MITTLEMAN, KAREN D.; RICCI, MATTHEW R.; BAILEY, STEPHEN P.
Decrements in prolonged exercise performance during heat stress have been attributed to reductions in blood or plasma volume(33,43), reductions in muscle blood flow(32,43), accelerated rates of muscle glycogen depletion (13), and blood lactate accumulation(13,26). More recently Nielsen et al.(36,37,44) have demonstrated that the earlier onset of fatigue during uphill treadmill walking in the heat(40°C) when compared with that in a cool environment (18°C) was not associated with the factors cited above. Nielsen (36) proposed that heat stress per se may have hastened fatigue through a reduction in the function of motor centers in the brain, alteration of motor unit recruitment, or a decreased motivation for activity. Brück and Olschewski (8) have also reported the drive to exercise is reduced when mean body temperature is elevated.
One possible mechanism for the occurrence of “central fatigue” during prolonged exercise has been described by Newsholme et al.(34,35). Briefly, this hypothesis suggests that the rise in the concentration of plasma free fatty acids (FFA) as a result of prolonged exercise (16) may lead to the displacement of the amino acid tryptophan (TRP) from albumin. Increases in the plasma concentration of unbound, or free tryptophan (F-TRP), result in increased transport of TRP across the blood brain barrier and synthesis of the neurotransmitter serotonin (5-hydroxytryptamine (5-HT)). Since F-TRP and the branched-chain amino acids (BCAA = leucine, isoleucine, and valine) use the same transport mechanism to cross the blood brain barrier (39), the ratio of F-TRP:BCAA has been proposed to be important in determining the rate of 5-HT synthesis(12). In addition to the potential rise inF-TRP, BCAA uptake and metabolism by skeletal muscle has been reported to be enhanced during prolonged exercise(1,17,47), thus further increasingF-TRP:BCAA. Elevated levels of 5-HT have been linked to feelings of lethargy in humans (49) and are associated with fatigue during prolonged exercise in the rat(2,3,6).
Several methods of altering the ratio of F-TRP:BCAA and thus delaying fatigue during prolonged exercise stress have been employed. Davis et al. (10) supplied various amounts of carbohydrate during cycle exercise and observed that attenuation of the increase in plasmaF-TRP and F-TRP:BCAA was associated with a delay in fatigue. Other researchers have used BCAA supplements to modify TRP availability to the brain in an attempt to delay fatigue(5,15,20,40,46). These investigations have produced equivocal results; however, differences in composition and timing of the BCAA supplements may have contributed to this lack of agreement. Also BCAA ingestion has been shown to increase plasma ammonia (27,28,46), a potential source of both peripheral and central fatigue during prolonged exercise(4).
Whether the diminished central drive associated with heat stress may have mechanisms similar to those proposed for prolonged exercise and thus could be influenced by altering the F-TRP:BCAA ratio is unknown. Also, peripheral ammonia (NH3) production and plasma FFA concentrations have been reported to be increased during heat stress at rest(24) or exercise (45), potentially contributing to a diminished performance. The purpose of the present study was to evaluate the influence of BCAA supplementation on the onset of fatigue during prolonged exercise in the heat. In addition, since previous research has suggested that females display a greater behavioral susceptibility to changes in brain serotonergic activity (25) and are at higher risk of serotonergic-related disorders (e.g., depression and anorexia nervosa (11,25), we investigated responses in both men and women.
Subjects. Sixteen healthy, moderately trained subjects (eight males, eight females) volunteered to participate in the study. Subjects were examined by a physician to rule out any contraindications to participation. All procedures were approved by the Rutgers University Institutional Review Board for the protection of human subjects, and participants provided their informed consent before the study.
Experimental protocol. Subjects initially reported to the laboratory to perform a graded exercise test for the determination of peak oxygen consumption (˙VO2peak) as well as the relative work rate(40% ˙VO2peak) used in subsequent experimental sessions. A Schwinn Velodyne ergometer, which enabled the subjects to ride their own bicycles during all experimental exercise tests, was used. Oxygen consumption(˙VO2) was determined using an indirect, open-circuit system. Expired fractions of O2 and CO2 were measured with an Applied Electrochemistry S-3A analyzer (Ametek, Pittsburgh, PA) and a Beckman LB-2 analyzer (Brea, CA), respectively. Ventilation (˙VE) was measured with a dry gas meter. All data were collected continuously on line using the Vista Turbofit software program (VacuMed, Ventura, CA). Body composition was assessed from skinfolds using a Lange skinfold caliper with percent body fat calculated from the equations of Jackson and Pollock(22) for men and Jackson et al.(23) for women.
Experimental sessions were conducted on two separate occasions, separated by at least 1 wk. Women were evaluated during the follicular phase of the menstrual cycle (cycle days 1-8), thus 1 month lapsed between trials. Three women were using oral contraceptives; however Grucza et al.(18) have shown that their use does not influence thermoregulatory function during the follicular phase of the menstrual cycle. Before each session, subjects were asked to refrain from caffeine and alcohol ingestion for at least 12 h and to refrain from strenuous exercise for 24 h.
On the morning of each trial, subjects reported to the laboratory at 8:00 a.m. at which time they were fed a meal consisting of 840 kcal (67% carbohydrate, 11% protein, and 22% fat). Subjects returned to the laboratory at 11:00 a.m. and body weight was determined after voiding. An indwelling venous catheter was placed in the brachial vein for subsequent blood draws, and the subject was instrumented for cardiovascular and thermoregulatory measurements described below. A baseline blood sample was taken after 30 min of seated rest in a comfortable room (Ta = 22.7 ± 1.6°C; rh= 38 ± 19%); then the subject entered a temperature controlled environmental chamber (Ta = 34.4 ± 1.8°C; rh = 39 ± 14%) and remained seated for 2 h. A resting heat phase was included to simulate natural conditions of heat exposure before exercise. Subjects then mounted the cycle ergometer and exercised at 40% ˙VO2peak until fatigue. This relative workload was selected in an effort to minimize the influence of cardiovascular and intermuscular metabolic factors on the development of fatigue, as well as maintain core temperature below 39°C. If subjects exceed a core temperature of 39°C, the exercise session was terminated according to the guidelines of the Rutgers University Institutional Review Board for the protection of human subjects. Fatigue was determined as the time point at which the subject was unable to maintain the desired workload for 1 continuous minute or requested to stop.
During each trial subjects received 5 mL·kg-1 body weight of a drink containing either 5.88 g·L-1 of BCAA (54% leucine, 19% isoleucine, 27% valine, (BCAA)) or 5.88 g·L-1 of polydextrose(PLAC) every 60 min during rest and every 30 min during exercise. Implementation of the drink treatment began after 60 min of rest in the heat. During the BCAA trial females consumed a total of 9.4 ± 0.8 g of BCAA, and males consumed a total of 15.8 ± 1.1 g of BCAA. The drinks were formulated to be indistinguishable in taste and appearance and were administered double-blinded using a Latin-square design. More specifically, 3.9 mL·L-1 of orange juice flavoring, 2 mL·L-1 of raspberry extract, and 0.05 g·L-1 of naringin were added to each drink to mask the typically bitter taste of amino acids.
Physiological measures. Heart rates (HR, beat·min-1) were measured continuously with a Vantage XL heart rate monitor (Polar Electro Inc., Port Washington, NY) and were recorded at 10-min intervals. Blood pressure was monitored by auscultation using a sphygmomanometer every 15 min during the trials. Mean arterial pressure (MAP, mm Hg) was calculated from systolic and diastolic pressures (1/3 pulse pressure plus diastolic pressure).
Surface thermocouples were placed at four sites (arm, chest, thigh, calf) to assess mean skin temperature (Tsk, °C) from the formula of Ramanathan (42). Core temperature (Tes, °C) was measured within the esophagus with a 30-gauge copper-constantin thermocouple embedded in an infant feeding tube. The flexible tube was inserted through the nasal passage to the approximate level of the heart determined by the subject's sitting height (31). Tsk and Tes were monitored continuously and recorded every 5 min during the trials (Thermocouple Datalogger, Omega, Stamford, CT). Relative humidity (rh,%) was determined every 30 min using a sling psychrometer (Fisher Scientific, Indiana, PA).
Collection of all physiologic measures began after placement of the indwelling catheter and continued until fatigue. All baseline measures are averages of data collected over the 30-min rest period in an ambient environment before entering the environmental chamber.
Psychological measures. To assess the potential influence of BCAA supplementation on subjective feelings of fatigue, ratings of perceived exertion (10-point scale) (RPE, (7), and ratings of perceived thermal sensations (PTS, (14)) were recorded every 30 min throughout the trials. The POMS (30) was administered during baseline, at the end of the rest phase in the heat, and at the end of exercise to fatigue. The total mood disturbance (TMD) score for the POMS was calculated according to the procedure of Prusaczyk et al.(41).
Blood analyses. Blood samples (10 cc) were collected every 30 min during the trials from a heplock catheter inserted into the brachial vein. For plasma NH3 and amino acid analyses, blood was collected in heparinized Vacutainer tubes; Vacutainer tubes containing EDTA were used for plasma FFA and glucose. Whole blood was analyzed for hematocrit in triplicate using microcapillary tubes and a microhematocrit centrifuge. The remaining blood was centrifuged for 15 min; then plasma was divided into aliquot samples and frozen at -70°C. Plasma NH3 was analyzed in triplicate immediately after the completion of each trial by the method of Kun and Kearney(9). The coefficient of variation for plasma NH3 measurements was 9.7%. Plasma glucose and FFA were assayed in duplicate using spectro-photometric methods (21,38). For amino acids, plasma samples were stored and sent to another laboratory for analysis by high pressure liquid chromatography (HPLC) according to procedures previously described (10). Changes in plasma volume(ΔPV) was calculated from changes in hematocrit.
Statistical analyses. A MANOVA with repeated measures design was used to evaluate all data. Main effects included sex, drink treatments, and time. When responses were similar between sexes, data were combined for comparison between drinks and over time. Data at fatigue were compared between sexes and drink treatments. A significance level of P < 0.05 was selected a priori. When significant main effects were observed, the least square means procedure was used to evaluate differences across treatments, sexes, and time as well as to examine interaction effects. When appropriate, standard contrast procedures were performed to examine specific differences between cell means. Data are means ± SEM unless noted otherwise.
Subjects. Physical characteristics of the seven men and six women who completed the study are shown in Table 1. The two women and one man who terminated the trials before fatigue cited gastrointestinal distress (N = 1), back discomfort (N = 1), and inability to tolerate the blood sampling procedure (N = 1) as reasons. The groups were similar in fitness (˙VO2peak) and were both relatively lean; however, the men had significantly less body fat(P = 0.04).
Cycle time to exhaustion. Cycling times until exhaustion during exercise at 40% ˙VO2peak in the heat were greater (P = 0.04) during the BCAA trial (153.1 ± 13.3 min) than in the PLAC trial(137.0 ± 12.2 min). Furthermore, 10 (5 men and 5 women) of the 13 subjects performed better during the BCAA trial than in the PLAC trial. No sex differences were observed. There was also no difference between cycle time to exhaustion in the first (144 ± 11 min) and second (147 ± 14) trials that the subjects completed in the experiment.
Thermoregulatory responses. Absolute temperature responses and the increases observed during rest and exercise in the heat were similar between men and women and were not influenced by the fluid treatments. Tes averaged 36.6 ± 0.1°C during baseline, 36.4 ± 0.1°C during rest in the heat, and increased to 37.1 ± 0.1°C throughout the exercise phase. Tsk for both trials increased from 31.5± 0.4°C at baseline to 34.8 ± 0.1°C during rest in the heat, with a further increase to 35.6 ± 0.1°C during exercise. Values at fatigue are reported in Table 2 for both Tes and Tsk. Tes at fatigue did not differ between men and women or between drink treatments. Although there were no significant main effects for drink or sex for Tsk at fatigue, a significant drink by sex interaction (F1,11 = 4.87, P = 0.05) was observed. For the men, Tsk at fatigue tended toward a lower value during BCAA, whereas the women had similar Tsk responses for both treatments. Sweat losses, calculated from changes in body weight corrected for fluid intake and urine output, were similar for men and women and between treatments (PLAC = 2.53 ± 0.36 L; BCAA = 2.53 ± 0.33 L).
Cardiovascular responses. HR, MAP, and ΔPV responses were also similar for both drink treatments and between sexes. HR averaged 61± 2 beats·min-1 and 64 ± 2 beats·min-1 during baseline and rest in the heat, respectively. HR increased to 142 ± 4 beats·min-1 during exercise in the heat. Values for HR at fatigue for both trials are reported inTable 2.
MAP was reduced during rest in the heat (80.7 ± 1.4 mm Hg) when compared with that at baseline (84.4 ± 1.7 mm Hg). MAP increased to 87.1 ± 1.4 mm Hg for both treatments during exercise. Although the main effect of the drink treatment was not significant, a significant drink by time interaction (F2,22 = 4.87, P = 0.01) was observed for MAP as the average values measured during rest in the heat were lower during the PLAC trial (79.3 ± 1.8 mm Hg) when compared with those during the BCAA trial (82.2 ± 2.1 mm Hg). MAP during exercise increased by 6.3 ± 1.4 mm Hg for both drink treatments. MAP at fatigue(Table 2) was similar between drink treatments and sexes.
During rest in the heat the hemodilution observed (ΔPV = 1.58± 0.83%) was reversed during exercise (ΔPV = -7.64 ± 0.68%). There were no differences between drink treatments or sexes. Fatigue values for ΔPV are displayed in Table 2.
Psychological responses. Data for the individual POMS scales and TMD at baseline, after rest in the heat, and at fatigue are shown inTable 3 for the eight subjects (six men and two women) who completed all questions at each time phase. At the initiation of the study the Symptoms Checklist-90-R (Clinical Psychometric Research) was administered to four women subjects; however, this scale was not deemed appropriate for the present study. The POMS was then administered to the remaining subjects. Since data from only two women were assessed, sex differences were not analyzed.
Depression, anger, and tension scores exhibited a significant drink effect(P < 0.05), with greater values measured during BCAA than PLAC. Closer examination indicated that differences in tension and anger between treatments existed only at baseline and that these differences did not exist following rest in the heat. Rest in the heat resulted in reduction in tension(F2,14 = 5.46, P = 0.04) that returned toward baseline following exercise for both trials. Confusion, fatigue, and TMD scores were similar during baseline and rest in the heat but were significantly elevated at fatigue (P < 0.04) for both drink treatments. Vigor scores were reduced at fatigue for both trials when compared with those at both baseline and rest in the heat (P < 0.001).
PTS and RPE responses for all 13 subjects were also similar between drink treatments. PTS averaged 4.7 ± 0.1 over the rest phase and significantly increased to 6.1 ± 0.1 throughout exercise in the heat. At fatigue, PTS was similar for PLAC (6.8 ± 0.2) and BCAA (6.6 ± 0.2). Although RPE averaged over the exercise phase was similar for both men and women for both drink treatments (PLAC = 5.2 ± 0.5; BCAA = 5.1± 0.4), RPE at fatigue was significantly greater in men (8.4 ± 0.2) when compared with that in women (6.2 ± 0.7).
Plasma variables. Figure 1 displays the data for glucose and FFA over time for the six men and three women who completed 2 h of exercise on both drink treatments. Data at fatigue are also displayed for all 13 subjects. Although FFA responses were similar for both men and women, a significant sex effect (F1,7 = 9.88, P = 0.02) was observed for glucose; thus data for each sex are presented separately. Drink treatment did not influence these results. For males, glucose at fatigue (4.0± 0.2 mM) was maintained at pre-exposure levels of 4.2 ± 0.1 mM. Fatigue glucose values for females (5.9 ± 0.6 mM) were also similar to their baseline values (5.5 ± 0.4 mM). For both sexes, rest in the heat resulted in a significantly greater plasma glucose that was returned toward its pre-exposure value by the first hour of exercise. Females exhibited higher glucose values at all time period. In contrast, for both men and women FFA remained at pre-exposure values (0.35 ± 0.03 mM) until the second hour of exercise when values reached 0.98 ± 0.09 mM. FFA at fatigue (1.88± 0.18 mM) were significantly greater than that at 120 min of exercise(P = 0.001).
Figure 1-Data (mean ...Image Tools
Data for the sum of plasma BCAA (Σ BCAA = leucine + isoleucine + valine) are shown in Figure 2. Lower concentrations were observed in the women when compared with those in the men at all time periods(F1,7 = 7.38, P = 0.03). Following the initial administration of the drink at the end of 1 h of rest in the heat, BCAA resulted in a significantly higher Σ BCAA when compared with PLAC(F1,7 = 107.15, P = 0.0001). In the men, Σ BCAA values reached a plateau after the first hour of exercise (1129 ± 110 μM) and were maintained throughout exercise to fatigue (1138 ± 113 μM). In contrast, the women exhibited a linear increase in Σ BCAA which peaked at 1023 ± 65 μM at fatigue. Fatigue values were similar between men and women (Fig. 2).
Figure 2-Data (mean ...Image Tools
F-TRP, Σ BCAA:F-TRP, and NH3 responses over time are presented in Figure 3. Data for men and women were combined because no differences were observed. F-TRP, which increased over time (F5,40 = 26.54, P = 0.0001), did not display a significant drink effect; however, a significant drink by time interaction (F5,40 = 3.21, P = 0.02) was evident. During PLAC, F-TRP followed a similar pattern to the FFA response, with the exception that F-TRP was significantly elevated above baseline by 1 h of exercise. In contrast, the rise inF-TRP was delayed until 2 h of exercise during the BCAA trial, and values at fatigue were lower during BCAA (9.6 ± 0.9 μM) when compared with those during PLAC (12.0 ± 1.3 μM). When the ratio ofΣ BCAA: F-TRP was computed, BCAA resulted in a significant reduction from its baseline value (0.013 ± 0.002 ND) by 2 h of rest, which was maintained throughout exercise until fatigue (0.009 ± 0.001 ND). During the PLAC trial, Σ BCAA:F-TRP ratios were maintained at baseline values (0.015 ± 0.002 ND) until fatigue, when a significant elevation was observed (0.025 ± 0.002 ND). Although there was a trend for plasma NH3 to be greater during the BCAA trial when compared with that during PLAC, these differences were not statistically significant. NH3 was slightly, but not significantly, elevated during the resting heat exposure and continued to increase during the exercise phase. After 60 min of exercise, plasma NH3 increased 2-fold from pre-exposure values and continued to rise during 2 h of exercise. Values at fatigue for BCAA (135.8 ± 22.0 μM) and PLAC (114.3 ± 17.6 μM) were similar to those observed at 120 min of exercise.
Figure 3-Mean (SEM) ...Image Tools
This study investigated the effects of BCAA supplementation on exercise time to fatigue in healthy, active men and women who were exposed to heat stress. Because the earlier onset of fatigue during heat stress has been linked to central mechanisms (36), we hypothesized that BCAA supplementation would prolong endurance performance in the heat via manipulation of the brain serotonergic system as has been proposed for prolonged exercise in comfortable environments (35).
The ingestion of the BCAA drink resulted in a two-fold increase in plasma BCAA concentrations, a blunted plasma F-TRP at fatigue, and a 50% reduction in the F-TRP:BCAA, when compared with the ingestion of the placebo drink. In addition, cycling time to exhaustion was increased by 14± 5%. Although some researchers have reported a beneficial effect of BCAA treatment on endurance performance in comfortable ambient temperatures(5,20), others have observed no ergogenic effect(15,40,46). Comparisons between previous studies and the present study must be made with caution as the environmental stress (35°C), exercise intensity (40% ˙VO2peak), and the form of BCAA supplementation (drink containing BCAA without glucose) were unique. Nonetheless, results from this study indicate that the earlier onset of fatigue during moderate exercise in the heat may be related to theF-TRP:BCAA and thus performance modestly improved with supplementation of BCAA.
The potentiation of plasma Σ BCAA in the present study(Fig. 2), with an average ingestion over the duration of the trial of 12.8 g, was similar to the ≈1250 μM reported by Blomstrand et al. (5) who observed an improvement in marathon performance. However van Hall et al. (46), who provided their cyclists with 23.4 g BCAA (plasma Σ BCAA ≈ 2400 μM), observed no improvement in endurance cycle times at 70-75%˙VO2max.
During both drink treatments, fatigue values were similar for cardiovascular, thermoregulatory, and substrate responses which have been linked to mechanisms of fatigue. Although muscle glycogen levels were not measured in the present study, the moderate exercise intensity performed is not likely to have resulted in depletion. Previous studies of the effect of heat stress on glycogen utilization are equivocal as both increases(13) and no change (37) have been reported. Plasma glucose was maintained at pre exposure concentrations during rest and exercise in the heat.
With few exceptions, the physiological responses to prolonged exercise during heat stress were similar in the men and women who were at similar levels of aerobic fitness. Plasma glucose was elevated and plasma Σ BCAA was reduced in the women when compared to that in the men for both drink treatments. The differential glucose response was somewhat surprising as the women were studied during the follicular phase of their menstrual cycles when estrogen, which has been linked to decreased carbohydrate metabolism(29), would be relatively low. However, since the breakfast provided to all subjects was identical, the 840 kcal meal may have maintained plasma glucose at higher levels in the women as compared with those in the men. Whether the higher glucose concentrations observed in the women may have indirectly reduced their plasma Σ BCAA via a greater insulin release or by attenuating endogenous release of BCAA into the blood is unknown and requires further study.
Plasma FFA, which were similar during baseline and rest in the heat, increased significantly following the first hour of exercise for both drink treatments. We had anticipated that rest in the heat would stimulate lipolysis as Jacob et al. (24) reported a 1.8-fold increase in circulating FFA concentrations at rest during hyperthermic conditions. Core temperatures following rest in the heat in our study were lower than those reported by Jacob et al. (24), potentially inducing a lesser environmental stimulus for lipolysis. Plasma F-TRP responded in a similar manner to FFA, suggesting that the mechanism for enhanced 5-HT synthesis was affected by this experimental protocol.
The lack of effect of BCAA supplementation on plasma NH3 concentrations was unexpected. It has been shown that BCAA ingestion before exercise results in an increase in the rise in plasma NH3 concentrations over placebo (27,28,48). While plasma NH3 concentrations tended to be higher with BCAA during exercise in this investigation, this elevation was not significant. During exercise at 70% ˙VO2peak, Snow et al. (45) observed a greater plasma ammonia during 40°C exposure when compared with that at 20°C. The lower exercise intensity or method of BCAA supplementation used in the present study may account for these differences.
Core temperature at fatigue was significantly elevated above baseline for both treatments, however, because of the moderate exercise intensity employed in our study. Tes did not approach 39°C, which Nielsen(36) has hypothesized will result in a diminished ability to recruit motor unit or affect motivation. Since Tes at fatigue in this investigation did not approach 39°C, it is difficult for us to assess accurately Nielsen's hypothesis.
An increase in skin temperature was also induced by 2 h of resting heat exposure, this effect was further enhanced by exercise at 40%˙VO2peak. It is possible that afferent information from skin receptors may have also contributed to the reduced motivation to work. This is supported by the research of Brück and Olschewski(8) who reported that an elevation in mean body temperature, which includes the contribution from both core and skin temperatures, reduces the drive to exercise.
BCAA supplementation had no effect on subjective feelings of perceived exertion or thermal sensation. It is unclear why the women reported lower RPE scores at fatigue than the men since relative workloads were similar. This sex difference was only evident at fatigue as similar values were observed for the men and women throughout the 2 h of exercise. Although initial POMS scores for depression, tension, and anger were elevated for the BCAA trial, changes in mood states because of rest and exercise in the heat were not influenced by the drink treatment. These data are in agreement with Petruzello et al.(40) who reported no effect of BCAA on POMS responses. In contrast, Hassmén et al. (19) reported BCAA improved POMS tension and depression scores when compared with those in the placebo treatment, during a 30-km competitive run. Prusaczyk et al.(41) also reported POMS scores were not affected by glycogen depletion or altered dietary carbohydrate consumption. Our data would support their suggestion that short-term manipulations of diet may not be sufficient to alter mood states during exercise.
The specific mechanism underlying the improved performance observed during prolonged cycling in the heat as a result of BCAA supplementation is unclear. If the improvement was a result of reductions in TRP transport across the blood brain barrier, secondary to increases in plasma BCAA levels, then plasmaF-TRP levels at fatigue would be expected to be greater and RPE throughout exercise might be expected to be lower during the BCAA trials. Neither of these results was observed in this investigation, in fact plasmaF-TRP levels at fatigue were actually lower during the BCAA trial. It has been suggested that BCAA supplementation during prolonged exercise may actually be detrimental to performance because of the increase in plasma NH3 levels which are seen in concert with this nutritional manipulation(4). Plasma NH3 itself is believed to have negative effects on central drive (4). The conclusion that the potential positive effect of BCAA supplementation on TRP transport into the brain was offset by the potential negative effects of increasing plasma NH3 levels would be attractive if plasma NH3 levels were elevated throughout the BCAA trial. While plasma NH3 levels tended to be higher during the BCAA trial, significant differences between treatments were not observed at any time point.
It is possible that the positive effects of BCAA supplementation were the result of its potential influence on energy supply to the muscle. If BCAA was being used to a greater extent for energy production during the BCAA trial, then plasma levels of glucose and NH3 would be expected to be higher during exercise and plasma levels of FFA would be expected to be lower. None of these results was observed in this investigation; however, it must be acknowledged that the experimental methods used in this investigation are not able to accurately evaluate differences in BCAA utilization during exercise under the two drink conditions.
In summary, supplementation of BCAA during prolonged, moderate exercise in the heat resulted in a modest improvement in performance in healthy, active men and women. The improvement seen in this investigation may be a result of the reduction in the F-TRP:BCAA ratio; however, other physiological and psychological data which would be supportive of this conclusion are equivocal. Consequently, the hypothesis that the earlier onset of fatigue during exercise in the heat may be of central origin(36) and similar to the “central fatigue” proposed for endurance exercise in comfortable ambient conditions(35) remains in question.
We appreciate the technical support provided by Dr. Christian Schwabe's laboratory, Ms. Layla Fakhrzadeh, and Ms. C. Michelle Miller. The authors are also grateful to Dr. Robert Monaco and Ms. Lynn Johnson for their medical assistance and to the dedicated students who served as subjects and laboratory assistants.
This work was supported by a Gatorade Sports Nutrition Research Grant from the American College of Sports Medicine Foundation.
Present address for Stephen P. Bailey: Department of Rehabilitation Sciences, College of Health Related Professions, Medical University of South Carolina, 171 Ashley Ave., Charleston, SC 29425.
Address for Correspondence: Karen D. Mittleman, Ph.D., Design-Write, Inc., 189 Wall St., Princeton, NJ 08540. E-mail:firstname.lastname@example.org.
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