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Relationship between hyperventilation and excessive CO2 output during recovery from repeated cycling sprints

T. Yano, T. Yunoki, R. Matsuura, T. Arimitsu

. 2009 ; 58 (4) : 529-535.

Jazyk angličtina Země Česko

Perzistentní odkaz   https://www.medvik.cz/link/bmc09004976

The purpose of the present study was to examine whether excessive CO2 output (V . co2excess) is dominantly attributable to hyperventilation during the period of recovery from repeated cycling sprints. A series of four 10-sec cycling sprints with 30-sec passive recovery periods was performed two times. The first series and second series of cycle sprints (SCS) were followed by 360-sec passive recovery periods (first recovery and second recovery). Increases in blood lactate (?La) were 11.17±2.57 mM from rest to 5.5 min during first recovery and 2.07±1.23 mM from the start of the second SCS to 5.5 min during second recovery. CO2 output (V . co2) was significantly higher than O2 uptake (V . o2) during both recovery periods. This difference was defined as V . co2excess. V . co2excess was significantly higher during first recovery than during second recovery. V . co2excess was added from rest to the end of first recovery and from the start of the second SCS to the end of second recovery (CO2excess). ?La was significantly related to CO2excess (r=0.845). However, ventilation during first recovery was the same as that during second recovery. End-tidal CO2 pressure (PETco2) significantly decreased from the resting level during the recovery periods, indicating hyperventilation. PETco2 during first recovery was significantly higher than that during second recovery. It is concluded that V . co2excess is not simply determined by ventilation during recovery from repeated cycle sprints.

Citace poskytuje Crossref.org

Bibliografie atd.

Lit.: 25

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$a The purpose of the present study was to examine whether excessive CO2 output (V . co2excess) is dominantly attributable to hyperventilation during the period of recovery from repeated cycling sprints. A series of four 10-sec cycling sprints with 30-sec passive recovery periods was performed two times. The first series and second series of cycle sprints (SCS) were followed by 360-sec passive recovery periods (first recovery and second recovery). Increases in blood lactate (?La) were 11.17±2.57 mM from rest to 5.5 min during first recovery and 2.07±1.23 mM from the start of the second SCS to 5.5 min during second recovery. CO2 output (V . co2) was significantly higher than O2 uptake (V . o2) during both recovery periods. This difference was defined as V . co2excess. V . co2excess was significantly higher during first recovery than during second recovery. V . co2excess was added from rest to the end of first recovery and from the start of the second SCS to the end of second recovery (CO2excess). ?La was significantly related to CO2excess (r=0.845). However, ventilation during first recovery was the same as that during second recovery. End-tidal CO2 pressure (PETco2) significantly decreased from the resting level during the recovery periods, indicating hyperventilation. PETco2 during first recovery was significantly higher than that during second recovery. It is concluded that V . co2excess is not simply determined by ventilation during recovery from repeated cycle sprints.
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