/or inspiratory flow resistive forces are higher than normal, also does not elicit changes in LVR or Q(leg).     

Prediction of maximal VO2 from a submaximal StairMaster test in young women

The StairMaster 4000 PT is a popular step ergometer which provides a submaximal test protocol (SM Predicted VO(2)max) for the prediction of VO(2)max (ml.kg(-1).min(-1)). The purpose of this study was to evaluate the SM Predicted VO(2)max protocol by comparing it to results from a VO(2)max treadmill test in 20 young healthy women aged 20-25 years. Subjects were 10 step-trained (ST) women who had performed aerobic activities and exercised on a step ergometer for 20-30 minutes at least 3 times per week for the past 3 months, and 10 non-step-trained (NST) women who had performed aerobic activities no more than twice a week during the past 3 months and had no previous experience on a step ergometer. The SM Predicted VO(2)max protocol used 2 steady state heart rates between approximately 115-150 b.min(-1) to estimate VO(2)max. The Bruce maximal treadmill protocol (Actual VO(2)max) was used to measure VO(2)max by open circuit spirometry. Each subject performed both tests within a 7-day period. The means and standard deviations for the Actual VO(2)max tests were 39.8 +/- 6.1 ml.kg(-1).min(-1) for the ST group, 37.6 +/- 6.3 ml.kg(-1).min(-1) for the NST group, and 38.7 +/- 6.2 ml.kg(-1).min(-1) for the Total group (N = 20); and for the SM Predicted VO(2)max tests, means and standard deviations were 40.78 +/- 14.0 ml.kg(-1).min(-1), 30.9 +/- 4.8 ml.kg(-1).min(-1) and 35.9 +/- 11.4 ml.kg(-1).min(-1). There was no significant difference (p > 0.05) between the means of the Actual VO(2)max and SM Predicted VO(2)max test for the Total group (N = 20) or the ST group (n = 10), but a significant difference (p < 0.05) was shown for the NST group. The coefficient of determination (R(2)) and standard error of estimate (SEE) for the SM Predicted VO(2)max and Actual VO(2)max tests were R(2) = 0.18, SEE = 5.72 ml.kg(-1).min(-1) for the Total group; R(2) = 0.00, SEE = 6.68 ml.kg(-1).min(-1) for the NST group; and R(2) = 0.33, SEE = 5.32 ml.kg(-1).min(-1) for ST group. In conclusion, the SM Predicted VO(2)max test has acceptable accuracy for the ST group, but significantly underpredicted the NST group by almost 7 ml; and, as demonstrated by the high SEEs, it has a low level of precision for both ST and NST subjects.     

Development of a submaximal test to predict elliptical cross-trainer VO2max

The purpose of this study was to develop an equation to predict VO2max from a submaximal elliptical cross-trainer test. Fifty-four apparently healthy subjects (25 men and 29 women, mean +/- SD age: 29.5 +/- 7.1 years, height: 173.3 +/- 12.6 cm, weight: 72.3 +/- 7.9 kg, percent body fat: 17.3 +/- 5.0%, and elliptical cross-trainer VO2max: 43.9 +/- 7.2 ml x kg(-1) x min(-1)) participated in the study and were randomly assigned to an original sample group (n = 40) and a cross-validation group (n = 14). Each subject completed an elliptical cross-trainer submaximal (3 5-minute submaximal stages) and a VO2max test on the same day, with a 15-minute rest period in between. Stepwise multiple regression analyses were used to develop an equation for estimating elliptical cross-trainer VO2max from the data of the original sample group. The accuracy of the equation was tested by using data from the cross-validation group. Because there was no shrinkage in R2 between the original sample group and the cross-validation group, data were combined in the final prediction equation (R2 = 0.732, standard error of the estimate = 3.91 ml x kg(-1) x min(-1), p < 0.05): VO2max = 73.676 + 7.383(gender) - 0.317(weight) + 0.003957(age x cadence) - 0.006452(age x heart rate at stage 2). The correlation coefficient between the predicted and measured VO2max values was r = 0.86. Dependent t-tests resulted in no significant differences (p > 0.05) between predicted (43.8 ml x kg(-1) x min(-1)) and measured (43.9 ml x kg(-1) x min(-1)) VO2max measurements. Results indicate that the protocol and equation developed in the current study can be used by exercise professionals to provide acceptably accurate estimates of VO2max in non-laboratory-based settings.     

Prolonged submaximal exercise and L-carnitine in humans

Changes in the main physiological parameters and circulating indicators of carbohydrate, protein, lipid (and ketone body) metabolism were measured in ten exercising subjects before L-carnitine (L-carn) loading, after 4 weeks of daily loading with 2 g L-carn, and 6-8 weeks after terminating L-carn administration. Measurements were made on venous blood samples collected during each experiment at fixed time intervals over an initial rest of 45 min, 60 min bicycle exercise performed near 50% VO2max and 120 min recovery. Free and total plasma carnitine levels reached a plateau corresponding to an average rise of 25% for both fractions, 9-10 days after the beginning of the L-carn diet. These levels returned to their initial values 6-8 weeks after cessation of the supply. Generally L-carn supplementation did not significantly modify the physiological parameters and circulating metabolites. No distinct increase of the relative participation of endogenous lipids in the fuel supply of prolonged submaximal exercise was observed. In normal human subjects the increased demand for fatty acid oxidation resulting from exercise seems to be adequately supported by endogenous levels of carnitine.     

VO2 kinetics in the horse during moderate and heavy exercise

Langsetmo, I., G. E. Weigle, M. R. Fedde, H. H. Erickson, T. J. Barstow, and D. C. Poole.O₂ kinetics in thehorse during moderate and heavy exercise. J. Appl.Physiol. 83(4): 1235-1241, 1997.The horse is asuperb athlete, achieving a maximalO₂ uptake (~160ml · min¹ · kg¹)approaching twice that of the fittest humans. Although equine O₂ uptake(O₂) kinetics arereportedly fast, they have not been precisely characterized, nor hastheir exercise intensity dependence been elucidated. To addressthese issues, adult male horses underwent incremental treadmill testingto determine their lactate threshold (T_lac) and peakO₂(O_{2 peak}),and kinetic features of their O₂ response to"square-wave" work forcings were resolved using exercisetransitions from 3 m/s to abelow-T_lac speed of 7 m/s or anabove-T_lac speed of 12.3 ± 0.7 m/s (i.e., between T_lac and O_{2 peak}) sustainedfor 6 min. O₂ andCO₂ output were measured using anopen-flow system: pulmonary artery temperature was monitored, and mixedvenous blood was sampled for plasma lactate.O₂ kinetics at work levelsbelow T_lac were well fit by atwo-phase exponential model, with a phase2 time constant(₁ = 10.0 ± 0.9 s) thatfollowed a time delay (TD₁ = 18.9 ± 1.9 s). TD₁ was similar tothat found in humans performing leg cycling exercise, but the timeconstant was substantially faster. For speeds aboveT_lac,TD₁ was unchanged (20.3 ± 1.2 s); however, the phase 2 time constantwas significantly slower (₁ = 20.7 ± 3.4 s, P < 0.05) than for exercise belowT_lac. Furthermore, in four of fivehorses, a secondary, delayed increase inO₂ became evident135.7 ± 28.5 s after the exercise transition. This "slowcomponent" accounted for ~12% (5.8 ± 2.7 l/min) of the netincrease in exercise O₂. Weconclude that, at exercise intensities below and aboveT_lac, qualitative features ofO₂ kinetics in the horseare similar to those in humans. However, at speeds belowT_lac the fast component of theresponse is more rapid than that reported for humans, likely reflectingdifferent energetics of O₂utilization within equine muscle fibers.

     

Effects of prior heavy exercise on VO(2) kinetics during heavy exercise are related to changes in muscle activity.

We hypothesized that the elevated primary O(2) uptake (VO(2)) amplitude during the second of two bouts of heavy cycle exercise would be accompanied by an increase in the integrated electromyogram (iEMG) measured from three leg muscles (gluteus maximus, vastus lateralis, and vastus medialis). Eight healthy men performed two 6-min bouts of heavy leg cycling (at 70% of the difference between the lactate threshold and peak VO(2)) separated by 12 min of recovery. The iEMG was measured throughout each exercise bout. The amplitude of the primary VO(2) response was increased after prior heavy leg exercise (from mean +/- SE 2.11 +/- 0.12 to 2.44 +/- 0.10 l/min, P < 0.05) with no change in the time constant of the primary response (from 21.7 +/- 2.3 to 25.2 +/- 3.3 s), and the amplitude of the VO(2) slow component was reduced (from 0.79 +/- 0.08 to 0.40 +/- 0.08 l/min, P < 0.05). The elevated primary VO(2) amplitude after leg cycling was accompanied by a 19% increase in the averaged iEMG of the three muscles in the first 2 min of exercise (491 +/- 108 vs. 604 +/- 151% increase above baseline values, P < 0.05), whereas mean power frequency was unchanged (80.1 +/- 0.9 vs. 80.6 +/- 1.0 Hz). The results of the present study indicate that the increased primary VO(2) amplitude observed during the second of two bouts of heavy exercise is related to a greater recruitment of motor units at the onset of exercise.     

Prior heavy-intensity exercise speeds VO2 kinetics during moderate-intensity exercise in young adults.

The effect of prior heavy-intensity warm-up exercise on subsequent moderate-intensity phase 2 pulmonary O2 uptake kinetics (tauVO2) was examined in young adults exhibiting relatively fast (FK; tauVO2 < 30 s; n = 6) and slow (SK; tauVO2 > 30 s; n = 6) VO2 kinetics in moderate-intensity exercise without prior warm up. Subjects performed four repetitions of a moderate (Mod1)-heavy-moderate (Mod2) protocol on a cycle ergometer with work rates corresponding to 80% estimated lactate threshold (moderate intensity) and 50% difference between lactate threshold and peak VO2 (heavy intensity); each transition lasted 6 min, and each was preceded by 6 min of cycling at 20 W. VO2 and heart rate (HR) were measured breath-by-breath and beat-by-beat, respectively; concentration changes of muscle deoxyhemoglobin (HHb), oxyhemoglobin, and total hemoglobin were measured by near-infrared spectroscopy (Hamamatsu NIRO 300). tauVO2 was lower (P < 0.05) in Mod2 than in Mod1 in both FK (20 +/- 5 s vs. 26 +/- 5 s, respectively) and SK (30 +/- 8 s vs. 45 +/- 11 s, respectively); linear regression analysis showed a greater "speeding" of VO2 kinetics in subjects exhibiting a greater Mod1 tauVO2. HR, oxyhemoglobin, and total hemoglobin were elevated (P < 0.05) in Mod2 compared with Mod1. The delay before the increase in HHb was reduced (P <0.05) in Mod2, whereas the HHb mean response time was reduced (P <0.05) in FK (Mod2, 22 +/- 3 s; Mod1, 32 +/- 11 s) but not different in SK (Mod2, 36 +/- 13 s; Mod1, 34 +/- 15 s). We conclude that improved muscle perfusion in Mod2 may have contributed to the faster adaptation of VO2, especially in SK; however, a possible role for metabolic inertia in some subjects cannot be overlooked.     

Plasma 2-hydroxycatecholestrogen responses to acute submaximal and maximal exercise in untrained women

De Crée, Carl, Peter Ball, Bärbel Seidlitz,Gerrit Van Kranenburg, Peter Geurten, and Hans A. Keizer. Plasma2-hydroxycatecholestrogen responses to acute submaximal and maximalexercise in untrained women. J. Appl.Physiol. 82(1): 364-370, 1997.Exercise-induced menstrual problems are accompanied by an increase in catecholestrogen (CE) formation. It has been hypothesized that hypoestrogenemia may besecondary to an increased turnover from estrogens to CE, which then maydisrupt luteinizing hormone release. In addition, the strong affinityof CE for the catecholamine-deactivating enzyme catechol-O-methyltransferase (COMT)has led to speculations about their possible role in safeguardingnorepinephrine from premature decomposition during exercise. Weinvestigated whether acute exercise on a cycle ergometer produces anychanges in CE homeostasis. Nine untrained eumenorrheic women (body fat,24.8 ± 3.1%) volunteered for this study. Baseline plasma CEaverages for total 2-hydroxyestrogens (2-OHE) were 218 ± 29 (SE)pg/ml during the follicular phase (FPh) and 420 ± 58 pg/ml duringthe luteal phase (LPh). 2-Methoxyestrogens (2-MeOE) measured 257 ± 17 pg/ml in the FPh and 339 ± 39 pg/ml in the LPh. Duringincremental exercise, total estrogens (E) increased, but 2-OHE and2-MeOE levels did not significantly change in either phase. The 2-OHE/Eratio (measure of CE turnover) decreased during exercise in bothmenstrual phases, whereas the 2-MeOE/2-OHE ratio (correlates with COMTactivity) did not significantly change. These findings suggest thatthere is insufficient evidence to conclude that brief incrementalexercise in untrained eumenorrheic females acutely produces increasedCE formation.