Maximal strength training (MST) reduces pulmonary oxygen uptake (V O2) at a given submaximal exercise work rate (i.e., efficiency). However, whether the increase in efficiency originates in the trained skeletal muscle, and therefore the impact of this adaptation on muscle blood flow and arterial-venous oxygen difference (a-vO 2diff), is unknown. Thus five trained subjects partook in an 8-wk MST intervention consisting of half-squats with an emphasis on the rate of force development during the concentric phase of the movement. Pre-and posttraining measurements of pulmonary V O2 (indirect calorimetry), single-leg blood flow (thermodilution), and single-leg a-vO2diff (blood gases) were performed, to allow the assessment of skeletal muscle V O2 during submaximal cycling [237 Ϯ 23 W; ϳ60% of their peak pulmonary V O2 (V O2peak)]. Pulmonary V O2peak (ϳ4.05 l/min) and peak work rate (ϳ355 W), assessed during a graded exercise test, were unaffected by MST. As expected, following MST there was a significant reduction in pulmonary V O2 during steady-state submaximal cycling (ϳ237 W: 3.2 Ϯ 0.1 to 2.9 Ϯ 0.1 l/min). This was accompanied by a significant reduction in single-leg V O2 (1,101 Ϯ 105 to 935 Ϯ 93 ml/min) and single-leg blood flow (6,670 Ϯ 700 to 5,649 Ϯ 641 ml/min), but no change in single-leg a-vO2diff (16.7 Ϯ 0.8 to 16.8 Ϯ0.4 ml/dl). These data confirm an MSTinduced reduction in pulmonary V O2 during submaximal exercise and identify that this change in efficiency originates solely in skeletal muscle, reducing muscle blood flow, but not altering muscle a-vO2diff. oxygen consumption; blood flow; work economy DURING CYCLE EXERCISE, at a given submaximal work rate (WR), pulmonary oxygen uptake (V O 2 ) is similar between individuals of varying aerobic capacities [peak V O 2 (V O 2peak )] (34). This is true despite the complex, systemwide metabolic costs of exercise, such as ventilatory and cardiac muscle work, ion transport, and exercise-induced alterations in thermoregulation and metabolism, each of which may influence the V O 2 /WR relationship (6,39,43). Thus work efficiency, measured as the ratio of pulmonary V O 2 to work accomplished during submaximal steady-state cycling, is a global assessment of metabolic demand and may be influenced by a change in any of these systems. Therefore, a perturbation or stressor, such as maximal strength training (MST), which has been determined to alter work efficiency (22,26,42), may not simply be attributed to a change in efficiency of the exercising muscle.For over a decade, studies have documented that the use of MST, which consists of high loads and few repetitions, with an emphasis on the maximal rate of force development, improves work efficiency in both sedentary (22) and aerobically trained individuals (26,42), and this MST-induced change is even more evident during high-intensity exercise (22). While it is reasonable to expect enhanced intramuscular efficiency to be a major contributor to this documented improvement in work efficiency, an attenuated O 2 cost, external ...