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This study examined the hypothesis that walking training (WT) could accelerate the slowed time constant (τ) of phase II in pulmonary oxygen uptake ( $$\dot {V}$$ O2) on-kinetics in older women. Also, we aimed to demonstrate that O2 delivery and O2 utilization were better matched at the site of gas exchange in exercising muscles when τ $$\dot {V}$$ O2 was shortened. 20 recreationally active older women underwent WT sessions of approximately 60 min, 3–4 times a week for 12 weeks. We assessed $$\dot {V}$$ O2, heart rate (HR) and deoxygenated-hemoglobin concentration ([HHb]) kinetics during a constant-load exercise test before training (0 week—Pre), and at 6 and 12 weeks (6 weeks—Mid, 12 weeks—Post) throughout the training period. Maximal oxygen uptake ( $$\dot {V}$$ O2max) was unchanged throughout the training program. τHR tended to decline at Mid (58.6 ± 22.0 s), and was significantly shorter at Post (51.7 ± 21.7 s, p = 0.01) compared to Pre (67.1 ± 23.8 s). τ $$\dot {V}$$ O2 significantly decreased from 38.9 ± 8.6 s for Pre, to 31.5 ± 7.9 s for Mid (p = 0.02), and 32.3 ± 10.5 s for Post (p = 0.03). The normalized [HHb] to $$\dot {V}$$ O2 ratio (Δ[HHb]/Δ $$\dot {V}$$ O2) at Pre (1.32 ± 0.93) gradually approached the perfectly matched value (= 1.0) at Mid (1.15 ± 0.61) and Post (1.07 ± 0.52). The restoration to baseline (≒ 30 s) of the slower τ $$\dot {V}$$ O2 due to WT, which may reflect better matching of O2 delivery and O2 utilization at the site of gas exchange, suggests that a longer period of WT could be a useful tool for improving exercise tolerance in older individuals.

Background: It has recently been reported that unilateral fatiguing exercise affects not only the motor area innervating the exercising muscle but also the ipsilateral motor area innervating homologous nonexercised muscle. Objective: This study was designed to clarify the effects of fatiguing intermittent lower limb exercise on the excitability of the motor cortex representation of nonexercised muscles in the arm. Methods: Eight subjects performed an intermittent leg press exercise composed of three bouts of 5-minute leg press (T1, T2, and T3) at 50% of maximal voluntary contraction separated by a 2-minute rest. Motor-evoked potentials (MEP), short interval intracortical inhibition (SICI), and intracortical facilitation (ICF), using paired-pulse transcranial magnetic stimulation, were assessed in two nonexercised arm muscles (first dorsal interosseous muscle: FDI, n = 8; biceps brachii muscle: BB, n = 6) and one exercised leg muscle (quadriceps femoris muscle: QF, n = 6) before and immediately after each bout of exercise and for 30 minutes during recovery after the end of the third exercise bout (Experiment 1). Experiment 2 was the same as Experiment 1, except that the test pulse intensity was adjusted to produce a given amplitude of MEPTEST at each time point. Results: MEPs and SICI in the exercised QF muscle were depressed at all time points during and after fatigue. In contrast, MEPs in nonexercised arm muscles were facilitated from T1-T3 (T3, only FDI), but were then depressed for up to 20 minutes in the recovery period. SICI was reduced in both muscles during T1-T3 and remained depressed until 20 minutes into recovery. ICF was unchanged in arm muscles but depressed in QF over T1-T3. Conclusions: The current study indicates that muscle fatigue induced by exercise of a large lower limb muscle group has powerful effects on the excitability of both SICI and the corticospinal projection to muscles of the nonexercised upper limb.

It has been hypothesized that the signals of near infrared spectroscopy (NIRS) would reflect muscle O(2) uptake (mVO(2)). Although it is not definite that NIRS signals accurately reflect mVO(2), there is every possibility that NIRS signals at least reflect regional O(2) uptake (rVO(2)). The phase II kinetics of pulmonary oxygen uptake (pVO(2)) is regarded as reflecting mVO(2) at the onset of exercise. To examine whether the rVO(2) on-kinetics measured by NIRS reflects the mVO(2) on-kinetics at the onset of exercise, we compared the rVO(2) as measured by NIRS with the phase II kinetics of pVO(2) at the onset of exercise. Twelve healthy male subjects cycled a Monark ergometer at three different intensities: below the ventilatory threshold (VT) level (below-VT), on the VT level (on-VT), and above the VT level (above-VT), for 6 minutes on three separate occasions. The rVO(2) was calculated from the concentration of oxyhemoglobin and deoxyhemoglobin, as measured by NIRS every 3 seconds. The pVO(2) was determined by the breath-by-breath method. A significant relationship between the amount of increases of pVO(2) and rVO(2) from rest to the end of exercise among all levels of exercise intensity was found (r=0.935, P0.001). The time constants of rVO(2) (rVO(2)-Tc: below-VT: 6.514+/-2.159 s, on-VT: 7.760+/-2.035 s, above-VT: 9.532+/-2.342 s) were significantly faster than the time constants of pVO(2) (pVO(2)-Tc: below-VT: 23.8+/-4.4 s, on-VT: 25.9+/-5.1 s, above-VT: 26.3+/-5.7 s) (P0.001). There was no significant relationship between rVO(2)-Tc and pVO(2)-Tc for each intensity (P0.05). We conclude that the rVO(2) on-kinetics measured by NIRS does not necessarily reflect the mVO(2) kinetics at the onset of 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.

The effect of bicarbonate ingestion on total excess volume of CO2 Output (CO2 excess), due to bicaronate 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

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 C02 excess per unit of body mass per unit of blood lactate accumulation (Ala−) in exercise (CO2 excess·mass−1·Δla−), 12-min ERP, VO2 at AT (AT-VO2) and VO2max on average were 0.8 ml·kg−1·l−1·mmol−1, 97.8m, 4.4 ml·kg−1· min−1 and 7.3 ml·kg−1·min−1, respectively. The percentage change in CO2 excess·mass−1·Δla− (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·Δla− and the absolute amount of change in AT-VO2 (r=0.94, P

Objective This study was designed to examine whether exhaustive grip exercise of the left hand affected intracortical excitability in ipsilateral motor cortex. Methods Ten healthy male subjects (aged 21-24 years) participated in experiment 1 in which paired-pulse transcranial magnetic stimulation (TMS) was used to test corticospinal and corticocortical excitability in right (relaxed) first dorsal interosseous (FDI) muscle during the recovery period after exhaustive forceful grip exercise of the left hand. Seven of the same subjects participated in experiment 2, in which the intensity of the test stimulus was adjusted so that the amplitude of motor evoked potential (MEP(TEST)) was kept constant throughout the measurement. Results In experiment 1, MEP(TEST) was slightly reduced from 5 to 15min after exercise whilst short interval intracortical inhibition (SICI) at interstimulus interval (ISI) of 2 and 3ms became less effective. Intracortical facilitation (ICF) was unchanged. In experiment 2 when the MEP(TEST) was maintained at a constant size there was again no change in ICF, and the reduction in SICI was still present at the same intervals. Conclusions We conclude that unilateral exhaustive grip exercise reduced the excitability of the corticospinal output of the ipsilateral motor cortex whilst simultaneously reducing the excitability of SICI. These results would be compatible with the idea that fatigue increases the tonic level of interhemispheric inhibition from the fatigued to the non-fatigued cortex. Significance Muscle fatigue to the point of exhaustion has lasting effects on the excitability of intracortical circuits in the non-exercised hemisphere, perhaps via changes in the tonic levels of activity in transcallosal pathways.

It has been reported that oxygen uptake (VO2) increases exponentially with levels of the pedal rate during cycling. The purpose of this study was therefore to test the hypothesis that the O2 cost for internal power output (Pint) exerted in exercising muscle itself would be larger than for an external power output (Pext) calculated from external load and pedal rate during cycling exercise under various conditions of Pint and Pext in a large range of pedal rates. The O2 cost (DeltaVO2/ Deltapower output) was investigated in three experiments that featured different conditions on a cycle ergometer that were carried out at the same levels of total power output (Ptot; sum of Pint and Pext) (Exp. 1), Pext (Exp. 2) and load (Exp. 3). Each experiment consisted of three exercise tests with three levels of pedal rate (40 rpm for a lower pedal rate: LP; 70-80 rpm for a moderate pedal rate: MP; and 100-120 rpm for a higher pedal rate: HP) lasting for 2-3 min of unloaded cycling followed by 4-5 min of loaded cycling. Blood lactate accumulations (2.3-3.4 mmol l(-1)) at the HP were significantly higher compared with the LP (0.6-0.9 mmol l(-1)) and MP (0.9-1.0 mmol l(-1)) except for the LP in Exp. 1. The VO2 (360-432 ml min(-1) for LP, 479-644 ml min(-1) for MP, 960-1602 ml min(-1) for HP) during unloaded cycling in the three experiments increased exponentially with increasing pedal rates regardless of Pext=0. Moreover, the slope of the VO2-Pint (13.7 ml min(-1) W(-1)) relation revealed a steeper inclination than that of the VO2-Pext (10.2 ml min(-1) W(-1)) relation. We concluded that the O2 cost for Pint was larger than for Pext during the cycling exercises, indicating that the O2 cost for Ptot could be affected by the ratio of Pint to Ptot due to the levels of pedal rate.

The purpose of this study was to investigate the muscular efficiency during cycling exercise under certain total power output (P tot) or external power output (P ext) experimental conditions that required a large range of pedal rates from 40 to 120 rpm. Muscular efficiency estimated as a ratio of P tot, which is sum of internal power output (P int) and P ext, to rate of energy expenditure above a resting level was investigated in two experiments that featured different conditions on a cycle ergometer, which were carried out at the same levels of P tot (Exp. 1) and P ext (Exp. 2). Each experiment consisted of three exercise tests with three levels of pedal rates (40, 80 and 120 rpm) lasting for 2–3 min of unloaded cycling followed by 4–5 min of loaded cycling. $$ \dot V{\text{O}}_2 $$ during unloaded cycling (∼430 ml min−1 for 40 rpm, ∼640 ml min−1 for 80 rpm, ∼1,600 ml min−1 for 120 rpm) and the P int (∼3 W for 40 rpm, ∼25 W for 80 rpm, ∼90 W for 120 rpm) in the two experiments were markedly increased with increasing pedal rates. The highest muscular efficiency was found at 80 rpm in the two experiments, whereas a remarkable reduction (19%) in muscular efficiency obtained at 120 rpm could be attributable to greater O2 cost due to higher levels of P int accompanying the increased pedal rates. We concluded that muscular efficiency could be affected by the differences in O2 cost and P int during cycling under the large range of pedal rates employed in this study.

This study was carried out to compare blood lactate changes in isocapnic buffering phase in an incremental exercise test between sprinters and long distance runners, and to seek the possibility for predicting aerobic or anaerobic potential from blood lactate changes in isocapnic buffering phase. Gas exchange variables and blood lactate concentration ([lactate]) in six sprinters (SPR) and nine long distance runners (LDR) were measured during an incremental exercise test (30 W.min-1) up to subject's voluntary exhaustion on a cycle ergometer. Using a difference between [lactate] at lactate threshold (LT) and [lactate] at the onset of respiratory compensation phase (RCP) and the peak value of [lactate] obtained during a recovery period from the end of the exercise test, the relative increase in [lactate] during the isocapnic buffering phase ([lactate]ICBP) was assessed. The [lactate] at LT (mean +/- SD) was similar in both groups (1.36 +/- 0.27 for SPR vs. 1.24 +/- 0.24 mmol.l-1 for LDR), while the [lactate] at RCP and the peak value of [lactate] were found to be significantly higher in SPR than in LDR (3.61 +/- 0.33 vs. 2.36 +/- 0.45 mmol.l-1 for RCP, P < 0.001, 10.18 +/- 1.53 vs. 8.10 +/- 1.61 mmol.l-1 for peak, P < 0.05). The [lactate]ICBP showed a significantly higher value in SPR (22.5 +/- 5.9%, P < 0.05) compared to that in LDR (14.2 +/- 5.0%) as a result of a twofold greater increase of [lactate] from LT to RCP (2.25 +/- 0.49 for SPR vs. 1.12 +/- 0.39 mmol.l-1 for LDR). In addition, the [lactate]ICBP inversely correlated with oxygen uptake at LT (VO2LT, r = -0.582, P < 0.05) and maximal oxygen uptake (VO2max, r = -0.644, P < 0.01). The results indicate that the [lactate]ICBP is likely to give an index for the integrated metabolic, respiratory and buffering responses at the initial stage of metabolic acidosis derived from lactate accumulation.

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·l−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 \(\dot V\)O2 (ml · kg−1 · min−) AT-WR, OBLS-\(\dot V\)O2 (ml · kg−1 · min−), and OBLA-WR, respectively. When AT-HR (X2) was added to the \(\dot V\)O2 (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·l−1.

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.

TANAKA, KIYOJI, YOSHIYUKI MATSUURA, AKIRA MATSUZAKA, KOHJI HIRAKOBA, SHUZO KUMAGAI, SUB O. SUN, and KATSUMI ASANO. A longitudinal assessment of anaerobic threshold and distance-running performance. Med. Sci. Sports Exerc., Vol. 16, No. 3, pp. 278–282, 1984. 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 (JOURNAL/mespex/beta/00005768-198406000-00020/ENTITY_OV0398/v/2017-05-02T160503Z/r/image-png 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≥0.75) between the DRP and AT-related attributes held up consistently over the 9-month training period. Anaerobic threshold (expressed as ml O2·min-1·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 JOURNAL/mespex/beta/00005768-198406000-00017/ENTITY_OV0312/v/2017-05-02T160503Z/r/image-pngO2@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 JOURNAL/mespex/beta/00005768-198406000-00017/ENTITY_OV0312/v/2017-05-02T160503Z/r/image-pngO2@AT and/or V@AT changes rather than changes in other physiological attributes.