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

For moderate work rates (i.e, below the lactate threshold, theta(L)), oxygen uptake ((V) over dot(O2)) approaches the steady state mono-exponentially. At higher work rates, the (V) over dot(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-theta(L) cycling (with a 6 min recovery) does not significantly affect the (V) over dot(O2) time course for a subsequent sub-theta(L) bout, it significantly speeds the (V) over dot(O2), response to a subsequent supra-theta(L) bout (Gausche, Harmon, Lamarra & Whipp, 1989; Gerbino, Ward & Whipp, 1996). 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 (V) over dot(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 'Delta LE' (the difference between maximum (V) over dot(O2).LE and theta(L,LE)). On one occasion this was preceded by a 6 min period of cycling at 50 % Delta LE and, on another, by a similar period of arm-crank exercise (arm exercise: AE) at 50 % Delta AE; 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 li,(V) over dot(O2) between minute 6 and 3 of each work bout (Delta(V) over dot(O2[6-3])) and the 'partial' O-2 deficit (O-2 Def) provided indices of the slow phase of (V) over dot(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 Delta(V) over dot(O2),([6 3]) and O-2 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: Delta(V) over dot(O2),([6-3]) averaging 32 and 56 % of control, respectively, and O-2 Def 71 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 (V) over dot(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.