Training Session 1
Sprint running times in 60, 80, and 100 meters were 6.88 ± 0.08, 8.94 ± 0.06, and 11.23 ± 0.13 seconds, respectively.
Figure 1 shows height in vertical jump and blood lactate and ammonia concentrations during training sessions 1 (Figure 1; session 1), 2 (Figure 1; session 2), and 3 (Figure 1; session 3). Figure 1 (session 1) shows that there was a marked increase in blood lactate concentration in both athletes between the sixth and the last running bout, although the increase was more pronounced in athlete 1 (from 13 to 16 mmol·L−1) than in athlete 2 (from 13.8 to 15 mmol·L−1). From the first running bout, blood ammonia levels progressively increased in athlete 1, reaching values near 75-100 μmol·L−1 during the last running bouts. However, in athlete 2, blood ammonia remained near resting values (≤50 μmol·L−1) throughout the training session. Jumping height remained relatively constant during the first 4-5 running bouts, and they later fell during the remaining work periods. The decline in jumping height was higher in the athlete showing higher initial jumping height values (19%; athlete 1) than in the athlete with lower initial levels (13%; athlete 2).
Training Session 2
Sprint running times during the 6 × 100-m running bouts (11.78 ± 0.15 seconds; range: 11.43-11.99 seconds) were slightly higher than those programmed (11.50 seconds; p < 0.01).
Figure 1 (session 2) shows that there was a gradual and parallel increase in blood lactate and ammonia concentrations in both athletes during the training session. At the end of the last running bout analyzed, athlete 3 presented higher blood lactate (15 vs. 13.6 mmol·L−1) and ammonia levels (90 vs. 75 μmol·L−1) than athlete 4. Jumping height remained relatively constant during the first 3-5 running bouts and later fell during the last 4 running bouts in athlete 3 and the last running bout in athlete 4. The decline in jumping height was higher in the athlete showing higher initial jumping height (11%; athlete 3) than in the athlete with lower initial levels (6%; athlete 4).
Training Session 3
Running times during the 8 × 200-m running bouts (25.68 ± 0.52 seconds; range: 24.64-26.66 seconds) were slightly lower than those programmed (26.00 seconds; p < 0.05).
Figure 1 (session 3) shows that blood ammonia concentrations presented a similar pattern in both athletes because they remained near resting values during the first 3 running bouts, after which the concentration tended to increase progressively. Blood ammonia and blood lactate concentrations in the athletes after the last running bout were near 100 μmol·L−1 and 19-20 mmol·L−1, respectively. Height in vertical jump remained relatively constant during the first 4 running bouts and later fell during the remaining work periods. It is noteworthy that the decline in jumping height (18%) at the end of the training session was similar in both athletes, who presented similar initial jumping height.
Training Session 4
Running times during the 6 × 300-m running bouts (40.66 ± 0.90 seconds; range: 39.60-42.11 seconds) were similar than those programmed (40.80 seconds). Athlete 7 could only complete 5 of the 6 programmed running bouts because of exhaustion.
Figure 2 shows vertical jumping height and blood lactate and ammonia concentrations during training sessions 4 (Figure 2; session 4), 5 (Figure 2; session 5), and 6 (Figure 2; session 6). Figure 2 (session 4) shows that blood lactate concentration rose sharply during the first 2 running bouts, followed by a more gradual increase. At the end of the exercise, blood lactate values were 19.2 mmol·L−1 (athlete 7) and 17 mmol·L−1 (athlete 8). From the first running bout, blood ammonia levels progressively increased in athlete 7, reaching values around 100 μmol·L−1 during the last running bouts. However, blood ammonia remained near resting values in athlete 8 throughout the training session. Jumping height remained relatively constant during the first 3-4 running bouts and later fell during the remaining work periods.
Training Session 5
Running times during the 3 × 3 × 300-m running bouts (40.88 ± 0.36 seconds; range: 40.03-41.35 seconds) were similar to the programmed time (40.80 seconds).
Figure 2 (session 5) shows that there was a progressive increase in blood lactate concentration in both athletes between the third and the last running bouts, although the increase was more pronounced in athlete 9 (from 12 to 18.5 mmol·L−1) than in athlete 10 (from 11 to 17 mmol·L−1). Blood ammonia concentration and height in vertical jump remained near resting values until the last 2 running bouts, after which the values tended to progressively increase (ammonia) and decrease (jumping height), respectively. The decline in jumping height was higher in the athlete with higher initial jumping height (10%; athlete 10) than in the athlete with lower initial levels (7%; athlete 9).
Training Session 6
Running times during the 12 × 300-m running bouts (43.11 ± 1.12 seconds; range: 41.80-45.28 seconds) were higher than those programmed (42.50 seconds; p < 0.05). Athlete 11 could only complete 11 of the 12 programmed running bouts because of exhaustion.
Figure 2 (session 6) shows that at the end of the last running bout (11th and 12th running bout for athlete 11 and 12, respectively), athlete 12 presented higher blood lactate concentrations (22 mmol·L−1) than athlete 11 (18 mmol·L−1). Blood ammonia and jumping height remained near resting values until the fourth (athlete 11) or the fifth (athlete 12) running bouts, after which the values tended to progressively increase (ammonia) and decrease (jumping height), respectively. The fall in jumping height after the last work repetition (11th) done by both athletes was higher in the athlete showing higher initial jumping height (9%; athlete 11) than in the athlete with lower initial levels (5%; athlete 12).
Relationships Among Height in Vertical Jump, Blood Lactate, and Blood Ammonia Concentration
Figure 3 shows the significant (p < 0.05; R2 = 0.51) curvilinear negative relationship between individual values of blood ammonia concentration and individual values of jumping height (expressed as a percentage of the individual maximum jumping height attained during the training sessions).
This relationship illustrates that when blood ammonia levels did not exceed the approximate upper limit of the rest reference range (40-50 μmol·L−1), jumping height did not change significantly from maximum values. However, when blood ammonia values approximately exceeded the upper limit of the rest reference range, the jumping height decreased sharply.
The significant (p < 0.05; R2 = 0.68) curvilinear negative relationship between the individual values of blood lactate concentration and the individual values of jumping height (expressed as a percentage of the individual maximum jumping height attained during the training sessions) is showed in Figure 4.
For blood lactate levels not exceeding 8-12 mmol·L−1, the jumping height did not change significantly from maximum values. However, when blood lactate concentrations approximately exceeded 8-12 mmol·L−1, the jumping height decreased sharply. The data are consistent with a sharp decrease in jumping height when whole blood lactate levels exceed approximately 8-12 mmol·L−1.
Figure 5 shows the curvilinear significant (p < 0.05; R2 = 0.80) positive relationship between individual values of blood lactate concentration and individual values of blood ammonia.
This relationship illustrates that blood ammonia levels did not change significantly from the upper limit of the rest reference range (40-50 μmol·L−1) for blood lactate concentrations not exceeding approximately 8-12 mmol·L−1. However, when blood lactate concentrations approximately exceeded the level of 8-12 mmol·L−1, a sharp increase in blood ammonia levels above the rest reference range was observed.
To our knowledge, this is the first study describing metabolic and neuromuscular performance characteristics of several typical training sessions in a group of elite 400-m running athletes. The present results show that, although the high-intensity intermittent training sessions programmed were very diverse in principle, their physiological responses were nevertheless quite similar because a similar pattern of high blood lactate (14-23 mmol·L−1) and ammonia levels (50-100 μmol·L−1) was observed at the end of all the training sessions. These extremely high levels of blood lactate have also been found in 400-m runners during high-intensity treadmill running sessions (23) or after official competitions (19) and have been associated with increased muscle lactate production (3,7,12,20) with large reductions in muscle glycogen (12,26), particularly in type IIx fibers (7), whereas blood and muscle pH can reach values as low as 7.0 (20) and 6.0 (3), respectively. This suggests that anaerobic glycogenolysis is extensively activated during these types of exercises, preferentially in type IIx muscle fibers (12). The training sessions analyzed in the present study may be considered as specific types of training because they allow the successful reproduction of the physiological responses observed during official 400-m running competitions in elite athletes (19).
The appearance of high blood ammonia levels during these types of high-intensity intermittent exercises is primarily considered as an effect of accelerated ammonia formation in muscle associated with the very specific role that phosphagens play during this type of exercise (17,31). Thus, the metabolic demand of such types of intermittent exercise requires a high skeletal muscle ATP turnover that usually results in large reductions in muscle PCr concentrations (3,7,12,20) and in the muscles' ability to match the rate of ATP supply with its rate of utilization, thereby causing a marked reduction of skeletal muscle ATP content (4,17,31), particularly in type IIx fibers (7). This fall in muscle ATP content is closely linked to an increase in muscle adenosine monophosphate (AMP) levels (17,31), its deamination by AMP deaminase, and a corresponding increase of muscle inosine monophosphate (IMP) levels and muscle and blood ammonia concentrations (17,31), resulting in an accelerated purine nucleotide degradation and a loss of total adenine nucleotides from the muscle (14). Therefore, it can be suggested that the high blood ammonia levels observed during the high-intensity intermittent exercises analyzed in this study may represent an extracellular marker of pronounced muscle ammonia production and its net diffusion in the blood, associated to a decline in muscle adenine nucleotide stores, mainly by a pronounced reduction in muscle ATP content (17,31).
A significant relationship was observed in the present study between individual levels of blood lactate and individual levels of blood ammonia (Figure 5). The curvilinear fashion of the curve reveals that blood ammonia remained near resting levels for blood lactate levels lower than 8-12 mmol·L−1, but when blood lactate concentration exceeded 8-12 mmol·L−1, blood ammonia levels increased abruptly from rest values compared with blood lactate concentrations. A threshold of a sharp upward break point in blood ammonia accumulation corresponding to whole blood lactate levels of approximately 12 mmol·L−1 or to plasma lactate levels of 14 mmol·L−1 has been observed in recreationally active subjects (28) and in low-level 400-m runners (27). This finding is compatible with some reports in humans (14), showing that muscle ammonia and H+ accumulation and release in blood during high-intensity exercise does not begin until high muscle and blood lactate levels are reached and muscle pH is below a certain level. The significant relationship observed between blood lactate and blood ammonia levels in the present study allows for elite 400-m runner coaches to indirectly estimate the magnitude of degree of blood ammonia accumulation during high-intensity intermittent exercises from blood lactate concentration values.
In the majority of the training sessions analyzed, the 400-m runners who showed the greatest initial vertical height values during vertical jump tended to have the largest decreases in vertical height values with successive sprints. This is in line with previous investigations performed with track and field jumpers (5) and national level sprint runners (24), where individuals with high initial performance of short duration, such as vertical jump (5,24) or peak power output during cycloergometer sprints (3), demonstrated greater susceptibility to fatigue (5,24) during high-intensity exercise than individuals with lower performance of short duration. This greater susceptibility to fatigue has been associated with a higher proportion of fast twitch (FT) fibers (5), lower capillary density (18), oxidative enzyme content (18), and endurance fitness status (3). From a practical point of view, this suggests that 400-m athletes with higher initial vertical jump performances have more rapid muscle contraction failure and recover more slowly because their muscles are probably made up of a high proportion of FT muscle fibers. Therefore, 400-m runners with higher initial vertical jump performances should rest for longer between-exercise bouts during high-intensity training sessions than athletes with lower initial vertical jump performances, to maintain the same relative capability of leg extensor muscles to generate more mechanical power throughout the training session. The large variation in vertical jump profiles observed among the 400-m runners stresses the importance of following an individualized modeling approach to monitor training sessions in elite athletes who are homogeneous in performance.
A common picture during the training sessions analyzed was that vertical jumping performance was maintained during the initial exercise bouts up to a point of further increase in the number of exercise bouts, caused a pronounced loss in vertical jumping performance. In addition, significant negative curvilinear relationships were found between the individual values of vertical jump performance (as a percentage of the individual maximum values) and individual values of blood ammonia, as well as individual values of blood lactate concentrations (Figures 3 and 4). It indicates that force generating capacity during vertical jump performance began to decrease sharply when blood ammonia concentrations approximately exceed physiological rest values (45-50 μmo·L−1) or when blood lactate concentrations exceed 8-12 mmol·L−1. Associations between vertical jump performance and blood lactate concentrations have also been found in lower level 400-m runners performing single sprints from 100 to 400 m, with rest periods of 5-24 hours between the runs, at the velocity of the 400 m (22). The observed relationship between decreases in vertical jump performance and increases in blood ammonia concentrations above rest values (an indirect marker of reduced skeletal ATP content (17,31)) support previous findings (1,2), which suggests that decreased availability of ATP or PCr levels or both in a substantial fraction of the fast or twitch high-glycolytic fibers may be a significant contribution factor of fatigue.
Although the concentrations of intramuscular ATP or PCr stores were not directly measured in this study, the relationships observed among blood ammonia, blood lactate concentration, and vertical jumping performance allow us to differentiate 2 main exercise modes in each of the studied training sessions, in terms of energy status. (a) The first exercise bout characterized by blood ammonia concentrations and vertical jumping performance not changing from physiological resting levels, while blood lactate levels do not exceed 8-12 mmol·L−1. Previous studies have shown that the energy status is maintained in this metabolic situation because muscular PCr levels fall by less than 60-70% (25,26), muscle ATP levels and adenine nucleotide pool values do not change (2,25,26), and maximal running velocity is maintained (1,2). (b) When the number of repetition bouts is increased, there is a given critical number of repetitions beyond which an increase in blood ammonia concentrations above rest values and a continuous increase in blood lactate that may reach values up to 13-30 mmol·L−1 at the end occur, although vertical jumping performance is progressively decreased. In this metabolic situation, exercise has been associated with signs of energetic deficiency and delayed functional recovery because muscle PCr stores are almost completely broken down (3,25,26), leading to a significant decrease in muscle ATP levels (20,26) and adenine nucleotide pool, particularly in type II fibers (7,25), whereas maximal running velocity is decreased (1,2,25). The practical application for an efficient control of training loads is that the measurement of vertical jumping performance could be used during high-intensity intermittent training sessions to indirectly estimate the functional state of the muscle contractile machinery associated with the ability to regenerate ATP at high rates.
As mentioned in the Introduction, 2 main different modes of high-intensity intermittent training sessions (leading either to medium or to high blood lactate levels) can be differentiated in terms of energy status. However, the fact is that the great majority of the usual training sessions programmed into the training schedule of 400-m elite athletes during the precompetition or competition phase usually lead to extremely high blood lactate and ammonia levels and decreased force generating capacity. These types of training sessions are very popular among athletes and coaches and are recommended mainly on the basis of subjective observations and experience in the field. The reason why 400-m running coaches conduct little, if any, high-intensity intermittent training sessions leading to middle-range blood lactate levels (8-12 mmol·L−1 or lower) is unknown. Few studies have examined the effects of intermittent training leading to blood lactate values stabilized around 8-12 mmol·L−1 on anaerobic performance (9,11,16,21,32). These studies have found, in physically active or endurance-trained subjects, that after training 3-4 times a week for 6-8 weeks, significant increases were observed in maximal voluntary strength of the knee extensor muscles (32), vertical jump (32), running sprint performance (9,16,21,32), buffer capacity (11), monocarboxylate transporter 1 (21), and the activity of high energy phosphate transferring enzymes (32), whereas the percentage of type II fibers (9,32) or the total amount of muscle phosphagen (9,16,32) was also increased or unchanged. Taking into consideration these positive effects observed on anaerobic performance, it is conceivable that increasing the frequency of this type of training with lower metabolic stress and decreasing the frequency of the traditional training leading to extremely high blood lactate levels should allow athletes to practice at competitive intensity of exercise for more frequent training sessions with lower fatigue. This lower fatigue should play a role in preventing or avoiding negative effects (e.g., increased generation of free radicals and cell necrosis (29), muscle protein wasting (8), increased type I muscle fiber percentage (10), unchanged buffering capacity (13) and performance (10), muscle purine loss from muscle exceeding the rate of purine salvage (12), and decreased resting levels of skeletal muscle adenine nucleotides (13,31)) observed after traditional training with extremely high anaerobic lactacid demands, when this type of training is repeated too frequently.
In conclusion, high blood lactate (14-23 mmol·L−1) and ammonia levels (50-100 μmol·L−1) were observed during 6 habitual high-intensity intermittent training sessions of varying duration and intensity performed by elite male 400-m athletes. Vertical jumping performance was maintained during the initial exercise bouts up to a point of further increase in the number of exercise bouts, caused a pronounced decrease in vertical jumping performance, particularly in subjects with the highest initial vertical jump. The relationships observed among blood ammonia, blood lactate, and vertical jumping performance suggest that vertical jumping performance approximately begins to decrease when blood lactate concentration exceeds 8-12 mmol·L−1 and blood ammonia levels increase abruptly from rest values. The decrease in vertical jumping performance may indirectly reflect a state of energy deficit of the muscle contractile machinery associated with the inability to regenerate ATP at high rates. Further studies are required to accurately determine the most efficient combination in an annual program of training sessions with and without signs of energy deficit resulting in the greatest improvement in 400-m running performance.
This study has practical importance in that it shows that (a) the high-intensity intermittent training sessions performed regularly by elite 400-m runners may be considered as specific types of training because they allow the successful reproduction of the physiological responses observed during official 400-m running competitions in elite athletes; (b) the significant relationship observed between blood lactate and blood ammonia levels in the present study allows for elite 400-m runner coaches to indirectly estimate the magnitude of degree of blood ammonia accumulation during high-intensity intermittent exercises from blood lactate concentration values; (c) 400-m runners with higher initial vertical jump performances should rest for longer between-exercise bouts during high-intensity training sessions than athletes with lower initial vertical jump performances, to maintain the same relative capability of leg extensor muscles to generate more mechanical power throughout the training session; (d) the measurement of vertical jumping performance could be used during high-intensity intermittent training sessions to indirectly estimate the functional state of the muscle contractile machinery associated with the ability to regenerate ATP at high rates; and (e) it is conceivable that increasing the frequency of high-intensity intermittent training sessions, leading either to medium blood lactate levels (lower than 8-12 mmol·L−1) and blood ammonia concentrations or vertical jumping performance not changing from physiological basal levels, and decreasing the frequency of the traditional training, leading to extremely high blood lactate levels, should allow athletes to practice at competitive intensity of exercise for more frequent training sessions with lower fatigue.
This study was supported in part by grants from Association of Olympics Sports (Madrid, Spain) and from the Instituto Navarro del Deporte (Gobierno de Navarra, Spain).
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Keywords:© 2010 National Strength and Conditioning Association
sprint training; track and field; metabolic response; explosive force