In trained cyclists, β-alanine supplementation did not significantly improve 4-min cycling performance; however, there may be a small meaningful improvement in performance. Acute NaHCO3 supplementation significantly improved 4-min cycling performance. There seemed to be a minimal additive effect of combined β-alanine and NaHCO3 supplementation.
Purpose: To compare the training-intensity distribution (TID) across an 8-week training period in a group of highly trained middle-distance runners employing 3 different methods of training-intensity quantification. Methods: A total of 14 highly trained middle-distance runners performed an incremental treadmill test to exhaustion to determine the heart rate (HR) and running speed corresponding to the ventilatory thresholds (gas-exchange threshold and respiratory-compensation threshold), as well as fixed rating of perceived exertion (RPE) values, which were used to demarcate 3 training-intensity zones. During the following 8 weeks, the TID (total and percentage of time spent in each training zone) of all running training sessions (N = 695) was quantified using continuous running speed, HR monitoring, and RPE. Results: Compared with the running-speed-derived TID (zone 1, 79.9% [7.3%]; zone 2, 5.3% [4.9%]; and zone 3, 14.7% [7.3%]), HR-demarcated TID (zone 1, 79.6% [7.2%]; zone 2, 17.0% [6.3%]; and zone 3, 3.4% [2.0%]) resulted in a substantially higher training time in zone 2 (effect size ± 95% confidence interval: −1.64 ± 0.53; P < .001) and lower training time in zone 3 (−1.59 ± 0.51; P < .001). RPE-derived TID (zone 1, 39.6% [8.4%]; zone 2, 31.9% [8.7%]; and zone 3, 28.5% [11.6%]) reduced time in zone 1 compared with both HR (−5.64 ± 1.40; P < .001) and running speed (−5.69 ± 1.9; P < .001), whereas time in RPE training zones 2 and 3 was substantially higher than both HR- and running-speed-derived zones. Conclusion: The results show that the method of training-intensity quantification substantially affects computation of TID.
β-alanine supplementation has become a common practice among competitive athletes participating in a range of different sports. Although the mechanism by which chronic β-alanine supplementation could have an ergogenic effect is widely debated, the popular view is that β-alanine supplementation augments intramuscular carnosine content, leading to an increase in muscle buffer capacity, a delay in the onset of muscular fatigue, and a facilitated recovery during repeated bouts of high-intensity exercise. β-alanine supplementation appears to be most effective for exercise tasks that rely heavily on ATP synthesis from anaerobic glycolysis. However, research investigating its efficacy as an ergogenic aid remains equivocal, making it difficult to draw conclusions as to its effectiveness for training and competition. The aim of this review was to update, summarize, and critically evaluate the findings associated with β-alanine supplementation and exercise performance with the most recent research available to allow the development of practical recommendations for coaches and athletes. A critical review of the literature reveals that when significant ergogenic effects have been found, they have been generally shown in untrained individuals performing exercise bouts under laboratory conditions. The body of scientific data available concerning highly trained athletes performing single competition-like exercise tasks indicates that this type of population receives modest but potentially worthwhile performance benefits from β-alanine supplementation. Recent data indicate that athletes may not only be using β-alanine supplementation to enhance sports performance but also as a training aid to augment bouts of high-intensity training. β-alanine supplementation has also been shown to increase resistance training performance and training volume in team-sport athletes, which may allow for greater overload and superior adaptations compared with training alone. The ergogenic potential of β-alanine supplementation for elite athletes performing repeated high-intensity exercise bouts, either during training or during competition in sports which require repeated maximal efforts (e.g., rugby and soccer), needs scientific confirmation.
Introduction The aim of this study was to determine whether muscle oxidative capacity is influenced by alterations in training volume in middle-distance runners. Methods Twenty-four highly trained middle-distance runners (n = 16 males; V˙O2peak = 73.3(4.3) mL·kg−1·min−1; n = 8 females, V˙O2peak = 63.2(3.4) mL·kg−1·min−1) completed 3 wk of normal training (NormTr), 3 wk of high-volume training (HVTr; a 10%, 20%, and 30% increase in training volume during each successive week from NormTr), and a 1-wk taper (TapTr; 55% exponential reduction in training volume from HVTr week 3). Before and immediately after each training period, the rate of recovery of muscle oxygen consumption (mV˙O2) of the gastrocnemius medialis was measured using near-infrared spectroscopy, with the rate constant indicating muscle oxidative capacity. Time to exhaustion (TTE) and V˙O2peak were determined during a maximal incremental treadmill test. Results Twelve subjects were classified as being functionally overreached (FOR) after HVTr (decreased running TTE and high perceived fatigue), whereas the other 12 subjects were classified as acutely fatigued (AF; no decrease in running TTE). The AF group demonstrated a significant increase in muscle oxidative capacity after HVTr (rate constant: 15.1% ± 9.7% min−1; P = 0.009), with no further improvement after TapTr, whereas there was no change in muscle oxidative capacity for FOR at any time point (P > 0.05). Compared with the FOR group, the AF group had substantially larger improvements in TTE from pre-HVTr to post-TapTr (FOR, 8.8% ± 3.7%; AF, 3.2% ± 3.0%; P = 0.04). Conclusion The present study was able to demonstrate that muscle oxidative capacity was increased in response to a period of HVTr, but only in runners who did not develop FOR. Furthermore, runners who did not develop FOR had substantially larger performance improvements after a taper period.
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