Eur J Appl Physiol DOI 10.1007/s00421-014-3000-0
ORIGINAL ARTICLE
The effect of prior exercise intensity on oxygen uptake kinetics during high‑intensity running exercise in trained subjects Paulo Cesar do Nascimento · Ricardo Dantas de Lucas · Kristopher Mendes de Souza · Rafael Alves de Aguiar · Benedito Sérgio Denadai · Luiz Guilherme Antonacci Guglielmo
Received: 22 March 2014 / Accepted: 15 September 2014 © Springer-Verlag Berlin Heidelberg 2014
Abstract Purpose The aim of this study was to compare the effects of two different kinds of prior exercise protocols [continuous exercise (CE) versus intermittent repeated sprint (IRS)] on oxygen uptake (VO2) kinetics parameters during highintensity running. Methods Thirteen male amateur futsal players (age 22.8 ± 6.1 years; mass 76.0 ± 10.2 kg; height 178.7 ± 6.6 cm; VO2max 58.1 ± 4.5 mL kg−1 min−1) performed a maximal incremental running test for the determination of the gas exchange threshold (GET) and maximal VO2 (VO2max). On two different days, the subjects completed a 6-min bout of high-intensity running (50 % Δ) on a treadmill that was 6-min after (1) an identical bout of high-intensity exercise (from control to CE), and (2) a protocol of IRS (6 × 40 m). Result We found significant differences between CE and IRS for the blood lactate concentration ([La]; 6.1 versus
10.7 mmol L−1, respectively), VO2 baseline (0.74 versus 0.93 L min−1, respectively) and the heart rate (HR; 102 versus 124 bpm, respectively) before the onset of highintensity exercise. However, both prior CE and prior IRS significantly increased the absolute primary VO2 amplitude (3.77 and 3.79 L min−1, respectively, versus control 3.54 L min−1), reduced the amplitude of the VO2 slow component (0.26 and 0.21 L min−1, respectively, versus control 0.50 L min−1), and decreased the mean response time (MRT; 28.9 and 28.0 s, respectively, versus control 36.9 s) during subsequent bouts. Conclusion This study showed that different protocols and intensities of prior exercise trigger similar effects on VO2 kinetics during high-intensity running. Keywords Priming exercise · Oxygen uptake kinetics · Blood lactate · High-intensity running
Communicated by Peter Krustrup. P. C. do Nascimento · R. D. de Lucas · K. M. de Souza · L. G. A. Guglielmo Physical Effort Laboratory, Sports Center, Federal University of Santa Catarina, Florianopolis, Brazil
R. A. de Aguiar Human Performance Research Group, Center of Health and Sport Sciences, Santa Catarina State University, Florianopolis, SC, Brazil
P. C. do Nascimento (*) · R. A. de Aguiar Rua Silvio Possobon, 70, apartamento 1009, Abraão, Florianopolis, Santa Catarina CEP 88085‑190, Brazil e-mail:
[email protected] B. S. Denadai Human Performance Laboratory, UNESP, Avenida 24 A, 1515, Bela Vista, Rio Claro, SP CEP 13506‑900, Brazil
R. D. de Lucas Rua Antonio Edu Vieira, Pantanal, CDS/UFSC, Florianopolis, SC 88000‑000, Brazil
L. G. A. Guglielmo Rua Vereador Ramon Filomeno No. 357, Itacorubi, Florianopolis, SC CEP 88034‑495, Brazil
K. M. de Souza Avenida Presidente Nereu Ramos, 1100, Apto 801, Campinas, São José, SC CEP 88101410, Brazil
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Abbreviations Ap Amplitude of the primary component As VO2 slow component amplitude CE Continuous exercise GET Gas-exchange threshold HR Heart rate IRS Intermittent repeated sprint [La] Blood lactate concentration MRT Mean response time O2 Oxygen PCr Muscular phosphocreatine PV Peak velocity τ VO2 time constant VO2 O2 uptake VO2max Maximal O2 uptake 50 % Δ 50 % of the difference between GET and VO2max Introduction It has been demonstrated that the performance of prior exercise, such as continuous exercise (CE) or sprint exercise, accelerates the “overall” oxygen uptake (VO2) kinetics during subsequent high-intensity exercise (Gerbino et al. 1996; Burnley et al. 2002a; Tordi et al. 2003; Wilkerson et al. 2004; Faisal et al. 2009; Lanzi et al. 2012). This is due to an increase in the absolute amplitude of the VO2 primary component (absolute Ap) and a reduction in the amplitude of the VO2 slow component (As) (Gerbino et al. 1996; Burnley et al. 2002a, 2006; Koppo and Bouckaert, 2001; Scheuermann et al. 2001; Bailey et al. 2009; Lanzi et al. 2012). However, the underlying mechanisms and the optimal prior exercise protocol remain to be resolved. Several studies postulate that the altered VO2 kinetics after prior high-intensity exercise might be attributed to an enhanced muscle O2 availability triggered by greater muscle vasodilatation and a rightward shift of the oxyhemoglobin dissociation curve resulting from the residual metabolic acidosis (Gerbino et al. 1996; Tschakovsky and Hughson 1999; Tordi et al. 2003; Wilkerson et al. 2004; Faisal et al. 2009). However, the results concerning this issue are somewhat controversial, as other mechanisms might be linked to the reduction of VO2 slow component amplitude (Lanzi et al. 2012). In fact, the “priming” effect on the VO2 kinetics has also been attributed to a partial relief of muscle oxidative metabolic inertia and/or alterations in motor unit recruitment profiles or muscle fatigue process (Burnley et al. 2002b; Wilkerson et al. 2004; Poole et al. 2008; Cannon et al. 2011; Lanzi et al. 2012). Nevertheless, the effect of prior high-intensity exercise on the VO2 kinetics has been investigated primarily using CE protocols performed at heavy- and severe-intensity domains (Burnley et al. 2002b; Jones et al. 2008; Faisal
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et al. 2009; Bailey et al. 2009). Moreover, some studies have analyzed the effect of prior sprint exercise on the VO2 kinetics, since it may induce mechanisms beyond those related to greater muscle perfusion (Burnley et al. 2002a; Tordi et al. 2003; Wilkerson et al. 2004; Lanzi et al. 2012). Indeed, sprint exercise protocols cause a significant decrease in the muscular phosphocreatine concentration ([PCr]) and greater muscle fatigue and/or greater motor unit recruitment (Gaitanos et al. 1993; Rossiter et al. 2001; Tomlin and Wenger 2001; Burnley et al. 2002a; Dupont et al. 2005; Lanzi et al. 2012), which could alter the muscle bioenergetics and motor unit recruitment profile during subsequent exercise and thus accelerate the VO2 kinetics. However, the majority of the studies have investigated the effect of prior high-intensity and sprint exercise on the VO2 kinetics using cycling exercise. Thus, there is limited data in the literature showing that prior high-intensity exercise could accelerate the VO2 kinetics during running (Draper et al. 2006; Jones et al. 2008; Buchheit et al. 2009). Overall, studies using prior CE have not demonstrated the effects on VO2 kinetics during subsequent high-intensity running exercise (Draper et al. 2006; Jones et al. 2008). Furthermore, it might be inappropriate to make inferences from results of prior exercise studies in cycling to running exercise, because the VO2 kinetics of these modes of exercise is different (Carter et al. 2000; Jones et al. 2008). At this time, only one study has investigated the effect of prior repeated sprint on the VO2 response in running (Buchheit et al. 2009). Buchheit et al. (2009) showed that prior repeated sprint (6 × 25 m, 25 s of active recovery) could decrease the τ of phase II (τp—the time taken to reach 63 % of the increase in VO2 above baseline) in subjects that are moderately fast (16 ≥ τ ≤ 30 s), but not in subjects with very fast VO2 kinetics (τ