Many studies (1,2,9,15–17,24) have compared the physiological responses of endurance trained with healthy, untrained subjects during submaximal exercise by attempting to normalize the exercise intensity relative to peak oxygen consumption (i.e., % V̇O2peak). Presumably, it was assumed that this would decrease the variability of the physiological response among subjects. The use of such a normalization process was likely based upon the historical perception that the ability to deliver and utilize oxygen in contracting skeletal muscle was the limiting factor for endurance exercise performance (35,40), and this convention continues to be used.
Whether selecting a work rate relative to V̇O2peak actually decreases the variability of the physiological response to exercise is unclear. Some studies (9,16) have demonstrated that physiological and metabolic responses to exercise at the same relative intensity are the same regardless of training status. In contrast, several other studies (1,2,15,17) have observed that the metabolic, cardiovascular, and hormonal changes differ between endurance trained and untrained individuals during exercise at the same relative oxygen consumption (45–75% V̇O2peak). Furthermore, Coyle et al. (6) observed that glycogen utilization and exercise performance can vary significantly in individuals with similar V̇O2peaks when cycling at the same percentage of V̇O2peak. Similarly, McLellan and Gass (28) observed that subjects with similar cardiovascular fitness, as measured by V̇O2peak, had different metabolic profiles during exercise at the same relative intensity. The findings from these experiments suggest that although the physiological stress imposed upon the subjects is assumed to be similar (i.e., of the same relative oxygen uptake), the physiological responses may differ. It appears therefore, that the intended purpose of the relative exercise intensity—to reduce variability in the physiological responses between individuals—is not necessarily achieved when relative oxygen consumption is used as the defining measure.
It is possible that the physiological differences between individuals may be related to the work rate and its relationship not with whole body oxygen consumption, but rather with the ability to generate the majority of ATP via oxidative processes, particularly in those muscles working at the highest rate. One measure of metabolic control is the so-called lactate threshold (LT). It has been reported (8,26) that the LT may vary from 45–85% V̇O2peak among individuals. Furthermore, it is well accepted that the LT occurs at a greater percentage of V̇O2peak in endurance trained individuals (4,12). Also, although the subjects in previous studies (6,28) had similar aerobic capacities (V̇O2peak), they had different LTs. Coyle et al. (6) observed a strong correlation between exercise performance and LT (r = 0.9), and glycogenolysis and LT (r = −0.91). It appears from these data that performance and metabolism may be more closely related to LT than to cardiovascular fitness, as measured by V̇O2peak. The individual variability of physiological response to submaximal exercise, therefore, could be reduced if the exercise intensity were normalized to the LT.
It is possible therefore, that some (1,2,15,18) but not all (9,16) previous researchers observed a difference in physiological responses because they tested the two groups of subjects at an intensity above the LT for the untrained group but below the LT of the trained group. Hence, the purpose of this investigation was to compare trained with untrained men during prolonged cycling at 70% V̇O2peak and 95% LT. We hypothesized that the physiological responses during exercise would not be different when comparing trained with untrained subjects at 95% LT, but at 70% V̇O2peak there would be marked differences between the two groups.
Seven endurance trained (TR) and six untrained (UT) males (Table 1) volunteered to participate in the present study after being fully informed of the experimental procedures and giving informed written consent. Subjects were designated as TR if they had a peak oxygen consumption (V̇O2peak) greater than 60 mL·kg−1·min−1 and UT if they had a V̇O2peak less than 50 mL·kg−1·min−1. In addition, average weekly training for the TR group consisted of 11 h of endurance exercise, which included approximately 175–200 km of cycling. In contrast, UT were sedentary. The Human Ethics Committee at the Royal Melbourne Institute of Technology approved this experiment.
V̇O2peak and LT.
V̇O2peak and LT were determined during incremental cycling exercise to volitional exhaustion on an electrically braked cycle ergometer (Lode, Groningen, The Netherlands). This test consisted of four 5-min stages at 50, 100, 150, and 200 W, followed by an increase of 25 W·min−1 until exhaustion, as previously described (1). Blood samples were collected at the conclusion of each incremental work rate and analyzed for lactate using an enzymatic spectrophotometric technique as previously described (36). The LT was determined using the method preferred by Coyle et al. (5). Briefly, LT was determined by plotting blood lactate concentration against V̇O2 and was defined as the point where blood lactate increased 1 mM above baseline concentration. Although we were able to determine the LT for the UT group accurately—it is possible that given an extremely sedentary group—there may be a risk that there will be a decreased sensitivity for determining the LT. Future studies may wish to use increments of 25 W (i.e., 25, 50, 75, 100 W) in the initial submaximal phase of the incremental test for the UT group. The V̇O2 versus work rate relationship obtained from the incremental exercise test was subsequently used to calculate the work rate for each of the exercise trials.
Each subject performed two submaximal exercise tests, conducted in random order, on the previously mentioned cycle ergometer. Subjects cycled for 60 min, either at a work rate corresponding to ∼ 70% V̇O2peak or ∼ 95% LT. The exercise intensity corresponding to ∼ 70% V̇O2peak was selected because it typically occurs between the LT for trained and untrained individuals (8). Additionally, ∼ 70% V̇O2peak is the work rate commonly used in the literature to compare trained and untrained individuals during prolonged submaximal exercise (1,2,9,15–17). Before these trials, subjects arrived at the laboratory after an overnight fast, having refrained from exercise, alcohol, tobacco, and caffeine for 24 h. The subjects were instructed to consume a high carbohydrate (CHO) diet and to record their total food and fluid intake before the first trial. This diet was replicated for the second trial.
Heart rate and pulmonary measurements.
Heart rate (HR) was recorded via telemetry (Sport tester, Polar, Finland) at rest, and after 5, 20, 40, and 60 min of exercise. Expired pulmonary gases were collected at 5, 30, and 60 min and analyzed as described previously (1). V̇O2 and respiratory exchange ratio (RER) were calculated from these measurements and CHO oxidation rate was subsequently calculated using V̇O2 and RER.
Blood sampling and analyses.
A catheter was inserted into an antecubital vein and blood was sampled immediately after each HR measurement was taken. The catheter was kept patent by flushing with 1 mL of saline containing 5 IU of heparin. Blood was placed in tubes containing lithium heparin and then spun by a centrifuge. Subsequently, an aliquot of plasma was added to ice-cold 3 M perchloric acid (PCA), the tubes were spun again and the supernatant was stored at −80°C before analysis for lactate. The remainder of the plasma was stored in liquid nitrogen for later ammonia and hypoxanthine analysis. The plasma stored for the measurement of hypoxanthine required deproteinization with 1.5 M PCA and subsequent neutralization with 2.1 M KHCO3 immediately before analysis. Plasma lactate was determined in duplicate, using an enzymatic spectrophotometric technique (25). Plasma ammonia analysis was performed in duplicate within 72 h of collection, using flow injection analysis (37). Plasma hypoxanthine was measured on neutralized PCA extracts, using a modification of the reverse-phase high-performance liquid chromatography (HPLC) method described by Wynants and Van Belle (41). Separation was achieved by a Merck Hibar Lichrosphere 100 CH-18/2 250 × 4-mm column.
A Student’s t- test of independent means was used to compare TR and UT subject characteristics. Performance data and plasma metabolite concentrations were compared using analysis of variance (ANOVA) with a between factor (training status) and two within factors (exercise intensity and time) (Biomedical Data Processing statistical software). Simple main effects analyses and Newman-Keuls post hoc tests were used to locate specific differences. Significance was accepted at the P < 0.05 level. All values are reported as means ± standard error of the mean (SE).
Performance and pulmonary variables.
V̇O2peak and LT were higher (P < 0.001) in TR compared with UT (Table 1). Of note, the work rate and relative exercise intensity (i.e., % V̇O2peak) for UT 95% LT were lower (P < 0.01) than for all of the other trials (Fig. 1). There were no differences in relative exercise intensity between the other trials (Fig. 1B). Although the work rate for UT 70% V̇O2peak was lower (P < 0.001) than for TR 70% V̇O2peak and TR 95% LT (Fig. 1A), average HR for the trial was higher (P < 0.01) throughout exercise in UT 70% V̇O2peak compared with all of the other trials (Fig. 2). There were no differences in the average RER for the four trials (Table 2). A power analysis calculation (beta = 0.2, alpha = 0.05, one-tailed test) indicated that a sample size of 6.7 would have been adequate to detect a significant difference in these data. The statistical analysis revealed no interaction for the CHO oxidation rate, however there was a main effect (P < 0.05) for training and exercise intensity. The CHO oxidation rate was greater (P < 0.05) in TR compared with UT, and also during exercise at 70% V̇O2peak compared with 95% LT (P < 0.05) (Table 2). There was also a trend (P = 0.07) for a main effect for RER to be greater at 70% V̇O2peak compared with 95% LT (Table 2).
Plasma metabolite concentrations.
The resting concentrations of all the plasma metabolites were not different between TR and UT in any trial (Fig. 3). Plasma lactate was greater (P < 0.01) at 20 and 40 min in UT 70% V̇O2peak compared with all of the other trials (Fig. 3A). Similarly, plasma ammonia concentration was higher (P < 0.01) at 40 and 60 min in the UT 70% V̇O2peak trial compared with the other three trials (Fig. 3B). There was a tendency (P = 0.077) for plasma hypoxanthine to be greater at 60 min in UT 70% V̇O2peak, compared with the other trials (Fig. 3C). A power analysis calculation (beta = 0.2, alpha = 0.05, one-tailed test) indicated that a sample size of 11.5 would have been adequate to detect a significant difference in these data. Importantly, at no time were the concentrations of plasma lactate, ammonia and hypoxanthine different among the UT 95% LT, TR 95% LT and TR 70% V̇O2peak trials (Fig. 3).
The results from the present study demonstrate that the physiological responses to exercise at 70% V̇O2peak were very different in TR compared with UT. These data indicate that TR were under less cardiac and metabolic stress compared with UT during exercise at this intensity. In contrast, relatively homogenous physiological responses were elicited among subjects with very different aerobic fitness levels when they cycled at 95% LT. It appears therefore, that if the aim is to compare TR with UT under similar physiological conditions, then 70% V̇O2peak should not be used as the exercise intensity.
Exercise at 70% V̇O2peak.
In the present study, the increased plasma ammonia concentrations, along with the tendency (P = 0.077) for an elevated plasma hypoxanthine concentration, provide indirect evidence that UT may have experienced an imbalance between muscle ATP synthesis and degradation during exercise at 70% V̇O2peak. Ammonia is produced in skeletal muscle via adenosine monophosphate (AMP) deamination to inosine monophosphate (IMP; 38), with the latter accumulating in contracting muscle when the rate of ATP demand exceeds the rate of ATP synthesis (38). A small proportion of the accumulated IMP may be degraded to produce hypoxanthine. Ammonia and hypoxanthine are able to diffuse across the sarcolemma and accumulate in the plasma (38). The results from the present study are consistent with cross-sectional (1,17) and longitudinal (21,22) endurance training studies which have demonstrated a reduced contracting muscle IMP accumulation, as well as attenuated plasma hypoxanthine and ammonia concentrations during prolonged submaximal exercise after training. The training-induced improvement in the matching of muscle ATP synthesis with demand probably results from the increase in muscle oxidative capacity associated with endurance training (11,23). Although this may be the best explanation for the observed training effect, other possible mechanisms cannot be discounted since Green et al. (21) reported a reduced IMP accumulation in contracting muscle after short-term endurance training with no evidence of an increase in muscle oxidative capacity. The increase in plasma ammonia concentration observed in UT during exercise at 70% V̇O2peak is best explained by an imbalance between muscle ATP supply and demand; however, this interpretation must be treated with some caution because ammonia may also be produced in contracting muscle from the catabolism of amino acids during submaximal exercise (20).
In the present study, UT also had higher (P < 0.01) plasma lactate concentrations than TR when exercising at 70% V̇O2peak (Fig. 3A). These data are in contrast with Deuster et al. (9), and the explanation for this conflict is unclear. The explanation may be related to the intermittent protocol employed by these previous researchers (20 min of treadmill running at 70% V̇O2peak: 30 s work, 30 s rest), because this type of exercise has been reported to increase plasma lactate levels and CHO oxidation compared with continuous exercise (3). It is therefore possible that endurance training metabolic adaptations are more difficult to observe with intermittent exercise protocols such as the one used by Deuster et al. (9). Our findings are consistent, however, with the results of others (2,17,24) who used a similar protocol to the present study and observed that endurance training attenuated plasma and muscle lactate accumulation during exercise at 65–75% V̇O2peak. Because UT in the present study were exercising at an intensity 13.2 ± 2.8% above their LT, whereas TR were cycling just below their LT (Table 1), it is not surprising that there was a difference in the plasma lactate concentration between TR and UT exercising at 70% V̇O2peak. It is well established that exercise performed above the LT results in a marked accumulation of plasma lactate, whereas during exercise below the LT there is little, if any, alteration in plasma lactate concentration from resting levels (6). The higher plasma lactate concentrations are probably due to an increased muscle lactate production and release (23), indicating that the contracting UT muscle utilized anaerobic glycolysis to a greater extent than TR at 70% V̇O2peak. This greater reliance on anaerobic glycolysis is most likely due to the limited capacity for UT muscle to match pyruvate oxidation rates with the rate of pyruvate production (23). The former appears to be limited by the comparatively lower mitochondria content found in UT muscle (23). It is also possible that the lower plasma lactate in TR 70% V̇O2peak resulted in part from an increased clearance from the circulation in these subjects (27,33).
Despite the fact that there were no differences in RER in the present study (Table 2), TR had a greater (P < 0.05) absolute CHO oxidation rate than UT across both exercise intensities (Table 2). The TR subjects maintained a higher work rate (Fig. 1A) throughout the exercise bouts; hence, the greater absolute CHO oxidation rate (Table 2). As mentioned above, TR also had an attenuated (P < 0.01) accumulation of plasma lactate in the 70% V̇O2peak trial compared with UT. Although speculative, these data provide evidence for a tendency away from anaerobic glycolysis and toward CHO oxidation in TR.
In this study, UT also had a higher (P < 0.01) HR throughout exercise at 70% V̇O2peak, compared with TR (Fig. 2). Higher HR values have been reported previously in UT during exercise at 70% V̇O2peak (17). This study doesn’t purport to investigate the regulation of heart activity in TR versus UT; however, these data support the concept that the degree of muscle stress during exercise is sensed by the afferent nerves and integrated into the cardiac adjustment to exercise (31).
Although the different physiological responses between TR and UT during exercise at 70% V̇O2peak are best explained by the training-enhanced oxidative capacity of TR, it is possible—because the present study employed a cross-sectional experimental design—that the differences may be partially due to genetic differences between the two groups in terms of fiber type distribution. For example, the lesser accumulation of plasma ammonia and lactate and the tendency for a lower plasma hypoxanthine observed in TR at 70% V̇O2peak may result from a greater reliance on Type I muscle fibers. It is well established that endurance trained individuals have a greater proportion of Type I fibers than the general population (34), which may be determined by a combination of genetics and training. It is possible therefore, that a predominance of Type I fibers in TR may thus diminish the metabolic response to exercise. In contrast, the UT subjects in the present study would be expected to recruit a greater number of Type II fibers during exercise at 70% V̇O2peak, compared with TR. This increased reliance on Type II fibers may have contributed significantly to the greater circulating ammonia, hypoxanthine, and lactate concentrations in UT at 70% V̇O2peak, because Type II fibers are associated with an increased muscle ATP loss (11,30), greater blood ammonia concentration (10,19), and lactate production (13).
Exercise at 95% LT.
In the present study, we attempted to test the two subject populations at a work rate sufficient to maintain metabolic control. Although there is some controversy surrounding the term “lactate threshold” and the methods for measuring such a phenomenon (39), we (14) and others (6) have demonstrated that the use of the method employed in the current study was successful in maintaining metabolic control and is an accurate predictor of endurance performance. The data from the 95% LT trials support these earlier studies since no differences in the accumulation of plasma ammonia, hypoxanthine, or lactate between TR and UT during exercise at 95% LT were observed (Fig. 3). In addition, the present data are similar to the findings of McLellan and Jacobs (29), who observed that expressing the exercise intensity relative to the onset of blood lactate accumulation (OBLA), rather than to V̇O2peak, decreased the individual variability of the blood lactate response during 30 min of exercise. The low concentrations of plasma ammonia and hypoxanthine (Fig. 3, B and C) in the present study suggest that both TR and UT were able to meet ATP demand during exercise at 95% LT. To our knowledge there are no published data comparing the accumulation of plasma ammonia and hypoxanthine between TR and UT at this intensity. Additionally, as there were no differences in HR (Fig. 2) between TR and UT during exercise at 95% LT, the cardiac stress appears to be similar between the groups at this intensity. To our knowledge there are no data comparing HR in TR and UT during exercise at 95% LT.
Although the present study is unable to determine the mechanism for the similar metabolic and cardiac responses between TR and UT when exercising at 95% LT, it is possible that the homogenous responses may be due to a similar fiber type recruitment pattern at this exercise intensity. There is substantial evidence (18,34) which demonstrates that Type I motor units are recruited first during prolonged submaximal exercise in humans. Furthermore, glycogen depletion is more pronounced in Type I than in Type II fibers during light (31% V̇O2peak) and moderate (61% V̇O2peak) submaximal exercise (18,34). In addition, Nagata et al. (32) observed a significant correlation (r = 0.92) between the electromyograph (EMG) threshold, as determined by the nonlinear increase in the integrated EMG (IEMG) and the blood lactate threshold. These researchers suggested that the nonlinear increase in the IEMG was probably due to increased recruitment of Type II motor units. Based on these data, Type I muscle fibers would be expected to be the predominant fiber type recruited during exercise at an intensity below the LT (95% LT) in both the TR and UT groups in the present study. If this is correct, the similar muscle fiber recruitment pattern during exercise at 95% LT may explain, at least in part, the similar metabolic responses observed between the groups. It should be noted that there are other factors, such as a similar distribution of power output and economy of movement (7) that may also partially account for the similar metabolic responses observed between TR and UT during exercise at 95% LT.
In conclusion, the present study demonstrates that the markers of exercise stress were greater in UT compared with TR when the exercise was performed at the same relative percentage of peak oxygen consumption (i.e., 70% V̇O2peak). In contrast, the metabolic and cardiac stress in TR and UT subjects were similar during exercise at 95% LT. These findings suggest that the frequently selected work rate of between 60 and 80% V̇O2peak may be inappropriate as a relative exercise intensity when comparing endurance trained with untrained subjects, because it may be below the LT in the trained, but well above the LT in the untrained group. In order to normalize the exercise intensity between individuals with different aerobic capacities, it may be more appropriate to select a work rate relative to the LT.
We thank the subjects for participating in this study, and Sue Fabris and Troy Flanagan for technical assistance. This work was funded, in part, by a grant from the Faculty of Biomedical and Health Sciences, R.M.I.T.
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