Low-intensity training increases peak arm VO2 by enhancing both convective and diffusive O2 delivery

AimIt is an ongoing discussion the extent to which oxygen delivery and oxygen extraction contribute to an increased muscle oxygen uptake during dynamic exercise. It has been proposed that local muscle factors including the capillary bed and mitochondrial oxidative capacity play a large role in prolonged low-intensity training of a small muscle group when the cardiac output capacity is not directly limiting. The purpose of this study was to investigate the relative roles of circulatory and muscle metabolic mechanisms by which prolonged low-intensity exercise training alters regional muscle VO2. MethodsIn nine healthy volunteers (seven males, two females), haemodynamic and metabolic responses to incremental arm cycling were measured by the Fick method and biopsy of the deltoid and triceps muscles before and after 42days of skiing for 6hday(-1) at 60% max heart rate. ResultsPeak pulmonary VO2 during arm crank was unchanged after training (2.380.19 vs. 2.18 +/- 0.2Lmin(-1) pre-training) yet arm VO2 (1.04 +/- 0.08 vs. 0.83 +/- 0.1Lmin(1), P<0.05) and power output (137 +/- 9 vs. 114 +/- 10 Watts) were increased along with a higher arm blood flow (7.9 +/- 0.5 vs. 6.8 +/- 0.6Lmin(-1), P<0.05) and expanded muscle capillary volume (76 +/- 7 vs. 62 +/- 4mL, P<0.05). Muscle O-2 diffusion capacity (16.2 +/- 1 vs. 12.5 +/- 0.9mLmin(-1)mHg(-1), P<0.05) and O-2 extraction (68 +/- 1 vs. 62 +/- 1%, P<0.05) were enhanced at a similar mean capillary transit time (569 +/- 43 vs. 564 +/- 31ms) and P-50 (35.8 +/- 0.7 vs. 35 +/- 0.8), whereas mitochondrial O-2 flux capacity was unchanged (147 +/- 6mLkgmin(-1) vs. 146 +/- 8mLkgmin(-1)). ConclusionThe mechanisms underlying the increase in peak arm VO2 with prolonged low-intensity training in previously untrained subjects are an increased convective O-2 delivery specifically to the muscles of the arm combined with a larger capillary-muscle surface area that enhance diffusional O-2 conductance, with no apparent role of mitochondrial respiratory capacity.