[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.
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Keywords:©2006The American College of Sports Medicine
HIGH REPETITION,; SHORT REST PERIOD,; HIGH INTENSITY,; BLOOD LACTATE