The metabolic effects of exercise

The metabolic effects of exercise have classically been considered in terms of the changing composition of the blood and it may be thought a little old-fashioned to perpetuate this approach. Nevertheless, I believe that the changes in the composition of the blood during exercise are more complex than has generally been credited and the time is opportune to re-examine them. The increase in the concentration of lactate is historically the first observation and the one which has excited the most interest, The classical theory of oxygen debt introduced by A. V. Hill held the expenditure of energy by the exercising muscle to exceed the energy available to it from oxidative catabolism, the balance or debt being made up by the anaerobic production of lactate. After exercise, the oxygen consumption remained high for a period of time and this was thought to be due to the combustion of the lactate which resulted in the repayment of the debt. Later observations made it necessary to modify the simplicity of the original concept. Early on, Margaria, Edwards & Dill (1933), for instance, divided the oxygen debt into a lactic and an alactic phase, and the most recent modification has been the calculation of ‘excess lactate’ by Huckabee (1958a,b). Such modifications are necessitated by discrepancies between fact and theory ; but fact must accompany theory, and, although it may seem surprising, through nearly half a century of investigation the simple observation of how the concentration of lactate in the blood changes during the course of exercise has only been made by a handful of authors. Such few observations as have been published record conflicting results (Bang, 1936; Lundin & Strom, 1947; Asmussen, 1950) and it is for this reason we have made a number of studies on the concentration of lactate in arterial blood during exercise. During the course of 30 min mild bicycling exercise in the recumbant position, it is usual for the concentration of lactate to rise rapidly for the first few minutes, reaching a maximum after about 5-10 min. From this time onwards it usually falls progressively and this decline is often not affected by the moment of stopping exercise. Such changes in the concentration of lactate occur while the external work, the ventilation and the oxygen uptake remain constant. If the subject bicycles for only 4 min, the concentration of lactate in the arterial blood follows a very similar course, reaching a maximum about 5-10 min after the beginning of exercise and then declining gradually. I n this instance the concentration of lactate continues to rise after the end of exercise and remains high long after the oxygen uptake has returned to its normal resting level. Such simple observations raise doubts about whether there is any relation between the increased uptake of oxygen after exercise and the concentration of lactate in the blood. Nor are such doubts dispelled by considering the lactate : pyruvate ratio or the ‘excess lactate’, both of which quantities can be shown to move independently of the oxygen uptake under such circumstances.