The oxygen uptake (V̇O2 ) or work rate just below that at which there is a systematic rise in blood lactate ([La]) concentration during incremental exercise is now referred to as the blood lactate threshold (TLa). Wasserman and his associates (25) used the term anaerobic threshold to describe this inflection point because they felt that the sudden increase in blood [La] was due to muscle tissue hypoxia and increased anaerobic glycolysis. In recent years, some investigators have challenged the concept of the anaerobic threshold and the idea that muscle hypoxia is the sole cause of the TLa. Factors that may play a role in the production of the lactate threshold that occurs during incremental exercise include muscle fiber recruitment (2,14,28), muscle anaerobiosis (8,25), a decreased rate of lactate removal from the blood (2), and hormonal regulation of muscle glycogenolysis and glycolysis (2,6,16,17,21–23,27).
Plasma epinephrine ([Epi]) and norepinephrine ([NE]) concentrations are also known to demonstrate inflection points (or thresholds) at submaximal work rates during incremental exercise (15–18,27). In addition, the abrupt increases in plasma [Epi] and blood [La] have been reported to occur at identical work rates during incremental exercise (16,17).
Epinephrine is known to activate phosphorylase and to stimulate muscle glycogenolysis (4,5). This will increase the rate of glycolytic flux, enhance muscle lactate production, and increase the rate of lactate appearance in the blood. Moreover, Epi infusion has been found to produce an increase in La output from contracting gastrocnemius muscle in dogs (22). Infusion of Epi in humans increases blood [La] both at rest (6,20,23) and during exercise (10,12,24). These studies suggest a causal relationship between increases in plasma [Epi] and La production during submaximal exercise. Thus, it has been argued that the rise in plasma [Epi] during graded exercise is the primary factor influencing the TLa (3,16,17,24).
Blomqvist et al. (1) and Davies et al. (7) found a lower plasma [Epi] at any given relative work intensity during incremental exercise performed with the arms than with the legs. These investigators did not attempt to determine a breakpoint for the rise in plasma [Epi] during incremental exercise, but their results suggest that the TEpi may occur at a higher % of V̇O2 peak for arm than for leg exercise. A study by Davis et al. (9) found a lower anaerobic threshold for arm cranking than for either cycling or running. They reported that the anaerobic threshold for arm cranking occurred at about 47% of V̇O2 peak, whereas the threshold for leg cycling occurred at 59% of V̇O2 peak. The findings of these studies suggest that TLa and TEpi may not occur together during arm exercise. Moreover, these findings suggest that TEpi may occur after TLa during arm-cranking exercise. Researchers have suggested that a dissociation of the thresholds indicates that they are not causally related (16–18).
However, analysis of threshold behavior without consideration of the actual concentration of lactate and epinephrine may provide an inaccurate assessment of the association between blood La and plasma Epi (27). During Epi infusion in resting subjects, several investigators have demonstrated that a critical plasma [Epi] was necessary before blood [La] rose above resting values (6,20,23). Weltman et al. (27) suggested that the critical [Epi] may occur at TLa but not necessarily at the point where an abrupt increase in plasma [Epi] occurs during incremental exercise (i.e., at the Epi threshold). Therefore, it would be inappropriate to conclude that a dissociation of TLa and TEpi during arm or leg exercise suggests that plasma Epi is not influencing blood lactate behavior.
No study has examined the relationship between TLa and TEpi during both arm cranking and leg cycling. The present study was conducted to examine the plasma Epi and blood La responses to incremental arm and leg exercise. The purpose was to determine if the blood lactate and epinephrine thresholds would occur together during both arm and leg exercise. A secondary objective was to determine whether the Epi concentrations observed at the TLa for arm and leg exercise are within the range of [Epi] values previously reported to increase blood [La] above resting values (150–288 pg·mL−1).
MATERIALS AND METHODS
Subjects.
Seven physically active, male subjects volunteered to participate in the present study. The mean (±SE) values for age, body mass and height were 25.4 ± 2.2 yr, 81.3 ± 2.7 kg, and 178 ± 2 cm, respectively. Written informed consent was obtained after a detailed description of the procedures was provided. Approval of the experimental procedures was granted by the Ethics Review Committee of Griffith University.
Experimental protocol.
Each subject was asked to complete two continuous, incremental exercise tests on separate days. Both exercise tests were performed using an electrically braked cycle ergometer (Lode, Excalibur Sport, Groningen, The Netherlands). One test consisted of 1-arm cranking with the subject’s dominant arm, whereas the other exercise test was 2-leg cycling. Subjects were familiarized with 1-arm cranking and the cycling protocol on a day before testing. The two exercise tests were performed in random order at least 1 wk apart. Subjects were tested at least 3 h postabsorptive, and all tests for each subject were performed at the same time of day. Before each testing session subjects had a 22-gauge catheter inserted into an antecubital or forearm vein (nondominant arm) and then sat quietly for 30 min. Blood samples were obtained from the nonexercising arm during 1-arm cranking and from the same arm and vein during 2-leg cycling. The catheter was kept patent by flushing with a heparinized saline solution.
Arm-crank and cycle ergometer exercise.
Each subject performed an incremental test using an electrically braked cycle ergometer modified for arm-cranking. The crank axis of the ergometer was aligned with the subject’s shoulder joint, and the seat was adjusted to allow for a slight bend in the elbow when the pedal was at its greatest distance from the subject. Enlarged, circular crank handles were used to provide a secure hand grip. The subject exercised using his dominant arm and blood was sampled from the nonexercising arm. Subjects were encouraged to exercise to volitional fatigue, but the exercise test was stopped when there was a significant amount of upper body movement during exercise. Thus, the results for arm cranking may not represent a peak exercise response.
After 3 min of unloaded arm-cranking at 60 rpm, the power output was increased by 5 W every 2 min until volitional exhaustion. The 2-leg cycling protocol consisted of 3 min of unloaded cycling at 60 rpm, followed by 20–25 W increments every 2 min. Protocols were designed to obtain 12–14 blood samples during both incremental exercise tests. During exercise, subjects breathed through a low-resistance Hans Rudolph valve with expired gas passing through a pneumotachograph (Hans Rudolph, Series 3830, Kansas City, MO) for determination of expired min ventilation. Gas samples were drawn from a mixing chamber for analysis of expired O2 and CO2 content using zirconia (O2) and infrared (CO2) analyzers (Clinical Engineering Solutions, Sydney, Australia). The pneumotachograph and the O2 and CO2 analyzers were calibrated before each test using a standard 3-L syringe and precision reference gases, respectively. Pulmonary minute ventilation (V̇E), V̇O2 and CO2 output (V̇CO2 ) were determined for each 30-s period of incremental exercise. Peak levels for all variables were defined as the highest value measured during the exercise test. Heart rate and rhythm were monitored continuously throughout exercise using a CM5 electrode placement and a Lohmeier (M 607, Munich, Germany) electrocardiograph.
Approximately 5 mL of blood were obtained during the last 30 s of each work stage from an indwelling catheter in an antecubital vein. One mL of blood was immediately deproteinized with 2 mL of iced 0.8% perchloric acid and centrifuged. The supernatant was separated and frozen at −70°C until analyzed for lactate concentration using an enzymatic technique (19).
The remainder of the 5 mL blood sample was placed in a heparinized tube containing 70 μL of a reduced glutathione and EGTA solution (2.5 g glutathione and 3.0 g EGTA mixed with 33.5 mL of distilled water). The plasma was separated and stored at −70°C until the samples could be analyzed for catecholamine levels. Plasma norepinephrine and epinephrine concentrations were determined by means of high-performance liquid chromatography (HPLC) with electrochemical detection (26). The between-day coefficients of variation were less than 5%, whereas within-day coefficients of variation were less than 3% for both epinephrine and norepinephrine.
Figure 1 illustrates the detection of the blood lactate, epinephrine, and norepinephrine thresholds during both modes of exercise in one subject. Two investigators selected the TLa in a blinded manner from graphs of lactate plotted against power output for arm and leg exercise. This method of detecting the TLa has been described by Schneider et al. (18) and Weltman et al. (27). Norepinephrine and epinephrine thresholds were determined in the same manner as the lactate thresholds. A third investigator was consulted in a few instances when the two investigators did not agree on threshold placement. Two of three investigators were able to agree on the selection of the thresholds in every subject (42 thresholds).
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Figure 1: Detection of the blood lactate, epinephrine, and norepinephrine thresholds during arm and leg exercise in one subject. The vertical line in each panel indicates the threshold.
Statistical analyses.
A two-way analysis of variance with repeated measures was used to compare threshold differences between and within 1-arm cranking and 2-leg cycling. A Tukey post hoc test was used when significant mean differences were observed. Relationships between plasma catecholamine concentrations and blood lactate levels were assessed using Pearson’s product-moment correlations. Paired t-tests were used to compare peak exercise values obtained for the two modes of exercise. Statistical significance was accepted as P < 0.05.
RESULTS
Peak values obtained during incremental exercise for 1-arm cranking and 2-leg cycling are presented in Table 1. All peak exercise values were significantly higher for 2-leg cycling than for 1-arm cranking (P < 0.01).
Table 1: Peak values obtained during incremental arm and leg exercise.
Oxygen uptake and power output values obtained at TLa, TEpi and TNE for the two modes of exercise are presented in Table 2. When the two modes of exercise were compared, TLa, TEpi, and TNE were all significantly lower for 1-arm cranking than for 2-leg cycling (P < 0.01). Within both modes of exercise, TLa, TEpi, and TNE were not found to be significantly different from each other (P > 0.05). In other words, the three thresholds occurred at the same level of V̇O2 during arm cranking and during leg cycling.
Table 2: Mean values obtained at the blood lactate, epinephrine, and norepinephrine thresholds during arm and leg exercise.
The relationship between TLa and TEpi for arm and leg exercise is presented in Figure 2. A significant correlation between the V̇O2 values measured at TLa and TEpi was obtained for both arm (0.917) and leg (0.929) exercise (P < 0.001). Table 3 provides the mean correlation coefficients for the relationship between blood [La] and catecholamine concentrations in all subjects during graded exercise for both modes of exercise. The correlation observed between blood [La] and plasma [Epi] determined at every work stage of incremental exercise was 0.925 ± 0.042 for arm and 0.964 ± 0.008 for leg exercise (P < 0.001). A significant correlation was also found between blood [La] and plasma [NE] for both incremental arm and leg exercise (P < 0.001).
Figure 2: Relationship between blood lactate threshold (T La) and epinephrine threshold (TEpi) during 1-arm cranking (upper panel) and 2-leg cycling (lower panel). The diagonal line in each panel is the linear regression.
Table 3: Mean correlation coefficients for the relationship between blood lactate and plasma catecholamines during incremental arm and leg exercise.
Blood lactate and plasma catecholamine concentrations obtained at the TLa during both arm and leg exercise are provided in Table 4. Blood La concentrations obtained at the TLa were not significantly different for arm and leg exercise. Moreover, plasma catecholamine concentrations measured at the La threshold were not found to be significantly different for the two modes of exercise.
Table 4: Blood lactate and plasma catecholamine concentrations observed at the lactate threshold during arm and leg exercise.
DISCUSSION
The present study demonstrated that TLa, TEpi and TNE shifted between exercise testing modes depending on the size of the muscle mass utilized. The blood La and catecholamine thresholds were found to be significantly lower for arm than for leg exercise. Furthermore, the breakpoint in plasma catecholamines moved in an identical manner and occurred simultaneously with that of TLa regardless of the mode of exercise (arm or leg). Other investigators (16) have found that TLa and TEpi occurred together during both running and cycling in trained subjects. The finding in the present study that the La and catecholamine thresholds occurred together for both arm and leg exercise supports the concept that the rise in plasma [Epi] during incremental exercise contributes to the La breakpoint.
In the present study, the correlation between the V̇O2 measured at TLa and TEpi was 0.917 for arm cranking and 0.929 for leg cycling. In addition, a significant correlation was observed between plasma [Epi] and blood [La] during graded arm (0.925) and leg (0.964) exercise. In agreement with these findings, Mazzeo and Marshall (16) reported a correlation of 0.974 between blood [La] and plasma [Epi] during incremental running and cycling. Furthermore, Podolin et al. (17) observed a significant relationship between plasma catecholamine levels and lactate during graded exercise performed under normal glycogen and glycogen-depleted conditions. Previous investigations and the findings of the present study indicate a strong association between blood La and Epi levels during exercise, but these data do not suggest that TEpi causes TLa. Weltman et al. (27) have shown that TEpi is often preceded by TLa, suggesting that although Epi may influence La accumulation, the actual Epi threshold does not necessarily cause the La threshold.
The influence of catecholamines on La production during exercise has been well established in the literature. Epinephrine acts through β-adrenergic receptors and cyclic AMP to activate phosphorylase and increase muscle glycogenolysis (4,5,21). As muscle glycogenolysis is increased, the rate of La production is augmented and La is released into the circulation. Beta-adrenergic blockade has been shown to reduce both the rate of muscle glycogen breakdown in humans (12,13) and lactate turnover during exercise in animals (11). In addition, Brooks and Gregg (3) found a very high correlation (r = 0.97) between lactate turnover and plasma [Epi] in rats during exercise.
It should be noted that a rise in plasma [NE] could also contribute to the development of the TLa by causing vasoconstriction and a subsequent redistribution of blood flow away from organs and tissues that normally remove La from the blood. A decrease in the rate of removal of blood La is one of several mechanisms that have been offered to explain the TLa (2).
A recent study by Weltman et al. (27) found that the TLa occurred at a significantly lower V̇O2 than either TEpi or TNE during both rowing and running. However, TLa occurred at a plasma [Epi] of about 200–250 pg·mL−1 for both modes of exercise. These Epi concentrations agree with those reported to produce a rise in blood [La] during Epi infusion at rest (6,20,23). Weltman et al. (27) concluded that although TLa and TEpi did not occur at the same V̇O2, the observation that TLa occurred at a plasma [Epi] of about 200–250 pg·mL−1, regardless of the mode of exercise, is consistent with the hypothesis that plasma [Epi] influences TLa.
In the present study, the [Epi] obtained at the lactate threshold was about 150 pg·mL−1 (0.150 ng·mL−1) for both arm and leg exercise. Although somewhat lower than the values reported by Weltman et al. (27), the Epi levels observed at the TLa in the present study are consistent with the critical plasma Epi concentrations (in the range of 150–288 pg·mL−1) reported to cause blood La to increase above resting levels (6,20,23). Although it may not be appropriate to apply observations made in resting subjects to exercise conditions, the findings of the present study support the argument that the rise in plasma [Epi] may contribute to the breakpoint in blood [La] that occurs during incremental exercise.
In summary, the catecholamine and blood La thresholds were significantly lower for arm cranking than for leg cycling. However, the threshold in [Epi] shifted in an identical manner and occurred together with the blood La threshold regardless of the mode of exercise (arm or leg). The Epi concentrations obtained at the TLa agree with those previously reported to elicit a rise in blood [La] during Epi infusion at rest. These findings are consistent with the hypothesis that a rise in plasma [Epi] may contribute to the breakpoint in blood [La] that occurs during a graded exercise test.
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