High-intensity exercise results in the production and accumulation of lactate (La−) and hydrogen ions (H+). Although recent evidence suggests that the effects of a decrease in intracellular pH (pHi) on muscle contractile force may be less than previously thought (31), a large decrease in pHi after intense exercise may negatively affect some metabolic/ionic processes (19). Therefore, a reduction in the accumulation of H+ may benefit those regularly participating in high-intensity exercise, including those involved in team sports, who are required to perform repeated sprints throughout a game.
The removal of H+ during intense muscle contractions occurs via a number of differing transport systems and via intracellular buffering (19). The buffering of H+ may be especially beneficial during sprint-type exercise, where there is a rapid H+ accumulation attributable to the high rate of nonmitochondrial ATP resynthesis required to maintain power output. In support of this hypothesis, a relationship has been reported between muscle buffer capacity (βm) and repeated-sprint ability (RSA) (4). Although high-intensity exercise and the accumulation of H+ during training have been suggested as important stimuli to increase βm (11), the effects of many training methods on βm and H+ regulation are still unclear.
Previous reports have shown that high-intensity interval training, rather than low-to moderate-intensity endurance training, results in an increase in βm (11). However, the effects of resistance training on H+ regulation are less clear. Strength-trained athletes have been reported to have better H+ regulation than healthy untrained subjects during intense isometric exercise (30). Resistance training has also been shown to result in both metabolic and ionic changes within the muscle that may contribute to improved H+ regulation (13,20,28). Metabolic changes reported after high-repetition, isometric resistance training include a large drop in pHi (postexercise pH ≈ 6.8) and an increase in blood lactate concentration ([La−]b) (postexercise [La−]b ≈ 14 mmol·L−1) (16,29), similar to that reported during intense interval training (9,11). Therefore, this type of resistance training may provide an adequate stimulus to improve βm and H+ regulation.
The purpose of the present study was to determine the effects of high-repetition, short-rest period resistance training on changes to βm and H+ regulation during high-intensity exercise. We measured βm using in vitro techniques (titration βmin vitro) on freeze-dried muscle tissue, thus measuring the buffering potential of the physicochemical buffers within the muscle (excluding bicarbonate, which is removed during the freeze-drying process). It was hypothesized that 5 wk of high-repetition, short-rest period resistance training would result in improved βmin vitro and H+ regulation.
Sixteen moderately trained female students (mean ± SD, age 18 ± 1 yr, mass 60.8 ± 7.2 kg, height 168.4 ± 7.6 cm, V˙O2peak 46.0 ± 5.0 mL·kg−1·min−1) volunteered to participate in the study. Subjects were ranked on RSA and strength, and then matched pairs were randomly allocated to a training or control group. Before this investigation, none of the subjects had participated in resistance training, but they had been recreationally involved in various team sports (hockey, netball, and soccer), in which they continued to participate throughout the study (2-3× wk−1). Subjects were informed of the study requirements, benefits, and risks before giving written informed consent. Approval for the study's procedures was granted by the institutional research ethics committee. Originally, there were 18 subjects (nine in each group), but in the first week of training, one subject left each group.
All of the subjects completed a familiarization trial of a graded exercise test (GXT), the 5 × 6-s cycle test of RSA and the 60-s constant-intensity exercise test (CIT60 ≈ 160% V˙O2peak) before baseline testing. Subjects also participated in two resistance-training familiarization sessions before beginning the training program. On the day of the CIT60, each subject had a muscle biopsy from the vastus lateralis muscle at rest and immediately on cessation of the exercise test. Pre- and posttraining tests were conducted at the same time of day. Subjects were asked to maintain their normal diet and training throughout the study. They were also required to consume no food or beverages (other than water) for 2 h before testing, and they were asked not to consume alcohol or to perform vigorous exercise in the 24 h before testing. Food diaries were given to each subject to record food and fluid consumption for 2 d before each test, and subjects were asked to replicate this during posttraining testing. All subjects were eumenorrheic and there were no differences in menstrual phase between the two groups at the beginning of the study.
The GXT was performed on an air-braked track-cycle ergometer (Evolution Pty. Ltd., Adelaide, Australia) and consisted of graded exercise steps (4-min stages) using an intermittent protocol (1-min break between stages). The test commenced at 50 W, and intensity was increased by 30 W every 4 min until volitional exhaustion. Capillary blood samples were taken at rest and immediately after each 4-min stage of the GXT. Both the lactate threshold (LT) and V˙O2peak were determined from the GXT (4). LT was calculated using the power output (W) at 4 mmol·L−1 (LT4mM) and the modified Dmax method (LTDmax) (5).
5 × 6-s cycle test.
Each subject completed a standardized warm-up before beginning the 5 × 6-s cycle test (Model Ex-10, Repco, Australia). Toe clips and heel straps were used to secure the feet to the pedals, and each sprint was performed in the standing position. The test consisted of five 6-s maximal sprints departing every 30 s. During the 24-s recovery between sprints, subjects rested (seated) until 5 s before the next sprint, when they assumed the ready position (standing). The method used to determine total work and the decrement (%) in power and work has been described in a previous report (4).
The CIT60 consisted of 60 s of continuous cycling at a set power output on an air-braked, front-access cycle ergometer (Model Ex-10, Repco, Australia). Toe clips and heel straps were used to secure the feet to the pedals, and the test was performed in the seated position. Strong verbal encouragement was provided to each subject during the test. The set power output for CIT60 was based on the mean power output achieved during the pretraining RSA test (5 × 6-s sprints, total of 30 s sprinting). Therefore, the 60-s test was performed at 50% of the mean power (W) recorded during the pretraining 5 × 6-s sprint test. This was an intensity equal to approximately 160% (range = 130-180%) of the pretraining V˙O2peak. The CIT60 was based on mean power during the 30 s of sprinting (5 × 6-s) rather than on the final power output of the extended V˙O2peak and LT test (six to eight 4-min incremental stages) because this better reflects the ability to perform short (60 s) and intense (> V˙O2peak) exercise (3).
3RM strength testing.
Strength of the legs was determined by measuring the maximum mass that could be lifted for three repetitions (3RM) on the horizontal leg press (2). The seat position on the leg press was adjusted so that each participant's knee angle visually appeared to be at 90° at the start of the lift. This seat position was recorded and subsequently used during training and for pre and post 3RM testing. The two familiarization resistance-training sessions were used to determine the appropriate lifting loads during training for all the other exercises.
Within 4-7 d of baseline testing, subjects within the RT group started the high-repetition (15-20) short-rest period (20 s) resistance-training program (5 wk), using a combination of free weights and machines. Both groups continued to perform their normal recreational training. The first six exercises of the resistance-training program involved the leg muscles and included squats (free weights), leg press (machine weight), leg extensions (machine weight), leg curls (machine weight), lunges (free weights), and weighted step-ups (free weights). Additional upper-body exercises were included for variety and completeness in the overall program. These exercises included the bench press (free weights), seated row (machine weights), shoulder press (free weights), lat pull-down (machine weights), and sit-ups. The order of exercise was performed as listed above. For each exercise, all of the stipulated sets were completed before moving onto the next exercise. Each exercise set was performed for 40 s, separated by a 20-s rest period. Because of the short rest periods between exercise bouts, a decline in load during a subsequent set of an exercise was required for the subjects to be able to complete 15-20 repetitions. Therefore, set 1 was performed at 70%, set 2 at 60%, and sets 3-5 at 50% of the 3RM load. Subjects performed two to three sets of each exercise during weeks 1-2 and three to five sets during weeks 3-5. When subjects could complete 20 repetitions of an exercise during two consecutive training sessions, the load was increased by the smallest increment available for that piece of equipment. The increase in weight lifted for the leg press each week was approximately 10%. Before training, each subject performed a 5-min cycle warm-up (~80 W). Training heart rate (polar heart rate monitor, Vantage NV, Finland) and [La−]b (see below) were measured during week 3 of the training program.
Capillary blood sampling and analysis.
A hyperemic ointment (Finalgon, Boehringer Ingelheim, Germany) was applied to the earlobe 5-7 min before initial blood sampling. Glass capillary tubes were used to collect 50 L of blood during the GXT and training (D957G-70-35, Clinitubes, Radiometer, Copenhagen, Denmark) and 100 L of blood during the CIT60 test (D957G-70-125, Clinitubes, Radiometer, Copenhagen, Denmark). Capillary blood samples were taken at rest and immediately after each 4-min stage of the GXT. Capillary blood samples were taken at rest and at the completion of the legs exercises of a training session during week 3. Capillary blood samples were also taken at rest, immediately, and 5 min after the CIT60 test. Blood H+ ([H+]b) and [La−]b were determined using a blood-gas analyzer (ABL 625, Radiometer, Copenhagen, Denmark).
Muscle sampling and analysis.
On the day of the CIT60 cycle test, one incision was made under local anesthesia (5 mL, 1% Xylocaine) into the vastus lateralis of each subject. The incision was used for the pretest biopsy and then closed with a steri strip and subsequently used for the posttest biopsy. Pre- and posttest biopsy samples were taken with the needle inserted at different angles, with manual suction applied for both samples. Every attempt was made to collect the muscle biopsy at the same depth before and after exercise. The first muscle sample was taken (before warm-up) during supine rest. The second muscle sample was taken immediately after the cessation of the CIT60 test, with the subject remaining on the cycle ergometer. All pretraining samples were taken from the right leg, and all posttraining samples were taken from the left leg from approximately the same position. The samples were then removed from the biopsy needle and stored at −80°C until subsequent analysis.
Titration βmin vitro and [H+].
Freeze-dried resting muscle samples (2-3 mg) were dissected free from visible blood, fat, and connective tissue and were homogenized on ice for 2 min in a solution containing sodium fluoride (10 mM) at a dilution of 30 mg of dry muscle per milliliter of homogenizing solution. The muscle homogenate was then placed in a circulating water bath at 37°C for 5 min before and during the measurement of pH. The pH ([H+]) measurements were made with a microelectrode (MI-415, Microelectrodes Inc, Bedford, NH) connected to a pH meter (SA 520, Orion Research Inc, Cambridge, MA). After initial pH measurement, muscle homogenates (rest samples) were adjusted to a pH of approximately 7.2 with a sodium hydroxide (NaOH) (0.02 M) solution and then titrated to a pH of approximately 6.2 by the serial addition of 2 μL of hydrochloric acid (10 mM). From the fitted titration trendline, the number of moles of H+ (per gram of dry muscle) required to change the pH from 7.1 to 6.5 were interpolated. This value was then normalized to the whole pH unit for final display as micromoles H+ per gram of dry muscle per unit of pH (μmol H+·g−1 d.w.muscle·pH−1) and determined as the subject's βmin vitro.
All values are reported as mean ± SD, except Figs. 1-4 (± SE). Two-way ANOVA with repeated measures for time were used to test for interaction and main effects. When an effect was found, LSD post hoc tests were performed to determine where the difference had occurred. The alpha level for statistical significance was set at 0.05.
[La−]b and heart rate during training.
Mean [La−]b and heart rate (as a percent of maximum heart rate) after the leg exercises during a typical training session were 9.1 ± 1.9 mmol·L−1 and 85 ± 2%, respectively.
Body mass, leg strength, and RSA.
There were no significant changes in body mass after the RT or C period (P = 0.56) (Table 1). There were significant increases in leg-press 3RM after the RT period (23%) but not the C period (2%) (P = 0.04; Table 1). There were significant improvements in total work (measured in joules and joules per kilogram of body mass) during the repeated-sprint test (5 × 6-s sprints) after RT (10 and 12%) but not after the C period (1 and 3%; P = 0.04 and 0.03, respectively; Fig. 3). There were also significant improvements in work and peak power during each of the five sprints after RT but not after the C period (P < 0.05, Fig. 4).
V˙O2peak and LT during the GXT.
After 5 wk, there was no significant change in absolute (L·min−1) or relative V˙O2peak (mL·kg−1·min−1) (P = 0.85 and 0.35, respectively) or power (W) at V˙O2peak (P = 0.64) for the RT group or the C group (Table 1). However, the RT group had a nonsignificant improvement in LTdmax (8%, P = 0.10) and significantly improved LT4mM (15%, P < 0.001), with no change for the C group (Table 1).
Changes in [La−]b, [H+]b, and [HCO3−]b during the CIT60.
There were no significant changes in resting [La−]b (P = 0.34), [H+]b (P = 0.31), or [HCO3−]b (P = 0.81) after the RT or C periods (Table 2). After the training period there was a significant reduction in immediate postexericse [La−]b (P < 0.001) and [H+]b (P = 0.01) and an increase in [HCO3−]b (P = 0.04) for the RT group, but not the C group (Table 2). There was also a reduction in 5-min postexercise [La−]b (P < 0.00) and [H+]b (P < 0.001) and an increase in [HCO3−]b (P = 0.02) for the RT group, but not the C group (Table 2).
Changes in V˙O2, CO2, and RER during the CIT60.
There were no significant differences in posttraining V˙O2 (RT: 1.58 ± 0.29, C: 1.68 ± 0.30; P > 0.05), CO2 (RT: 1.53 ± 0.33, C: 1.59 ± 0.37; P > 0.05), or RER (RT: 0.96 ± 0.05, C: 0.94 ± 0.06; P > 0.05) between the two groups during the CIT60. There were also no significant differences in any of these values from pre- to posttraining (P > 0.05).
βmin vitro and [H+]i during the CIT60.
There were no changes in βmin vitro for the RT (132 ± 23 to 135 ± 19 μmol H+·g−1 d.w.muscle·pH−1) or C groups (128 ± 18 to 120 ± 18 μmol H+·g−1 d.w.muscle·pH−1) (P = 0.78). There were also no differences in βmin vitro between the RT and C groups before or after the 5-wk training period (P = 0.28, Fig. 1). However, there was a significant decrease in postexercise [H+]i after RT but not after C (P = 0.05, Fig. 2).
The main finding of the present study was that high-repetition, short-rest period resistance training did not result in significant improvements in βmin vitro but did reduce [H+]i after 60 s of intense exercise (~160% V˙O2peak). The RT group also had a significant reduction in [H+]b and [La−]b during the CIT60. Similar to some previous reports (6), resistance training did not result in significant improvements in V˙O2peak; however, resistance training did improve the LT4mM and leg-press 3RM. The changes in H+ regulation, muscle strength, and the LT4mM are likely to have contributed to the improved repeated-sprint performance after the training period.
High-intensity exercise, and subsequently, a large accumulation of H+, has been suggested to be an important stimulus to increase βmin vitro (11). Despite this, the high-repetition, short-rest period resistance-training program employed in the present study did not increase βmin vitro. Similarly, previous protocols employing leg-extension training have reported no change in βmin vitro (21,25). However, these studies used a single-limb, single-joint exercise design, leaving a greater proportion of inactive tissue, which has been shown to improve lactate/H+ removal compared with multijoint movements or multilimb exercise (1). Consequently, the H+ accumulation during these previous reports may have been insufficient to adequately stress the buffering capacity of the muscle. Therefore, we employed a training protocol that involved both single- and multilimb movements of both legs for extended periods, thus causing a greater H+ accumulation both locally and systemically. The posttraining (after completion of leg exercises) blood lactate data (9.1 ± 1.9 mmol·L−1) indicate that there was a greater systemic H+ accumulation and, therefore, a likely greater muscle H+ accumulation than in previous studies using single-limb, single-joint training (blood lactate 3-4 mmol·L−1) (25). Nevertheless, we did not find significant changes in βmin vitro after training, suggesting that H+ accumulation remained insufficient or that factors in addition to high-intensity exercise and H+ accumulation may significantly affect changes in βmin vitro.
In contrast to the present study, previous research has reported significant improvements in βmin vitro after interval cycle training using short rest periods (1 min) between high-intensity efforts (80-100% V˙O2peak) lasting 2-5 min (11,32). In addition to larger improvements in βmin vitro, high-intensity interval training also resulted in a greater training [La−]b (~16 vs 5 mmol·L−1) than moderate-intensity training (11). Although the blood lactate levels in the present investigation are higher than those reported after moderate-intensity training, they are approximately two thirds of those reported after high-intensity interval training, which did improve βmin vitro. Despite the intense nature of our resistance-training protocol, the H+ accumulation that occurred may still have been insufficient to stimulate changes in βmin vitro.
Compared with a previous investigation that reported an improvement in βmin vitro, the present study employed a different mode of exercise (resistance exercise vs cycling), a different interval length (40 s vs 2 min), and a different between-set recovery (20 s vs 1 min) (11). Also, the total time performing lower-body exercise was less (~40%). Therefore, subjects in the present study may not have spent enough time exercising with a large accumulation of H+ within their muscle to stimulate changes in βmin vitro. The short rest periods used in the present study also required a drop in the training load from set 1 to set 3 of a given exercise (70 to 50% of 3RM). This may have reduced the use of fast-twitch glycolytic fibers and increased the reliance on slow-twitch oxidative fibers, decreasing the accumulation of H+. Therefore, our findings suggest that something more than intense work bouts with short rest periods may be needed to effect changes in βmin vitro.
Although previous resistance training studies have measured changes in βmin vitro and proteins involved in H+ regulation (20,21), this is the first to also measure changes in [H+]i during intense exercise. Although there were no significant improvements in βmin vitro in the present study, there were significant reductions in the accumulation of [H+]b, [La−]b, and [H+]i after the CIT60, indicating an improved H+ regulation. A cross-sectional report has also shown that strength-trained athletes have better H+ regulation than untrained controls during isometric exercise (30). Furthermore, Harber et al. (16) found that [La−]b after a resistance-training session was significantly lower after 10 wk of circuit resistance training (one to three sets of 12-20 reps, 10-30 s of rest, 40-60% 1RM). These and our findings may be attributable to a reduction in H+ production during a given load and/or enhanced H+ removal in resistance-trained subjects.
There was no change in V˙O2peak or in the relative intensity (as a percentage of V˙O2peak) of the CIT60 after training. Furthermore, total V˙O2 during the CIT60 did not change after training. These findings would normally be interpreted to indicate a similar provision of energy from both anaerobic and aerobic metabolism during the CIT60 before and after training. However, previous authors have reported a reduced anaerobic contribution during constant-load, fixed-duration cycling after heavy resistance and sprint training, without changes in whole-body V˙O2 (13,17). These findings may be attributable to a reduced V˙O2 of accessory muscles (i.e., respiratory muscles) or to altered fiber recruitment during the exercise task (13,17). Such adaptations may allow for an elevated oxygen use within the leg muscles used during cycling, without significant changes to whole-body V˙O2, resulting in a reduced reliance on anaerobic energy sources (and less H+ production) during high-intensity exercise.
Although reports employing heavy resistance training (three to five sets of two to eight reps at approximately 80% 1RM) have not typically reported changes in aerobic enzymes or V˙O2peak (15), training studies using longer work bouts (six sets of 15-20 repetitions or repeated isokinetic knee extension for 30 s) similar to those used in the present study have reported an increase in aerobic enzymes, despite little change in V˙O2peak (8,28). Although we did not measure aerobic enzymes in the present report, we did find an increase in the LT after training, suggesting that there may have been an increase in the oxidative capacity within the muscle of the RT group (18). Therefore, the reduced H+ accumulation during high-intensity exercise in the present study may be associated with an altered mitochondrial potential of the muscle (28) not detected by changes in V˙O2peak.
The lower H+ accumulation after training is more likely related to an improved ion-transport capacity of the muscle. Previously, 5 wk of moderate-intensity resistance training was reported not to increase the content of the Na+/H+ exchanger (10), although it did increase the content of the La−/H+ cotransporter (20). The subjects employed in these studies were sedentary and much older compared with the active young adults employed in the present study. Nevertheless, resistance training can increase the content/activity of other ion-transport proteins (i.e., Na+/K+ pump) in young and well-trained adults and, therefore, may also increase the content/activity of H+-transport proteins in young adults such as those recruited for the present study (14). Such changes to H+-transport proteins in the present study may have contributed to the decrease in H+ accumulation during exercise at the same absolute load.
The findings from the present study and from a previous report (21) suggest that high-repetition resistance training does not increase βmin vitro and, therefore, that changes to the buffering of H+ within the muscle did not contribute to the improved muscle H+ regulation by our subjects. Similarly, others have reported improved muscle H+ regulation during intense exercise (130% V˙O2peak), without changes to βmin vitro, after sprint training (17). They suggested that other regulatory mechanisms may have affected H+ accumulation, such as a reduction in the disturbance to the strong ion difference ([SID]). Although the effects of resistance training on the [SID] are unknown, previous reports suggest that sprint- and endurance training can positively affect the [SID], reducing the accumulation of H+ during high-intensity exercise (22,26). Resistance training increases the content of proteins involved in the regulation of strong ions (i.e., La− and K+ regulation) (10,14,20) and, subsequently, may alter the [SID], thereby reducing the [H+]i during intense exercise.
We show for the first time that resistance training can improve the ability to perform short (5 × 6 s) repeated sprints interspersed by short recovery periods (24 s) similar to those encountered in some team sports. Although little research has investigated the effects of resistance training on repeated-sprint performance, previous reports have identified a relationship between maximal strength and single-sprint performance in team-sport athletes (r = 0.71, P < 0.05) (23). There was, however, no such relationship reported between strength and sprint decrement during repeated sprints in team-sport athletes (23). Furthermore, although sprint training has been shown to improve sprint performance (17), the effects of heavy resistance training on single-sprint performance are mixed. Heavy resistance training has been shown to increase the initital but not the later performance during a long (60 s) single sprint (8). These findings may be attributable to the positive relationship that has previously been reported between initial sprint performance and the power decrement during repeated sprints, which is likely attributable to a greater metabolic disturbance by those with a greater initial power output (7). This suggests that although heavy resistance training may improve an initial sprint, it may not improve repeated-sprint performance.
Our results show that high-repetition resistance training that includes a high metabolic load (because of short rest periods) can improve repeated-sprint performance (peak and mean power). Furthermore, improvements in total work during short repeated sprints after our high-repetition short-rest period resistance training (10-12%) were similar to those reported after high-intensity interval (13%) (12) and sprint training (12%) (24). However, in contrast to the previously reported interval training, our subjects did not improve their V˙O2peak. A high V˙O2peak has been associated with the recovery of sprint performance in untrained subjects, and therefore, changes in V˙O2peak have been thought to be important to improve RSA (4). However, similar to Ortenblad et al. (24), who employed a repeated-sprint training protocol, the results of the present study show that improvements in brief (< 10 s) repeated sprints with short recovery periods (< 30 s) may occur independently of changes in V˙O2peak.
The only other resistance-training study to measure RSA recruited resistance-trained males and employed moderate to heavy resistance-training methods (five sets of 10 repetitions) (27). Despite a differing subject population and training methods, they reported improvements in RSA similar to those seen in the present study (total work, ~9%). Although they show that heavy resistance training can improve repeated sprints with long recovery periods between efforts (15 × 5 s, 50 s of rest between sprints), we have also shown that high-repetition resistance training can increase RSA with short recovery periods between efforts (5 × 6 s, 24 s of rest between sprints), similar to what is encountered in some team-sport situations. Indeed, because of the short rest period used in the present study, our subjects had large decreases in performance from sprints 1 to 5, before and after training (Fig. 4). However, the improvement in performance after training was similar for sprints 1 to 5 (Fig. 4), indicating that the training intervention not only improved single-sprint performance but also improved the performance of subsequent sprints. The increase in both initial and later sprint performance in the present study may have been caused by the metabolic adaptations that had occurred. Indeed, previous authors have identified an association between H+ regulation, LT, and repeated-sprint performance (4); therefore, these changes may have contributed to the improved RSA in the present study.
We did not find improvements in βmin vitro after 5 wk of high-repetition (15-20) short-rest period (20 s) resistance training. Despite no improvement in βm, there was a reduced accumulation of H+ within the muscle and blood after intense exercise (~160% V˙O2peak intensity; CIT60). This may have been caused by a reduced production of H+ and/or improved H+ removal. Although it did not improve V˙O2peak, the resistance training program did significantly improve LT4mM and strength. It is likely that the increases in strength, H+ regulation, and LT contributed to the improvement in repeated-sprint performance after training.
1. Ahlborg, G., L. Hagenfeldt, and J. Wahren. Substrate utilization by the inactive leg during one-leg or arm exercise. J. Appl. Physiol.
2. Baechle, T. R., R. W. Earle, and D. Wathen. Resistance training. In: Essentials of Strength Training and Conditioning,
T. R. Baechle and R. W. Earle (Eds.). Champaign, IL: Human Kinetics, 2000, pp. 407-412.
3. Barnett, C., D. Jenkins, L. T. Mackinnon, and S. Green. A new method for calculation of constant supra-VO2 peak power outputs. Med. Sci. Sports Exerc.
4. Bishop, D., J. Edge, and C. Goodman. Muscle buffer capacity and aerobic fitness are associated with repeated-sprint ability in women. Eur. J. Appl. Physiol.
5. Bishop, D., D. G. Jenkins, and L. T. Mackinnon. The relationship between plasma lactate parameters, Wpeak and 1-h cycling performance in women. Med. Sci. Sports Exerc.
6. Bishop, D., D. G. Jenkins, L. T. Mackinnon, M. McEniery, and M. F. Carey. The effects of strength training on endurance performance and muscle characteristics. Med. Sci. Sports Exerc.
7. Bishop, D., and M. Spencer. Determinants of repeated-sprint ability in well-trained team-sport athletes and endurance-trained athletes. J. Sports Med. Phys. Fitness
8. Costill, D. L., E. F. Coyle, W. Fink, G. R. Lesmes, and F. A. Witzmann. Adaptations in skeletal muscle following strength training. J. Appl. Physiol.
9. 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.
10. Dela, F., M. Holten, and C. Juel. Effect of resistance training on Na,K pump and Na+/H+ exchange protein densities in muscle from control and patients with type 2 diabetes. Pflugers Arch.
11. Edge, J., D. Bishop, and C. Goodman. The effects of training intensity on muscle buffer capacity in females. Eur. J. Appl. Physiol.
12. Edge, J., D. Bishop, C. Goodman, and B. Dawson. Effects of high- and moderate-intensity training on metabolism and repeated sprints. Med. Sci. Sports Exerc.
13. Goreham, C., H. J. Green, M. Ball-Burnett, and D. Ranney. High-resistance training and muscle metabolism during prolonged exercise. Am. J. Physiol.
14. Green, H., A. Dahly, K. Shoemaker, C. Goreham, E. Bombardier, and M. Ball-Burnett. Serial effects of high-resistance and prolonged endurance training on Na+-K+ pump concentration and enzymatic activities in human vastus lateralis. Acta Physiol. Scand.
15. Green, H., C. Goreham, J. Ouyang, M. Ball-Burnett, and D. Ranney. Regulation of fiber size, oxidative potential, and capillarization in human muscle by resistance exercise. Am. J. Physiol.
16. Harber, M. P., A. C. Fry, M. R. Rubin, J. C. Smith, and L. W. Weiss. Skeletal muscle and hormonal adaptations to circuit weight training in untrained men. Scand. J. Med. Sci. Sport
17. Harmer, A. R., M. J. McKenna, J. R. Sutton, et al. Skeletal muscle metabolic and ionic adaptations during intense exercise following sprint training in humans. J. Appl. Physiol.
18. Ivy, J. L., R. T. Withers, P. J. Van Handel, D. H. Elger, and D. L. Costill. Muscle respiratory capacity and fiber type as determinants of the lactate threshold. J. Appl. Physiol.
19. Juel, C. Muscle pH regulation: role of training. Acta Physiol. Scand.
20. Juel, C., M. K. Holten, and F. Dela. Effects of strength training on muscle lactate release and MCT1 and MCT4 content in healthy and type 2 diabetic humans. J. Physiol.
21. Mannion, A. F., P. M. Jakeman, and P. L. T. Willan. Effects of isokinetic training of the knee extensors on high-intensity exercise performance and skeletal muscle buffering. Eur. J. Appl. Physiol.
22. McKenna, M. J., G. J. F. Heigenhauser, R. S. McKelvie, J. D. MacDougall, and A. M. Jones. Sprint training enhances ionic regulation during intense exercise in men. J. Physiol.
23. Newman, M. A., K. M. Tarpenning, and F. E. Marino. Relationships between isokinetic knee strength, single-sprint performance, and repeated-sprint ability in football players. J. Strength Cond. Res.
24. Ortenblad, N., P. K. Lunde, K. Levin, J. L. Anderson, and P. K. Pederson. Enhanced sarcoplasmic reticulum calcium release following intermittent sprint training. Am. J. Physiol.
25. Pilegaard, H., K. Domino, T. Noland, et al. Effect of high-intensity exercise training on lactate/hydrogen ion transport capacity in human skeletal muscle. Am. J. Physiol.
26. Putman, C. T., N. L. Jones, and G. J. Heigenhauser. Effects of short-term training on plasma acid-base balance during incremental exercise in man. J. Physiol.
27. Robinson, J. M., M. H. Stone, R. L. Johnson, C. M. Penland, B. J. Warren, and D. R. Lewis. Effects of different weight training exercise/rest intervals on strength, power, and high intensity exercise endurance. J. Strength Cond. Res.
28. Sale, D. G., J. D. MacDougall, I. Jacobs, and S. Garner. Interaction between concurrent strength and endurance training. J. Appl. Physiol.
29. Schott, J., K. McCully, and O. M. Rutherford. The role of metabolites in strength training. Eur. J. Appl. Physiol.
30. Sinoway, L. I., R. F. Rea, T. J. Mosher, M. B. Smith, and A. L. Mark. Hydrogen ion concentration is not the sole determinant of muscle metaboreceptor responses in humans. J. Clin. Invest.
31. Westerblad, H., D. G. Allen, and J. Lannergren. Muscle fatigue: lactic acid or inorganic phosphate the major cause? News Physiol. Sci.
32. Weston, A. R., K. H. Myburgh, F. H. Lindsay, S. C. Dennis, T. D. Noakes, and J. A. Hawley. Skeletal muscle buffering capacity and endurance performance after high-intensity interval training by well-trained cyclists. Eur. J. Appl. Physiol.