Effects of prior arm exercise on pulmonary gas exchange kinetics during high-intensity leg exercise in humans

Abstract

For moderate work rates (i.e. below the lactate threshold, θ(L)), oxygen uptake (V̇(O2)) approaches the steady state mono-exponentially. At higher work rates, the V̇(O2) kinetics are more complex, reflecting the delayed superimposition of an additional, slow component. The mechanisms of this 'slow' component are poorly understood. It has been demonstrated, however, that while a prior bout of supra-θ(L) cycling (with a 6 min recovery) does not significantly affect the V̇(O2) time course for a subsequent sub-θ(L) bout, it significantly speeds the V̇(O2) response to a subsequent supra-θ(L) bout. These investigators proposed that this speeding was a result of improved muscle perfusion during the exercise transient, possibly related to the residual metabolic acidaemia still present at the start of the subsequent exercise bout. To determine whether speeding of the V̇(O2) kinetics could also be induced by a bout of prior high-intensity exercise performed at a remote site (e.g. the arms), subjects each performed two 6 min bouts of high-intensity cycling (leg exercise: LE at a work rate equivalent to 50% of 'ΔLE' (the difference between maximum V̇(O2,LE) and θ(L,LE)). On one occasion this was preceded by a 6 min period of cycling at 50% ΔLE and, on another, by a similar period of arm-crank exercise (arm exercise: AE) at 50% ΔAE; in each case, the work bouts were separated by 6 min of unloaded pedalling. Pulmonary gas exchange variables were derived breath-by-breath. During unloaded pedalling and at minute 6 of each work bout, arterialized venous blood samples were drawn from the dorsum of the heated hand or at the wrist for analysis of pH, lactate, pyruvate, noradrenaline (NAdr), adrenaline (Adr), and potassium (K+). The difference in V̇(O2) between minute 6 and 3 of each work bout (ΔV̇(O2,[6.3])) and the 'partial' O2 deficit (O2 Def) provided indices of the slow phase of V̇(O2) kinetics. The initial AE and LE bouts resulted in similar degrees of metabolic (lactic) acidaemia; the residual acidaemia at the end of the subsequent 6 min recovery phase was also similar for the two protocols, as were [K+], [Adr] and [NAdr]. The subsequent LE bouts were associated with reductions in both ΔV̇(O2,[6.3]) and O2 Def, relative to control, with the effect being more marked when the work was preceded by a prior LE bout than a prior AE bout: ΔV̇(O2,[6.3]) averaging 32 and 56% of control, respectively, and O2 Def71 and 81%. Consequently, the increase in [lactate] and decrease in pH induced in this second LE bout were smaller when preceded by prior leg exercise than prior arm exercise. It is therefore concluded that while metabolic, acidaemia induced at a site remote from the legs is associated with a less prominent slow phase of the V̇(O2) kinetics for high-intensity leg exercise, a component specific to the involved contractile units appears to exert the dominant effect. The mechanisms underlying this response are, however, presently uncertain.