Influence of pre-exercise acidosis and alkalosis on the kinetics of acid-base recovery following intense exercise

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Robergs and Siegler are with the Exercise Physiology Laboratories, Dept.of PP&D, Johnson Center, Albuquerque, NM 87131. Hutchinson, Hendee, and Madden are with Inlight Solutions, Albu-querque, NM 87106.

International Journal of Sport Nutrition and Exercise Metabolism, 2005, 14, 1-© 2005 Human Kinetics Publishers, Inc.

Influence of Pre-Exercise Acidosis and Alkalosison the Kinetics of Acid-Base Recovery

Following Intense Exercise

Robert Robergs, Keith Hutchinson, Shonn Hendee,Sean Madden, and Jason Siegler

The purpose of this study was to measure the recovery kinetics of pH and lactate for the conditions of pre-exercise acidosis, alkalosis, and placebo states. Twelve trained male cyclists completed 3 exercise trials (110% workload at VO2max), ingesting either 0.3 g/kg of NH4Cl (ACD), 0.2 g/kg of Na+HCO3

- and 0.2 g/kg of sodium citrate (ALK), or a placebo (calcium carbonate) (PLAC). Blood samples (heated dorsal hand vein) were drawn before, during, and after exercise. Exercise-induced acidosis was more severe in the ACD and PLAC trials (7.15 ± 0.06, 7.21 ± 0.07, 7.16 ± 0.06, P < 0.05, for ACD, ALK, PLAC, respectively). Recovery kinetics for blood pH and lactate, as assessed by the monoexponential slope constant, were not different between all trials (0.057 ± 0.01, 0.050 ± 0.01, 0.080 ± 0.02, for ACD, ALK, PLAC, respec-tively). Complete recovery of blood pH from metabolic acidosis can take longer than 45 min. Such a recovery profile is nonlinear, with 50% recovery occurring in approximately 12 min. Complete recovery of blood lactate can take longer than 60 min, with 50% recovery occurring in approximately 30 min. Induced alkalosis decreases metabolic acidosis and improves pH recov-ery compared to acidodic and placebo conditions. Although blood pH and lactate are highly correlated during recovery from acidosis, they recover at significantly different rates.

Key Words: fatigue, metabolic acidosis, sodium bicarbonate, metabolism, lactate

The capability to sustain high-intensity exercise depends largely on the body’s ability to minimize increases in cellular and blood hydrogen ion concentrations ([H+]). Mechanisms such as acid excretion by the kidney, hyperventilation, and blood bicarbonate (HCO3

-), work to offset the increasing production/release of H+ during catabolism. Once the body’s energy demands exceed that of its H+ buffering capacity, however, the rise in [H+] decreases blood and muscle pH (8) and eventu-ally contributes to fatigue.

The effectiveness of buffering free H+ during intense exercise has been assessed directly by measuring changes in muscle or arterial blood pH, or the

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3 Influence of Pre-Exercise Acidosis and Alkalosis

blood buffering capacity, and indirectly via muscle or blood lactate concentrations (14). Whether or not blood lactate is a valid indirect marker of increased non-mito-chondrial ATP turnover in contracting skeletal muscle is unclear. Furthermore, the presence of the proton-lactate transporter (monocarboxylate transporter), which functions to remove a lactate molecule and a proton from the cell is interpreted to be causal to similar profiles of lactate and blood pH change during and following intense exercise (2, 3).

The majority of research on blood acidosis and intense exercise has focused on the metabolic by-products that cause the acidosis and subsequent fatigue (12, 25, 29). Such research has assessed the ergogenic potential of inducing a pre-exer-cise alkalosis by ingestion or infusion of sodium bicarbonate (Na+HCO3

-), sodium citrate (Na+(CH2)2COH(COO-)3), or both. Enhancing the body’s blood buffering capacity in this manner has led to mixed results. Methodological discrepancies, such as treatment dose, ingestion profile, and mode of exercise have all made comparisons across studies difficult (17). Most investigators agree that perfor-mance notwithstanding, pre-exercise ingestion of Na+HCO3

- increases blood pH or retards the decrease in blood pH during exercise (17). Of the investigations that have specifically quantified blood pH changes in response to dietary or exercise interventions, however, none have measured blood pH changes during recovery. Understanding the recovery kinetics of blood pH is essential for multiple sprint or intermittent activities such as soccer, rugby, or hockey. Once the recovery kinetics is known, interventions can be developed to improve blood pH recovery kinetics and subsequent sports performance.

Therefore, we studied the effects of pre-exercise, diet-induced acidosis or alkalosis on the acid-base response to and recovery from high-intensity exercise to exhaustion. We hypothesized that the recovery kinetics of both blood pH and lactate, as seen through slope and time constants, would differ between the acidodic and alkalotic conditions, as well as compared to each other.

Methods

Twelve healthy competitive male cyclists (age 25.3 ± 3.7 y; height 170.2 ± 10.2 cm; weight 70.6 ± 5.5 kg; VO2max 72.5 ± 8.1 mL · kg-1· min-1) completed three exercise trials, each separated by at least 1 wk. Subjects signed an approved consent form after being informed of the procedures and possible risks and side effects. Participants were excluded on the basis of self-reported pre-existing medical condi-tions contraindicative to the study’s testing regimen. The study was approved by an institutional review board. All testing was conducted at an altitude of 1570 m.

General Procedures

Subjects were instructed in the importance of nutritional intake and told to control, record, and duplicate intake for all 3 trials. All participants kept written logs of food intake the evening prior to the first trial, and were told to avoid spicy foods and excessive intake of meat protein. On the morning of each exercise trial, the subjects ingested 2 cans of liquid meal replacement (Slim-FastTM) 3 h before exercise to standardize caloric, acid, and base dietary intake. The trials were randomized using the Latin least squares design.

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Step 1 Step 2 Step 3 Step 4 Step 5 Step 6 Step 7

10 min Catheter 10 min 60 min 5 min Exercise 60 min warm- insertion- supplement seated rest warm-up bout at 110% seated hand bath arterialized ingestion and subse- on cycle VO2max recovery hand vein (ACD, ALK, quent ergometer (approx. and subse- PLAC)– blood draws at 70 rpm 2-3 min) quent blood water ad lib draws

A flow chart depicting a typical trial is presented as steps 1 through 7:

Acid-Base Intervention

Prior to the acid-base intervention, a catheter was inserted into a heated dorsal hand vein. Resting baseline blood samples (2 mL discard followed by a 1 mL sample [blood pH]) were obtained before all trials. Subjects then ingested the acid-base supplement (pills). Blood samples were obtained at 15, 30, 45, and 60 min after ingestion while the subject sat quietly in an upright, seated position.

The acid-base interventions were as follows:

a) Nutritional acidosis (ACD). Subjects ingested 0.3 g/kg of NH4Cl with purified water over 10 min.

b) Nutritional alkalosis (ALK). Subjects ingested capsules providing a total dose of 0.2 g/kg of Na+HCO3

- and 0.2 g/kg of sodium citrate with purified water over 10 min.

c) Placebo (PLAC). Subjects ingested calcium carbonate with purified water over 10 min.

Exercise Protocol

VO2max. One week prior to the exercise trials, all subjects performed a VO2max test on a Lode cycle ergometer (Varberg, Sweden). The participants breathed through a low resistance, low dead-space two-way nonrebreathing valve (Hans-Rudolph, Kansas City, MO) into a 3 L plastic mixing bag for expired gas sampling. Venti-lation (VE) was measured using a low-resistance turbine connected in series on the expired side of the mouthpiece and interfaced with a data collection software system. Expired gas fractions for O2 and CO2 were measured from the mixing bag by metabolic analyzers (AEI Technologies, Pittsburgh, PA) and data for VO2 and VCO2 were computed each breath throughout exercise. The analyzers were cali-brated prior to each exercise test with known concentrations of N2, O2, and CO2. The expired airflow turbine was calibrated prior to each test using a 3 L calibration syringe (Hans Rudolph). The analyzers were interfaced to a computer and data was processed in real time using custom software that continuously displayed metabolic variables on a computer monitor throughout exercise. VO2max for all subjects was defined as the attainment of a plateau in VO2 where an increase in VO2 of ≤ 50 mL/min occurred with increasing workload. Heart rate was monitored continuously

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and recorded every 15 s throughout the exercise trial using an electrocardiography system (model Q4000, Quinton Cardiology, Inc., Bothell, WA).

Exercise Trials. Subjects first completed a 5 min warm-up on an upright cycle ergometer (Monark model 824, Monark AG, Stockholm, Sweden) at 70 rev/min at an intensity of 50 W. After the warm-up, the subjects performed a bout of intense cycle exercise with a cadence of 80 rpm and power output equivalent to 110% workload at VO2max. Workloads were pre-determined using the maximal watt output from the initial VO2max test. This intensity was designed to cause volitional fatigue after 2 to 3 min of exercise, and is slightly lower than used in other studies (120% VO2max) due to the terrestrial altitude of our location (22).

Recovery

Immediately on termination of exercise, the subjects were seated in a chair and post-exercise blood draws commenced. Blood samples were drawn every 2 min for 20 min. Subsequent blood draws were taken every 4 min for 40 min (total recovery time = 60 min). Blood oxygen-hemoglobin saturation (SaO2) data were measured continuously on the opposite hand during recovery using a finger pulse oximeter (Sportstat, Plymouth, MN).

Blood Sampling and Analysis

All catheters were placed in a heated dorsal hand vein (10 min, 35 °C hot water bath). The hand remained heated throughout the test using a fan-forced heater. The catheter was connected to a three-way stopcock and the stopcock and catheter were flushed with 2 mL of sterile saline between blood draws. Blood samples (2 mL flush and 1 mL sample) were drawn in separate syringes. The 1 mL samples were drawn into a heparin-coated 1 mL syringe, immediately capped, and placed on ice until subsequent (performed immediately following collection) blood gas and acid-base analyses using a clinical blood gas analyzer (Bayer Rapidlab model 865, Pittsburgh, PA). The blood remaining after blood gas analysis was capped and refrigerated for later analysis of lactate using enzymatic spectrophotometry.

Statistical Analyses

Data are presented as mean ±standard deviation. Prior to analysis, all data were assessed for normal distribution, homogeneity of variance, and independence of errors. Dependent variables considered were blood pH, bicarbonate, and lactate. The blood data were analyzed using multiple (baseline [BASE] vs. pre-exercise [PE], and PE vs. immediate post-exercise [IPE] vs. end recovery [ER]) two-way repeated measures ANOVA designs, where one effect was the condition (ACD, ALK, PLAC) and the second effect was time. Three-way repeated measures ANOVA design was used to assess recovery kinetics (monoexponential slope, time constants [t0.5]) (factor 1) between trials (factor 2) and between pH and lactate (factor 3). Raw data for blood pH and lactate were fit with third-order polynomial func-tions using commercial software (Prism 3, Graphpad Software, Tulsa, OK). Post hoc analysis was done using Tukey’s HSD. Statistical significance was set at P < 0.05.

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Results

Data Presentation

Due to the different phases of blood acid-base and lactate change (pre-exercise [PE], exercise performance, immediate-post recovery [IPE], and end recovery [ER]), and the fact that prior research has often reported data for such changes as independent categories, data could be presented for the specific phases of the study for each dependent variable, or for the changes across time or study phases. We chose to do the latter, as this approach was consistent with the statistical analyses. Nevertheless, data are first presented for the influence of nutritional intervention on blood acid-base balance, and the differences in exercise performance between trials.

Pre-Exercise Nutrition and Acid-Base Balance

The effects of pre-exercise supplementation with acid (NH4Cl), base (Na+HCO3- and

Na+Citrate-), or placebo (calcium carbonate) on blood pH, HCO3- and lactate are

presented in Figures 1a through 1c. Ingestion of Na+HCO3- significantly increased

both blood pH and blood HCO3- when compared to PLAC and ACD (P < 0.05).

Conversely, ingestion of NH4Cl significantly lowered blood pH when compared to the ALK and PLAC trials (P < 0.05). Blood lactate remained unchanged from baseline to pre-exercise values for all trials.

Performance

For the performance trial, subjects exercised at 409.1 ± 29.2 W. Figure 2 presents the exercise times to exhaustion for each trial. Time to exhaustion in both the PLAC and ALK trials were significantly longer compared to ACD (P < 0.05). Despite the greater pre-exercise blood HCO3

- and pH in the ALK trial compared to PLAC, time to exhaustion was no different than PLAC.

Changes Across the Study Phases

Data for the changes in each of blood pH, HCO3- and lactate across the study phases are presented in Figures 3a through 3c.

Blood pH. The post-exercise time to peak change for blood pH was 5.0 ± 2.4, 3.19 ± 1.3, and 3.5 ± 2.2 for ACD, ALK, PLAC, respectively. The interaction between time and trial was significant [F(6,48) = 11.78; P < 0.001] (Figure 3a). At IPE, the ALK trial induced a higher blood pH compared to ACD and PLAC. The higher pH of the ALK trial remained from IPE throughout recovery (ER)(P < 0.05).

Blood HCO3-. Post-exercise time to peak change for HCO3- was 5.1 ± 2.4, 4.0 ± 2.0, and 4.7 ± 4.3 for ACD, ALK, PLAC, respectively. The interaction between time and trial was significant [F(6,48) = 9.67; P < 0.001) (Figure 3b). At ER, HCO3- differed among all conditions (ACD, ALK, PLAC), with ALK having the highest concentration of HCO3-, followed by PLAC and ACD (P < 0.05).

Blood Lactate. Post-exercise time to peak change for blood lactate was 5.0 ± 2.3, 6.0 ± 2.1, and 3.8 ±2.5 for ACD, ALK, PLAC, respectively. Blood lac-tate concentrations were similar between trials for all time points of post-exercise and recovery (Figure 3c).

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Figure 1—Pre-exercise data for a) pH, b) HCO3-, and c) lactate between the three trials. *

Indicates different from baseline within the trial (P < 0.05); ^ Indicates different from all other trials for the same condition (P < 0.05).

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Figure 2—Exercise time to fatigue across trials (min). * Indicates different from ACD trial (P < 0.05).

Recovery Kinetics

The recoveries of blood pH, HCO3-, and lactate were best fit with nonlinear expo-

nential functions. Raw data for blood pH, HCO3-, and lactate for select individuals

are presented in Figures 4a through 4c. Note that time data are different for each trial due to the different times to peak change in blood acid-base balance induced by the pre-exercise nutrition intervention.

Exponential curves for time-normalized data from all subjects are presented in Figures 5a through 5c. Data for the exponential slopes and half-time recovery constants (t0.5) for both blood pH and lactate are presented in Table 1. No differ-ences existed for either slope or time constant data between trials for either blood pH and lactate. Blood pH time constant data were significantly lower for pH than lactate for all trials (P < 0.01).

Relationship Between Blood pH and Lactate Recovery

Blood pH and lactate recovery correlations were assessed for all trials. Linear correlations revealed averaged correlation coefficients of 0.88, 0.74, and 0.86 for ACD, ALK, and PLAC, respectively. Differences between correlations were sig-nificant [F(2,16) = 13.34; P < 0.001]. Data for 2 subjects are presented in Figure 6. Application of a third-order polynomial function to the data sets for each trial revealed complex relationships between blood pH and lactate. For the ALK and PLAC trials, blood pH recovered more rapidly than lactate during the initial 10 min of recovery. Also, blood lactate recovery remained approximately 50% complete after blood pH was near complete recovery. These figures support the kinetic data of Table 1.

Discussion

The unique findings of this study were that a) pre-exercise alterations of blood HCO3

- alters time to peak change in acid-base balance recovery; b) complete blood

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Figure 3—Changes from pre-exercise (PE) to post-exercise (IPE) and end recovery (ER) for a) pH, b) HCO3

-, and c) lactate. PE to IPE, and IPE to ER changes were different for all trials. * Indicates different from PE within the trial (P < 0.05); ̂ Indicates different from all other trials for the same condition; # Indicates different from ACD and PLAC for the same condition (P < 0.05); � Indicates different from ACD for the same condition (P < 0.05).

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Figure 4—Representative data from one subject, showing the different recovery kinetics between the three trials for a) pH, b) HCO3

-, and c) lactate.

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Figure 5—The resulting curves for all data from all subjects between the three trials for the recovery of a) pH, b) HCO3

-, and c) lactate.

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Figure 6—The relationships between blood pH and lactate for two representative subjects for each of the ACD, ALK, and PLAC trials. Data were fit with a third-order polynomial function. Note the complex function between pH and lactate, with a more linear fit only apparent for the ACD trial.

Table 1 Data for the Mono-Exponential Slopes and Half Time Recovery Constants for Each Blood Acid-Base Parameter

Slope t0.5

Trial pH Lactate pH Lactate

ACD 0.057 ± 0.01 0.040 ± 0.02 12.67 ± 3.50* 23.37 ± 9.47PLAC 0.080 ± 0.02 0.030 ± 0.03 9.83 ± 2.73* 35.81 ± 24.58ALK 0.050 ± 0.01 0.020 ± 0.01 15.51 ± 3.45* 36.63 ± 19.66

Note. Values are mean ±_ standard deviation; ACD, acidosis; PLAC, placebo; ALK, alkalosis; * = significantly different from lactate (P < 0.01).

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pH recovery requires more than 45 min, has a t0.5 approximating 12 min, and is best modeled using a nonlinear function having 2 components (fast and slow); c) complete blood lactate recovery requires greater than 60 min, has a t0.5 approximat-ing 30 min, and recovers based on a mild mono-exponential function; d) blood HCO3

- was elevated during pre-exercise and recovery conditions for the ALK trial when compared with ACD and PLAC trials; and e) lactate recovery curves were similar between conditions.

Pre-Exercise Acid-Base Manipulation

Oral ingestion of Na+HCO3- has been reported to require a minimum of 1 h to pass

through the stomach and be detected in the bloodstream (14). Thus, timing of peak HCO3

- levels and the subsequent exercise bouts have been of central focus in many studies (8, 10, 27). Peak blood HCO3

- levels are also affected by the amount ingested.

In the current study, the time between ingestion and exercise was 60 min. Peak pre-exercise pH and HCO3

- values were 7.461 ± 0.03 and 26.38 ± 2.00 for the ALK trial, respectively. Blood pH values were similar to those reported by Horswill et al.; however, pre-exercise HCO3

- values were lower in the current study (approximately 26 mmol/L to 30 mmol/L) (8). Nevertheless, HCO3

- was still significantly higher than pre-ingestion levels (P < 0.05) and significantly higher when compared to the PLAC and ACD conditions.

Intense Exercise Performance

The effects of increased HCO3- on intense exercise performance are inconclusive.

In this study, the time to exhaustion was not different between PLAC and ALK trials, indicating no performance enhancement. Also, mean power output (409.1 ± 29.2 W) was unchanged throughout conditions. These results are similar to those reported in previous studies (8, 9, 18, 27). Variations in exercise intensity, dura-tion, and ingested bicarbonate dosage appear to have an effect on performance outcome measures. Based on pilot research prior to the current study, the dosage (200 mg/kg) was sufficient to induce a significant increase in blood pH, with peak levels observed at the onset of exercise. Pilot work also showed that peak blood pH levels were not further raised using 300 mg/kg.

Due to the exponential rise in the concentration of H+ during intense exer-cise, it is expected that an eventual limiting factor during such a bout is depletion of one’s blood buffering capacity. It has been shown that the greater the exercise intensity the more rapid the diminishment of the buffering capacity (12, 31). Many studies have been conducted investigating the effect on blood buffering capaci-ties for various intensities of exercise and induced pre-exercise alkalosis (28, 30). Exercise intensities have ranged from 95 to 125% workload at VO2max (28, 30) and durations of 1 to 3 min (13, 23). Two such investigations using a similar workload percentage as that of the current study produced comparable results. Katz et al. in 1984 and Horswill et al. in 1988 both prescribed 200 mg · kg-1 · body weight (BW) -1 bicarbonate ingestion and had subjects cycle to exhaustion (~ 2 min) (8, 10). Although total work was not indicated, both studies reported no change in onset of fatigue when compared to controls. In this study, we observed no change in either time to fatigue or power output (Figure 2).

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The only consistency in the literature with regard to induced pre-exercise alkalosis and performance duration are those studies whose methodology included intermittent exercise protocols (6, 16, 33). The bouts were approximately 1 min in duration (5 bouts total), with 5 min passive rest between bouts (6, 16, 33). Pre-sumably, the rest interval in multiple bout exercise conditions allows greater blood flow and therefore HCO3

- exchange between blood and muscle, thus facilitating improved recovery of intramuscular acidosis and delaying processes of acid-base related fatigue in the subsequent bout of exercise.

An important variable influencing the effectiveness of pre-exercise alkalosis is the amount of base ingested. Tolerable levels of Na+HCO3

- appear to be ≤300 mg · kg-1 · BW-1. Dosages lower that 200 mg · kg-1· BW-1 do not appear effective, however (8). The current dosage of 200 mg · kg-1 · bw-1, was tolerated by all subjects. This dosage, however, might not have been sufficient to delay the onset of fatigue. One reason for this could have been the highly trained state of our subject popula-tion. It has been reported that pre-exercise alkalosis might not have the purported effect when individuals are highly trained (24). Many studies have shown that buffering capacities could be enhanced with training, almost in effect maximiz-ing the already existing buffering capabilities and therefore rendering bicarbonate ingestion less effective (24).

Peak Changes in Blood Acid-Base and Lactate

The peak changes in blood acid-base in this study were consistent with results from other studies (6, 8, 20, 26). Peak (or nadir) blood pH values differed between the alkalosis and the other 2 conditions (Figure 4a), with the average nadir pH value being higher. With a supposed enhancement of blood buffering capacity and increased facilitation of H+ out of the muscle (2), one might expect higher pH values in the alkalosis-induced state. One could also assume, then, that there would be a delayed onset of fatigue. This was not the case, however, as was previously reported.

Peak lactate values were similar to those reported by Brooks et al. (2). Lactate facilitation out of the working muscle appears to be increased under the conditions of induced alkalosis. Brooks contends that lactate facilitation might be affected by pH and could be temperature dependent (2). Blood pH values in this study would concur with such findings, in that blood pH was highest in the alkalotic state (Figure 3a). Such trends in lactate concentration, although not significant, were also observed in the current study, with lactate concentrations being highest in the alkalotic condition (Figure 3c).

Recovery Kinetics of Acid-Base Balance

Previous studies observing the recovery kinetics of acid-base balance have not addressed adequate durations of recovery (15, 29). It might be misleading to base conclusions of acid-base recovery on time frames of 15 min or less. In the cur-rent study, the duration of recovery was 60 min, thereby allowing the detection of more complex recovery kinetics to be analyzed using nonlinear and two-segment analyses (Figures 4 and 5). This finding is unique in that no study has followed pH recovery for such an extended time period.

A comparative look at the 60 min pH recoveries of the ACD, ALK, and PLAC trials reveals a similar first recovery segment. All 3 trials had similar pH

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recovery slopes, as well as similar half-time constants (t0.5 ~ 12 min). The important comparison that must be addressed, however, is that although the recovery slopes were similar in nature, the low values of pH were significantly lower during the ACD and PLAC trials than ALK trials [7.15±0.06, 7.21 ±0.07, and 7.16 ±0.06 ACD, ALK, and PLAC, respectively (Figure 3a)]. Also significantly different was the pH value between ACD, ALK, and PLAC at the end of the 60 min recovery segment (Figure 3a), with the ALK trial resulting in the highest pH.

The second recovery segment for blood pH followed a similar pattern. ACD, ALK, and PLAC trials had a comparable slope, however, overall pH values were higher for the ALK trial when compared to the other conditions. Although the higher pH values seen in the ALK trials weren’t indicative of increased time to exhaus-tion, these values might be of importance during recovery from intense exercise, especially if the exercise is intermittent in nature. A higher recovery pH could affect performance in latter bouts, and should be addressed in further investigations.

Another unique finding from the perspective of a 60 min recovery time frame was revealed in the HCO3

- kinetics. The two-segment recovery regressions that were prominent in the blood pH kinetics were not apparent in the HCO3

- kinetics for any of the conditions (Figure 4b). This suggests very different mechanisms for pH and for HCO3

- recovery.

Recovery Kinetics of Blood Lactate

The recovery pattern for blood lactate followed similar patterns to that of past research (1, 7, 19). The curvilinear response has been presented in many studies, both in a passive or active recovery mode (1, 7, 19). Peak blood lactate values are also similar to those reported in past research for similar exercise intensities (7).

Peak blood lactate values during recovery have been reported highest during alkalotic-induced states (2). Brooks et al. has reported that with the addition of Na+HCO3

-, lactate facilitation out of the working muscle is enhanced (2). If this is the case, then the results of this study would add merit to such a claim. Peak blood lactate was highest in the ALK trials when compared to the PLAC and ACD conditions (Figure 4c).

Another important finding of this study was that blood lactate recovery was very slow compared to blood pH (Table 1), with almost triple the t0.5. As for the HCO3

- recovery data, there are obviously different mechanisms involved in the recovery of blood lactate and pH. This is logical, as there is no stoichiometry between blood lactate efflux and muscle proton efflux from working muscle (1), and blood pH recovery is complicated by the combination of cellular and pulmonary-related alterations in proton buffering potential. The applied interpretations of the disparate recovery kinetics between blood pH and lactate is that the decrease in blood lactate after intense exercise should not be used to infer concomitant changes in blood acid-base balance. Similarly, researchers, coaches, and athletes alike should realize that recovery from acidosis might take as long as 10 min to 50% recovery (PLAC trial), and the presence of elevated blood lactate could be irrelevant.

Conclusions

The results of this study indicate the need for further quantification of blood pH recovery kinetics. The 60 min recovery time frame revealed that a two-segment

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recovery might be necessary to fully appreciate blood pH recovery from intense exercise. Also, with the addition of Na+HCO3

-, blood pH was enhanced throughout when compared to the PLAC and ACD conditions. This could be of importance when addressing training or sporting events requiring multiple sprint/recovery bouts. Further study using multiple sprint bout designs might aid in further explanation of blood recovery kinetics during intermittent exercise.

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Influence of pre-exercise acidosis and alkalosis on the kinetics of acid-base recovery following intense exercise

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