Effects of submaximal cycling at different exercise intensities on maximal isometric force output of the non-exercised elbow flexor muscles.

The purpose of this study was to examine the effects of submaximal cycling at different exercise intensities on maximal isometric force output of the non-exercised elbow flexor muscles after the cycling. A total of 8 healthy young men performed multiple maximal voluntary contractions by the right elbow flexion before, immediately after, 5 min after, and 10 min after a 6-min submaximal cycling at ventilatory threshold (LI), 70% [Formula: see text] (MI), and 80% [Formula: see text] (HI) with both arms relaxed in the air. Force and surface electromyogram (EMG) of the right biceps brachii muscle during the multiple MVCs, blood lactate concentration ([La]), cardiorespiratory responses, and sensations of fatigue for legs (SEF-L) were measured before, immediately after, 5 min after, and 10 min after the submaximal cycling with the three different exercise intensities. Immediately after the submaximal cycling, [La], cardiorespiratory responses, and SEF-L were enhanced in proportion to an increase in exercise intensity of the cycling. Changes in force and EMG activity during the multiple MVCs were not significantly different across the three conditions. The findings imply that group III/IV muscle afferent feedback after the submaximal cycling does not determine the magnitude of MVC force loss of the non-exercised upper limb muscles.

Effect of low-intensity training on transient kinetics of pulmonary oxygen uptake during moderate-intensity cycle exercise.

AIM: It is unclear whether the slowed time constant of phase II in pulmonary oxygen uptake on-kinetics (V̇O2τ) in unfit and inactive men would be shortened by low exercise intensity (low-intensity) walking training. We therefore tested the hypothesis that the slowed V̇O2τ in sedentary population would speed up due to low-intensity walking training with high volume. METHODS: Ten unfit and inactive male subjects (aged 26 to 50 yrs) underwent a low-intensity (30-40% of V̇O2max), long-duration (>60 min) training in the form of walking exercise 3-4 times a week for 12 weeks. We prospectively collected data on anthropometric, maximal oxygen uptake (V̇O2max), time constant of heart rate (HRτ) and V̇O2τ before training (0 wk; Pre) and every six weeks (6 wk; Mid, 12 wk; Post) from the beginning of the training. RESULTS: Anthropometric variables and V̇O2max showed no significant changes throughout the training program, whereas HRτ showed a tendency to be shortened with a progress of the training with no significant change. The slowed V̇O2τ at Pre (47.6±5.6 s) remained almost unchanged at Mid (48.8±4.9 s), but had a significant decrease at Post (40.5±7.9 s, P<0.05). CONCLUSION: In this study acceleration of the slowed V̇O2τ due to low-intensity walking training is thought to occur presumably owing to an improved matching of oxygen delivery to oxygen utilization at the site of gas exchange in active muscle tissue. We concluded that low-intensity walking training at beginning stage of training could contribute to the acceleration of the slowed V̇O2τ in unfit and inactive subjects.

Effect of different pedal rates on oxygen uptake slow component during constant-load cycling exercise.

AIM: We hypothesized that an extremely high pedal rate would induce much more type II muscle fibers recruitment even at an early phase of the same absolute work rate compared with normal pedal rates, and would result in changed amplitude of the pulmonary oxygen uptake slow component (VO(2)SC) during heavy constant-load exercise. METHODS: Two square-wave transitions of constant-load exercise were carried out at an exercise intensity corresponding to a VO(2) of 130% of the ventilatory threshold. The amplitude of the VO(2)SC in phase III during heavy constant-load exercise was determined at normal (60 rpm) and extremely high pedal rates (110 rpm). The VO(2) kinetics were analyzed by nonlinear regression. RESULTS: Although the absolute work rates were almost identical in the two pedal rates cycling exercise, the amplitude of the VO(2) in phase II (phase II amplitude), end-exercise VO(2) (EEVO(2)) and blood lactate accumulation ([La]) were significantly greater at 110 rpm than at 60 rpm (2 260+/-242 vs 1.830+/-304 mL.min(-1) for phase II amplitude; P<0.01, 2 350+/-265 vs 1 709+/-342 mL.min(-1) for EEVO(2); P<0.01, 6.4+/-1.3 vs 3.2+/-1.3 mmol.L(-1) for [La]; P<0.01, respectively). The amplitude of the VO(2)SC in phase III also revealed a significantly higher value at 110 rpm compared with 60 rpm (416+/-73 vs 201+/-89 mL.min(-1), P<0.01). In spite of the appearance of greater VO(2)SC at 110 rpm, no corresponding changes in integrals of the electromyography (EMG) signal and mean power frequency were observed. CONCLUSIONS: The results of this study indicate that the amplitude of the VO(2)SC was greater in higher pedal rate during the same work rate constant-load cycling exercise, which might be associated with a progressive increase in the adenosine triphosphate requirement of already recruited muscle fibers in exercising muscle.

Phosphocreatine content in single fibers of human muscle after sustained submaximal exercise.

The effect of sustained submaximal exercise on muscle energetics has been studied on the single-fiber level in human skeletal muscle. Seven subjects cycled to fatigue (mean 77 min) at a work rate corresponding to approximately 75% of maximal O2 uptake. Biopsies were taken from the vastus lateralis muscle at rest, at fatigue, and after 5 min of recovery. Muscle glycogen decreased from 444 +/- 40 (SE) mmol glucosyl units/kg dry wt at rest to 94 +/- 16. Postexercise glycogen was inversely correlated (P < 0.01) to muscle content of inosine monophosphate, a catabolite of ATP. Phosphocreatine (PCr) in mixed-fiber muscle decreased at fatigue to 37% but was restored above the initial value (106.5%, P < 0.025) after 5 min of recovery. The overshoot was localized to type I fibers. The rapid reversal of PCr is in contrast to the slow recovery in contraction force. Pi increased at fatigue but less than that expected from the changes in PCr and other phosphate compounds. Mean PCr at rest was approximately 20% higher in type II than in type I fibers (86.4 +/- 3.6 and 71.6 +/- 1.8 mmol/kg dry wt, respectively, P < 0.05), but at fatigue similar PCr contents were observed in the two fiber types. Reduction in PCr in all fibers at fatigue suggests that all fibers were recruited at the end of exercise. PCr content in single fibers showed a great variability in samples at rest, exercise, and recovery. The variability was more pronounced than for ATP, and the data suggest that it is due to interfiber physiological-biochemical differences. At fatigue ATP was maintained relatively high in all single fibers, but a pronounced depletion of PCr was observed in a large number of fibers, and this may contribute to fatigue through the associated increases in Pi or/and free ADP. It is noteworthy that the increase in calculated free ADP at fatigue was similar to that after high-intensity exercise.

Prediction of blood lactate accumulation from excess CO2 output during constant exercise.

To determine the predictability of blood lactate accumulation from excess CO2 output derived from bicarbonate buffering of lactic acid during constant exercise, eight normal active volunteers were studied during three stages of constant exercise on a cycle ergometer. Three work rates consisted of 100% (stage I), 120% (stage II) and 150% (stage III) of each subject's anaerobic threshold (AT), each of which was lasted for 4 min. Excess CO2 output (Ex CO2, ml) at each stage of constant exercise was estimated form the integral of difference between total VCO2 and aerobic VCO2 (from regression line for VCO2 and VO2 at exercise intensities below the AT obtained in incremental exercise test). Ex CO2 per body mass (Ex CO2-mass-1) was increased progressively with blood lactate (La) accumulation from rest to each stage of constant exercise. Mean values (+/-SD) in the measured La accumulation (delta La,measured) and predicted La accumulation (delta La,predicted) at three stages of constant exercise were 1.82 +/- 0.83 vs 3.19 +/- 1.70 for stage 1, 5.58 +/- 3.47 vs 7.09 +/- 3.28 for stage II and 12.19 +/- 2.36 vs 12.74 +/- 1.83 mmol.l-1 for stage III, respectively. There was a significant difference between delta La,measured and delta La,predicted at stage I (p < 0.05), but no significant differences between these two variables at stage II and III. The averaged difference from delta La,predicted to delta La,measured at stage III (0.55 mmol.l-1) showed a tendency to be smaller than stage I (1.38 mmol.l-1) and II (1.50 mmol.l-1). On the other hand, delta La,predicted was found to correlate very closely with delta La,measured (r = 0.954, P < 0.001, n = 20). The results of this study suggest that the changes of La accumulation could be predicted from excess CO2 output generated in constant exercises above the AT.

Effect of acute sodium bicarbonate ingestion on excess CO2 output during incremental exercise.

The effect of bicarbonate ingestion on total excess volume of CO2 output (CO2 excess), due to bicarbonate buffering of lactic acid in exercise, was studied in eight healthy male volunteers during incremental exercise on a cycle ergometer performed after ingestion (0.3 g.kg-1 body mass) of CaCO3 (control) and NaHCO3 (alkalosis). The resting arterialized venous blood pH (P < 0.05) and bicarbonate concentration ([HCO3-]b; P < 0.01) were significantly higher in acute metabolic alkalosis [AMA; pH, 7.44 (SD 0.03); [HCO3-]b, 29.4 (SD 1.5) mmol.l-1] than in the control [pH, 7.39 (SD 0.03); [HCO3-]b, 25.5 (SD 1.0) mmol.l-1]. The blood lactate concentrations ([la-]b) during exercise below the anaerobic threshold (AT) were not affected by AMA, while significantly higher [la-]b at exhaustion [12.29 (SD 1.87) vs 9.57 (SD 2.14) mmol.l-1, P < 0.05] and at 3 min after exercise [14.41 (SD 1.75) vs 12.26 (SD 1.40) mmol.l-1, P < 0.05] were found in AMA compared with the control. The CO2 excess increased significantly from the control [3177 (SD 506) ml] to AMA [3897 (SD 381) ml; P < 0.05]. The CO2 excess per body mass was found to be significantly correlated with both the increase of [la-]b from rest to 3 min after exercise (delta[la-]b; r = 0.926, P < 0.001) and with the decrease of [HCO3-]b from rest to 3 min after exercise (delta [HCO3-]b; r = 0.872, P < 0.001), indicating that CO2 excess per body mass increased linearly with both delta [la-]b and delta [HCO3-]b.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of endurance training on excessive CO2 expiration due to lactate production in exercise.

We attempted to determine the change in total excess volume of CO2 output (CO2 excess) due to bicarbonate buffering of lactic acid produced in exercise due to endurance training for approximately 2 months and to assess the relationship between the changes of CO2 excess and distance-running performance. Six male endurance runners, aged 19-22 years, were subjects. Maximal oxygen uptake (VO2max), oxygen uptake (VO2) at anaerobic threshold (AT), CO2 excess and blood lactate concentration were measured during incremental exercise on a cycle ergometer and 12-min exhausting running performance (12-min ERP) was also measured on the track before and after endurance training. The absolute magnitudes in the improvement due to training for CO2 excess per unit of body mass per unit of blood lactate accumulation (delta la-) in exercise (CO2 excess.mass-1.delta la-), 12-min ERP, VO2 at AT (AT-VO2) and VO2max on average were 0.8 ml.kg-1.l-1.mmol-1, 97.8 m, 4.4 ml.kg-1. min-1 and 7.3 ml.kg-1.min-1, respectively. The percentage change in CO2 excess.mass-1.delta la- (15.7%) was almost same as those of VO2max (13.7%) and AT-VO2 (13.2%). It was found to be a high correlation between the absolute amount of change in CO2 excess.mass-1.delta la-, and the absolute amount of change in AT-VO2 (r = 0.94, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

A longitudinal assessment of anaerobic threshold and distance-running performance.

Longitudinal changes in the anaerobic threshold (AT) and distance-running performances (DRP) were assessed with a 4.5-month interval between the pre-, mid-, and post-tests in a relatively homogeneous (in terms of both maximal aerobic power and DRP) sample of 21 male, trained, endurance runners (means age = 18.5 yr) than had been employed previously. ANOVA with repeated measures followed by the Newman- Keuls post-hoc comparison revealed that there were significant alterations in both DRP and AT. Even in this improved state, higher relationships (r greater than or equal to 0.75) between the DRP and AT-related attributes held up consistently over the 9-month training period. Anaerobic threshold (expressed as ml O2 X min-1 X kg-1) showed a correlation higher than 0.80 with 10,000-m race time in every set of tests. When the relationships between the absolute amount of change in the Vo2@AT and the absolute amount of change in DRP were evaluated, significant correlations (r = -0.56 to -0.83) were found in several different time periods. Running velocity at AT (V@AT) also improved significantly, and was closely related to DRP changes. It is speculated that DRP changes are more directly accounted for by the Vo2@AT and/or V@AT changes rather than changes in other physiological attributes.

Relationships of anaerobic threshold and onset of blood lactate accumulation with endurance performance.

This study was undertaken to compare the contribution of both the anaerobic threshold (AT) and onset of blood lactate accumulation (OBLA) with endurance performance in eleven non-endurance trained active male adults. AT determination was based upon both blood lactate and gas exchange criteria, while OBLA was determined as the point corresponding to a blood lactate concentration of 4 mmol X 1(-1). A dependent t-test revealed significantly higher values for OBLA related variables as compared with corresponding AT related variables, thereby validating the comparison of these two categories of variables in relation to endurance performance. Approximately 67, 60, 37, and 50% of the variance in endurance performance were accounted for by AT-VO2 (ml X kg-1 X min-1), AT-WR, OBLA-VO2 (ml X kg-1 X min-1), and OBLA-WR, respectively. When AT-HR (X2) was added to the AT-VO2 (X1) as another predictor, the contribution of these variables to endurance performance increased appreciably to 84%. The resultant multiple regression equation was Y = -4.564 X1 + 2.68 IX2 + 90.6 (SEE = 9.9 s). Consequently, it is suggested that variables related to an abrupt increase in blood lactate, together with several gas exchange responses, could explain endurance performance in a shorter distance to a greater extent than variables related to a rigid threshold of 4 mmol X 1(-1).

Relationships of the anaerobic threshold with the 5 km, 10 km, and 10 mile races.

The purpose of present study was to assess the relationship between anaerobic threshold (AT) and performances in three different distance races (i.e., 5 km, 10 km, and 10 mile). AT, VO2 max, and related parameters for 17 young endurance runners aged 16--18 years tested on a treadmill with a discontinuous method. The determination of AT was based upon both gas exchange and blood lactate methods. Performances in the distance races were measured within nearly the same month as the time of experiment. Mean AT-VO2 was 51.0 ml . kg-1 . min-1 (2.837 l . min-1), while VO2 max averaged 64.1 ml . kg-1 . min-1 (3.568 l . min-1). AT-HR and %AT (AT-VO2/VO2 max) were 174.7 beats . min-1 and 79.6%, respectively. The correlations between VO2 max (ml . kg-1 . min-1) and performances in the three distance races were not high (r = -0.645, r = -0.674, r = -0.574), while those between AT-VO2 and performances was r = -0.945, r = -0.839, and r = -0.835, respectively. The latter results indicate that AT-VO2 alone would account for 83.9%, 70.4%, and 69.7% of the variance in the 5 km, 10 km, and 10 mile performances, respectively. Since r = -0.945 (5 km versus AT-VO2) is significantly different from r = -0.645 (5 km versus VO2 max), the 5 km performance appears to be more related to AT-VO2 than VO2 max. It is concluded that individual variance in the middle and long distance races (particularly the 5 km race) is better accounted for by the variance in AT-VO2 expressed as milliliters of oxygen per kilogram of body weight than by differences in VO2 max.