The Effect of Acidosis on Peak Power After a Simulated 4000-m Individual Pursuit on a Bicycle Ergometer
| aut.embargo | No | en_NZ |
| aut.thirdpc.contains | No | en_NZ |
| dc.contributor.advisor | Cairns, Simeon | |
| dc.contributor.advisor | Plews, Daniel | |
| dc.contributor.author | Mildenhall, Mathew | |
| dc.date.accessioned | 2019-10-17T21:44:40Z | |
| dc.date.available | 2019-10-17T21:44:40Z | |
| dc.date.copyright | 2019 | |
| dc.date.issued | 2019 | |
| dc.date.updated | 2019-10-17T09:15:37Z | |
| dc.description.abstract | Background: Large reductions in plasma and muscle pH have been associated with fatigue during supramaximal exercise. The ingestion of sodium bicarbonate (NaHCO3) has often been used to attenuate plasma acidosis and provide an ergogenic effect. Due to the importance of the end-spurt in supramaximal events an understanding of what limits the ability to produce power late into a race could provide a competitive advantage. Additionally, the anaerobic power reserve (APR) has been put forth as a noninvasive tool for quantification and prediction of the anaerobic capabilities above aerobic capacity. However, limited research has related the model to changes in acid-base balance commonly seen over supramaximal exercise. Aims: To determine: 1) the effect of NaHCO3 on plasma acidosis and changes in anaerobic peak power output (PPO) after a 3-min fixed-intensity supramaximal cycling time-trial (based on the intensity requirements of a 4000-m individual pursuit) 2) the role of blood lactate concentration (blood [La-]), plasma potassium concentration (plasma [K+]), plasma calcium concentration (plasma [Ca2+]), plasma sodium concentration (plasma [Na+]), and peripheral oxygen saturation (SpO2) on changes in PPO 3) the relationship between APR and changes in PPO and plasma measures. Methods: Twelve elite cyclists from both sprint and endurance backgrounds were recruited to participate. Participants performed an initial testing session to determine APR, and two experimental intervention trials. During the intervention trials participants firstly ingested 0.3 g.kg-1 body mass (BM) of either NaHCO3 (BIC) or placebo (PLA) in a double-blind, randomized crossover design, 75 min prior to a standardized warm up. Performance testing then included an initial PPO (PPO1) followed by a fixed-intensity time-trial, simulating ~75% (or 3 min) of a 4000-m individual pursuit at 105% of the power at V̇ O2peak (pV̇ O2peak) followed by a second PPO (PPO2). All trials were performed on a magnetically braked cycle ergometer. Results: No difference in the percentage decrease of PPO (between PPO1 and PPO2) (45.7 ± 13.7% PLA vs. 42.3 ± 12.6% BIC, P > 0.05), peak torque (P = 0.34) or peak cadence (P = 0.42) was observed between PLA and BIC. Plasma bicarbonate concentration ([HCO3-]) was higher in BIC vs. PLA immediately following PPO1 (33.9 ± 2.7 vs. 27.0 ± 2.2 mmol.L-1, P < 0.001), and PPO2 (26.7 ± 2.9 vs. 22.1 ± 2.7 mmol.L-1, P < 0.001). Plasma pH was also higher in BIC at PPO1 (7.38 ± 0.05 vs. 7.29 ± 0.03 pH units, P < 0.001) and PPO2 (7.20 ± 0.12 vs. 7.13 ± 0.14 pH units, P < 0.001). No relationship was found between the percentage decrease of PPO and plasma pH at PPO2 (r = -0.112, P > 0.05) or the absolute change in plasma pH from PPO1 to PPO2 (r = -0.016, P > 0.05). Blood [La-] was higher in BIC at PPO2 (19.6 ± 4.5 PLA vs. 22.1 ± 3.3 mmol.L-1, P = 0.011). Plasma [K+] increased from rest to PPO1 in both trials (1.1 ± 0.6 mmol.L-1 PLA, P < 0.001 and 0.8 ± 0.7 mmol.L-1 BIC, P = 0.01), however no further increases were seen from PPO1 to PPO2 (PLA, P > 0.05 or BIC, P = 0.12). SpO2 decreased throughout the fixed-intensity time-trial (99.6 ± 0.7 to 96.0 ± 2.5% PLA, P = 0.02 and 99.5 ± 0.8 to 96.3 ± 3.7% BIC, P = 0.02). However, no difference was seen between trials (P > 0.05). A strong positive correlation was found between APR and the percentage decrease of PPO (r = 0.79, P = 0.002). APR was negatively correlated to the absolute increase in blood [La-] from PPO1 to PPO2 (r = -0.59, P = 0.045), and positively correlated to the absolute decrease in plasma [HCO3-] from PPO1 to PPO2 (r = 0.60, p = 0.039). Moderate but non-significant relationships were seen between APR and the absolute changes in plasma pH from PPO1 to PPO2 (r = 0.52, P = 0.08). Conclusion: Differences in plasma acidosis do not appear to affect the decrease in PPO following a simulated 4000-m individual pursuit cycling time-trial. Additionally, these findings question the rise in plasma [K+] and decrease in SpO2 as limiting factors dictating the ability to sprint at the end of a 4000-m individual pursuit. Furthermore, the inverse relationship between the APR and the increase in blood [La-], as well as a non-significant relationship between APR and the change in plasma pH suggest that a higher APR does not reflect the capacity of the anaerobic glycolytic pathway. Instead, this implies that the ATP-PCr pathway is a major determinate of the APR. | en_NZ |
| dc.identifier.uri | https://hdl.handle.net/10292/12918 | |
| dc.language.iso | en | en_NZ |
| dc.publisher | Auckland University of Technology | |
| dc.rights.accessrights | OpenAccess | |
| dc.subject | Supramaximal | en_NZ |
| dc.subject | Acidosis | en_NZ |
| dc.subject | Peak power | en_NZ |
| dc.subject | Cycling | en_NZ |
| dc.title | The Effect of Acidosis on Peak Power After a Simulated 4000-m Individual Pursuit on a Bicycle Ergometer | en_NZ |
| dc.type | Thesis | en_NZ |
| thesis.degree.grantor | Auckland University of Technology | |
| thesis.degree.level | Masters Theses | |
| thesis.degree.name | Master of Sport and Exercise | en_NZ |