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Basic Sciences: Original Investigations

Effect of induced alkalosis on exhaustive leg press performance


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Medicine & Science in Sports & Exercise: April 1998 - Volume 30 - Issue 4 - p 523-528
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Fatigue has been defined as a failure to maintain the required or expected force, leading to a reduced performance of a given task(5). For over 100 years scientists have been pursuing the mechanisms that cause fatigue in order to enhance physical performance. Although this topic has been extensively studied, it is difficult to draw conclusions because of the multitude of factors that play a role in the fatigue process. However, the accumulation of hydrogen ions (H+) is frequently referred to as the major cause of fatigue during short term high intensity activity. Several mechanisms have been proposed to explain this effect of H+ on muscle function (6). There is also some evidence that the lactate anion inhibits muscle force production by an undetermined mechanism (1,9).

Several investigators have shown that an increased concentration of extracellular bicarbonate ([HCO3-]) will increase the rate of H+ and lactate efflux out of muscle and possibly delay fatigue(8,10,11). As a result of these findings in isolated muscles, numerous studies have used alkalinizing agents (primarily sodium bicarbonate, NaHCO3) through either ingestion or infusion in an attempt to enhance human performance (13).

To our knowledge only four studies have investigated the effects of NaHCO3 on resistance exercise performance(2,12,14,20), and these have reported conflicting results. Of special note, Webster et al. (20) had subjects ingest 0.3 g·kg-1 of either NaHCO3 or white flour (placebo) 105 min before an exercise test on a leg press machine. The subjects performed four sets of 12 repetitions and then a fifth set to volitional fatigue with approximately 70% of their one repetition maximum (1 RM). Although four out of the six subjects in the bicarbonate trial improved performance by an average of three repetitions (approximately 16%), overall there was no statistically significant effect on performance. However, after completion of the first four sets, blood pH was still within the normal range of 7.35-7.45. After the fifth, exhaustive set, blood pH was still 7.32, which is approximately 0.10-0.15 units higher than the values found by both Costill et al. (3) and Wijnen et al. (21), who used a similar protocol with cycling. Webster et al.(20) hypothesized that a protocol resulting in greater changes in pH and lactate concentration ([La-]) similar to those of Costill et al. (3) and Wijnen et al.(21) would increase the likelihood that NaHCO3 would improve resistance exercise performance. Also, a post-hoc power analysis predicted that a greater number of subjects would be required for a satisfactory statistical power (20).

Therefore, the purpose of this study was to examine the effects of NaHCO3 on five maximal sets of leg press exercise utilizing a more intense protocol and a greater number of subjects than Webster et al.(20).


Subjects. Fifteen males completed the study, and each provided written informed consent before the start of the experiment. Physical characteristics of the subjects (mean ± SE) were as follows: age 21.5± 0.4 yr; height 177.2 ± 2.2 cm; weight 81.0 ± 2.8 kg. All subjects had been involved in a regular weight training program that included lower body lifts for a minimum of 2 yr before the study. However, none were competitive strength or bodybuilding athletes.

Protocol familiarization. Before experimental testing, each subject's one repetition maximum (1 RM) for seated leg extension was determined on a leg press machine (Universal, Cedar Rapids, IA). Chair position was adjusted to allow an 80-85° flexion at the knee when the feet were resting on the machine's upper foot pads. After determination of the subject's 1 RM, a series of familiarization sessions were performed. The exercise performed in these sessions was identical to that in the experimental sessions. Each session was separated by 3 to 6 d to ensure adequate recuperation. Before performing the testing protocol, subjects performed a 10-min standardized warm-up based on their 1 RM with 5 min rest before the start of the protocol. After the warm-up and rest, each subject performed five consecutive sets with each set ending when the subject was unable to complete another repetition. The first set of the protocol was performed with a load equal to approximately 85% of the subject's 1 RM. During the following sets the load was determined by the number of repetitions the subject had performed in the previous set. The load remained unchanged if the subject was capable of performing 13 or more repetitions, whereas the load was decreased by approximately 5% if the subject performed 12 repetitions or less. One and one tenth kg weights (2.5 lb) were added to the weight stack to be as precise as possible in setting the load. This protocol was established during extensive pilot work to maintain the number of repetitions per set for each subject at approximately 12 repetitions (± 4 repetitions). This number of repetitions is similar to that performed in each set by bodybuilders during typical workouts. Each set was separated by 90 s of unloaded leg presses to prevent blood pooling. Each repetition was performed with a complete stop before initiating the next repetition. When the total number of repetitions for the five sets was within 10% on two consecutive sessions, the subject was then tested after the ingestion of gelatin capsules (Lilly, Indianapolis, IN, size 0) containing either a placebo (white flour) or the experimental substance, NaHCO3.

Experimental testing sessions. Subjects reported to the laboratory on two separate occasions separated by 3-6 d. Two treatments were given, one before each exhaustive resistance exercise testing session. One treatment was a placebo (white flour) and the other was NaHCO3 (baking soda). Both treatments were administered in gelatin capsules (Lilly, size 0) in the amount of 0.3 g·kg-1 and were ingested over a period of 5 min. Subjects were instructed to arrive at each testing session in a euhydrated state. The subjects were encouraged to drink as much water as possible throughout the experiment without becoming uncomfortably full; this amount of water was measured. Although the subjects were not required to duplicate their water consumption during their second trial, water consumption was not significantly different between trials. Ninety minutes after ingestion of either placebo or NaHCO3, the standardized warm-up was performed. Five minutes after the warm-up, each subject performed five maximal sets with the weights which had been previously determined in the familiarization sessions. Exactly the same weights were used in both the placebo and NaHCO3 trials. The order of the tests was randomized for each subject and the tests were conducted in a double blind fashion.

Blood collection. Before the ingestion of either treatment, a 21-gauge indwelling catheter was inserted into a prominent forearm vein. Arterialized venous blood samples were taken at the following times: preingestion, 30, 60, 90, and 105 min after ingestion (the 105-min sample was pre-exercise and post-warm-up), 1 min after each set, and at 3, 5, 7, 9, and 15 min in recovery after the fifth set. Arterialization of venous blood was attempted by warming the subject's hand and lower arm in a heated box that was maintained at ≈ 65°C. It has been shown (20) that at least 60 s of recovery are necessary after this type of exercise before the blood samples are once again “arterialized.” The hand and arm were heated to increase blood flow sufficiently to attain a venous PO2 ≥ 70 mm Hg at rest before the exercise. The heated box allowed the subjects to grip a support bar while the hand and forearm were surrounded by circulating hot air.

Blood analyses. All samples were analyzed for pH, PCO2, and PO2 with an automated blood gas, pH analyzer (IL 1304). Percent oxygen saturation of hemoglobin [%O2Hb] and hemoglobin concentration[Hb] were measured spectrophotometrically using a CO-oximeter (IL 282). Plasma[HCO3-] was calculated from the Henderson-Hasselbalch equation. Hemoglobin concentrations in mmol·L-1 were combined with values for pH and PCO2 and fitted to the Siggaard-Andersen alignment nomogram for an estimate of base excess (17). To correct these values for partial oxygen-hemoglobin desaturation, the following correction factor (C) was subtracted from the value obtained from the alignment nomogram: C = {(0.15) [Hb]} × {(100% -% saturation)/100}(15). The corrected values are referred to as oxygenated base excess (OxyBE) which is defined as the number of mEq·L-1 of fixed acid or base necessary to bring a sample of fully oxygenated blood at 37°C and a PCO2 of 40 mm Hg to a pH of 7.40. A positive value indicates an excess of base or an alkalosis, while a negative value indicates a deficit of base or an acidosis (17). The described correction factor is quite small for “arterialized” venous blood since it is highly saturated with oxygen. In addition, a portion of each sample was immediately pipeted into ice-cold perchloric acid, centrifuged at 800g for 15 min, and the supernatant stored in cryotubes at-80°C until subsequent analysis for [La-]. All samples were analyzed in duplicate using modifications of standard spectrophotometric methods (7).

Statistical analyses. All statistical analyses were standard two-way (treatment X time) repeated measures ANOVA procedures. The analyses were done with Super-ANOVA (Abacus Concepts, Berkeley, CA), a statistical package for the MacIntosh computer. Pairwise post-hoc contrasts were used when necessary to determine where significant differences occurred. The 0.05 level was used for statistical significance. All results are reported as means ± SE.


In an attempt to minimize the possibility of gastrointestinal distress that has been reported with NaHCO3 ingestion in some studies, subjects were instructed to arrive at each testing session in a euhydrated state. Subjects also were encouraged to drink frequently after the ingestion of either placebo or NaHCO3. There was no significant difference between treatments(placebo = 1.35 ± 0.13 L, NaHCO3 = 1.46 ± 0.28 L) for the amount of water consumed. To our knowledge this is the largest fluid intake reported during any NaHCO3 study. Four of the 15 subjects reported some slight gastrointestinal distress in the NaHCO3 treatment. During the sets of leg extensions, venous blood was never “arterialized”(PO2 = 64 ± 2 mm Hg). This was probably the result of the strong isometric contraction which was required in grasping the support bars. However, arterialization was successful (PO2 ≥ 70 mm Hg) before exercise and during recovery from exercise.

Blood parameters pre-exercise. All control values for pH,[HCO3-], OxyBE, and [La-] were within normal range and not significantly different between treatments before ingestion of either treatment (pH: NaHCO3 = 7.40 ± 0.01, placebo = 7.40 ± 0.01; [HCO3-]: NaHCO3 = 22.8 ± 0.2, placebo = 23.0± 0.2 mEq·L-1; OxyBE: NaHCO3 = -1.3 ± 0.2, placebo = -1.1 ± 0.2 mEq·L-1; [La-]: NaHCO3= 1.3 ± 0.1, placebo = 1.1 ± 0.0 mM) (Fig. 1). The ingestion of NaHCO3 resulted in a statistically significant increase in all the above mentioned acid-base parameters except for[La-]. Peak values for pH occurred immediately before exercise (7.47± 0.01), whereas both [HCO3-] (28.0 ± 0.4 mEq·L-1) and OxyBE (4.3 ± 0.4 mEq·L-1) demonstrated peak values 15 min earlier. Overall, the subjects were significantly more alkaline during the NaHCO3 trial than during the placebo trial immediately before initiating the exercise test. The ingestion of NaHCO3 had no effect on [La-] before initiation of the warm-up period (1.1 ± 0.1 mM).

Figure 1-Acid-base parameters pre-exercise, during exercise, and in recovery from exercise. * indicates sodium bicarbonate and placebo treatment means are significantly different (:
P < 0.05).

Blood parameters in response to exercise. After the first set of exercise both experimental groups experienced an immediate statistically significant decline in pH, [HCO3-], and OxyBE, and a significant increase in [La-] (Fig. 1). Each subsequent set produced a further decline in pH, [HCO3-], and OxyBE, and a further increase in [La-]. At the completion of each set; pH,[HCO3-], and OxyBE were significantly higher in the NaHCO3 treatment. Lactate concentrations were significantly higher in the NaHCO3 treatment after sets four and five. There was a significantly higher PCO2 (not shown) after every set in the NaHCO3 trial.

Blood parameters in recovery from exercise. Acid-base parameters decreased further during recovery from the fifth (final) set(Fig. 1). By minute 7 all acid-base parameters began to rise but did not reach pre-exercise values by 15 min of recovery. Values for pH, [HCO3-], OxyBE, and [La-] were significantly higher at every sample time in recovery for the NaHCO3 trial in comparison with those in the placebo trial. There was a significantly higher PCO2 at every sample time during recovery for the NaHCO3 trial. Although PCO2 was significantly higher throughout exercise and recovery for the NaHCO3 trial (≈ 2.5 mm Hg), it is questionable whether this small difference has any physiological importance.

Exercise performance. The total number of repetitions completed by each subject during the five sets is shown in Table 1 along with the number of repetitions for each individual set. Although 7 of the 15 subjects performed more repetitions after the ingestion of NaHCO3, the mean difference between treatments was not statistically significant (P = 0.66). There was no order effect for total repetitions or repetitions for any single set.

Repetitions completed in each exercise bout after the ingestion of either placebo or NaHCO3.


In the first study of NaHCO3 ingestion and isotonic resistance exercise, Webster et al. (20) found no improvement in performance in six male subjects with prior weight training experience as a result of NaHCO3 ingestion (0.3 g·kg-1). In that study(20), the subjects performed five sets of repetitions with a weight equaling approximately 70% of their 1 RM. In the first four sets, 12 repetitions were performed and then as many repetitions as possible were done in the fifth set. Therefore, the first four sets were not exhaustive. As a result, Webster et al. (20) speculated that NaHCO3 might have been more effective as an ergogenic agent if the resistance exercise had been more intense. In addition, a post-hoc power analysis revealed that a pool of 18 subjects, rather than only six, would have resulted in a statistically significant performance improvement in the NaHCO3 trial if all 18 subjects had responded the same on the average as the actual six subjects had performed.

These considerations of Webster et al. (20) prompted the present study which used a more intense resistance exercise protocol and a greater number of subjects. In this study, 15 weight trained male subjects also performed five sets of repetitions. However, the weight ranged from approximately 65%-85% of 1 RM and each set was performed to exhaustion. This exercise protocol was more intense than that of Webster et al.(20) as evidenced by a lower [HCO3-](placebo: present study 14.0 vs Webster et al. 15.4 mEq·L-1) and OxyBE (placebo: present study -12.3 vs Webster et al. -10.7 mEq·L-1), and by a higher [La-] (placebo: present study 11.3 vs Webster et al. 9.8 mM) after the fifth (final) bout. Because of the exhaustive nature of this protocol, several subjects became pale, dizzy, and nauseous in the early recovery period. Despite the larger number of subjects and the more intense resistance exercise protocol, NaHCO3 ingestion still had no statistically significant effect on performance.

As has been noted, this area of study has consistently reported contradictory results (20). Although Webster et al.(20) found no statistical improvement with NaHCO3 ingestion, three of their six subjects improved resistance exercise performance by 10% with NaHCO3 ingestion. In the present study, only two of our 15 subjects showed 10% improvement with NaHCO3 ingestion. Given the time (protocol familiarization and testing) and effort (blood sampling and analysis) for the researchers and the inconvenience (and small risk) for the subjects, only 15 subjects (rather than the 18 suggested by Webster et al. (20) were studied once it became clear that the majority of the subjects were not showing improvements with bicarbonate.

Despite the fact that the protocol in the present study was more intense than that used by Webster et al. (20) as described above, this resistance exercise regimen was not as metabolically challenging (at the whole body level) as the typical cycle ergometer protocols that employ repeated bouts of “all-out” cycling. Resistance exercise requires high force outputs but usually does not elicit whole body metabolic rates greater than 50% of ˙VO2max(4,18,22). In contrast, short term high intensity cycling exercise such as that for which NaHCO3 ingestion has been shown to improve performance, typically requires an energy expenditure that exceeds 100% of ˙VO2max. This difference in metabolic response is illustrated in Figure 2 which compares the [La-] and pH responses of repeated bouts of intense cycling (3) with those for resistance exercise in the present study. Although this comparison is imperfect because of the slightly different sampling times and methods of sampling (arterialized samples in the present study vs venous samples by Costill et al. (3), it does reflect the differences between resistance exercise and cycling exercise. Note that the[La-] was similar during the first four bouts although these cycling bouts were not performed to exhaustion. After the fifth exhaustive cycling bout, the [La-] was much higher than that found after five exhaustive resistance exercise bouts. Also blood pH was always lower during cycling exercise with the difference becoming progressively greater as the number of bouts increased, reaching almost 0.2 units lower by the fifth bout. This contrast in metabolic cost and acid-base response between high intensity cycling and high force resistance exercise may explain the differing ergogenic effects of NaHCO3 for the two types of exercise.

Figure 2-Comparison of blood pH and lactate responses between present study of exhaustive leg press performance and study by Costill et al.:
(3) of repeated high intensity cycling. Data from both studies are for placebo trials. Reference 3. Costill, D. L., F., Verstappen, H. Kuipers, E. Janssen, and W. Fink. Acid-base balance during repeated bouts of exercise: influence of HCO3. Int. J. Sports Med. 5:228-231, 1984.

It should be noted that our results do not agree with the preliminary report of Marsit et al. (12) who found that sets of 10 repetitions of leg press exercise at 67.5% of 1 RM were improved with dosages of both 0.2 and 0.3 g·kg-1 of NaHCO3. Also Maughan et al.(14) have reported a positive effect on static endurance at 20% of MVC but not at 50% or 80% of MVC. Finally, Coombes and McNaughton(2) found not only an increase in work output during 85 s of maximal isokinetic knee flexion and extension following NaHCO3 ingestion but also an increase in peak torque. The increase in peak torque is especially difficult to explain since the mechanism for such an effect is unclear. It is well accepted that an increased extracellular pH and[HCO3-] can promote lactate and H+ efflux from muscle during contraction and recovery (8,10,11). However, intramuscular pH before exercise or contraction is apparently not affected by NaHCO3 ingestion(3,10,16,19), nor is intramuscular[HCO3-] (19). Accordingly, the basis for any improvement in peak torque is unknown.

In summary, NaHCO3 ingestion failed to improve resistance exercise performance in 15 weight trained male subjects. Despite the high force output required to complete the resistance exercise regimen, the metabolic response as reflected by blood [La-] and pH was not as dramatic as that reported for repeated bouts of maximal cycling in which NaHCO3 ingestion has been found to provide an ergogenic effect. It may be that a slower rate of lactate and H+ production in resistance exercise (perhaps because of the use of a smaller muscle mass than during cycling) minimizes the possible benefits of increased extracellular pH and [HCO3-].

This work was supported in part by National Institute of Arthritis and Musculoskeletal and Skin Diseases Grant No. 1R01AR-40342.

Current addresses are: Mr. Kevin J. Portington, 33 Whitman Street, Carteret, NJ 07008; Dr. Michael J. Webster, School of Human Performance and Recreation, Box 542, University of Southern Mississippi, Hattiesburg, MS 39406; Dr. Rodney M. Rutland, Life College, School of Chiropractic, 1269 Barclay Circle, Marietta, GA 30060.

Address for correspondence: Dr. L. Bruce Gladden, Department of Health& Human Performance, 2050 Memorial Coliseum, Auburn, AL 36849-5323. E-mail: [email protected].


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