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The article presents a research which investigates the effectiveness of inspiratory threshold loading (ITL) and inspiratory muscle training (IMT) in meliorating and regulating the lactate concentration in the blood of the cyclists after maximal cycling. The participants of the study include 18 cyclists and cites the tools used by researchers including maximal incremental cycling tests and physicochemical approach to determine the participants' lactate concentration. Furthermore, researchers found that ITL can affect the recovery of lactate concentration in muscles.

Although reduced blood lactate concentrations ([lac−]B) have been observed during whole-body exercise following inspiratory muscle training (IMT), it remains unknown whether the inspiratory muscles are the source of at least part of this reduction. To investigate this, we tested the hypothesis that IMT would attenuate the increase in [lac−]B caused by mimicking, at rest, the breathing pattern observed during high-intensity exercise. Twenty-two physically active males were matched for 85% maximal exercise minute ventilation $$ \left( {\dot V_{{\text{E}}} \max } \right) $$ and divided equally into an IMT or a control group. Prior to and following a 6 week intervention, participants performed 10 min of volitional hyperpnoea at the breathing pattern commensurate with 85% $$ \dot V_{{\text{E}}} \max . $$ The IMT group performed 6 weeks of pressure-threshold IMT; the control group performed no IMT. Maximal inspiratory mouth pressure increased (mean ± SD) 31 ± 22% following IMT and was unchanged in the control group. Prior to the intervention in the control group, [lac−]B increased from 0.76 ± 0.24 mmol L−1 at rest to 1.50 ± 0.60 mmol L−1 ( P < 0.05) following 10 min volitional hyperpnoea. In the IMT group, [lac−]B increased from 0.85 ± 0.40 mmol L−1 at rest to 2.02 ± 0.85 mmol L−1 following 10 min volitional hyperpnoea ( P < 0.05). After 6 weeks, increases in [lac−]B during volitional hyperpnoea were unchanged in the control group. Conversely, following IMT the increase in [lac−]B during volitional hyperpnoea was reduced by 17 ± 37% and 25 ± 34% following 8 and 10 min, respectively ( P < 0.05). In conclusion, increases in [lac−]B during volitional hyperpnoea at 85% $$ \dot V_{{\text{E}}} \max $$ were attenuated following IMT. These findings suggest that the inspiratory muscles were the source of at least part of this reduction, and provide a possible explanation for some of the IMT-mediated reductions in [lac−]B, often observed during whole-body exercise. [ABSTRACT FROM AUTHOR]

Ventilatory work during heavy endurance exercise has not been thought to influence systemic lactate concentration. We evaluated the effect of maximal isocapnic volitional hyperpnoea upon arterialised venous blood lactate concentration ([lac−]B) during leg cycling exercise at maximum lactate steady state (MLSS). Seven healthy males performed a lactate minimum test to estimate MLSS, which was then resolved using separate 30 min constant power tests (MLSS=207±8 W, mean ± SEM). Thereafter, a 30 min control trial at MLSS was performed. In a further experimental trial, the control trial was mimicked except that from 20 to 28 min maximal isocapnic volitional hyperpnoea was superimposed on exercise. Over 20–28 min minute ventilation, oxygen uptake, and heart rate during the control and experimental trials were 87.3±2.4 and 168.3±7.0 l min−1 ( P<0.01), the latter being comparable to that achieved in the maximal phase of the lactate minimum test (171.9±6.8 l min−1), 3.46±0.20 and 3.83 ± 0.20 l min−1 ( P<0.01), and 158.5±2.7 and 166.8±2.7 beats min−1 ( P<0.05), respectively. From 20 to 30 min of the experimental trial [lac−]B increased from 3.7±0.2 to 4.7±0.3 mmol l−1 ( P<0.05). The partial pressure of carbon dioxide in arterialised venous blood increased approximately 3 mmHg during volitional hyperpnoea, which may have attenuated the [lac−]B increase. These results show that, during heavy exercise, respiratory muscle work may affect [lac−]B. We speculate that the changes observed were related to the altered lactate turnover in respiratory muscles, locomotor muscles, or both. [ABSTRACT FROM AUTHOR]

Several studies have reported that improvements in endurance performance following respiratory muscle training (RMT) are associated with a decrease in blood lactate concentration ([Lac]B). The present study examined whether pressure threshold inspiratory muscle training (IMT) elicits an increase in the cycling power output corresponding to the maximum lactate steady state (MLSS). Using a double-blind, placebo-controlled design, 12 healthy, non-endurance-trained male participants were assigned in equal numbers to an experimental (IMT) or sham training control (placebo) group. Cycling power output at MLSS was initially identified using a lactate minimum protocol followed by a series of constant power output rides (2.5% increments) of 29.5 min duration; MLSS was reassessed following six weeks of IMT or sham IMT. Maximum inspiratory mouth pressure increased significantly (26%) in the IMT group, but remained unchanged in the placebo group. The cycling power output corresponding to MLSS remained unchanged in both groups after the intervention. After IMT, [Lac]B decreased significantly at MLSS power in the IMT group [-1.17 (1.01) mmol l-1 after 29.5 min of cycling; mean (SD)], but remained unchanged in the placebo group [+0.37 (1.66) mmol l-1]. These data support previous observations that IMT results in a decrease in [Lac]Bat a given intensity of exercise. That such a decrease in [Lac]B was not associated with a substantial (>2.5%) increase in MLSS power is a new finding suggesting that RMT-induced increases in exercise tolerance and reductions in [Lac]B are not ascribable to a substantial increase in the ‘lactate threshold’. [ABSTRACT FROM AUTHOR]

Purpose: This study examined whether metabolite accumulation, induced by prior upper body exercise, affected the power-duration relationship for leg cycle ergometry. Methods: Seven males performed, to the limit of tolerance and both without (L) and with (AL) prior severe-intensity arm-cranking exercise, an incremental cycling test and four constant power cycling tests to determine the parameters of the power-duration relationship: critical power (CP) and W'. Results: At the onset of cycling exercise plasma lactate (L vs AL: 1.2±0.1 vs 11.6 + 2.9mEq-L-1)')and hydrogen ion (40.4+ 1.3 vs 53.1 + 4.3 nEq-L-1), concentrations were higher during AL compared with L, whereas the strong ion difference (37.8 + 1.8 vs 32.4 ± 2.0 mEq-L-1) and bicarbonate concentration (25.7 ± 0.7 vs 18.3+ 1.9 mEq-L-1) were lower during AL compared with L (P<0.01). During incremental exercise, maximum cycling power (358 ± 15 vs 332 ± 21 W) and peak oxygen uptake (VO2peak) (4-31 ± 0.36 vs 3.71 ± 0.44 L-min-1)) were lower during AL compared with L (P < 0.05). The rate of increase in plasma potassium concentration during constant power cycling was greater during AL compared with L (0.09 ± 0.08 vsO. 14 ± 0.13 mEq-L-1) min-1) (P < 0.05), and exercise duration was 35 ± 15% shorter (P< 0.01). CP was not different between L and AL (267 ± 19 vs 264 ± 20 W), whereas W was lower in AL (17.3 ± 5.7 vs 11.8 + 4.2 kJ) (P < 0.01). Conclusion: The reduced W' after prior upper body exercise indicates that the magnitude of W ' is partly dependent on metabolite accumulation. [ABSTRACT FROM AUTHOR]

The article reports on research which was conducted to investigate the effect different pressure threshold inspiratory loads had on on lactate clearance and plasma acid-base balance during recovery from maximal exercise. Researchers evaluated eight moderately trained male athletes who performed cycling tests. They found that in athletes who had achieved moderate enduring training status, inspiratory loading did not appear to accelerate lactate clearance or modify plasma acid-base balance during recovery from maximal exercise.

Michael A. Johnson, Peter I. Brown and Graham R. Sharpe respond to a letter to the editor submitted in response to their article "Inspiratory Loading Intensity Does Not Influence Lactate Clearance During Recovery"