Oxygen deficit at the onset of submaximal exercise is not due to a delayed oxygen transport.
Six subjects cycled on two occasions for 10 min at power output of 188 +/- 11 W (means +/- SEM), which corresponded to 70 +/- 2% of their maximal oxygen uptake (VO2 max). The exercise intensity was either increased gradually in a stepwise manner over about 15 min (slow transition-S), or increased directly (direct transition-D) to the predetermined power output. Muscle samples from the quadriceps femoris muscle were taken at rest and immediately after exercise in both trials. During exercise with both D and S muscle lactate increased approximately 10 times (P less than 0.01), phosphocreatine decreased about 50% (P less than 0.01) and ADP increased about 20% (P less than 0.05). There were no significant differences between S and D (P greater than 0.05). Furthermore, blood lactate, O2 deficit, O2 debt, and the calculated increase in muscle content of inorganic phosphate (Pi) were all similar between D and S (P greater than 0.05). It is concluded that the O2 deficit and the anaerobic energy utilization is not affected by the rate of transition from rest to exercise. Consequently, the O2 deficit at the onset of exercise is not due to a delay in O2 transport, but may be due to a limited peripheral O2 utilization as a result of metabolic adjustments at the cellular level. Increases in ADP and Pi are suggested to be primary metabolic regulators which activate both aerobic and anaerobic energy production resulting in the O2 deficit.
Sahlin
K
K
Department of Clinical Physiology, Karolinska Institute, Huddinge University Hospital, Sweden.
Ren
J M
JM
Broberg
S
S
D000328:Adult; D004734:Energy Metabolism; D015444:Exercise; D006801:Humans; D007773:Lactates / Q000378:metabolism; D008297:Male; D009132:Muscles / Q000378:metabolism; D010101:Oxygen Consumption; D010725:Phosphocreatine / Q000378:metabolism
D007773:Lactates; D010725:Phosphocreatine