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During maximal whole body exercise V[O.sub.2 peak] is limited by [O.sub.2] delivery. In turn, it is though that blood flow at near-maximal exercise must be restrained by the sympathetic nervous system to maintain mean arterial pressure. To determine whether enhancing vasodilation across the leg results in higher [O.sub.2] delivery and leg V[O.sub.2] during near-maximal and maximal exercise in humans, seven men performed two maximal incremental exercise tests on the cycle ergometer. In random order, one test was performed with and one without (control exercise) infusion of ATP (8 mg in 1 ml of isotonic saline solution) into the fight femoral artery at a rate of 80 [micro]g x kg body [mass.sup.-1] x [min.sup.-1]. During near-maximal exercise (92% of V[O.sub.2peak]), the infusion of ATP increased leg vascular conductance (+43%, P < 0.05), leg blood flow (+20%, 1.7 l/min, P < 0.05), and leg [O.sub.2] delivery (+20%, 0.3 l/min, P < 0.05). No effects were observed on leg or systemic V[O.sub.2]. Leg [O.sub.2] fractional extraction was decreased from 85 [+ or -] 3 (control) to 78 [+ or -] 4% (ATP) in the infused leg (P < 0.05), while it remained unchanged in the left leg (84 [+ or -] 2 and 83 [+ or -] 2%; control and ATP; n = 3). ATP infusion at maximal exercise increased leg vascular conductance by 17% (P < 0.05), while leg blood flow tended to be elevated by 0.8 l/min (P = 0.08). However, neither systemic nor leg peak V[O.sub.2] values where enhanced due to a reduction of [O.sub.2] extraction from 84 [+ or -] 4 to 76 [+ or -] 4%, in the control and ATP conditions, respectively (P < 0.05). In summary, the V[O.sub.2] of the skeletal muscles of the lower extremities is not enhanced by limb vasodilation at near-maximal or maximal exercise in humans. The fact that ATP infusion resulted in a reduction of [O.sub.2] extraction across the exercising leg suggests a vasodilating effect of ATP on less-active muscle fibers and other noncontracting tissues and that under normal conditions these regions are under high vasoconstrictor influence to ensure the most efficient flow distribution of the available cardiac output to the most active muscle fibers of the exercising limb. muscle sympathetic nerve activity; fatigue; performance doi:10.1152/ajpregu.00746.2005

To determine whether conditions for [O.sub.2] utilization and [O.sub.2] off-loading from the hemoglobin are different in exercising arms and legs, six cross-country skiers participated in this study. Femoral and subclavian vein blood flow and gases were determined during skiing on a treadmill at ~76% maximal [O.sub.2] uptake (V[O.sub.2 max]) and at V[O.sub.2 max] with different techniques: diagonal stride (combined arm and leg exercise), double poling (predominantly arm exercise), and leg skiing (predominantly leg exercise). The percentage of [O.sub.2] extraction was always higher for the legs than for the arms. At maximal exercise (diagonal stride), the corresponding mean values were 93 and 85% (n = 3; P < 0.05). During exercise, mean arm [O.sub.2] extraction correlated with the P[O.sub.2] value that causes hemoglobin to be 50% saturated ([P.sub.50]: r = 0.93, P < 0.05), but for a given value of [P.sub.50], [O.sub.2] extraction was always higher in the legs than in the arms. Mean capillary muscle [O.sub.2] conductance of the arm during double poling was 14.5 (SD 2.6) ml x [min.sup.-1] x mm[Hg.sup.-1], and mean capillary P[o.sub.2] was 47.7 (SD 2.6) mmHg. Corresponding values for the legs during maximal exercise were 48.3 (SD 13.0) ml x [min.sup.-1]. mm[Hg.sup.-1] and 33.8 (SD 2.6) mmHg, respectively. Because conditions for [O.sub.2] off-loading from the hemoglobin are similar in leg and arm muscles, the observed differences in maximal arm and leg [O.sub.2] extraction should be attributed to other factors, such as a higher heterogeneity in blood flow distribution, shorter mean transit time, smaller diffusing area, and larger diffusing distance, in arms than in legs. diffusing capacity; fatigue; oxygen extraction; performance; training

To unravel the mechanisms by which maximal oxygen uptake (V[O.sub.2 max]) is reduced with severe acute hypoxia in humans, nine Danish lowlanders performed incremental cycle ergometer exercise to exhaustion, while breathing room air (normoxia) or 10.5% [O.sub.2] in [N.sub.2] (hypoxia, ~5,300 m above sea level). With hypoxia, exercise Pa[O.sub.2] dropped to 31-34 mmHg and arterial [O.sub.2] content (Ca[O.sub.2]) was reduced by 35% (P < 0.001). Forty-one percent of the reduction in Ca[O.sub.2] was explained by the lower inspired [O.sub.2] pressure (PI[O.sub.2]) in hypoxia, whereas the rest was due to the impairment of the pulmonary gas exchange, as reflected by the higher alveolar-arterial [O.sub.2] difference in hypoxia (P < 0.05). Hypoxia caused a 47% decrease in V[O.sub.2 max] (a greater fall than accountable by reduced Ca[O.sub.2]). Peak cardiac output decreased by 17% (P < 0.01), due to equal reductions in both peak heart rate and stroke volume (P < 0.05). Peak leg blood flow was also lower (by 22%, P < 0.01). Consequently, systemic and leg [O.sub.2] delivery were reduced by 43 and 47%, respectively, with hypoxia (P < 0.001) correlating closely with V[O.sub.2 max] (r = 0.98, P < 0.001). Therefore, three main mechanisms account for the reduction of V[O.sub.2 max] in severe acute hypoxia: 1) reduction of PI[O.sub.2], 2) impairment of pulmonary gas exchange, and 3) reduction of maximal cardiac output and peak leg blood flow, each explaining about one-third of the loss in V[O.sub.2 max]. cardiac output; fatigue; performance; cardiovascular physiology

Acute hypoxia (AH) reduces maximal [O.sub.2] consumption (V[O.sub.2 max]), but after acclimatization, and despite increases in both hemoglobin concentration and arterial [O.sub.2] saturation that can normalize arterial [O.sub.2] concentration ([[O.sub.2]]), V[O.sub.2 max] remains low. To determine why, seven lowlanders were studied at V[O.sub.2 max] (cycle ergometry) at sea level (SL), after 9-10 wk at 5,260 m [chronic hypoxia (CH)], and 6 mo later at SL in AH (FI[O.sub.2] = 0.105) equivalent to 5,260 m. Pulmonary and leg indexes of [O.sub.2] transport were measured in each condition. Both cardiac output and leg blood flow were reduced by ~15% in both AH and CH (P < 0.05). At maximal exercise, arterial [[O.sub.2]] in AH was 31% lower than at SL (P < 0.05), whereas in CH it was the same as at SL due to both polycythemia and hyperventilation. [O.sub.2] extraction by the legs, however, remained at SL values in both AH and CH. Although at both SL and in AH, 76% of the cardiac output perfused the legs, in CH the legs received only 67%. Pulmonary V[O.sub.2 max] (4.1 [+ or -] 0.3 l/min at SL) fell to 2.2 [+ or -] 0.1 l/min in AH (P < 0.05) and was only 2.4 [+ or -] 0.2 l/min in CH (P < 0.05). These data suggest that the failure to recover V[O.sub.2 max] after acclimatization despite normalization of arterial [[O.sub.2]] is explained by two circulatory effects of altitude: 1) failure of cardiac output to normalize and 2) preferential redistribution of cardiac output to nonexercising tissues. Oxygen transport from blood to muscle mitochondria, on the other hand, appears unaffected by CH. cardiac output; fatigue; performance; exercise; cardiovascular physiology; maximal oxygen consumption

To study the role of muscle mass and muscle activity on lactate and energy kinetics during exercise, whole body and limb lactate, glucose, and fatty acid fluxes were determined in six elite cross-country skiers during roller-skiing for 40 min with the diagonal stride (Continuous Arm + Leg) followed by 10 min of double poling and diagonal stride at 72-76% maximal [O.sub.2] uptake. A high lactate appearance rate ([R.sub.a] 184 [+ or -] 17 [micro]mol*[kg.sup.-1]*[min.sup.-1]) but a low arterial lactate concentration (~2.5 mmol/l) were observed during Continuous Arm + Leg despite a substantial net lactate release by the arm of ~2.1 mmol/min, which was balanced by a similar net lactate uptake by the leg. Whole body and limb lactate oxidation during Continuous Arm + Leg was ~45% at rest and ~95% of disappearance rate and limb lactate uptake, respectively. Limb lactate kinetics changed multiple times when exercise mode was changed. Whole body glucose and glycerol turnover was unchanged during the different skiing modes; however, limb net glucose uptake changed severalfold. In conclusion, the arterial lactate concentration can be maintained at a relatively low level despite high lactate [R.sub.a], during exercise with a large muscle mass because of the large capacity of active skeletal muscle to take up lactate, which is tightly correlated with lactate delivery. The limb lactate uptake during exercise is oxidized at rates far above resting oxygen consumption, implying that lactate uptake and subsequent oxidation are also dependent on an elevated metabolic rate. The relative contribution of whole body and limb lactate oxidation is between 20 and 30% of total carbohydrate oxidation at rest and during exercise under the various conditions. Skeletal muscle can change its limb net glucose uptake severalfold within minutes, causing a redistribution of the available glucose because whole body glucose turnover was unchanged. lactate dehydrogenase; cross-country skiing; tracers

We hypothesized that reliance on lactate as a means of energy distribution is higher after a prolonged period of acclimatization (9 wk) than it is at sea level due to a higher lactate [R.sub.a] and disposal from active skeletal muscle. To evaluate this hypothesis, six Danish lowlanders (25 [+ or -] 2 yr) were studied at rest and during 20 min of bicycle exercise at 146 W at sea level (SL) and after 9 wk of acclimatization to 5,260 m (Alt). Whole body glucose [R.sub.a] was similar at SL and Alt at rest and during exercise. Lactate [R.sub.a] was also similar for the two conditions at rest; however, during exercise, lactate [R.sub.a] was substantially lower at SL (65 [micro]mol*[min.sup.-1]*kg body [wt.sup.-1]) than it was at Alt (150 [micro]mol*[min.sup.-l]*kg body [wt.sup.-1]) at the same exercise intensity. During exercise, net lactate release was ~6-fold at Alt compared with SL, and related to this, tracer-calculated leg lactate uptake and release were both 3- or 4-fold higher at Alt compared with SL. The contribution of the two legs to glucose disposal was similar at SL and Alt; however, the contribution of the two legs to lactate [R.sub.a] was significantly lower at rest and during exercise at SL (27 and 81%) than it was at Alt (45 and 123%). In conclusion, at rest and during exercise at the same absolute workload, CHO and blood glucose utilization were similar at SL and at Alt. Leg net lactate release was severalfold higher, and the contribution of leg lactate release to whole body lactate [R.sub.a] was higher at Alt compared with SL. During exercise, the relative contribution of lactate oxidation to whole body CHO oxidation was substantially higher at Alt compared with SL as a result of increased uptake and subsequent oxidation of lactate by the active skeletal muscles. glucose; isotopes; [1-[sup.13]C]lactate

During exercise in humans, the alveolar-arterial O2 tension difference ((A-a)DO2) increases with exercise intensity and is an important factor determining the absolute level of oxygen binding to hemoglobin and therefore the level of systemic oxygen transport. During exercise in hypoxia, the (A-a)DO2 is accentuated. Using the multiple inert gas elimination technique it has been shown that during exercise in acute hypoxia the contribution of ventilation-perfusion inequality to (A-a)DO2 is rather small and in the absence of pulmonary edema intrapulmonary shunts can be ruled out. This implies that the main mechanism limiting pulmonary gas exchange is diffusion limitation. It is presumed that an elevation of cardiac output during exercise in acute hypoxia should increase the (A-a)DO2. However, no studies have examined how variations in cardiac output independently affect pulmonary diffusion with increases in exercise intensity. We have consistently observed that during steady-state, submaximal (100-120 W) exercise on the cycle ergometer in hypoxia the lung can accommodate an increase in cardiac output of ~2 L·min-1 without any significant effect on pulmonary gas exchange. This result contrasts with the predicted effect of cardiac output on (A-a)DO2 using the model of Piiper and Scheid, and thus indicates that an elevation of cardiac output is not necessarily accompanied by a reduction of mean transit time and (or) diffusion limitation during submaximal exercise in acute hypoxia. It remains to be determined what is the influence of changes in cardiac output per se on pulmonary gas exchange during high-intensity exercise. [ABSTRACT FROM AUTHOR]

Acute hypoxia (AH) reduces maximal O[sub 2] consumption (Vo[sub 2 max]), but after acclimatization, and despite increases in both hemoglobin concentration and arterial O[sub 2] saturation that can normalize arterial O[sub 2] concentration ([O[sub 2]]), VO[sub 2 max] remains low. To determine why, seven lowlanders were studied at VO[sub 2 max] (cycle ergometry) at sea level (SL), after 9-10 wk at 5,260 m [chronic hypoxia (CH)], and 6 mo later at SL in AH (FI[sub O[sub 2]] = 0.105) equivalent to 5,260 m. Pulmonary and leg indexes of O[sub 2] transport were measured in each condition. Both cardiac output and leg blood flow were reduced by ∼15% in both AH and CH (P < 0.05). At maximal exercise, arterial [O[sub 2]] in AH was 31% lower than at SL (P < 0.05), whereas in CH it was the same as at SL due to both polycythemia and hyperventilation. O[sub 2] extraction by the legs, however, remained at SL values in both AH and CH. Although at both SL and in AH, 76% of the cardiac output per. fused the legs, in CH the legs received only 67%. Pulmonary VO[sub 2 max] (4.1 ± 0.3 1/min at SL) fell to 2.2 ± 0.1 l/min in AH (P < 0.05) and was only 2.4 ± 0.2 l/min in CH (P < 0.05). These data suggest that the failure to recover VO[sub 2 max] after acclimatization despite normalization of arterial [O[sub 2]] is explained by two circulatory effects of altitude: 1) failure of cardiac output to normalize and 2) preferential redistribution of cardiac output to nonexercising tissues. Oxygen transport from blood to muscle mitochondria, on the other hand, appears unaffected by CH. [ABSTRACT FROM AUTHOR]

Evaluates the effects of severe acute hypoxia on exercise performance and metabolism during 30-second Wingate tests. Estimation of oxygen deficit from submaximal cycling economy tests by use of a nonlinear model; Impact of hypoxia on peak power output, fatigue index and exercise femoral vein blood lactate concentrations.