Date of Award


Degree Type


Degree Name

Doctor of Philosophy (PhD)


Medical Sciences


Dr. N.L. Jones


The acidosis accompanying short-term maximal exercise has been quantified and the mechanisms contributing to its control examined. Maximal exercise lasting 30 s was performed on a constant-velocity cycle ergometer. In 3 subjects, acid-base changes were examined across the working quadriceps femoris muscle after arterial and femoral venous catheterisation (Part A). The acid-base changes across the inactive forearm muscle were examined in 6 subjects following arterial and deep forearm venous catheterisation. Gas exchange was measured breath-by-breath during exercise and recovery (Part B). Muscle biopsies were taken from the quadriceps femoris muscle in 6 subjects and analysed for intracellular strong ion changes using neutron activation analysis (Part C).

The intracellular acid load was due to both increased CO₂ production and strong anion production; the muscle [lactate] increased to 30 mmol/kg w.w. after 30 s exercise. The CO₂ and strong ion concentration contributed 25% and 75%, respectively, to the increase in intracellular [H⁺]. The weak acid concentration was assumed not to change during exercise and recovery. CO₂ and strong ions were removed from the intracellular fluid during recovery.

Initially CO₂ output from the muscle reduced the intracellular PCO₂; the femoral venous PCO₂ increased to 105 mm Hg. The increased CO₂ flux to the lungs increased the CO₂ elimination from the body; the CO₂ output increased to 3060 ml/min by the end of exercise. The lungs were effective in removing the excess CO₂ delivered to them as the arterial PCO₂ was less than resting levels throughout recovery. Elimination of excess CO₂ from muscle was complete by 3 min recovery.

Strong ion exchange occurred more slowly; lactate disappeared at a rate of 2 mmol/kg w.w./min. Immediately after exercise the intracellular-femoral venous [lactate] gradient was 40 mmol/l and favoured diffusion of lactate into the circulation. Approximately 55-60% of the lactate diffused from the muscle, the remaining lactate was oxidised or converted to glycogen. Lactate was taken up by the inactive forearm muscle; the v-a [lactate] difference was approximately 4.5 mmol/l. Only about 45% of the lactate taken up by the inactive tissue was oxidised, the remaining lactate was metabolised to other metabolic end points. Lactate uptake by inactive tissue reduced the anion concentration of the body and increased the strong ion difference across the inactive tissue. Recovery of acid-base balance is not complete until all the lactate has been removed from the body.

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