UNLABELLED: Five healthy non-smoking men, aged 22.2 +/- 0.8 years (mean SD), VO2 max 50.2 +/- 6.2 ml.min-1.kg-1) performed two 6 minutes constant power output (PO) bouts of cycling at 70 rev.min-1, separated by a 20 minutes of rest. The power output during the first bout of exercise corresponded to 40% VO2max, while the second exercise corresponded to 75% VO2max. The first bout of exercise was performed at a power output below the lactate threshold (LT)--determined during an incremental exercise test. In the second bout of exercise the subjects exercised above the LT. This experimental protocol was performed twice. Once as a control test (test C) and on a separate day, at about 90 minutes after ingestion of 3 mmol.kg-1 BW of NH4Cl (test A). Ingestion of ammonium chloride developed a state of metabolic acidosis. Antecubital venous blood samples taken every one minute of cycling were analysed for pH, HCO-3, BE, pO2, pCO2 and plasma lactate concentration [La]pl. Oxygen uptake was measured continuously using breath by breath system. The obtained acidotic shift of blood acid-base balance was also present throughout the 6 minutes bouts of exercise. No significant difference in VO2 during the exercise corresponding to 40% VO2 max in the test C and the test A was observed. The total oxygen consumed throughout the 6 min cycling at the PO corresponding to 75% of VO2 max was not significantly different in test C and test A (13.532 vs. 13.422 l O2, respectively). The slow component of VO2 kinetics as expressed by the delta VO2(6-3 min) of exercise was significantly higher (p = 0.03) in test A than in test C (183 +/- 97 vs. 106 +/- 53 ml.min-1 O2, respectively). It should be noted that in each subject, the magnitude of the slow component of VO2 kinetics after pre-exercise acidification was consistently higher than in control experiment. IN CONCLUSION: The original finding of our study is that pre-exercise acidification induced by ingestion of 3 mmol.kg-1 B.W. of NH4Cl was accompanied by a significant increase in the magnitude of the slow component of VO2 kinetics. This is why we postulate that acidosis may play a significant role in the physiological mechanism responsible for the slow component of VO2 kinetics in humans.
UNLABELLED: Five healthy non-smoking men, aged 22.2 +/- 0.8 years (mean SD), VO2 max 50.2 +/- 6.2 ml.min-1.kg-1) performed two 6 minutes constant power output (PO) bouts of cycling at 70 rev.min-1, separated by a 20 minutes of rest. The power output during the first bout of exercise corresponded to 40% VO2max, while the second exercise corresponded to 75% VO2max. The first bout of exercise was performed at a power output below the lactate threshold (LT)--determined during an incremental exercise test. In the second bout of exercise the subjects exercised above the LT. This experimental protocol was performed twice. Once as a control test (test C) and on a separate day, at about 90 minutes after ingestion of 3 mmol.kg-1 BW of NH4Cl (test A). Ingestion of ammonium chloride developed a state of metabolic acidosis. Antecubital venous blood samples taken every one minute of cycling were analysed for pH, HCO-3, BE, pO2, pCO2 and plasma lactate concentration [La]pl. Oxygen uptake was measured continuously using breath by breath system. The obtained acidotic shift of blood acid-base balance was also present throughout the 6 minutes bouts of exercise. No significant difference in VO2 during the exercise corresponding to 40% VO2 max in the test C and the test A was observed. The total oxygen consumed throughout the 6 min cycling at the PO corresponding to 75% of VO2 max was not significantly different in test C and test A (13.532 vs. 13.422 l O2, respectively). The slow component of VO2 kinetics as expressed by the delta VO2(6-3 min) of exercise was significantly higher (p = 0.03) in test A than in test C (183 +/- 97 vs. 106 +/- 53 ml.min-1 O2, respectively). It should be noted that in each subject, the magnitude of the slow component of VO2 kinetics after pre-exercise acidification was consistently higher than in control experiment. IN CONCLUSION: The original finding of our study is that pre-exercise acidification induced by ingestion of 3 mmol.kg-1 B.W. of NH4Cl was accompanied by a significant increase in the magnitude of the slow component of VO2 kinetics. This is why we postulate that acidosis may play a significant role in the physiological mechanism responsible for the slow component of VO2 kinetics in humans.
Authors: Jerzy A Zoladz; Joanna Majerczak; Bruno Grassi; Zbigniew Szkutnik; Michał Korostyński; Sławomir Gołda; Marcin Grandys; Wiesława Jarmuszkiewicz; Wincenty Kilarski; Janusz Karasinski; Bernard Korzeniewski Journal: PLoS One Date: 2016-04-22 Impact factor: 3.240