Effect of prior exercise on pulmonary O2 uptake and estimated muscle capillary blood flow kinetics during moderate-intensity field running in men

Martin Buchheit, Paul B. Laursen, Said Ahmaidi
2009 Journal of applied physiology  
Buchheit M, Laursen PB, Ahmaidi S. Effect of prior exercise on pulmonary O2 uptake and estimated muscle capillary blood flow kinetics during moderate-intensity field running in men. The effect of prior exercise on pulmonary O 2 uptake (V O2 p) and estimated muscle capillary blood flow (Q m) kinetics during moderate-intensity, field-based running was examined in 14 young adult men, presenting with either moderately fast (16 s Ͻ V O2 p Ͻ 30 s; MFK) or very fast V O2 p kinetics (V O2 p Ͻ 16 s;
more » ... (i.e., primary time constant, V O2 p). On four occasions, participants completed a square-wave protocol involving two bouts of running at 90 -95% of estimated lactate threshold (Mod1 and Mod2), separated by 2 min of repeated supramaximal sprinting. V O2 p was measured breath by breath, heart rate (HR) beat to beat, and vastus lateralis oxygenation {deoxy-hemoglobin/myoglobin concentration (deoxy-[HbϩMb])} using near-infrared spectroscopy. Mean response time of Q m (Q m MRT) was estimated by rearranging the Fick equation, using V O2 p and deoxy-[HbϩMb] as proxies of muscle O2 uptake (V O2) and arteriovenous difference, respectively. HR, blood lactate concentration, total hemoglobin, and Q m were elevated before Mod2 compared with Mod1 (all P Ͻ 0.05). V O2 p was shorter in VFK compared with MFK during Mod 1 (13.1 Ϯ 1.8 vs. 21.0 Ϯ 2.5 s, P Ͻ 0.01), but not in Mod2 (12.9 Ϯ 1.5 vs. 13.7 Ϯ 3.8 s, P ϭ 1.0). Q m MRT was shorter in VFK compared with MFK in Mod1 (8.8 Ϯ 1.9 vs. 17.0 Ϯ 3.4 s, P Ͻ 0.01), but not in Mod 2 (10.1 Ϯ 1.8 vs. 10.5 Ϯ 3.5 s, P ϭ 1.0). During Mod 2, HR kinetics were slowed, whereas mean deoxy-[HbϩMb] response time was unchanged. The difference in V O2 p between Mod1 and Mod2 was related to Q m MRT measured at Mod 1 (r ϭ 0.71, P Ͻ 0.01). Present results suggest that local O2 delivery (i.e., Q m) may be a factor contributing to the V O2 kinetic during the onset of moderate-intensity, field-based running exercise, at least in subjects exhibiting moderately fast V O2 kinetics. oxygen uptake dynamics; near-infrared spectroscopy; muscle deoxygenation; repeated sprint exercise; warm-up COMMENCEMENT OF EXERCISE INSTIGATES an increase in O 2 delivery to working muscles to support the required increase in muscle oxygen uptake (V O 2 ; V O 2 m ). However, the kinetics supporting the V O 2 m at exercise onset, now shown convincingly to be inferred from the pulmonary V O 2 (V O 2 p ) (27, 37), are still debated (40). Resolution of our knowledge surrounding whether V O 2 m is limited by adequate delivery of O 2 and/or other substrates required for mitochondrial oxidative phosphorylation (i.e., metabolic inertia) is essential for understanding metabolic control in health, the mechanics of impaired (slowed) V O 2 m kinetics found in patient populations (25, 26) , and, eventually, for the design of appropriate exercise training interventions (3). The current viewpoint surrounding the O 2 delivery/metabolic inertia debate is that it is a false dichotomy; that is, there may be a "tipping point" in the relationship between the speed of the V O 2 p kinetics [expressed using the time constant () of the primary component (i.e., phase II) of V O 2 p (V O 2 p )] and muscle O 2 delivery (40). As highlighted by Poole et al. (40) , the kinetics to the left of this tipping point (i.e., short V O 2 p ) appear to be more essentially O 2 -delivery dependent, whereas the right side is more likely determined by the availability of other substrates limiting O 2 utilization. It is, however, worth noting that the tipping point is more of a terminological concept than a real physiological variable or a parameter that we can currently measure. Mechanistic exploration into the basis of V O 2 p kinetics have used "priming" exercises in the past (e.g., Refs. 7, 10, 11, 19, 24, 28, 29) . Compared with exercise transition without warm-up, V O 2 p kinetics upon initiation of heavy exercise subsequent to intense exercise appear consistently accelerated (the "overall" V O 2 p kinetics being significantly faster, due predominantly to a marked reduction in the amplitude of the so-called V O 2 p "slow component"). Mechanisms put forward to explain this phenomenon hint at enhanced muscle O 2 supply and delivery [i.e., increased cardiac output, muscle blood flow (Q m ) and total hemoglobin (tHb), or blood acidosis enhancing O 2 dissociation from Hb], and/or partial relief of muscle oxidative metabolic inertia {i.e., faster enzyme activation and improved substrate provision, illustrated by a shorter time delay (TD) before near-infrared spectroscopy (NIRS) muscle deoxygenation; deoxy-Hb/myoglobin concentration (deoxy-[HbϩMb])}, and/or alterations in motor unit recruitment profiles (for review, see Ref. 12). Studies examining the effect of prior heavy exercise on V O 2 p adaptation at the onset of moderate-intensity exercise have been conflicting. Heavy-intensity warm-up exercise has been shown to have no effect on subsequent moderate-intensity V O 2 p exercise kinetics in young adults (11, 22, 24 ), yet quickened V O 2 p in older adults (19, 44) , reinforcing the assumption that V O 2 p kinetics in the moderate-intensity domain might be age-or at least "V O 2 p kinetic dependent" (i.e., related to the initial V O 2 p value; the initial speed of V O 2 p adaptation). Indeed, subjects with a poor (slow) initial O 2 delivery capacity are most likely to present with shorter V O 2 p after heavy exercise (19, 28, 29, 44) . In contrast, Gurd et al. (29) recently reported that prior heavy cycling exercise hastened the V O 2 p adaptation, even in young subjects presenting with fast (i.e., Ͻ30 s) V O 2 p kinetics. However, subjects classified as having "fast V O 2 p kinetics" (i.e., 26 s on average) in the study by Gurd et al. had, in fact, rather moderately fast
doi:10.1152/japplphysiol.91625.2008 pmid:19498090 fatcat:4h4c5vzcnzf7pbbrktfjqt44pm