Physiological responses to cycling for 60 minutes at maximal lactate steady state.

Changes in physiological variables during a 60-min continuous test at maximal lactate steady state (MLSS) were studied using highly conditioned cyclists (1 female and 9 males, aged 28.3 +/- 8.1 years). To determine power at MLSS, we tested at 8-min increments and interpolated the power corresponding to a blood lactate value of 4 mmol/L. During the subsequent 60-min exercise at MLSS, we observed a sequential increase of physiological parameters, in contrast to stable blood lactate. Heart rate drifted upward from beginning to end of exercise. This became statistically significant after 30 min. From 10-60 min of exercise, a change of +12.6 +/- 3.2 bpm was noted. Significant drift was seen after 30 min for the respiratory exchange ratio, after 40 min for the rate of perceived exertion using the Borg scale, and after 50 min for % VO(2)max/kg and minute ventilation. This slow component of VO(2)max may be the result of higher recruitment of type II fibers.     

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.     

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.     

(.)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.     

Haemodynamic responses to exercise, ATP infusion and thigh compression in humans: insight into the role of muscle mechanisms on cardiovascular function

The muscle pump and muscle vasodilatory mechanism are thought to play important roles in increasing and maintaining muscle perfusion and cardiac output ((.)Q) during exercise, but their actual contributions remain uncertain. To evaluate the role of the skeletal muscle pump and vasodilatation on cardiovascular function during exercise, we determined leg and systemic haemodynamic responses in healthy men during (1) incremental one-legged knee-extensor exercise, (2) step-wise femoral artery ATP infusion at rest, (3) passive exercise (n=10), (4)femoral vein or artery ATP infusion (n=6), and (5) cyclic thigh compressions at rest and during passive and voluntary exercise (n=7). Incremental exercise resulted in progressive increases in leg blood flow (DeltaLBF 7.4 +/- 0.7 l min(-1)), cardiac output (Delta (.)Q 8.7 +/- 0.7 l min(-1)), mean arterial pressure (DeltaMAP 51 +/- 5 mmHg), and leg and systemic oxygen delivery and (.)VO2 . Arterial ATP infusion resulted in similar increases in (.)Q , LBF, and systemic and leg oxygen delivery, but central venous pressure and muscle metabolism remained unchanged and MAP was reduced. In contrast,femoral vein ATP infusion did not alter LBF, (.)Q or MAP. Passive exercise also increased blood flow (DeltaLBF 0.7 +/- 0.1 l min(-1)), yet the increase in muscle and systemic perfusion, unrelated to elevations in aerobic metabolism, accounted only for approximately 5% of peak exercise hyperaemia.Likewise, thigh compressions alone or in combination with passive exercise increased blood flow (DeltaLBF 0.5-0.7 l min(-1)) without altering (.)Q, MAP or (.)VO2. These findings suggest that the skeletal muscle pump is not obligatory for sustaining venous return, central venous pressure,stroke volume and (.)Q or maintaining muscle blood flow during one-legged exercise in humans.Further, its contribution to muscle and systemic peak exercise hyperaemia appears to be minimal in comparison to the effects of muscle vasodilatation.     

Respiratory factors do not limit maximal symptom-limited exercise in patients with mild cystic fibrosis lung disease

To evaluate whether respiratory factors limit exercise capacity in patients with mild cystic fibrosis (CF) lung disease (mean FEV(1) = 76 +/- 7.7% predicted) we stressed the respiratory system of seven patients using added dead space (V(D)). Primary outcomes were exercise duration (Ex(dur)) and maximal oxygen uptake (VO(2max)). Dyspnoea/leg-discomfort were assessed at end-exercise. Ex(dur) was identical between control and V(D) studies (520 +/- 152 versus 511 +/ -166 s, p = NS) as was VO(2max)(1.6 +/- 0.5 versus 1.6 +/- 0.6 L/min, p = NS). Significant resting, sub-maximal and maximal workload increases in minute ventilation (V(E)) were detected (70.8 +/- 13.7 versus 79.5 +/- 16.9 L/min, p < 0.05). Analysis of breathing pattern revealed increases in V(E) were attributable to increases in tidal volume (2.0 +/- 0.5 versus 2.2 +/- 0.6 L, p < 0.05) with no change in respiratory frequency. There was no difference in dyspnoea/leg discomfort between tests. The increase in V(E) in response to V(D), with no change in [Exdur/VO(2max) suggests maximal symptom-limited exercise limitation is not primarily limited by respiratory factors in mild CF lung disease. Focused investigation and treatment of non-respiratory factors contributing to exercise limitation may improve exercise rehabilitation in this patient group.     

The differences in CO2 kinetics during incremental exercise among sprinters, middle, and long distance runners

The purpose of this study was to investigate the differences in kinetics of CO2 output (VCO2) during incremental exercise in sprinters (S), middle (MD), and long distance runners (LD). In the steady state exercise, the VCO2 was linearly related to the O2 uptake (VO2). In the incremental exercise below anaerobic threshold (AT), the VCO2 was also linearly related to the VO2. The difference between the VCO2 estimates from the regression lines obtained in steady state and incremental exercise was added from the start of exercise up to a given time. The added values were defined as CO2 stores. The CO2 stores per body weight were significantly related to mixed venous CO2 pressure (PVCO2) determined by the CO2 rebreathing method. The slopes of the regression lines between PVCO2 and CO2 stores per body weight were not different among three groups. If VCO2 above AT is estimated from the VO2 using the regression line obtained in incremental exercise below AT, the estimated VCO2 is lower than the measured VCO2. The sum of the differences in VCO2 up to a given time was defined as CO2 excess. The CO2 excess per body weight was significantly related to delta LA (the difference between blood lactates at 5 min after exercise and at rest). The ratios of CO2 excess per body weight to delta LA were 3.30 +/- 1.49, 4.16 +/- 2.33, and 5.55 +/- 2.05 for sprinters, middle, and long distance runners, respectively. This ratio obtained in sprinters was significantly lower than that in long distance runners (p less than 0.01).     

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.     

Reduced oxygen uptake increase to work rate increment (DeltaVO2/DeltaWR) is predictable by VO2 response to constant work rate exercise in patients with chronic heart failure

Patients with reduced peak oxygen uptake (VO2) due to chronic heart failure (CHF) exhibit abnormal VO2 kinetics even during mild to moderate exercise. This is characterized by a reduced ratio of the VO2 increase to the work rate increment (DeltaVO2/DeltaWR) during ramp exercise, and by a slow increase in VO2 during constant work rate exercise. Because the slow kinetics alone is unlikely to explain the reduced DeltaVO2/DeltaWR on theoretical grounds, we can postulate that the linearity between work rate and VO2 may be impaired when exercise is imposed in a ramp fashion. The present study was designed to address this issue. In 21 CHF patients and 17 normal controls, we performed both symptom-limited exercise testing (15 W. min(-1) ramp) and a constant work rate exercise test (0 W followed by 50-W step). The VO2 step response was used to mathematically derive the hypothetical VO2 ramp response by time integration. Although peak VO2 and work rate were both significantly lower in patients, the attenuation in peak VO2 was more prominent ( p<0.05), which could be explained by a lower DeltaVO2/DeltaWR in patients compared with controls [8.1 (SD 1.0) and 9.8 (0.5) ml. min(-1). W(-1), p<0.01]. The hypothetical DeltaVO2/DeltaWR derived from the VO2 step response was also significantly lower in patients [8.7 (1.0) and 10.0 (0.7) ml. min(-1). W(-1), p<0.01]. The hypothetical and measured DeltaVO2/DeltaWR were highly correlated ( r=0.78, p<0.001). Thus, we can reasonably predict the VO2 ramp response from the VO2 response to a step increase in work rate, indicating that linearity between VO2 and work rate is held constant irrespective of loading patterns. Additional studies, such as those including evaluation of anaerobic bioenergetics, are needed to further elucidate the precise mechanism(s) of this phenomenon.     

Hyperoxia does not increase peak muscle oxygen uptake in small muscle group exercise.

We examined the influence of hyperoxia on peak oxygen uptake (VO2peak) and peripheral gas exchange during exercise with the quadriceps femoris muscle. Young, trained men (n=5) and women (n=3) performed single-leg knee-extension exercise at 70% and 100% of maximum while inspiring normal air (NOX) or 60% O2 (HiOX). Blood was sampled from the femoral vein of the exercising limb and from the contralateral artery. In comparison with NOX, hyperoxic arterial O2 tension (PaO2) increased from 13.5 +/- 0.3 (x +/- SE) to 41.6 +/- 0. 3 kPa, O2 saturation (SaO2) from 98 +/- 0.1 to 100 +/- 0.1%, and O2 concentration (CaO2) from 177 +/- 4 to 186 +/- 4 mL L-1 (all P < 0. 01). Peak exercise femoral venous PO2 (PvO2) was also higher in HiOX (3.68 +/- 0.06 vs. 3.39 +/- 0.7 kPa; P < 0.05), indicating a higher O2 diffusion driving pressure. HiOX femoral venous O2 saturation averaged 36.8 +/- 2.0% as opposed to 33.4 +/- 1.5% in NOX (P < 0.05) and O2 concentration 63 +/- 6 vs. 55 +/- 4 mL L-1 (P < 0.05). Peak exercise quadriceps blood flow (Qleg), measured by the thermo-dilution technique, was lower in HiOX than in NOX, 6.4 +/- 0. 5 vs. 7.3 +/- 0.9 L min-1 (P < 0.05); mean arterial blood pressure at inguinal height was similar in NOX and HiOX at 144 and 142 mmHg, respectively. O2 delivery to the limb (Qleq times CaO2) was not significantly different in HiOX and NOX. VO2peak of the exercising limb averaged 890 mL min-1 in NOX and 801 mL min-1 in HiOX (n.s.) corresponding to 365 and 330 mL min-1 per kg active muscle, respectively. The VO2peak-to-PvO2 ratio was lower (P < 0.05) in HiOX than in NOX suggesting a lower O2 conductance. We conclude that the similar VO2peak values despite higher O2 driving pressure in HiOX indicates a peripheral limitation for VO2peak. This may relate to saturation of the rate of O2 turnover in the mitochondria during exercise with a small muscle group but can also be caused by tissue diffusion limitation related to lower O2 conductance.     

Effects of ischaemia on subsequent exercise-induced oxygen uptake kinetics in healthy adult humans

Leg muscles were occluded (33 kPa) prior to exercise to determine whether the induced metabolic changes, and reactive hyperaemia upon occlusion release just prior to the exercise, would accelerate the subsequent oxygen consumption (VO2) response. Eight subjects performed double bouts (6 min duration, 6 min rest in-between) of square wave leg cycle ergometry both below and above their lactate threshold (LT). Prior to exercise, large blood pressure cuffs were put around the upper thighs. Occlusion durations were 0 min (control), 5 min and 10 min. Ischaemia was terminated within 5 s prior to exercise onset. Heart rate, VO2, ventilatory rate (V(E)), electromyogram (EMG) and haemoglobin/myoglobin (Hb/Mb) saturation were recorded continuously. Single exponential modelling demonstrated that, compared to control (time constant = 53.9 +/- 13.9 s), ischaemia quickened the VO2 response (P < 0.05) for the first bout of exercise above LT (time constant = 48.3 +/- 14.5 s) but not to any other exercise bout below or above LT. The 3-6 min integrated EMG (iEMG) slope was correlated to the 3-6 min VO2 slope (r = 0.73). Hb/Mb saturation verified the ischaemia but did not show a consistent relation to the VO2 time course. Reactive hyperaemia induced a faster VO2 response for work rates above LT. The effect, while significant, was not large considering the expected favourable metabolic and circulatory changes induced by ischaemia.     

Effects of blood gas, pH, lactate, potassium on the oxygen uptake time courses during constant-load bicycle exercise.

Changes in the time courses of VO2 during constant-load exercise were examined in connection with other cardiorespiratory and blood chemical parameters. Eleven healthy male subjects performed a ramp exercise and three to six constant-load exercises at varying degrees of load using an electro-braked bicycle ergometer. Heart rate, ventilation, and gas exchange were measured during both types of exercise, and chemical parameters of the subject's blood (blood gas, pH, lactate, and electrolytes) were determined during two intensities of constant-load exercise. The time courses of cardiorespiratory and blood chemical data 3 min after the onset of constant-load exercise were fitted by linear regressions to see whether these parameters had reached the steady state or not. Heart rate increased significantly at a lower intensity of constant-load exercise than VE, VO2, and VCO2. While the increase in VCO2 was slower than that of VO2, a definite difference in time courses was not found between VE and VO2. The time courses of changes in blood gas, pH, bicarbonate, and lactate were not correlated with those of VO2. However, changes in blood potassium concentration were closely correlated with those of VO2 in terms of time courses and magnitude. This suggests the possibility that blood potassium may play an important role in the control of VO2 time course during constant-load exercise.     

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.     

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.     

The influence of exercise test protocol on perceived exertion at submaximal exercise intensities in children.

This study examined ratings of perceived exertion (RPE) using Borg's 6-20 scale at 50 W, 80 W, and ventilatory threshold (VT) in 10-year-old children (n = 15) during two different graded exercise tests. Power output was increased by 10 W.min(-1) in one protocol and by 30 W.3 min(-1) in the other. The cardiorespiratory responses at VT and peak exercise were similar between protocols. At 50 W and 80 W the cardiorespiratory responses were generally lower (P < 0.05) in the 10W trial. However, RPE was 11.5 +/- 2.9 and 12.1 +/- 3.2 at 50 W and 15.1 +/- 2.7 and 15.3 +/- 2.8 at 80 W in the 10-W and 30-W trials, respectively (P > 0.05). The RPE at VT was 13.9 +/- 2.4 in the 10-W trial and 12.4 +/- 2.4 in the 30-W trial (P < 0.05). In that variations in submaximal RPE did not coincide with variations in central mediators of exertion, locals cues of exertion may have provided the dominate sensory signal.     

Dopaminergic modulation of exercise hyperpnoea via D(2) receptors in mice

Dopamine is related to behaviour (including arousal, motivation and motor control of locomotion), and its turnover in the brain is increased during exercise. We examined the hypothesis that dopamine D(2) receptors contribute to exercise hyperpnoea via central neural pathways using the D(2)-like receptor antagonist, raclopride. We simultaneously measured ventilation and pulmonary gas exchange for the first time in mice. Mice injected with saline and raclopride (2 mg (kg body weight)(-1); i.p.) were compared for respiratory responses to constant-load exercise at 6 m min(-1). Each mouse was set in an airtight treadmill chamber. In the resting state, raclopride-treated mice had reduced respiratory frequency (f(R)) and minute ventilation (V) compared with saline-treated mice, but arterial P(CO(2)) and pulmonary gas exchange were not affected, showing that alveolar ventilation was maintained. Inhalation of hyperoxic gas maintained V in saline-treated mice, and hypercapnic ventilatory responses between the two groups were similar. Treadmill exercise produced an abrupt increase in V to a maximal level within 1 min and declined to a steady-state level in both groups. Raclopride-treated mice had reduced f(R) and V compared with saline-treated mice during steady states, but showed a similar increase in f(R) and V at exercise onset. Minute ventilation in the steady state was controlled, along with the increase in pulmonary O(2) uptake in both groups, but was lowered in raclopride-treated mice. Thus, D(2) receptors participate in resting breathing patterns to raise f(R) and exercise hyperpnoea in the steady state, probably through behavioural control and not central motor command, at exercise onset.     

Oxygen Uptake Kinetics of Older Humans are Slowed with Age but are Unaffected by Hyperoxia

Cross-sectional studies have compared the oxygen uptake (VO2) kinetics during the on-transient of moderate intensity exercise in older and younger adults. The slower values in the older adults may have been due to an age-related reduction in the capacity for O2 transport or alternatively a reduced intramuscular oxidative capacity. We studied: (1) the effects of ageing on VO2 kinetics in older adults on two occasions 9 years apart, and (2) the effect of hyperoxia on VO2 kinetics at the second test time. After a 9 year period, follow-up testing was undertaken on seven older adults (78 +/- 5 years, mean +/- S.D.). They each performed six repeats of 6 min bouts of constant-load cycle exercise from loadless cycling to 80% of their ventilatory threshold. They breathed one of two gas mixtures (euoxia: inspired O2 fraction, FI,O2, 0.21; hyperoxia: FI,O2, 0.70) on different trials determined on a random basis. Breath-by-breath VO2 data were time aligned and ensemble averaged. VO2 kinetics, modelled with a single exponential from phase 2 onset (+20 s) to steady state and described by the exponential time constant (tau) were compared with data collected from the same adults 9 years earlier. One-way repeated measures analysis of variance revealed that tau was slowed significantly with age (from 30 +/- 8 to 46 +/- 10 s), but was unaffected by hyperoxia (43 +/- 15 s). We concluded that: (1) in older adults studied longitudinally over a 9 year period, the on-transient VO2 kinetics are slowed, in agreement with, but to a greater extent, than from cross-sectional data; and (2) the phase 2 time constant (tau) for these older adults was not accelerated by hyperoxic breathing. Thus the expected hyperoxia-induced increase in the capacity for O2 transport was not associated with faster on-transient VO2 kinetics suggesting either that O2 transport may not limit VO2 kinetics during the 8th decade, or that O2 transport was not improved with hyperoxia.     

Exhaled nitric oxide level during and after heavy exercise in athletes with exercise-induced hypoxaemia

Endogenous nitric oxide (NO) is an important mediator of vasodilatation, bronchodilatation and lung inflammation. We hypothesised that the exhaled NO level may be modified in some endurance-trained athletes during and after intense exercise. Nine athletes with exercise-induced hypoxaemia (EIH), 12 athletes without EIH and 10 untrained subjects exercised for 15 min at 90% maximal oxygen consumption (VO(2)max). Exhaled NO was measured during exercise, and after 1 h and 22 h of recovery. Exhaled NO concentration ( C(NO)) decreased significantly during exercise in all subjects and returned to basal values after 1 h of recovery with no further modification. Exhaled NO output (V(NO)) rose significantly during exercise, rapidly dropped down following exercise and was similar to resting values after 1 h and 22 h of recovery. The results also showed that C(NO) and V(NO) were significantly lower in the athletes with EIH in comparison with the untrained subjects (V(NO) was 5.32 +/- 0.77 nmol/min versus 3.61 +/- 0.72 nmol/min at rest, 18.52 +/- 1.50 nmol/min versus 15.00 +/- 2.06 nmol/min during heavy exercise, and 5.52 +/- 1.04 nmol/min versus 3.79 +/- 0.76 nmol/min after 22 h recovery, in untrained subjects and EIH athletes, respectively). These findings do not confirm the hypothesis of pulmonary inflammation associated with EIH. However, potential NO epithelial down-regulation may occur and contribute to the development of gas exchange abnormality in some endurance-trained athletes.     

Gender differences in temperature and vascular characteristics during exercise recovery.

Temperature and vascular responses during exercise recovery were examined in men and women of similar age and fitness status (VO2max: 76 +/- 5 vs 73 +/- 5 mL O2 / kg Fat Free Mass x min). Forearm blood flow (venous occlusion plethysmography; FBF), rectal (Trectal) and forearm skin (Tskin) temperatures (degree C) were measured before and every 15 min up to 105 min (t105) during recovery from a 45-min run at 75% of VO2max. Results indicate Trectal decreased to pre-exercise levels within 25 min in men but reached and remained at values lower than baseline between 60 and 105 min of recovery in women. From 90 to 105 min of recovery, Tskin was lower in women than men (t105 : 29.0 +/- 1.3 vs 30.7 +/- 1.5; p <.05). Recovery FBF (mL/100mL x min) was higher in men than women from the start (6.2 +/- 1.9 vs 4.9 +/- 1.9) to the end of recovery (t105 = 1.7 +/- 0.6 vs 2.6 +/- 1.1) (p <.05). Heat flux calculated at the forearm was higher in women and increased throughout the last hour of recovery (p <.05). Further investigations are needed to examine mechanisms underlying failure of post-exercise core and skin temperatures in women to stabilize at pre-exercise levels.