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.     

Oxygen uptake kinetics during exercise are slowed in patients with peripheral arterial disease.

Patients with peripheral arterial disease (PAD) have arterial occlusions that limit peripheral blood flow. This study evaluated the dynamic response in O(2) consumption (VO(2)) at the onset of constant-load exercise (VO(2) kinetics) in patients with PAD. Eight patients with bilateral PAD, seven patients with unilateral PAD, nine age-matched nonsmoking controls, and seven smoking controls performed graded treadmill exercise to assess peak VO(2). Subjects also performed constant-load exercise tests at 2.0 miles/h at 0 and 4% grade to determine VO(2) kinetics. Peak VO(2) was reduced 50% in patients with PAD compared with both control groups (P < 0.05). At 4% grade, phase 2 VO(2) kinetics were significantly slowed for the PAD groups compared with controls (60.1 +/- 15.7 and 58.7 +/- 8.3 s, unilateral and bilateral PAD groups, respectively; compared with 28. 4 +/- 19.3 and 27.9 +/- 8.1 s, nonsmoking and smoking controls, respectively; P < 0.05). No relationship was found between VO(2) kinetics and disease severity. These data demonstrate that VO(2) kinetics are markedly slowed in patients with PAD. The impairment in VO(2) kinetics is not related to smoking status or arterial disease severity and therefore may reflect altered control of skeletal muscle metabolism.     

Standard exercise test to assess peripheral arterial disease.

The fall in ankle systolic pressure after exercise serves as an objective indicator of the severity of haemodynamically important peripheral arterial disease. Twenty-six patients were studied to establish the effects of different work loads on the pressure response and to develop a test to standardise these effects. The patients walked for one or two minutes at 4 km/h and one or two minutes at 6 km/h, and the fall in pressure was the same when measured immediately after exercise. The time taken for the pressure to return to the pre-exercise value varied. As the fall in pressure occurs after only one minute of exercise at 4 km/h on a 10% slope, this might be adopted as a standard test. It is acceptable to the patient, since claudication, angina, and shortness of breath rarely occur. It is sensitive enough to detect mild or asymptomatic disease and is useful in following up patients.     

O2 transport in ponies during treadmill exercise

We assessed cardiovascular variables and blood O2 contents in order to characterize O2 transport in ponies during treadmill exercise. In normal ponies at 1.8, 3, and 6 mph, respectively, cardiac output (Qc) increased from 12 l/min at rest to maximum levels of 19.7, 28.7, and 39.9 l/min between 30 and 60 s. Qc then decreased to steady-state levels of 18.2, 24.6, and 32.7 l/min by 4 min. Heart rate (HR) showed a similar biphasic response in the 1st min of exercise. Systolic and diastolic arterial blood pressure (BP) decreased at the onset of exercise by 20-25 Torr (P less than 0.05) and then increased to a steady-state by 60 s. Mean right ventricular pressures (MRVBP) increased from approximately 9.7 Torr at rest to 15.9 (1.8 mph), 15.2 (3 mph), and 23.6 Torr (6 mph) by 1 min and then decreased throughout the remainder of the 8 min of exercise (P less than 0.05). At 3 and 6 mph, respectively, arterial O2 content (CaO2) increased from 11.6 vol% at rest to 12.7 and 15.0 vol% by 45 s and 13.1 and 16.6 vol% by 7 min. At 7 min of 9.3 mph exercise, it increased to 20.34 vol%. Hemoglobin (Hb) at 3 mph increased from 9.6 g/100 ml at rest to 10.5 g/100 ml by 45 s and 11.7 g/100 ml by 7 min. At 6 mph, Hb increased to 12 g/100 ml at 45 s and 13.0 g/100 ml by 7 min of exercise. These data demonstrate that the rapid, work load-dependent increase in CaO2 represents an important mechanism to increase O2 transport in exercising ponies.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dynamic linearity of VO2 responses during aerobic exercise.

The multifrequent pseudorandom binary sequence (PRBS) technique is a useful tool for studying oxygen uptake (VO2) kinetics within the aerobic range. However, the validity of this multifrequent test may be limited by nonlinearities generated by the circulatory and pulmonary system. To check for such nonlinear effects, we compared the frequency responses computed from two PRBS protocols with the results of pure sinusoidal frequencies varying in amplitude and mean values (periods between 50 s and 450 s). According to our results the VO2 frequency response does not seem to depend on the type of testing--PRBS or sine--or the changes within each test, i.e. mean power and power amplitude of the sine tests and the switching frequency of the PRBS. In the range of higher frequencies small differences between the test conditions may have been obscured by the greater scatter of dynamic responses. It was concluded that the VO2 frequency response was quasi-linear for periods down to the least 100 s. However, even in this range nonlinearities can be provoked by rest-exercise transitions, by a varying contribution of lactate or by an insufficient noise reduction.     

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.     

Pulmonary gas exchange during exercise in highly trained cyclists with arterial hypoxemia.

The causes of exercise-induced hypoxemia (EIH) remain unclear. We studied the mechanisms of EIH in highly trained cyclists. Five subjects had no significant change from resting arterial PO(2) (Pa(O(2)); 92.1 +/- 2.6 Torr) during maximal exercise (C), and seven subjects (E) had a >10-Torr reduction in Pa(O(2)) (81.7 +/- 4.5 Torr). Later, they were studied at rest and during various exercise intensities by using the multiple inert gas elimination technique in normoxia and hypoxia (13.2% O(2)). During normoxia at 90% peak O(2) consumption, Pa(O(2)) was lower in E compared with C (87 +/- 4 vs. 97 +/- 6 Torr, P < 0.001) and alveolar-to-arterial O(2) tension difference (A-aDO(2)) was greater (33 +/- 4 vs. 23 +/- 1 Torr, P < 0. 001). Diffusion limitation accounted for 23 (E) and 13 Torr (C) of the A-aDO(2) (P < 0.01). There were no significant differences between groups in arterial PCO(2) (Pa(CO(2))) or ventilation-perfusion (VA/Q) inequality as measured by the log SD of the perfusion distribution (logSD(Q)). Stepwise multiple linear regression revealed that lung O(2) diffusing capacity (DL(O(2))), logSD(Q), and Pa(CO(2)) each accounted for approximately 30% of the variance in Pa(O(2)) (r = 0.95, P < 0.001). These data suggest that EIH has a multifactorial etiology related to DL(O(2)), VA/Q inequality, and ventilation.     

Dietary nitrate supplementation enhances exercise performance in peripheral arterial disease

Peripheral arterial disease (PAD) results in a failure to adequately supply blood and oxygen (O(2)) to working tissues and presents as claudication pain during walking. Nitric oxide (NO) bioavailability is essential for vascular health and function. Plasma nitrite (NO(2)(-)) is a marker of vascular NO production but may also be a protected circulating source that can be converted to NO during hypoxic conditions, possibly aiding perfusion. We hypothesized that dietary supplementation of inorganic nitrate in the form of beetroot (BR) juice would increase plasma NO(2)(-) concentration, increase exercise tolerance, and decrease gastrocnemius fractional O(2) extraction, compared with placebo (PL). This was a randomized, open-label, crossover study. At each visit, subjects (n = 8) underwent resting blood draws, followed by consumption of 500 ml BR or PL and subsequent blood draws prior to, during, and following a maximal cardiopulmonary exercise (CPX) test. Gastrocnemius oxygenation during the CPX was measured by near-infrared spectroscopy. There were no changes from rest for [NO(2)(-)] (152 ± 72 nM) following PL. BR increased plasma [NO(2)(-)] after 3 h (943 ± 826 nM; P ≤ 0.01). Subjects walked 18% longer before the onset of claudication pain (183 ± 84 s vs. 215 ± 99 s; P ≤ 0.01) and had a 17% longer peak walking time (467 ± 223 s vs. 533 ± 233 s; P ≤ 0.05) following BR vs. PL. Gastrocnemius tissue fractional O(2) extraction was lower during exercise following BR (7.3 ± 6.2 vs. 10.4 ± 6.1 arbitrary units; P ≤ 0.01). Diastolic blood pressure was lower in the BR group at rest and during CPX testing (P ≤ 0.05). These findings support the hypothesis that NO(2)(-)-related NO signaling increases peripheral tissue oxygenation in areas of hypoxia and increases exercise tolerance in PAD.     

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.

     

Is the gender difference in peak VO2 greater for arm than leg exercise?

Based on observations that the difference between men and women in estimates of arm musculature is greater than the difference in leg musculature, it was hypothesized that the gender difference in peak oxygen uptake (VO2; l.min-1) would be greater for arm exercise than leg exercise. To test this hypothesis, 19 (10 men, 9 women) highly trained swimmers (HT) and 20 (10 men, 10 women) untrained students (UT) were tested for peak VO2 on cycle and arm-crank ergometers. Arm and leg fat-free volumes (FFV) were measured to provide an estimate of muscle distribution. No gender difference was observed in either the arm-to-leg peak VO2 ratio (0.699 for the men vs 0.696 for the women) or in the arm-to-leg FFV ratio (0.410 for the men vs 0.402 for the women). Although the proportion of musculature in the arms as assessed by the FFV appeared to be the same in men and women, the similarity in muscle distribution was probably not responsible for the identical average arm-to-leg peak VO2 ratios. The variance in the muscle distribution accounted for only 2-4% of the variance in the arm-to-leg peak VO2 differences within individuals. We conclude that factors other than arm and leg muscle dimensions account for the variability in the arm-to-leg peak VO2 ratio and that the gender difference in peak VO2 is the same for arm and leg exercise.     

Hemodynamic responses during exercise at and above VO2max in swine

Mean arterial pressure (Pa), heart rate, cardiac output (Q), and Q distribution (with radiolabeled microspheres) were measured in miniature swine as they ran at high levels on a motor-driven treadmill. Each animal ran on two occasions: once during exercise at maximal O2 uptake (VO2max) and once at an intensity estimated to require approximately 115% VO2max. The purpose was to assess these cardiovascular variables to determine whether the calculated resistance to blood flow during supramaximal exercise was different from that during maximal exercise. A total of 114 tissues/organs were dissected for blood flow analysis. Pa and Q were unaltered between the two exercise conditions. Blood flow to all but one of the 62 skeletal muscles sampled was unchanged between conditions as were the blood flows to the visceral organs and brain. The results demonstrate that vascular resistance was constant in all these tissues between maximal and supramaximal exercise intensities. Elevated blood flows were measured in 7 of the 11 coronary sites sampled. Calculated resistance to blood flow indicated that a decrease in resistance occurred in most of the samples having elevated blood flow. Because heart rate was elevated during the supramaximal exercise, the increase in blood flow was probably in response to the greater myocardial work and concomitant elevation in O2 demand. In summary, it was shown that Pa, Q, and Q distribution in most tissues remained unchanged during exercise at intensities above VO2max. Thus a precise matching occurs between the increasingly powerful vasoconstrictor drive initiated by the sympathetic nervous system and the elevated local vasodilatory drive responding to the greater O2 demand during the supramaximal exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Decreased VO2 consumption during exercise with elicitation of the relaxation response.

Oxygen consumption is usually considered to be predictable and unalterable at a fixed work intensity. The relaxation response is hypothesized to be an integrated hypothalamic response which results in generalized decreased sympathetic nervous system activity. One physiologic manifestation of the relaxation response is decreased oxygen consumption. The possibility that the elicitation of the relaxation response could decrease oxygen consumption at a fixed work intensity was investigated. Oxygen consumption was decreased 4 percent (p less than 0.05) in eight subjects working at a fixed intensity when the relaxation response was simultaneously elicited.     

Prediction of VO2max during cycle exercise in pregnant women

We measured maximal O2 uptake (VO2max) during stationary cycling in 40 pregnant women [aged 29.2 +/- 3.9 (SD) yr, gestational age 25.9 +/- 3.3 wk]. Data from 30 of these women were used to develop an equation to predict the percent VO2max from submaximal heart rates. This equation and the submaximal VO2 were used to predict VO2max in the remaining 10 women. The accuracy of VO2max values estimated by this procedure was compared with values predicted by two popular methods: the Astrand nomogram and the VO2 vs. heart rate (VO2-HR) curve. VO2max values estimated by the derived equation method in the 10 validation subjects were only 3.7 +/- 12.2% higher than actual values (P greater than 0.05). The Astrand method overestimated VO2max by 9.0 +/- 19.4% (P greater than 0.05), whereas the VO2-HR curve method underestimated VO2max by only 1.6 +/- 10.3% in the same 10 subjects (P greater than 0.05). Both the Astrand and the VO2-HR curve methods correlated well with the actual values when all 40 subjects were considered (r = 0.77 and 0.85, respectively), but the VO2-HR curve method had a lower SE of prediction than the Astrand method (8.7 vs. 10.4%). In a comparison group of 10 nonpregnant sedentary women (29.9 +/- 4.5 yr), an equation relating %VO2max to HR nearly identical to that obtained in the pregnant women was found, suggesting that pregnancy does not alter this relationship. We conclude that extrapolating the VO2-HR curve to an estimated maximal HR is the most accurate method of predicting VO2max in pregnant women.     

Influence of acute plasma volume expansion on VO2 kinetics, VO2 peak, and performance during high-intensity cycle exercise.

The purpose of this study was to examine the influence of acute plasma volume expansion (APVE) on oxygen uptake (V(O2)) kinetics, V(O2peak), and time to exhaustion during severe-intensity exercise. Eight recreationally active men performed "step" cycle ergometer exercise tests at a work rate requiring 70% of the difference between the gas-exchange threshold and V(O2max) on three occasions: twice as a "control" (Con) and once after intravenous infusion of a plasma volume expander (Gelofusine; 7 ml/kg body mass). Pulmonary gas exchange was measured breath by breath. APVE resulted in a significant reduction in hemoglobin concentration (preinfusion: 16.0 +/- 1.0 vs. postinfusion: 14.7 +/- 0.8 g/dl; P < 0.001) and hematocrit (preinfusion: 44 +/- 2 vs. postinfusion: 41 +/- 3%; P < 0.01). Despite this reduction in arterial O(2) content, APVE had no effect on V(O2) kinetics (phase II time constant, Con: 33 +/- 15 vs. APVE: 34 +/- 12 s; P = 0.74), and actually resulted in an increased V(O2peak) (Con: 3.90 +/- 0.56 vs. APVE: 4.12 +/- 0.55 l/min; P = 0.006) and time to exhaustion (Con: 365 +/- 58 vs. APVE: 424 +/- 64 s; P = 0.04). The maximum O(2) pulse was also enhanced by the treatment (Con: 21.3 +/- 3.4 vs. APVE: 22.7 +/- 3.4 ml/beat; P = 0.04). In conclusion, APVE does not alter V(O2) kinetics but enhances V(O2peak) and exercise tolerance during high-intensity cycle exercise in young recreationally active subjects.