Kinetics of pulmonary $$\dot{V} \hbox{O}_{2}$$ and femoral artery blood flow and their relationship during repeated bouts of heavy exercise

Abstract

The mechanism that alters the pulmonary VO2 response to heavy-intensity exercise following prior heavy exercise has been frequently ascribed to an improvement in pre-exercise blood flow (BF) or O(2) delivery. Interventions to improve O(2) delivery have rarely resulted in a similar enhancement of VO2. However, the actual limb blood flow and VO2 dynamics in the second bout of repeated exercise remain equivocal. Seven healthy female subjects (21-32 years) performed consecutive 6-min (separated by 6 min of 10 W exercise) bilateral knee extension (KE) exercise in a semisupine position at a work rate halfway between the lactate threshold (LT) and VO2peak. Femoral artery blood flow (FBF) was measured by Doppler ultrasound simultaneously with breath-by-breath VO2 each protocol being repeated at least four times for precise kinetic characterization. The effective time-constant (tau') of the VO2 response was reduced following prior exercise (bout 1: 61.0 +/-10.5 vs. bout 2: 51.6+/-9.0 s; mean +/- SD; P<0.05), which was a result of a reduced slow component (bout 1: 16.0+/-8.0 vs. bout 2: 12.5+/-6.7 %; P<0.05) and an unchanged 'primary' tau. FBF was consistently faster than VO2. However, there was no bout-effect on tau' FBF (bout 1: 28.2+/-12.0 vs. bout 2: 34.2+/-8.5 s). The relationship between the exercise-associated VO2 (i.e., deltaVO2) and Delta FBF was similar between bouts, with a tendency (N.S: P>0.05) for deltaVO2/deltaFBF to be increased during the transition to bout 2 rather than decreased, as hypothesized. The return of VO2 kinetics toward first order, therefore, was associated with an 'appropriate', not enhanced, BF to the working muscles. Whether a relative prior-hyperemia in bout 2 enables a more homogeneous intramuscular distribution of BF and/or metabolic response is unclear, however, these data are consistent with events more proximal to the exercise muscle in mediating the VO2 response during repeated heavy-intensity KE exercise.

Prior heavy exercise elevates pyruvate dehydrogenase activity and muscle oxygenation and speeds O2uptake kinetics during moderate exercise in older adults

“…These findings are consistent with previous studies examining prior exercise in both young and older adults and suggest a greater muscle perfusion prior to and throughout Mod 2 (12,22,24). A greater muscle oxygenation is consistent with previous demonstrations of elevated HR in older adults (12,51) and greater limb conduit artery blood flow in young adults (16,17,41) during baseline exercise following heavy-intensity exercise and very early in the transition to a subsequent bout of exercise. There is evidence that O 2 availability is impaired during the transition to exercise in muscle from older animals and human subjects (3,11,12,14,39,43,44,49), and thus prior exercise in older adults likely improves O 2 availability in Mod 2 compared with Mod 1 .…”

Effect of hyperventilation and prior heavy exercise on O2 uptake and muscle deoxygenation kinetics during transitions to moderate exercise

“…4 in Gurd et al 2006). After HVY exercise, heart rate (DeLorey et al 2004;Gurd et al 2005;Scheuermann et al 2002) and NIRS-derived measures of oxy-and total hemoglobin/myoglobin [reflecting greater local (microvascular) perfusion] (DeLorey et al 2007;DeLorey et al 2004;Gurd et al 2005Gurd et al , 2006 remained elevated prior to and throughout the subsequent bout of exercise, while conduit artery muscle (i.e., bulk) blood flow remained elevated at baseline and during the immediate onset of exercise (DeLorey et al 2007;Endo et al 2005;Fukuba et al 2004;Hughson et al 2003;Jones et al 2006;MacDonald et al 2001;Paterson et al 2005). Based on these findings, it was argued that the speeding of _ VO 2p kinetics seen after HVY in these individuals is due, in part, to the removal of the constraint imposed by an inadequate local microvascular blood flow distribution and O 2 delivery during the exercise on-transition.…”

“…However, as demonstrated recently, the reduction in s _ VO 2p after prior HVY priming exercise was related directly to how ''slow'' the _ VO 2p response was to the ''unprimed'' state (Gurd et al 2005(Gurd et al , 2006, and thus failure to observe a measurable reduction in s _ VO 2p in these studies was not unexpected. A prior bout of HVY was shown previously to increase heart rate (DeLorey et al 2004;Gurd et al 2005;Scheuermann et al 2002) and cardiac output (Faisal et al 2009); to increase muscle perfusion, as shown by elevated bulk muscle blood flow (determined using Doppler ultrasonography) (DeLorey et al 2007;Endo et al 2005;Fukuba et al 2004;Hughson et al 2003;MacDonald et al 2001;Paterson et al 2005) and elevated local muscle oxyand total hemoglobin concentrations (measured using NIRS) (DeLorey et al 2004(DeLorey et al , 2007Gurd et al 2006;Gurd et al 2005;Jones et al 2006); and to increase mitochondrial PDH activity (Gurd et al 2006). In the present study, the speeding of _ VO 2p kinetics in MOD2 in HYPO (and CON), without a change in deoxygenation kinetics, along with a greater D[Hb TOT ] and D[O 2 Hb], suggest that greater muscle perfusion and distribution prior to and during MOD2 resulted in a higher muscle blood flow-to-O 2 utilization ratio during the exercise transition which would maintain a higher microvascular PO 2 and greater diffusive delivery of O 2 into the muscle.…”

Effects of recovery time on phosphocreatine kinetics during repeated bouts of heavy-intensity exercise

“…Furthermore, during heavy-intensity exercise performed in a supine or prone position, where muscle perfusion pressure is reduced, studies have consistently suggested that O 2 availability is a limiting factor of muscle O 2 consumption at the onset of exercise (Endo et al 2005;Fukuba et al 2004;Hughson et al 1993;Jones et al 2006;Perrey et al 2001). For example, Jones et al (2006) used the relative total haemoglobin/myoglobin concentration (D[Hb tot ]) measured using near-infrared spectroscopy to indicate that O 2 delivery was enhanced at the onset of a repeated bout of supine cycling, and an increased O 2 availability in the muscle was attributed to the reduction in the time constant (tau, s) of the fundamental, phase II VO 2 kinetic response (s 38 vs. 24 s).…”