Determinants of oxygen uptake kinetics in older humans following single-limb endurance exercise training

We hypothesised that the observed acceleration in the kinetics of exercise on-transient oxygen uptake (VO2) of five older humans (77 +/- 7 years (mean +/- S.D.) following 9 weeks of single-leg endurance exercise training was due to adaptations at the level of the muscle cell. Prior to, and following training, subjects performed constant-load single-limb knee extension exercise. Following training VO2 kinetics (phase 2, tau) were accelerated in the trained leg (week 0, 92 +/- 44 s; week 9, 48 +/- 22 s) and unchanged in the untrained leg (week 0, 104 +/- 43 s; week 9, 126 +/- 35 s). The kinetics of mean blood velocity in the femoral artery were faster than the kinetics of VO2, but were unchanged in both the trained (week 0, 19 +/- 10 s; week 9, 26 +/- 11 s) and untrained leg (week 0, 20 +/- 18 s; week 9, 18 +/- 10 s). Maximal citrate synthase activity, measured from biopsies of the vastus lateralis muscle, increased (P < 0.05) in the trained leg (week 0, 6.7 +/- 2.0 micromol x (g wet wt)(-1) x min(-1); week 9, 11.4 +/- 3.6 micromol x (g wet wt)(-1) x min(-1)) but was unchanged in the untrained leg (week 0, 5.9 +/- 0.5 micromol x (g wet wt)(-1) x min(-1); week 9, 7.9 +/- 1.9 micromol x (g wet wt)(-1) x min(-1)). These data suggest that the acceleration of VO2 kinetics was due to an improved rate of O2 utilisation by the muscle, but was not a result of increased O2 delivery.     

The Effects of Caffeine on the Kinetics of O2Uptake, CO2Production and Expiratory Ventilation in Humans During the On-Transient of Moderate and Heavy Intensity Exercise

In order to test the hypothesis that glycogen sparing observed early during exercise following caffeine ingestion was a consequence of tighter metabolic control reflected in faster VO2 kinetics, we examined the effect of caffeine ingestion on oxygen uptake (VO2), carbon dioxide production (VCO2) and expiratory ventilation (VE) kinetics at the onset of both moderate (MOD) and heavy (HVY) intensity exercise. Male subjects (n = 10) were assigned to either a MOD (50% VO2,max, n = 5) or HVY (80% VO2,max, n = 5) exercise condition. Constant-load cycle ergometer exercise was performed as a step function from loadless cycling 1 h after ingestion of either dextrose (placebo, PLAC) or caffeine (CAFF; 6 mg (kg body mass)-1). Alveolar gas exchange was measured breath-by-breath. A 2- or 3-component exponential model, fitted through the entire exercise transient, was used to analyse gas exchange and ventilatory data for the determination of total lag time (TLT: the time taken to attain 63% of the total exponential increase). Caffeine had no effect on TLT for VO2 kinetics at either exercise intensity (MOD: 36 +/- 14 s (PLAC) and 41 +/- 10 s (CAFF); HVY: 99 +/- 30 s (PLAC) and 103 +/- 26 (CAFF) (mean +/- S.D.)). TLT for VE was increased with caffeine at both exercise intensities (MOD: 50 +/- 20 s (PLAC) and 59 +/- 21 s (CAFF); HVY: 168 +/- 35 s (PLAC) and 203 +/- 48 s (CAFF)) and for VCO2 during MOD only (MOD: 47 +/- 14 s (PLAC) and 53 +/- 17 s (CAFF); HVY: 65 +/- 13 s (PLAC) and 69 +/- 17 s (CAFF)). Contrary to our hypothesis, the metabolic effects of caffeine did not alter the on-transient VO2 kinetics in moderate or heavy exercise. VCO2 kinetics were slowed by a reduction in CO2 stores reflected in pre-exercise and exercise endtidal CO2 pressure (PET,CO2) and plasma PCO2 which, we propose, contributed to slowed VE kinetics.     

Age-related heart rate response to exercise in heart transplant recipients. Functional significance

The heart rate (HR) and O(2) uptake (VO(2)) responses to cycle ergometer exercise and the role of O(2) transport in limiting submaximal and maximal aerobic performance were assessed in 33 heart transplant recipients (HTR) [14 children (P-HTR), 11 young adults (YA-HTR) and 8 middle-age adults (A-HTR)] and in 28 age-matched control subjects (CTL). In 7 P-HTR ("responders") the HR response to the onset of exercise (on-response) was as fast as that of CTL, whereas in all other patients ("non-responders") the HR on-response was typical of the denervated heart. Compared with non-responder P-HTR, responder P-HTR were also characterized by a normal peak HR (177+/- 16 vs. 151+/- 25 beats/min), an equally slow time constant for the VO(2) on-response (tau: 54 +/- 11 vs. 62+/- 13 s) and a similar low (approximately 60% of that of CTL) peak VO(2) (28 +/- 7 vs. 26 +/- 10 ml/kg per min). On the other hand non-responder YA-HTR and A-HTR were characterized by a relatively low peak HR (151 +/- 21 and 144 +/- 29 beats/min, respectively), a slow tau for the on-response (63 +/- 12 and 70 +/- 11 s) and a low peak (28 +/- 7 and 19 +/- 6 ml/kg per min). In conclusion, a sizeable number of paediatric patients (responder P-HTR) may reacquire the normal HR response to exercise, both in terms of kinetics and maximal level. Despite the almost complete recovery of cardiovascular function, and, probably, oxygen delivery, both the kinetics of the VO(2) on-response and the maximal aerobic power of the responder P-HTR were similar to those of non-responder P-HTR. The latter finding is probably attributable to peripheral limitations, due to inborn and/or pharmacological muscle deterioration.     

Effect of prior heavy exercise on muscle deoxygenation kinetics at the onset of subsequent heavy exercise

This study examines the effect of prior heavy exercise on muscle deoxygenation kinetics at the onset of heavy-intensity cycling exercise. Ten young male adults (20 +/- 2 years) performed two repetitions of step transitions (6 min) from 35 W to heavy-intensity exercise preceded by either no warm-up or by a heavy-intensity exercise. VO2 was measured breath-by-breath, and muscle deoxygenation (HHb) and total hemoglobin (Hb(tot)) were monitored continuously by near-infrared spectroscopy. We used a two-exponential model to describe the VO2 kinetics and a mono-exponential model for the HHb kinetic. The parameters of the phase II VO2 kinetics (TD1 VO2, tau1 VO2 and A1 VO2) were unaffected by prior heavy exercise, while some parameters of local muscle deoxygenation kinetics were significantly faster (TD HHb: 7 +/- 2 vs. 5 +/- 2 s; P < 0.001, MRT HHb: 20 +/- 3 vs. 15+/- 4 s; P < 0.05). Blood lactate, heart rate and Hb(tot) values were significantly higher before the second bout of heavy exercise. These results collectively suggest that the prior heavy exercise probably increased muscle O2 availability and improved O2 utilization at the onset of a subsequent bout of heavy exercise.     

The effect of hypoxia on pulmonary O2 uptake, leg blood flow and muscle deoxygenation during single-leg knee-extension exercise

The effect of hypoxic breathing on pulmonary O(2) uptake (VO(2p)), leg blood flow (LBF) and O(2) delivery and deoxygenation of the vastus lateralis muscle was examined during constant-load single-leg knee-extension exercise. Seven subjects (24 +/- 4 years; mean +/-s.d.) performed two transitions from unloaded to moderate-intensity exercise (21 W) under normoxic and hypoxic (P(ET)O(2)= 60 mmHg) conditions. Breath-by-breath VO(2p) and beat-by-beat femoral artery mean blood velocity (MBV) were measured by mass spectrometer and volume turbine and Doppler ultrasound (VingMed, CFM 750), respectively. Deoxy-(HHb), oxy-, and total haemoglobin/myoglobin were measured continuously by near-infrared spectroscopy (NIRS; Hamamatsu NIRO-300). VO(2p) data were filtered and averaged to 5 s bins at 20, 40, 60, 120, 180 and 300 s. MBV data were filtered and averaged to 2 s bins (1 contraction cycle). LBF was calculated for each contraction cycle and averaged to 5 s bins at 20, 40, 60, 120, 180 and 300 s. VO(2p) was significantly lower in hypoxia throughout the period of 20, 40, 60 and 120 s of the exercise on-transient. LBF (l min(-1)) was approximately 35% higher (P > 0.05) in hypoxia during the on-transient and steady-state of KE exercise, resulting in a similar leg O(2) delivery in hypoxia and normoxia. Local muscle deoxygenation (HHb) was similar in hypoxia and normoxia. These results suggest that factors other than O(2) delivery, possibly the diffusion of O(2,) were responsible for the lower O(2) uptake during the exercise on-transient in hypoxia.     

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 .     

Human femoral artery and estimated muscle capillary blood flow kinetics following the onset of exercise

The purpose of this study was to compare the kinetics of estimated capillary blood flow (Qcap) to those of femoral artery blood flow (QFA) and estimated muscle oxygen uptake (VO2m). Nine healthy subjects performed a series of transitions from rest to moderate (below estimated lactate threshold, 6 min bouts) knee extension exercise. Pulmonary oxygen uptake (VO2) was measured breath by breath, (QFA) was measured continuously using Doppler ultrasound, and deoxyhaemoglobin ([HHb]) was estimated by near-infrared spectroscopy over the rectus femoris throughout the tests. The time course of (Qcap) was estimated by rearranging the Fick equation (i.e. Qcap = VO2m/(a-v)O2), (arterio - venous O2 difference) using the primary component of VO2 to represent VO2m and [HHb] as a surrogate for (a - v)O2. The overall kinetics of QFA (mean response time, MRT, 13.7 +/- 7.0 s), VO2m (tau, 27.8 +/- 9.0 s) and Qcap (MRT, 41.4 +/- 19.0 s) were significantly (P < 0.05) different from each other. We conclude that for moderate intensity knee extension exercise, conduit artery blood flow (QFA) kinetics may not be a reasonable approximation of blood flow kinetics in the microcirculation (Qcap), the site of gas exchange. This temporal dissociation suggests that blood flow may be controlled differently at the conduit artery level than in the microcirculation.     

Influence of blood donation on O2 uptake on-kinetics, peak O2 uptake and time to exhaustion during severe-intensity cycle exercise in humans

We hypothesized that the reduction of O2-carrying capacity caused by the withdrawal of approximately 450 ml blood would result in slower phase II O2 uptake (VO2) kinetics, a lower VO2peak and a reduced time to exhaustion during severe-intensity cycle exercise. Eleven healthy subjects (mean +/- S.D. age 23 +/- 6 years, body mass 77.2 +/- 11.0 kg) completed 'step' exercise tests from unloaded cycling to a severe-intensity work rate (80% of the difference between the predetermined gas exchange threshold and the VO2peak) on two occasions before, and 24 h following, the voluntary donation of approximately 450 ml blood. Oxygen uptake was measured breath-by-breath, and VO2 kinetics estimated using non-linear regression techniques. The blood withdrawal resulted in a significant reduction in haemoglobin concentration (pre: 15.4 +/- 0.9 versus post: 14.7 +/- 1.3 g dl(-1); 95% confidence limits (CL): -0.04, -1.38) and haematocrit (pre: 44 +/- 2 versus post: 41 +/- 3%; 95% CL: -1.3, -5.1). Compared to the control condition, blood withdrawal resulted in significant reductions in VO2peak (pre: 3.79 +/- 0.64 versus post: 3.64 +/- 0.61 l min(-1); 95% CL: -0.04, - 0.27) and time to exhaustion (pre: 375 +/- 129 versus post: 321 +/- 99 s; 95% CL: -24, -85). However, the kinetic parameters of the fundamental VO2 response, including the phase II time constant (pre: 29 +/- 8 versus post: 30 +/- 6 s; 95% CL: 5, -3), were not altered by blood withdrawal. The magnitude of the VO2 slow component was significantly reduced following blood donation owing to the lower VO2peak attained. We conclude that a reduction in blood O2-carrying capacity, achieved through the withdrawal of approximately 450 ml blood, results in a significant reduction in VO2peak and exercise tolerance but has no effect on the fundamental phase of the VO2 on-kinetics during severe-intensity exercise.     

Effects of chronic heart failure in rats on the recovery of microvascular PO2 after contractions in muscles of opposing fibre type

Chronic heart failure (CHF) impairs muscle O2 delivery (QO2) and, at a given O2 uptake (VO2), lowers microvascular O2 pressures (PmvO2: determined by the QO2-to-VO2 ratio), which may impair recovery of high-energy phosphates following exercise. Because CHF preferentially decreases QO2 to slow-twitch muscles, we hypothesized that recovery PmvO2 kinetics would be slowed to a greater extent in soleus (SOL: approximately 84% type I fibres) than in peroneal (PER: approximately 14% type I) muscles of CHF rats. PmvO2 dynamics were determined in SOL and PER muscles of control (CON: n= 6; left ventricular end-diastolic pressure, LVEDP: approximately 3 mmHg), moderate CHF (MOD: n= 7; LVEDP: approximately 11 mmHg) and severe CHF (SEV: n= 4; LVEDP: approximately 25 mmHg) following cessation of electrical stimulation (180 s; 1 Hz). In PER, neither the recovery PmvO2 values nor the mean response time (MRT; a weighted average of the time to 63% of the overall response) were altered by CHF (CON: 66.8 +/- 8.0, MOD: 72.4 +/- 11.8, SEV: 69.1 +/- 9.5 s). In marked contrast, SOL PmvO2, at recovery onset, was reduced significantly in the SEV group ( approximately 6 Torr) and PmvO2 MRT was slowed with increased severity of CHF (CON: 45.1 +/- 5.3, MOD: 63.2 +/- 9.4, SEV: 82.6 +/- 12.3 s; P < 0.05 CON vs. MOD and SEV). These data indicate that CHF slows PmvO2 recovery following contractions and lowers capillary O2 driving pressure in slow-twitch SOL, but not in fast-twitch PER muscle. These results may explain, in part, the slowed recovery kinetics (phosphocreatine and VO2) and pronounced fatigue following muscular work in CHF patients.     

Role of respiratory system impedance in the difference of ventilatory control between children and adults

How children are able to adapt their ventilation to the intensity of exercise faster than adults remain unclear. We hypothesized that differences of VE observed between children and adults depend on either peripheral chemoreceptors or central command activity. We examined ventilatory control parameters in either normoxic or hypoxic condition (FI 02 =0.15). We analyzed the adaptability of the respiratory exchanges by (i) the measurement of ventilatory kinetics time-constant and (ii) the central command by the mouth-occlusion pressure (P0.1). A group of nine pre-pubescent children (mean age 9.5+/-1 years) and a group of eight adults (mean age 24+/-3.1 years) performed a constant-load exercise. In normoxia, children had significantly shorter time-constant (tau) VCO2 (respectively, 38.5+/-4.3 and 53.1+/-5.3s; P<0.001), tau VE (respectively, 52.5+/-13.1s vs. 66.1+/-12.3s; P<0.001), and tau P0.1 (57.4+/-15.4 and 61.0+/-12.9s, respectively; P<0.001) than adults. In hypoxia, children exhibited shorter tau P0.1/VT/Ti compare to adults. Reinforced by the significant correlation between tau VE and tau P0.1/VT/Ti for children but not adults, we concluded that ventilatory response differences could be due in part to the respiratory system impedance.     

Matching of blood flow to metabolic rate during recovery from moderate exercise in humans

It is unclear whether measurement of limb or conduit artery blood flow during recovery from exercise provides an accurate representation of flow to the muscle capillaries where gas exchange occurs. To investigate this, we: (a) examined the kinetic responses of femoral artery blood flow (QFA), estimated muscle capillary blood flow (Qcap) and estimated muscle oxygen uptake (VO2m) following cessation of exercise; and (b) compared these responses to verify the adequacy of O2 delivery during recovery. Pulmonary VO2 (VO2p) was measured breath by breath, QFA was measured using Doppler ultrasonography, and deoxy-haemoglobin/myoglobin (deoxy-[Hb/Mb]) was estimated by near-infrared spectroscopy over the rectus femoris in nine healthy subjects during a series of transitions from moderate knee-extension exercise to rest. The time course of Qcap was estimated by rearranging the Fick equation [i.e. Qcap(t) alpha VO2m(t)/deoxy-[Hb/Mb](t)], using the primary component of Vo2p to represent VO2m and deoxy-[Hb/Mb] as a surrogate for arteriovenous O2 difference. There were no significant differences among the overall kinetics of VO2m (tau, 31.4+/-8.2 s), QFA [mean response time (MRT), 34.5+/-20.4 s] and Qcap (MRT, 31.7+/-14.7 s). The VO2m kinetics were also significantly correlated (P<0.05) with those of both QFA and Qcap. Both QFA and Qcap appear to be coupled with VO2m during recovery from moderate knee-extension exercise, such that extraction falls (thus cellular energetic state is not further compromised) throughout recovery.     

Exercise gas transport determinants in elderly normotensive and hypertensive humans

This study examined the effect of the phenylalkylamine calcium channel blocker verapamil, on resting left ventricular (LV) function and O2 uptake rate (VO2) during exercise at maximal and submaximal work rates. Nine older hypertensive (71 years; OH), 10 older sedentary normotensive (69 years; OS), 10 older active (71 years; OA) and 10 young (24 years; Y) individuals volunteered. Studies were completed in the control condition and 4-6 h following 240 mg verapamil SR per os. Resting LV systolic (fractional shortening; FS) and diastolic (early: late (E/A) flow velocity ratio and isovolumic relaxation time (IVRT) were measured by Doppler echocardiography. Maximal oxygen uptake (VO2,max) and, on subsequent test days, four transitions to and from a 6 min square wave exercise perturbation at a sub-anaerobic threshold intensity of 40 W (OH, OS, OA) or 100 W (Y) for determination of VO2 kinetics were performed on a cycle ergometer. Breath-by-breath VO2 transients were fitted with a monoexponential equation, starting at phase 2 of the response, while heart rate (HR) was fitted from phase 1, for the determination of the time constant of VO2 (tau VO2) and HR (tau HR). Baseline left ventricular FS was significantly greater in the OS (32%), OA (34%) and Y (34%) than in the OH (23%) groups, while E/A was significantly greater in the OA (1.16) and Y (2.34) than in the OH (0.9) and OS (0.82) groups (P < 0.05). Baseline VO2,max was higher and tau VO2 faster in the young (41.4 ml kg-1 min-1; 25.2 s) than in the older groups and in the OA (28.8 ml kg-1 min-1; 44.3 s) than in both OH (20.8 ml kg-1 min-1; 71.3 s) and OS (22.0 ml kg-1 min-1; 59.5 s) groups (P < 0.05). Heart rate kinetics showed similar differences to VO2 kinetics among the groups. After verapamil, no significant changes in FS, E/A or IVRT were observed in the OA and Y groups. In the OH group, FS (32%) and E/A (1.15) increased while IVRT decreased significantly (from 0.103 to 0.07; P < 0.05). In the OS group, only E/A increased significantly (0.82 to 1.0; P < 0.05). None of the exercise variables (VO2,max, tau VO2 or tau HR) were altered for the OA or Y groups. VO2,max increased (from 20.8 to 22.8 ml kg-1 min-1) in the OH and (from 22.0 to 24.1 ml kg-1 min-1) in the OS (P < 0.05). tau VO2 was accelerated from 71.3 to 49.2 s in the OH group and from 59.5 to 48.2 s in the OS group (P < 0.05). These results suggest that VO2 responses at maximal and submaximal work rates may be dependent upon the initial cardiac pump function of the study population.     

The off-transient pulmonary oxygen uptake (VO(2)) kinetics following attainment of a particular VO(2) during heavy-intensity exercise in humans

The oxygen uptake response to moderate-intensity exercise (i.e. < anaerobic threshold (an)) has been characterised with a gain (i.e. response amplitude per increment of work rate) and time constant that do not vary appreciably at different work rates or between the on- and off-transients. Above an, the response becomes more complex with an early component that typically projects to a value that has a gain similar to that of the < an response, but which is supplemented by the addition of a delayed slow kinetic component. We therefore established a constant target VO2 (VO21) for each subject such that with different imposed work rates the contribution to VO21 from the slow phase varied over a wide range. Work rates were chosen so that VO21 was attained at 2-24 min. Five subjects (aged 21-58 years) cycled at four to five different work rates. VO2 was measured breath-by-breath, at VO21 the work rate was abruptly reduced and the subject recovered by cycling unloaded for 15 min. Unlike the on-transient, for which the slow component shows a long delay, the off-transient was best fitted as two simultaneous exponential components. The slower off-transient component had a small amplitude and long time constant, but did not differ significantly among the various tests. The off-transient kinetics for VO2 therefore was independent of the magnitude of the contribution to the slow phase from the on-transient kinetics.     

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.     

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.     

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.     

Change in O2 uptake during rebreathing in hyperoxia in man

In pertaining to PO2 dependency of the pulmonary CO diffusing capacity during rebreathing, the O2 uptake (VO2) and cardiac output (Q) were measured at three different PO2 levels between 100 and 500 Torr. Since the VO2 measured by an O2 injection method is strongly influenced in hyperoxia by a gas exchange ratio (R), a simulation method using a R-PCO2 relation during rebreathing was developed. Gas volume in the lung-bag-system needed in the computation was measured from the difference in O2 concentration between before and after injecting a known amount of O2 into the rebreathing circuit. The accuracy of the volume was checked by comparing it with the volume measured successively with a body box. The VO2 was determined by comparing the simulated O2 and CO2 concentrations in rebreathing gas with the measured ones. The VO2 significantly increased by rebreathing in hyperoxia. To analyze the VO2 increase, the Q was computed by dividing the VO2 by the arteriovenous O2 content difference, which in turn was obtained by dividing the slope of the CO2 dissociation curve by that of the R-PCO2 line. The Q was almost linearly related to the VO2. Since there was no difference in VO2 in steady state breathing between normoxia and hyperoxia, the increase in VO2 and Q seemed to occur transiently. This finding is very important in evaluating the PO2 dependency of the pulmonary diffusing capacity for CO.     

Left ventricular diastolic filling and cardiovascular functional capacity in older men

We investigated anaerobic threshold (< theta(L)) gas exchange kinetics and maximal oxygen uptake (VO2,max) among older men with reduced left ventricular end-diastolic filling (LVDF). Ten men (mean age, 73 years) with LVDF impairment and low fitness, but without other cardiovascular dysfunction were studied. Treatments compared to control included: 5 days, high intensity exercise training protocol; 5 days, calcium channel blockade (240 mg verapamil); 21 days, detraining/washout; and 5 days, combined treatments. Results indicated no changes in resting left ventricular systolic function with any treatment. Significant resting diastolic function changes included increased early:late flow velocity (control, 0.87; training, 1.28; verapamil, 1.32), and a decreased isovolumic relaxation time (control, 0.10 s; training, 0.08 s; verapamil, 0.08 s). The combined treatments were not additive. Sub-threshold oxygen uptake kinetics (tauVO2, s) were significantly faster following either training or verapamil (tauVO2,control, 62+/-12; tauVO2,training, 44+/-9; tauVO2,verapamil, 48+/-10) and combined treatments (tauVO2, 41+/- 8). V O2,max (ml kg(-1) min(-1)) was significantly increased (control, 21.8+/-2.2; training, 27.3+/-2.2; verapamil, 25.2+/-3.4; combined treatments, 26.9+/-2.3). Increasing ventricular preload with either exercise training or calcium channel blockade was coincident with faster tauVO2 and increased VO2,max.     

Dynamics of skeletal muscle oxygenation during sequential bouts of moderate exercise

In rat muscle, faster dynamics of microvascular P(O2) (approximately blood flow (Q(m) to O2 uptake (V(O2) ratio) after prior contractions that did not alter blood [lactate] have been considered to be a consequence of faster V(O2) kinetics. However, in humans, prior exercise below the lactate threshold does not affect the pulmonary V(O2) kinetics. To clarify this apparent discrepancy, we examined the effects of prior moderate exercise on the kinetics of muscle oxygenation (deoxyhaemoglobin, [HHb] alpha V(O2m)/Q(m)) and pulmonary V(O2) (V(O2p) in humans. Eight subjects performed two bouts (6 min each) of moderate-intensity cycling separated by 6 min of baseline pedalling. Muscle (vastus lateralis) oxygenation was evaluated by near-infrared spectroscopy and V(O2p) was measured breath-by-breath. The time constant (tau) of the primary component of V(O2p) was not significantly affected by prior exercise (21.5 +/- 9.2 versus 25.6 +/- 9.7 s; Bout 1 versus 2, P= 0.49). The time delay (TD) of [HHb] decreased (11.6 +/- 2.6 versus 7.7 +/- 1.5 s; Bout 1 versus 2, P < 0.05) and tau[HHb] increased (7.0 +/- 3.5 versus 10.2 +/- 4.6 s; Bout 1 versus 2, P < 0.05), while the mean response time (TD + tau) did not change (18.6 +/- 2.7 versus 17.9 +/- 3.9 s) after prior moderate exercise. Thus, prior moderate exercise resulted in shorter onset and slower rate of increase in [HHb] during subsequent exercise. These data suggest that prior exercise altered the dynamic interaction between V(O2m)and Q(m) following the onset of exercise.     

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.