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Muscle metabolic responses during 16 hours of intermittent heavy exercise

The alterations in muscle metabolism were investigated in response to repeated sessions of heavy intermittent exercise performed over 16 h. Tissue samples were extracted from the vastus lateralis muscle before (B) and after (A) 6 min of cycling at approximately 91% peak aerobic power at repetitions...

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Bibliographic Details
Published in:Canadian journal of physiology and pharmacology 2007-06, Vol.85 (6), p.634-645
Main Authors: Green, H.J, Duhamel, T.A, Holloway, G.P, Moule, J, Ouyang, J, Ranney, D, Tupling, A.R
Format: Article
Language:English
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Summary:The alterations in muscle metabolism were investigated in response to repeated sessions of heavy intermittent exercise performed over 16 h. Tissue samples were extracted from the vastus lateralis muscle before (B) and after (A) 6 min of cycling at approximately 91% peak aerobic power at repetitions one (R1), two (R2), nine (R9), and sixteen (R16) in 13 untrained volunteers (peak aerobic power = 44.3 ± 0.66 mL·kg -1 ·min -1 , mean ± SE). Metabolite content (mmol·(kg dry mass) -1 ) in homogenates at R1 indicated decreases (p < 0.05) in ATP (21.9 ± 0.62 vs. 17.7 ± 0.68) and phosphocreatine (80.3 ± 2.0 vs. 8.56 ± 1.5) and increases (p < 0.05) in inosine monophosphate (IMP, 0.077 ± 0.12 vs. 3.63 ± 0.85) and lactate (3.80 ± 0.57 vs. 84.6 ± 10.3). The content (µmol·(kg dry mass) -1 ) of calculated free ADP ([ADP f ], 86.4 ± 5.5 vs. 1014 ± 237) and free AMP ([AMP f ], 0.32 ± 0.03 vs. 78.4 ± 31) also increased (p < 0.05). No differences were observed between R1 and R2. By R9 and continuing to R16, pronounced reductions (p < 0.05) at A were observed in IMP (72.2%), [ADP f ] (58.7%), [AMP f ] (85.5%), and lactate (41.3%). The 16-hour protocol resulted in an 89.7% depletion (p < 0.05) of muscle glycogen. Repetition-dependent increases were also observed in oxygen consumption during exercise. It is concluded that repetitive heavy exercise results in less of a disturbance in phosphorylation potential, possibly as a result of increased mitochondrial respiration during the rest-to-work non-steady-state transition.
ISSN:0008-4212
1205-7541
DOI:10.1139/Y07-039