A comparison of modelling techniques used to characterise oxygen uptake kinetics during the on-transient of exercise

We compared estimates for the phase 2 time constant (tau) of oxygen uptake (VO2) during moderate- and heavy-intensity exercise, and the slow component of VO2 during heavy-intensity exercise using previously published exponential models. Estimates for tau and the slow component were different (P < 0.05) among models. For moderate-intensity exercise, a two-component exponential model, or a mono-exponential model fitted from 20 s to 3 min were best. For heavy-intensity exercise, a three-component model fitted throughout the entire 6 min bout of exercise, or a two-component model fitted from 20 s were best. When the time delays for the two- and three-component models were equal the best statistical fit was obtained; however, this model produced an inappropriately low DeltaVO2/DeltaWR (WR, work rate) for the projected phase 2 steady state, and the estimate of phase 2 tau was shortened compared with other models. The slow component was quantified as the difference between VO2 at end-exercise (6 min) and at 3 min (DeltaVO2 (6-3 min)); 259 ml x min(-1)), and also using the phase 3 amplitude terms (truncated to end-exercise) from exponential fits (409-833 ml x min(-1)). Onset of the slow component was identified by the phase 3 time delay parameter as being of delayed onset approximately 2 min (vs. arbitrary 3 min). Using this delay DeltaVO2 (6-2 min) was approximately 400 ml x min(-1). Use of valid consistent methods to estimate tau and the slow component in exercise are needed to advance physiological understanding.     

The effect of pedal rate on pulmonary O2 uptake kinetics during very heavy intensity exercise in trained and untrained teenage boys

This study tested the hypothesis that the VO2 kinetic response would be slowed in untrained (UT) but not trained (T) teenage participants whilst cycling at 115 rev min(-1) compared to 50 rev min(-1). Eight UT and seven T boys completed two square-wave transitions to very heavy-intensity exercise pedalling at 50 rev min(-1) and 115 rev min(-1). In UT at the higher pedal rate, the phase II VO2 was significantly (P < 0.01) slower (50 rev min(-1): 32 ± 5 vs. 115 rev min(-1): 42 ± 11 s) and the relative VO2 slow component was significantly (P < 0.01) elevated (50 rev min(-1): 10 ± 3 vs. 115 rev min(-1): 16 ± 5%). The phase II VO2 (50 rev min(-1): 26 ± 4 vs. 115 rev min(-1): 22 ± 6s) and relative VO2 slow component (50 rev min(-1): 14 ± 5 vs. 115 rev min(-1): 17 ± 3%) were unaltered by pedal rate in T (P > 0.05). These data are consistent with the notion that VO2 kinetics are influenced by muscle fibre recruitment in youth but this effect is attenuated in endurance trained teenage boys.     

Effects of Prior Exercise and Recovery Duration on Oxygen Uptake Kinetics During Heavy Exercise in Humans

Prior heavy exercise (above the lactate threshold, LT) reduces the amplitude of the pulmonary oxygen uptake (VO2) slow component during heavy exercise, yet the precise effect of prior heavy exercise on the phase II VO2 response remains to be established. This study was designed to test the hypotheses that (1) prior heavy exercise increases the amplitude of the phase II VO2 response independently of changes in the baseline VO2 value and (2) the effect of prior exercise depends on the amount of external work done during prior exercise, irrespective of the intensity of the prior exercise. Nine subjects performed two 6 min bouts of heavy cycling exercise separated by 6 min baseline pedalling recovery (A), two 6 min heavy exercise bouts separated by 12 min recovery (6 min rest and 6 min baseline pedalling, B), and a bout of moderate exercise (below the LT) in which the same amount of external work was performed as during the prior heavy exercise, followed by 6 min heavy exercise (C). In both tests A and B, prior heavy exercise significantly increased the absolute VO2 amplitude at the end of phase II (by approximately 150 ml x min(-1)), and reduced the amplitude of the VO2 slow component by a similar amount. Following 12 min of recovery (B), baseline VO2, but not blood [lactate], had returned to pre-exercise levels, indicating that these effects occurred independently of changes in baseline VO2. Prior moderate exercise (C) had no effect on either the VO2 or blood [lactate] responses to subsequent heavy exercise. The VO2 response to heavy exercise was therefore dependent on the intensity of prior exercise, and the effects on the amplitudes of the phase II and slow VO2 components persisted for at least 12 min following prior heavy exercise.     

Effect of high-intensity interval training and detraining on extra {\dot{{V}}\hbox{O}_{2}} and on the {\dot{{V}}\hbox{O}_{2}} slow component

To examine the effect of 6-week of high-intensity interval training (HIT) and of 6-week of detraining on the VO2/Work Rate (WR) relationship and on the slow component of VO2, nine young male adults performed on cycle ergometer, before, after training and after detraining, an incremental exercise (IE), and a 6-min constant work rate exercise (CWRE) above the first ventilatory threshold (VT1). For each IE, the slope and the intercept of the VO2/WR relationship were calculated with linear regression using data before VT1. The difference between VO2max measured and VO2max expected using the pre-VT1 slope was calculated (extra VO2). The difference between VO2 at 6th min and VO2 at 3rd min during CWRE (DeltaVO2(6'-3')) was also determined. HIT induced significant improvement of most of the aerobic fitness parameters while most of these parameters returned to their pre-training level after detraining. Extra VO2 during IE was reduced after training (130 +/- 100 vs. -29 +/- 175 ml min(-1), P = 0.04) and was not altered after detraining compared to post-training. DeltaVO2(6'-3') during CWRE was unchanged by training and by detraining. We found a significant correlation (r2 = 0.575, P = 0.02) between extra VO2 and DeltaVO2(6'-3') before training. These results show that an alteration of extra VO2 can occur without any change in the VO2 slow component, suggesting a possible dissociation of the two phenomena. Moreover, the fact that extra VO2 did not change after detraining could indicate that this improvement may remain after the loss of other adaptations.     

Rat Muscle Microvascular PO2 Kinetics During the Exercise Off-Transient

Dependent upon the relative speed of pulmonary oxygen consumption (VO2) and blood flow (Q) kinetics, the exercise off-transient may represent a condition of sub- or supra-optimal perfusion. To date, there are no direct measurements of the dynamics of the VO2/Q relationship within the muscle at the onset of the work/recovery transition. To address this issue, microvascular PO2 (PO2,m) dynamics were studied in the spinotrapezius muscles of 11 female Sprague-Dawley rats (weight approximately 220 g) during and following electrical stimulation (1 Hz) to assess the adequacy of Q. relative to VO2 post exercise. The exercise blood flow response (radioactive microspheres: muscle Q increased approximately 240 %), and post-exercise arterial blood pH (7.40 +/- 0.02) and blood lactate (1.3 +/- 0.4 mM x l(-1)) values were consistent with moderate-intensity exercise. Recovery PO2,m (i.e. off-transient) rose progressively until baseline values were achieved ((Delta)end-recovery exercise PO2,m, 14.0 +/- 1.9 Torr) and at no time fell below exercising PO2,m. The off-transient PO2,m was well fitted by a dual exponential model with both fast (tau = 25.4 +/- 5.1 s) and slow (tau = 71.2 +/- 34.2 s) components. Furthermore, there was a pronounced delay (54.9 +/- 10.7 s) before the onset of the slow component. These data, obtained at the muscle microvascular level, support the notion that muscle VO2 falls with faster kinetics than muscle Q during the off-transient, such that PO2,m increases systematically, though biphasically, during recovery.     

Oxygen uptake kinetics during severe exercise: a comparison between young and older men

This study examined the relationship between the slow component of oxygen uptake (VO2) kinetics and muscle electromyography (EMG) during severe exercise in nine young (21.7+/-0.9 yr) and nine older (71.6+/-0.8 yr) men. Oxygen uptake (VO2) and surface EMG activity of the left vastus lateralis muscle were measured during a 7-min square-wave bout of severe exercise on a cycle ergometer. The absolute amplitude of the VO2 slow component was greater and occurred approximately 60 s earlier in the young compared to older subjects. However, the rate of increase in the slow component, expressed as a percentage of the total VO2 response per unit time, was not different between young and older subjects (young: 4.8+/-0.5%.min(-1); older: 4.9+/-0.6%.min(-1)). The mean power frequency (MPF) of the EMG increased significantly during the slow component phase of exercise by 6.4+/-1.0% in the young and by 5.4+/-0.7% in the older group and this rise was not significantly different between the two groups. These results indicate that normal ageing may not alter the VO2 slow component (measured as the rate of increase in VO2) and that this finding may be related to similar muscle fibre recruitment patterns in the two groups during severe-intensity exercise.     

Kinetics of estimated human muscle capillary blood flow during recovery from exercise

The kinetic characteristics of muscle capillary blood flow (Qcap) during recovery from exercise are controversial (e.g. one versus two phases). Furthermore, it is not clear how the overall Qcap kinetics are temporally associated with muscle oxygen uptake (VO2m) kinetics. To address these issues, we examined the kinetics of Qcap estimated from the rearrangement of the Fick equation (Qcap=VO2m/C(a-v)O2) using the kinetics of pulmonary VO2 (VO2p, primary component) and deoxy-haemoglobin concentration ([HHb]) as indices of VO2m and C(a - v)O2 (arterio-venous oxygen difference) kinetics, respectively. VO2p (l min-1) was measured breath by breath and [HHb] (microm) was measured by near infrared spectroscopy during moderate (M; below lactate threshold, LT) and heavy exercise (H, above LT) in nine subjects. The kinetics of Qcap were biphasic, with an initial fast phase (tauI; M=9.3+/-4.9 s and H=6.0+/-3.8 s) followed by a slower phase 2 (tauP; M=29.9+/-8.6 s and H=47.7+/-26.0 s). For moderate exercise, the overall kinetics of Qcap (mean response time [MRT], 36.1+/-8.6 s) were significantly slower than the kinetics of VO2p (tauP; 27.8+/-5.3 s) and [HHb] (MRT for [HHb]; 16.2+/-6.3 s). However, for heavy exercise, there was no significant difference between MRT-[HHb] (34.7+/-10.4 s) and tauP for VO2p (32.3+/-6.7 s), while MRT for Qcap (48.7+/-21.8 s) was significantly slower than MRT for [HHb] and tauP for VO2p. In conclusion, during recovery from exercise the estimated Qcap kinetics were biphasic, showing an early rapid decrease in blood flow. In addition, the overall kinetics of Qcap were slower than the estimated VO2m kinetics.     

Pressor response to static and dynamic knee extensions at equivalent workload in humans

Static exercise has been thought to induce greater pressor response than dynamic exercise, but in contrast it has been recently reported that repetitive muscle contraction recruiting small muscles evokes greater response than sustained contraction. It remained unknown whether sustained contraction induces greater pressor response if large muscles were recruited. Nine subjects performed three types of isometric knee extensions recruiting the large muscle group, i.e., 2-min sustained (20% and 40% maximal voluntary contraction [MVC]) and 4-min repetitive (40% MVC, duty cycle = 1:1 s) muscle contractions. Compared under the equivalent TTI and exercising duration (2 min), the changes in femoral arterial blood flow and VO(2) from baseline (Delta BF, Delta VO(2)) were significantly less during sustained contraction than during repetitive contraction (sustained vs. repetitive; Delta BF: +92 +/- 195 vs. +1,174 +/- 269 ml.min(-1), Delta VO(2): +53 +/- 12 vs. +180 +/- 32 ml.min(-1), mean +/- SE, p < 0.05), although the change in mean arterial pressure (Delta MAP) was greater during sustained contraction (+24 +/- 3 vs. +19 +/- 3 mmHg). Compared under the equivalent TTI and peak tension (40% MVC), Delta BF and Delta VO(2) were less and Delta MAP was greater during sustained contraction (Delta BF: -296 +/- 176 vs. +868 +/- 272 ml.min(-1); Delta VO(2): +104 +/- 16 vs. + 212 +/- 46 ml.min(-1); Delta MAP: +37 +/- 8 vs. +20 +/- 4 mmHg). Moreover Delta MAP during postexercise occlusion of the active limb was significantly greater after sustained contraction than after repetitive contraction (+17.0 +/- 2.8 vs. +9.5 +/- 4.4 mmHg). These results demonstrated that pressor response is greater during sustained than during repetitive contraction, recruiting a large muscle group. This finding should be mainly due to the greater accumulation of metabolites in active muscles during sustained contraction.     

The VO2 response to submaximal ramp cycle exercise: Influence of ramp slope and training status

The aim of the study was to test whether ramp slope and training status interact in the oxygen uptake (VO2) response during submaximal ramp exercise. Eight cyclists (VO2 peak=67.8+/-3.7 ml min(-1)kg(-1)) and eight physically active students (PA students) (VO2 peak=49.1+/-4.3 ml min(-1)kg(-1)) performed several ramp protocols, respectively, 25 and 40 W min(-1) for the cyclists and 10, 25 and 40 W min(-1) for the PA students. Vo(2) was plotted as a function of time and work rate up to the gas exchange threshold (GET). Faster ramp elicited a significantly shorter mean response time (MRT) in both groups, and MRT was significantly longer for each ramp protocol in the PA students (126+/-32s, 76+/-15s and 50+/-6s for ramp 10, ramp 25 and ramp 40, respectively) compared to the cyclists (61+/-9s and 40+/-11s for ramp 25 and ramp 40, respectively). Ramp 40 showed less steep Delta VO2/Delta W than ramp 25 in both groups (p<0.01) and Delta VO2/Delta W was less steep for each ramp protocol in PA students (p<0.01) (9.82+/-0.30 ml min(-1)W(-1) and 9.33+/-0.45 ml min(-1)W(-1) for ramp 25 and ramp 40, respectively) compared to cyclists (10.31+/-0.40 ml min(-1)W(-1) and 10.05+/-0.48 ml min(-1)W(-1) for ramp 25 and ramp 40, respectively). In the PA students, Delta VO2/Delta W did not differ between ramp 10 and ramp 25. Statistical analysis showed no interaction effects between ramp slope and training status for MRT (p=0.62) and Delta VO2/Delta W (p=0.35).     

(.)VO(2) and EMG activity kinetics during moderate and severe constant work rate exercise in trained cyclists.

The purpose of this study was to compare O(2) uptake ((.)VO(2)) and muscle electromyography activity kinetics during moderate and severe exercise to test the hypothesis of progressive recruitment of fast-twitch fibers in the explanation of the VO(2) slow component. After an incremental test to exhaustion, 7 trained cyclists (mean +/- SD, 61.4 +/- 4.2 ml x min(-1) x kg(- 1)) performed several square-wave transitions for 6 min at moderate and severe intensities on a bicycle ergometer. The (.)VO(2) response and the electrical activity (i.e., median power frequency, MDF) of the quadriceps vastus lateralis and vastus medialis of both lower limbs were measured continuously during exercise. After 2 to 3 min of exercise onset, MDF values increased similarly during moderate and severe exercise for almost all muscles whereas a (.)VO(2) slow component occurred during severe exercise. There was no relationship between the increase of MDF values and the magnitude of the (.)VO(2) slow component during the severe exercise. These results suggest that the origin of the slow component may not be due to the progressive recruitment of fast-twitch fibers.     

Effects of recovery time on phosphocreatine kinetics during repeated bouts of heavy-intensity exercise

The purpose of this study was to examine the kinetics of phosphocreatine (PCr) breakdown in repeated bouts of heavy-intensity exercise separated by three different durations of resting recovery. Healthy young adult male subjects (n = 7) performed three protocols involving two identical bouts of heavy-intensity dynamic plantar flexion exercise separated by 3, 6, and 15 min of rest. Muscle high-energy phosphates and intracellular acid-base status were measured using phosphorus-31 magnetic resonance spectroscopy. In addition, the change in concentration of total haemoglobin (Delta[Hb(tot)]) and deoxy-haemoglobin (Delta[HHb]) were monitored using near-infrared spectroscopy. Prior exercise resulted in an elevated (P < 0.05) intracellular hydrogen ion ([H(+)](i)) after 3 min (182 +/- 72 (SD) nM; pH 6.73) and 6 min (112 +/- 19 nM; pH 6.95) but not after 15 min (93 +/- 8 nM; pH 7.03) compared to pre-exercise in Con (90 +/- 3 nM; pHi 7.05). The on-transient time constant (tau) of the PCr primary component was not different amongst the exercise bouts. However, in each of the subsequent bouts the amplitude of the PCr slow component, total PCr breakdown, and rise in [H(+)](i) were reduced (P < 0.05). At exercise onset, Delta[Hb(tot)] was increased (P < 0.05) and the Delta[HHb] kinetic response was slowed (P < 0.05) in the exercise after 3 min, consistent with improved muscle perfusion. In summary, neither the level of acidosis or muscle perfusion at the onset of exercise appeared to be directly related to the time course of the on-transient PCr primary component or the magnitude of the PCr slow component during subsequent bouts of exercise.     

Expression of a flt-4 (VEGFR3) splicing variant in primary human prostate tumors. VEGF D and flt-4t(Delta773-1081) overexpression is diagnostic for sentinel lymph node metastasis

Utilizing a cDNA expression library established from human prostate PC-3ML tumor cells, we have cloned a truncated flt-4 gene, termed flt-4t(Delta773-1081). We have then utilized RNase protection and ELISA to measure the relative levels of VEGF B, C, D and flt-1, KDR, flt-4 and flt-4t(Delta773-1081) expression in freshly isolated benign prostatic hyperplasia or BPH tissue (n=21), primary prostate cancers (n=82) and matching sentinel lymph node metastases from stage T2a-T2b/T3 tumors (n=52). Comparisons of the primary tumors with BPH showed that there was a significant upregulation of VEGF-B (P=0.003), VEGF D (P=0.005), flt-1 (P=0.003), KDR (P=0.002), flt-4 (P=0.007), and flt-4t(Delta773-1081) (P=0.001), but not VEGF-C (P=0.543). There was no correlation between VEGF-B and its receptor flt-1 (P=0.545), or VEGF-C and flt-4 (P=0.16) and KDR (P=0.23) receptor expression in tumor specimens. Conversely, there was no significant relationship between VEGF-D and the flt-4t(Delta773-1081) receptor (P=0.516) expression. Statistical analysis further showed that there was no significant correlation between VEGF-B, VEGF-C, VEGF-D, flt-1, KDR, flt-4 and flt-4t(Delta773-1081) with patient age (P>0.10), stage (P>0.10), PSA value (P>0.15) or tumor size (P>0.15). Likewise, there was no significant correlation between VEGF-B, VEGF-C, flt-1, KDR, and flt-4 with Gleason score (P>0.15). In comparison, flt-4t(Delta773-1081) levels clearly increased significantly in Gleason score 7 and Gleason score 8-10 tumors as well as in stage T2a-T2b/T3 tumors. The studies were extended to compare gene expression profiles in T2a-T2b and T3 tumors with (n=26) and without (n=26) matching sentinel lymph node metastases. The data showed that VEGF D and flt-4t(Delta773-1081) expression levels were significantly elevated in primary tumors with sentinel lymph node involvement compared to those lacking lymph node involvement (P>0.0022 and 0.006, respectively). These data suggest that targeting VEGF D and flt-4t(Delta773-1081) receptors may be particularly effective in the prevention of lymph node metastases.     

Physiological responses in tennis and running with similar oxygen uptake

The purpose of the study was to compare selected physiological responses during singles tennis match play and continuous running at a similar mean oxygen uptake ( ). The study consisted of two main parts, which were separated by 1 week. In the first part, 12 nationally ranked senior tennis players [six females and six males; 47.2 (6.6) years old and 47.0 (5.4) years old, respectively] each completed a 2-h singles tennis match (TE). Mean during TE [23.1 (3.1) ml·kg^–1·min^–1 for the women and 25.6 (2.8) ml·kg^–1·min^–1 for the men] was measured by a portable spirometry-telemetry system and corresponded to 56% (women) or 54% (men) of their respective maximum . In the second part, the relative data measured during TE were used to set a similar workload during a 2-h treadmill run at a constant level (RU). At the measured time points, heart rate [140.1 (15.5) beats·min^–1 vs 126.4 (15.1) beats·min^–1], lactate concentration [1.53 (0.65) mmol·l^–1 vs 1.01 (0.38) mmol·l^–1] and glucose concentration [5.45 (0.84) mmol·l^–1 vs 4.34 (0.56) mmol·l^–1] in capillary blood, as well as the respiratory exchange ratio [0.93 (0.03) vs 0.88 (0.03)], were higher (P<0.05) in TE compared to RU. Serum concentrations of free fatty acids increased (P<0.05) during both work loads [from 0.25 (0.15) mmol·l^–1 to 1.31 (0.44) mmol·l^–1 in TE and from 0.22 (0.17) mmol·l^–1 to 1.24 (0.35) mmol·l^–1 in RU]. Post-exercise urine concentrations of epinephrine [0.17 (0.14) μmol·l^–1 vs 0.08 (0.04) μmol·l^–1] and norepinephrine [1.27 (0.59) μmol·l^–1 vs. 0.55 (0.33) μmol·l^–1] were higher in TE (P<0.05). These results indicate a stronger metabolic emphasis on glycolysis and glycogenolysis and an overall enhanced sympathoadrenal activity during tennis match play compared to continuous running exercise at a similar mean . Electronic Publication     

Effect of a 15% increase in preferred pedal rate on time to exhaustion during heavy exercise.

The aim of this study was to evaluate the effect of a 15% increase in preferred pedal rate (PPR) on both time to exhaustion and pulmonary O(2) uptake (VO(2)) response during heavy exercise. Seven competitive cyclists underwent two constant-power tests (CPT) at a power output that theoretically requires 50% of the difference in VO(2) between the second ventilatory threshold and VO(2)max (Pdelta50). Each cyclist cycled a CPT at PPR (CPTPPR) and a CPT at +15% of PPR (CPT+15%) in a randomized order. The average PPR value was 94 +/- 4 rpm, and time to exhaustion was significantly longer in CPTPPR compared with CPT+15% (465 +/- 139 vs. 303+/- 42 s, respectively; p = 0.01). A significant decrease in VO(2) values in the first minutes of exercise and a significant increase in VO(2) slow component was reported in CPT+15% compared with CPT(PPR). These data indicate that the increase of 15% PPR was associated with a decrease in exercise tolerance and a specific VO(2) response, presumably due to an increase of negative muscular work, internal work, and an altering of motor unit recruitment patterns.     

Effect of training on the activity of five muscle enzymes studied on elite cross-country skiers

This study examines the effect of training intensity on the activity of enzymes in m. vastus lateralis. Elite junior cross-country skiers of both sexes trained 12-15 h weeks-1 for 5 months at either moderate (60-70% of VO2max, MIG) or high training intensity (80-90% of the VO2max, close to the lactate threshold; HIG). Muscle biopsies for enzyme analyses and fibre typing were taken before and after the training period. Histochemical analyses on single fibres were done for three enzymes (succinate dehydrogenase [SDH], hydroxybutyrate dehydrogenase [HBDH], glycerol-3-phosphate dehydrogenase [GPDH]), while the activity of citrate synthase [CS] and phosphofructokinase [PFK] was measured on whole biopsies. The activity of GPDH was low in ST fibres and high in FT fibres. The activity of SDH and HBDH was high in both ST and FTa fibres but low in the FTb fibres. The HIG increased their performance more than the MIG did during the training period as judged from scores on a 20-min run test. The SDH activity rose by 6% for the HIG (P < 0.02). No effects of training were found in the activities of CS, HBDH or GPDH, neither in the two training groups nor for the two genders (P > or = 0.16). The PFK activity fell by 10% for the HIG (P=0.02), while no change was found for the MIG. For GPDH, CS and SDH the women's activity was approximately 20% less than the value for the men (P < 0.03). For PFK and HBDH there was no sex difference (P > or = 0.27). There were positive correlations between the activity of three of the enzymes (CS, SDH and GPDH) and the performance parameters (VO2max, cross-country skiing and running performance; r > or = 0.6, P < 0.01). No correlations were found between the PFK or HBDH activities and the performance parameters (r < or = 0.16, P > 0.05). This study suggests that intensities near the lactate threshold affect biochemical and physiological parameters examined in this study as well as the performance of elite skiers, and that the rate-limiting enzymes may be more sensitive to training than non-rate-limiting enzymes.     

Early effects of exercise training on \mathop V\limits^ \cdot {\rm O}_2 on- and off-kinetics in 50-year-old subjects

We tested the hypothesis that, in healthy middle-aged subjects ( n=11, age 51.0 +/- 3.0 years, x +/- SD), the effects of exercise training on pulmonary O(2) uptake (VO(2)) on- and off-kinetics would appear earlier than those on peak. The subjects underwent a standard training program (combined endurance and resistance training) in a health club, and were evaluated before training ("time 0", T0), and after 7 (T7), 15 (T15), 30 (T30), 60 (T60) and 90 (T90) days of training. Breath-by-breath pulmonary O(2) uptake (VO(2)), heart rate (HR), systolic (SBP) and diastolic blood pressure, and capillary blood lactate concentration ([La](b)) were determined at rest and at each workload (w during a cycle ergometer incremental exercise test. The "heart rate x blood pressure product" was calculated as (HR x SBP). The day following the incremental test, the subjects performed three repetitions of a square-wave exercise at 50% of VO(2), for the determination of pulmonary VO(2) on- and off-kinetics. VO(2) and [La](bpeak) tended to increase with training; the increases became significant at T60 or T90. HR(peak)and (HR x SBP)(peak) were unaffected by training. The time constant of the "primary" component of the VO(2) on-kinetics (tau(2)) was 46.9 +/- 17.3 s (T0), 38.1 +/- 14.2 s (T7), 34.4 +/- 12.6 s (T15), 28.8 +/- 6.8 s (T30), 30.2 +/- 8.0 s (T60), and 30.4 +/- 12.4 s (T90); a significant difference compared to T0 was observed from T15 onward. From T15 onward, tau(2) were not significantly different from values obtained (29.2 +/- 5.3 s) from a group of healthy untrained young controls ( n=7, 21.6 +/- 0.5 years). The same pattern of change as a function of training was described for the VO(2) off-kinetics. It is concluded that in 50-year-old subjects VO(2) on- and off-kinetics are more sensitive to exercise training than other physiological variables determined at peak exercise.     

Beta-endorphin and adrenocorticotropin response to supramaximal treadmill exercise in trained and untrained males

The response of plasma beta-endorphin (beta-EP) and adrenocorticotropin (ACTH) was studied in seven well-trained (T) young endurance athletes and seven untrained (UT) age- and weight-matched males during treadmill exercise. Subjects ran continuously for 7 min at 60% VO2max, 3 min at 100% VO2max and 2 min at 110% VO2max. Arterialized blood was obtained periodically from a cannulated heated (41 degrees C) hand vein. Plasma beta-EP was measured by radio-immunoassay (RIA) which incorporated an antibody that did not cross-react (less than 1.5%) with beta-lipotropin. Plasma beta-EP was similar between groups at rest (T = 4.3 +/- 0.8 fmol ml-1, mean +/- SE, UT = 3.3 +/- 0.6 fmol ml-1) and did not change at the 60% VO2max stage. Beta-endorphin significantly increased at 100% VO2max with both groups responding similarly. A further increase occurred at 110% VO2max (T = 10.8 + 2.0 and UT = 6.6 + 1.0 fmol ml-1, P less than 0.05 for between group differences). This between group difference persisted 1 min after exercise when the highest beta-EP levels were reached (T = 18.7 +/- 4.7 and UT = 12.8 +/- 3.1 fmol ml-1, P less than 0.05). Plasma ACTH responses were similar to beta-EP with the highest values (T = 61.5 +/- 7.2, UT = 45.7 +/- 6.8 fmol ml-1, P less than 0.05 for between group differences) occurring at 1 min post-exercise. A positive correlation, r = 0.85, P less than 0.05, was found between beta-EP and ACTH using the 1 min post-exercise values. The enhanced response of beta-EP and ACTH in T may indicate a training-induced adaptation which increases the response capacity to extreme levels of stress.     

Caffeine ingestion attenuates the VO(2) slow component during intense exercise

The purpose of this study was to analyze the effects of caffeine ingestion on the slow component of oxygen uptake (DeltaVO(2)) during high-intensity endurance exercise. Nine subjects (8 male and 1 female; age: 21 +/- 1 years; VO(2 max): 57.9 +/- 1.5 ml kg(-1) min(-1)) performed two 9-min tests on a treadmill at a running velocity eliciting 90% of their VO(2 max), 60 min after ingesting either a placebo capsule (PLAC) or a capsule containing a caffeine dose of 5 mg (kg body mass)(-1) [CAFF]. The mean values of DeltaVO(2) were significantly lower in CAFF than in PLAC (83 +/- 31 ml min(-1) vs. 167 +/- 26 ml min(-1), respectively; p < 0.05). These findings suggest that the ergogenic effect of caffeine in a high-intensity endurance exercise shown in previous research may be partly mediated by a possible attenuation of the VO(2) slow component.     

Variation of haemoglobin extinction coefficients can cause errors in the determination of haemoglobin concentration measured by near-infrared spectroscopy

Near-infrared spectroscopy or imaging has been extensively applied to various biomedical applications since it can detect the concentrations of oxyhaemoglobin (HbO(2)), deoxyhaemoglobin (Hb) and total haemoglobin (Hb(total)) from deep tissues. To quantify concentrations of these haemoglobin derivatives, the extinction coefficient values of HbO(2) and Hb have to be employed. However, it was not well recognized among researchers that small differences in extinction coefficients could cause significant errors in quantifying the concentrations of haemoglobin derivatives. In this study, we derived equations to estimate errors of haemoglobin derivatives caused by the variation of haemoglobin extinction coefficients. To prove our error analysis, we performed experiments using liquid-tissue phantoms containing 1% Intralipid in a phosphate-buffered saline solution. The gas intervention of pure oxygen was given in the solution to examine the oxygenation changes in the phantom, and 3 mL of human blood was added twice to show the changes in [Hb(total)]. The error calculation has shown that even a small variation (0.01 cm(-1) mM(-1)) in extinction coefficients can produce appreciable relative errors in quantification of Delta[HbO(2)], Delta[Hb] and Delta[Hb(total)]. We have also observed that the error of Delta[Hb(total)] is not always larger than those of Delta[HbO(2)] and Delta[Hb]. This study concludes that we need to be aware of any variation in haemoglobin extinction coefficients, which could result from changes in temperature, and to utilize corresponding animal's haemoglobin extinction coefficients for the animal experiments, in order to obtain more accurate values of Delta[HbO(2)], Delta[Hb] and Delta[Hb(total)] from in vivo tissue measurements.     

Muscle glycogen reduction in man: relationship between surface EMG activity and oxygen uptake kinetics during heavy exercise

The purpose of this study was to determine whether muscle glycogen reduction prior to exercise would alter muscle fibre recruitment pattern and change either on-transient O2 uptake (VO2) kinetics or the VO2 slow component. Eight recreational cyclists (VO2peak, 55.6 +/- 1.3 ml kg (-1) min(-1)) were studied during 8 min of heavy constant-load cycling performed under control conditions (CON) and under conditions of reduced type I muscle glycogen content (GR). VO2 was measured breath-by-breath for the determination of VO2 kinetics using a double-exponential model with independent time delays. VO2 was higher in the GR trial compared to the CON trial as a result of augmented phase I and II amplitudes, with no difference between trials in the phase II time constant or the magnitude of the slow component. The mean power frequency (MPF) of electromyography activity for the vastus medialis increased over time during both trials, with a greater rate of increase observed in the GR trial compared to the CON trial. The results suggest that the recruitment of additional type II motor units contributed to the slow component in both trials. An increase in fat metabolism and augmented type II motor unit recruitment contributed to the higher VO2 in the GR trial. However, the greater rate of increase in the recruitment of type II motor units in the GR trial may not have been of sufficient magnitude to further elevate the slow component when VO2 was already high and approaching VO2peak .