LACTATE AND H+ EFFLUXES FROM HUMAN SKELETAL-MUSCLES DURING INTENSE, DYNAMIC EXERCISE

1. Lactate and H+ efflux from skeletal muscles were studied with the one-legged knee extension model under conditions in which blood flow, arterial lactate and the muscle-blood lactate concentration gradient were altered. Subjects exercised one leg twice to exhaustion (EX1, EX2), separated by a 10 min recovery and a period of intense intermittent exercise. After 1 h of recovery the exercise protocol was repeated with the other leg. Low-intensity exercise was performed with one leg during the recovery periods, while the other leg was passive during its recovery periods. 2. Prior to, and immediately after, EX1 and EX2 and then 3 and 10 min after EX1, a biopsy was taken from the vastus lateralis of the exercised leg for lactate, pH, muscle water and fibre-type determinations. Measurements of leg blood flow and venous-arterial differences for lactate (whole blood and plasma), pH, partial pressure of CO2 (P(CO2)), haemoglobin, saturation and base excess (BE) were performed at the end of exercise and regularly during the recovery period after EX1. 3. The lactate release was linearly related (r = 0.96; P < 0.05) to the muscle lactate gradient over a range of muscle lactate from 0 to 45 mmol (kg wet wt)-1. The muscle lactate transport was evaluated from the net femoral venous-arterial differences (V-A(diff)) for lactate. This rose with increases in the muscle lactate gradients, but as the gradient reached higher levels the V-A(diff) lactate responded less than at smaller gradients. Thus, the lactate transport over the muscle membrane appears to be partly saturated at high muscle lactate concentrations. 4. The percentage of slow twitch (% ST) fibres was inversely related to the muscle lactate gradient, but it was not correlated to the lactate release at the end of the exercises. In spite of a significantly higher blood flow during active recovery, the lactate release was the same whether the leg was resting or performed low-intensity exercise in the recovery periods. In several other conditions the muscle lactate and H+ gradients would have predicted that the V-A(diff) lactate would have been greater than it actually was. Thus, a variety of factors affect muscle lactate transport, including arterial lactate concentration, muscle perfusion, muscle contraction pattern and muscle morphology. 5. The muscle and femoral venous pH declined during EX1 to 6.73 and 7.14-7.15, respectively, and they increased to resting levels during 10 min of either passive or active recovery. The ratio between proton release and lactate efflux was estimated from the BE difference across the muscle, adjusted for changes in reduced haemoglobin. This was 1.4-1.6 at the end of each exercise and remained greater than unity during recovery. Thus, proton release appears to be faster than the lactate efflux both during exercise and recovery.