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This Article Full Text Full Text (PDF) All Versions of this Article: 577/3/985    most recent jphysiol.2006.112706v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Gurd, B. J. Articles by Kowalchuk, J. M. Search for Related Content PubMed PubMed Citation Articles by Gurd, B. J. Articles by Kowalchuk, J. M. Related Collections Skeletal Muscle and Exercise

¹ Canadian Centre for Activity and Aging
² School of Kinesiology, Faculty of Health Sciences
³ Department of Physiology and Pharmacology
⁴ Departments of Clinical Neurological Sciences and Rehabilitation Medicine, Faculty of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada N6A 5B9
⁵ Department of Medicine, McMaster University, Hamilton, Ontario, Canada L8N 3Z5
⁶ Faculty of Applied Health Sciences, Brock University, St Catharines, Ontario, Canada L2S 3A1

The adaptation of pulmonary oxygen uptake during the transition to moderate-intensity exercise (Mod) is faster following a prior bout of heavy-intensity exercise. In the present study we examined the activation of pyruvate dehydrogenase (PDHa) during Mod both with and without prior heavy-intensity exercise. Subjects (n = 9) performed a Mod₁–heavy-intensity–Mod₂ exercise protocol preceded by 20 W baseline. Breath-by-breath kinetics and near-infrared spectroscopy-derived muscle oxygenation were measured continuously, and muscle biopsy samples were taken at specific times during the transition to Mod. In Mod₁, PDHa increased from baseline (1.08 ± 0.2 mmol min^–1 (kg wet wt)^–1) to 30 s (2.05 ± 0.2 mmol min^–1 (kg wet wt)^–1), with no additional change at 6 min exercise (2.07 ± 0.3 mmol min^–1 (kg wet wt)^–1). In Mod₂, PDHa was already elevated at baseline (1.88 ± 0.3 mmol min^–1 (kg wet wt)^–1) and was greater than in Mod₁, and did not change at 30 s (1.96 ± 0.2 mmol min^–1 (kg wet wt)^–1) but increased at 6 min exercise (2.70 ± 0.3 mmol min^–1 (kg wet wt)^–1). The time constant of was lower in Mod₂ (19 ± 2 s) than Mod₁ (24 ± 3 s). Phosphocreatine (PCr) breakdown from baseline to 30 s was greater (P < 0.05) in Mod₁ (13.6 ± 6.7 mmol (kg dry wt)^–1) than Mod₂ (6.5 ± 6.2 mmol (kg dry wt)^–1) but total PCr breakdown was similar between conditions (Mod₁, 14.8 ± 7.4 mmol (kg dry wt)^–1; Mod₂, 20.1 ± 8.0 mmol (kg dry wt)^–1). Both oxyhaemoglobin and total haemoglobin were elevated prior to and throughout Mod₂ compared with Mod₁. In conclusion, the greater PDHa at baseline prior to Mod₂ compared with Mod₁ may have contributed in part to the faster kinetics in Mod₂. That oxyhaemoglobin and total haemoglobin were elevated prior to Mod₂ suggests that greater muscle perfusion may also have contributed to the observed faster kinetics. These findings are consistent with metabolic inertia, via delayed activation of PDH, in part limiting the adaptation of pulmonary and muscle O₂ consumption during the normal transition to exercise.

(Received 2 May 2006; accepted after revision 21 September 2006; first published online 21 September 2006)
Corresponding author J. M. Kowalchuk: Canadian Centre for Activity and Aging, School of Kinesiology, Faculty of Health Sciences, HSB 411C, The University of Western Ontario, London, Ontario, Canada N6A 5B9. Email: jkowalch{at}uwo.ca

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