After effects of chronic hypoxia on VO2 kinetics and on O2 deficit and debt

Single breath O2 consumption (PB = 730, FI02 = 0.21) was measured at rest, during 10 min cycloergometric exercise at 125 W, and in the following recovery phase in seven subjects before, and 12 days after 6 weeks at 5,200 m or above. Peak blood lactate after exercise (Lab) was measured. O2 deficits and debts and half times (t1/2) of the VO2 on- and off-kinetics were calculated. Before acclimatization, the VO2 on- and off-responses were close to a single exponential with t1/2 = 30 s. After return to sea level, the VO2 on-response curves were less steep in the initial phase, becoming closer to sigmoid. The t1/2, independent of the shape of the underlying function, was approximately 10 s longer. The VO2 off-responses during the initial 4 min of recovery were the same before and after acclimatization. Average O2 deficit was approximately 320 ml larger after acclimatization: the fast component of O2 debt was similar. Since steady state VO2 and Lab were the same, the O2 deficit difference can be attributed to a greater utilization of O2 stores. Of these, about 1/3 is explained in terms of increased mixed venous blood O2 stores, due to increased [Hb] (16.6 vs 14.9 g X dl-1), while the remainder is ascribed essentially to increased Mb-bound O2. O2 stores utilization and replenishment is presumed to occur when muscle metabolism is low; as a consequence, while it is clearly detectable from the shape of the initial phase of the VO2 on-response, during recovery it is spread throughout, thus becoming more difficult to appreciate.     

Effects of priming exercise on VO2 kinetics and O2 deficit at the onset of stepping and cycling

Breath-by-breath O2 uptake (VO2) kinetics and increase of blood lactate concentration (delta Lab) were determined at the onset of square-wave stepping (S) or cycling (C) exercise on six male subjects during 1) transition from rest (R) to constant work load, 2) transition from lower to heavier work loads, wherein the baseline VO2 (VO2 s) was randomly chosen between 20 and 65% of the subjects' maximal O2 uptake (VO2 max), and 3) inverse transition from higher to lower work loads and/or to rest. VO2 differences between starting and arriving levels were 20-60% VO2 max. In C, the VO2 on-response became monotonically slower with increasing VO2 s, the half time (t1/2) increasing from approximately 22 s for VO2 s = R to approximately 63 s when VO2 s approximately equal to 50% VO2 max. In S, the fastest VO2 kinetics (t1/2 = 16 s) was attained from VO2 s = 15-30% VO2 max, the t1/2 being approximately 25 s when starting from R or from 50% VO2 max. The slower VO2 kinetics in C were associated with a much larger delta Lab. The VO2 kinetics in recovery were essentially the same in all cases and could be approximated by a double exponential with t1/2 of 21.3 +/- 6 and 93 +/- 45 s for the fast and slow components, respectively. It is concluded that the O2 deficit incurred is the sum of three terms: 1) O2 stores depletion, 2) O2 equivalent of early lactate production, and 3) O2 equivalent of phosphocreatine breakdown.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of specific muscle training on VO2 on-response and early blood lactate

The relationship between half time of the O2 uptake on-response (t1/2 VO2on, seconds) and early blood lactate accumulation (delta Lab, mmol.1(-1) at the onset of submaximal arm and/or leg exercise was the object of a cross-sectional study of sedentary subjects (S,n = 3), and kayakers (K, n = 8), and of a longitudinal study on 11 untrained subjects of specific arm vs. leg training. In supine arm cranking (W = 125 watts) S had an average t1/2 VO2on of 82 s and a delta Aab of 9.2 mmol.1(-1) compared to 47 +/- 7 s and 4 +/- 1.4 mmol.1(-1), respectively, for K. In longitudinal trainees shorter t1/2 VO2on was accompanied by lower Lab for the trained limbs. Specific limb conditioning in swimmers and runners resulted in shorter t1/2 VO2on. A linear relationship was observed between delta Lab and t1/2 VO2on having an intercept on the time axis at congruent to 20 s and a slope proportional to muscle mass. Trained muscles were grouped closest to the intercept indicating local acceleration of the rate of O2 transfer approaching the t1/2 VO2on for isolated perfused muscle at the onset of work. Since t1/2 VO2on, we conclude that factors distal to the capillary are specifically involved in the local training response.     

Influence of respiratory muscle work on VO(2) and leg blood flow during submaximal exercise.

The work of breathing (W(b)) normally incurred during maximal exercise not only requires substantial cardiac output and O(2) consumption (VO(2)) but also causes vasoconstriction in locomotor muscles and compromises leg blood flow (Q(leg)). We wondered whether the W(b) normally incurred during submaximal exercise would also reduce Q(leg). Therefore, we investigated the effects of changing the W(b) on Q(leg) via thermodilution in 10 healthy trained male cyclists [maximal VO(2) (VO(2 max)) = 59 +/- 9 ml. kg(-1). min(-1)] during repeated bouts of cycle exercise at work rates corresponding to 50 and 75% of VO(2 max). Inspiratory muscle work was 1) reduced 40 +/- 6% via a proportional-assist ventilator, 2) not manipulated (control), or 3) increased 61 +/- 8% by addition of inspiratory resistive loads. Increasing the W(b) during submaximal exercise caused VO(2) to increase; decreasing the W(b) was associated with lower VO(2) (DeltaVO(2) = 0.12 and 0.21 l/min at 50 and 75% of VO(2 max), respectively, for approximately 100% change in W(b)). There were no significant changes in leg vascular resistance (LVR), norepinephrine spillover, arterial pressure, or Q(leg) when W(b) was reduced or increased. Why are LVR, norepinephrine spillover, and Q(leg) influenced by the W(b) at maximal but not submaximal exercise? We postulate that at submaximal work rates and ventilation rates the normal W(b) required makes insufficient demands for VO(2) and cardiac output to require any cardiovascular adjustment and is too small to activate sympathetic vasoconstrictor efferent output. Furthermore, even a 50-70% increase in W(b) during submaximal exercise, as might be encountered in conditions where ventilation rates and/or inspiratory flow resistive forces are higher than normal, also does not elicit changes in LVR or Q(leg).     

Influence of body CO2 stores on ventilatory dynamics during exercise

Pulmonary CO2 flow (the product of cardiac output and mixed venous CO2 content) is purported to be an important determinant of ventilatory dynamics in moderate exercise. Depletion of body CO2 stores prior to exercise should thus slow these dynamics. We investigated, therefore, the effects of reducing the CO2 stores by controlled volitional hyperventilation on cardiorespiratory and gas exchange response dynamics to 100 W cycling in six healthy adults. The control responses of ventilation (VE), CO2 output (VCO2), O2 uptake (VO2), and heart rate were comprised of an abrupt increase at exercise onset, followed by a slower rise to the new steady state (t1/2 = 48, 43, 31, and 33 s, respectively). Following volitional hyperventilation (9 min, PETCO2 = 25 Torr), the steady-state exercise responses were unchanged. However, VE and VCO2 dynamics were slowed considerably (t1/2 = 76, 71 s) as PETCO2 rose to achieve the control exercise value. VO2 dynamics were slowed only slightly (t1/2 = 39 s), and heart rate dynamics were unaffected. We conclude that pulmonary CO2 flow provides a significant stimulus to the dynamics of the exercise hyperpnea in man.     

Water immersion delays the oxygen uptake response to sitting arm-cranking in humans

We investigated the effect of central hypervolaemia during water immersion up to the xiphoid process on the oxygen uptake (VO2) and heart rate (HR) response to arm cranking. Seven men performed a 6-min arm-cranking exercise at an intensity requiring a VO2 at 80% ventilatory threshold both in air [C trial, 29 (SD 9) W] and immersed in water [WI trial, 29 (SD 11) W] after 6 min of sitting. The VO2 (phase 2) and HR responses to exercise were obtained from a mono-exponential fit [f(t) = baseline + gain x (1 - e(-(t-TD)/tau))]. The response was evaluated by the mean response time [MRT; sum of time constant (tau) and time delay (TD)]. No significant difference in VO2 and HR gains between the C and WI trials was observed [VO2 0.78 (SD 0.1) vs 0.80 (SD 0.2) l x min(-1), HR 36 (SD 7) vs 37 (SD 8) beats x min(-1), respectively]. Although the HR MRT was not significantly different between the C and WI trials [17 (SD 3), 19 (SD 8) s, respectively), VO2 MRT was greater in the WI trial than in the C trial [40 (SD 6), 45 (SD 6) s, respectively; P < 0.05]. Assuming no difference in VO2 in active muscle between the two trials, these results would indicate that an increased oxygen store and/or an altered response in muscle blood distribution delayed the VO2 response to exercise.     

Arm blood flow at rest and during arm exercise

To test the applicability of a dye-dilution method to quantitate total arm blood flow at rest and during arm exercise, indocyanine green was infused at a constant rate into the brachial artery. Eight subjects performed continuous 30-min arm exercises with an increase in intensity every 10 min (30, 60, and 90 W). The loads corresponded to 29 +/- 1, 48 +/- 2, and 78 +/- 4% (means +/- SE) of the maximal O2 uptake (VO2max 2.13 +/- 0.08 l/min) during arm exercise. VO2max during arm exercise was 61 +/- 1.7% of that during leg exercise. The dye concentration was analyzed in blood samples from three arm veins, two ipsi- and one contralateral, at shoulder level. Corresponding dye concentrations in both ipsilateral veins and a stable concentration difference between ipsi- and contralateral veins were achieved. Total arm blood flow was calculated to be 0.21 +/- 0.04 l/min at rest and 2.43 +/- 0.14 l/min at 90 W. Arm O2 uptake rose from 9 +/- 2 to 323 +/- 21 ml/min. Arm blood flow and O2 uptake each correlated linearly with both work load (r = 0.98) and pulmonary O2 uptake (r greater than or equal to 0.98). Mechanical efficiency for the arm and body was 34-44 and 16-19%, respectively. We conclude that arm blood flow can be determined by continuous infusion of indocyanine green.     

Pulmonary and leg VO2 during submaximal exercise: implications for muscular efficiency.

Insights into muscle energetics during exercise (e.g., muscular efficiency) are often inferred from measurements of pulmonary gas exchange. This procedure presupposes that changes of pulmonary O2 (VO2) associated with increases of external work reflect accurately the increased muscle VO2. The present investigation addressed this issue directly by making simultaneous determinations of pulmonary and leg VO2 over a range of work rates calculated to elicit 20-90% of maximum VO2 on the basis of prior incremental (25 or 30 W/min) cycle ergometry. VO2 for both legs was calculated as the product of twice one-leg blood flow (constant-infusion thermodilution) and arteriovenous O2 content difference across the leg. Measurements were made 3-5 min after each work rate imposition to avoid incorporation of the VO2 slow component above the lactate threshold. For all 17 subjects, the slope of pulmonary VO2 (9.9 +/- 0.2 ml O2.W-1.min-1) was not different (P greater than 0.05) from that for leg VO2 (9.2 +/- 0.6 ml O2.W-1.min-1). Estimation of "delta" efficiency (i.e., delta work accomplished divided by delta energy expended, calculated from slope of VO2 vs. work rate and a caloric equivalent for O2 of 4.985 cal/ml) using pulmonary VO2 measurements (29.1 +/- 0.6%) was likewise not significantly different (P greater than 0.05) from that made using leg VO2 measurements (33.7 +/- 2.4%). These data suggest that the net VO2 cost of metabolic "support" processes outside the exercising legs changes little over a relatively broad range of exercise intensities. Thus, under the conditions of this investigation, changes of VO2 measured from expired gas reflected closely those occurring within the exercising legs.     

Effect of carbohydrate feedings during high-intensity exercise

To determine the upper limits of steady-state exercise performance and carbohydrate oxidation late in exercise, seven trained men were studied on two occasions during prolonged cycling that alternated every 15 min between approximately 60% and approximately 85% of VO2max. When fed a sweet placebo throughout exercise, plasma glucose and respiratory exchange ratio (R) declined (P less than 0.05) from 5.0 +/- 0.1 mM and 0.91 +/- 0.01 after 30 min (i.e., at 85% VO2max) to 3.7 +/- 0.3 mM and 0.79 +/- 0.01 at fatigue (i.e., when the subjects were unable to continue exercise at 60% VO2max). Carbohydrate feeding throughout exercise (1 g/kg at 10 min, then 0.6 g/kg every 30 min) increased plasma glucose to approximately 6 mM and partially prevented this decline in carbohydrate oxidation, allowing the men to perform 19% more work (2.74 +/- 0.13 vs. 2.29 +/- 0.09 MJ, P less than 0.05) before fatiguing. Even when fed carbohydrate, however, by the 3rd h of exercise, R had fallen from 0.92 to 0.87, accompanied by a reduction in exercise intensity from approximately 85% to approximately 75% VO2max (both P less than 0.05). These data indicate that carbohydrate feedings enable trained cyclists to exercise at up to 75% VO2max and to oxidize carbohydrate at up to 2 g/min during the later stages of prolonged intense exercise.     

Endurance training reduces the magnitude of exercise-induced hyperammonemia in humans

The purpose of this study was to determine the influence of endurance-type exercise training on alterations of the ammonia content of blood in exercising humans. Seven females and four males trained 6 days/wk for 7 wk alternating days of continuous cycling (40 min) and interval running (five 5-min bouts). The NH3 content of blood was determined before and during cycle ergometer (CE) exercise (4 min) at power outputs (PO) of 119, 172, and 241 W pretraining and of 163, 230, and 271 W posttraining. These PO for each occasion represent relative work loads of approximately 65, 90, and 115% of peak CE maximum O2 uptake (PCE VO2), respectively. Training increased (P less than 0.05) PCE VO2 approximately 32% (2.72 +/- 0.25 to 3.56 +/- 0.29 l/min or 38.5 +/- 1.9 to 51.2 +/- 2.3 ml X kg-1 X min-1). Both pre- and posttraining the NH3 content of blood increased (P less than 0.05) with increasing intensity of exercise. Training did not influence the measure of these responses during exercise at the same relative intensity. During exercise at the same absolute PO, approximately 168 or 235 W, however, increases in blood NH3 were less (P less than 0.05) after training. The results indicate that the magnitude of increase in blood NH3 during exercise is determined by the energy requirement of the absolute work load, relative to an individual's aerobic power.     

Effects of previous exercise on the ventilatory determination of the aerobic threshold

To study the effects of previous submaximal exercise on the ventilatory determination of the Aerobic Threshold (AeT), 16 men were subjected to three maximal exercise tests (standard test = ST, retest = RT, and test with previous exercise = TPE ) on a cycle ergometer. The protocol for the three tests consisted of 3 min pedalling against 25 W, followed by increments of 25 W every minute until volitional fatigue. TPE was preceded by 10 min cycling at a power output corresponding to the AeT as determined in ST, followed by a recovery period pedalling against 25 W until VO2 returned to values consistent with the initial VO2 response to 25 W. AeT was determined from the gas exchange curves (ventilatory equivalent for O2, fraction of expired O2, excess of VCO2, ventilation, and respiratory gas exchange ratio) printed every 30 s. The results showed good ST X RT reliability (r = 0.89). TPE showed significantly higher AeT values (2.548 +/- 0.44 1 X min-1) when compared with ST (2.049 +/- 0.331 X min-1) and RT (2.083 +/- 0.30 1 X min-1). There were no significant differences for the sub-threshold respiratory gas exchange ratios among the trials. The sub-threshold VO2 response showed significantly higher values for TPE at power outputs above 50 W. It was concluded that the performance of previous exercise can increase the value for the ventilatory determination of the AeT due to a faster sub-threshold VO2 response.     

Exercise and nasal patency

Nasal airflow resistances were studied in 20 healthy subjects at rest, with exercise, and during recovery from exercise. Resistances were first measured under resting conditions. As a basis for comparison 0.1% xylometazoline was applied by insufflation; it reduced nasal resistance by an average of 49%. On a subsequent occasion, the degree and time course of changes in resistance were measured 1) during 5-min exercise bouts at rest 25, 50, and 75% of predicted maximum O2 intake (VO2max), 2) during 5-, 10-, and 15-min exercise bouts at 50% of VO2max, and 3) during recovery from exercise. Resistance decreased with intensity but not duration of exercise; an initial sudden decrease was followed by a more gradual but progressive decrease, which continued for several minutes following vigorous short duration exercise. Thus following 5 min of effort at 75% of VO2max, resistance reached a nadir (46% fall) 5 min after cessation of exercise. Recovery of preexercise values required 5 min after 5 min of exercise at 25% of VO2max and 10 min after 5 min of exercise at 50% of VO2max. Some decrease persisted 15 min after 5 min of exercise at 75% of VO2max.     

Blood flow and muscle oxygen uptake at the onset and end of moderate and heavy dynamic forearm exercise

We hypothesized that forearm blood flow (FBF) during moderate intensity dynamic exercise would meet the demands of the exercise and that postexercise FBF would quickly recover. In contrast, during heavy exercise, FBF would be inadequate causing a marked postexercise hyperemia and sustained increase in muscle oxygen uptake (VO(2musc)). Six subjects did forearm exercise (1-s contraction/relaxation, 1-s pause) for 5 min at 25 and 75% of peak workload. FBF was determined by Doppler ultrasound, and O(2) extraction was estimated from venous blood samples. In moderate exercise, FBF and VO(2musc) increased within 2 min to steady state. Rapid recovery to baseline suggested adequate O(2) supply during moderate exercise. In contrast, FBF was not adequate during heavy dynamic exercise. Immediately postexercise, there was an approximately 50% increase in FBF. Furthermore, we observed for the first time in the recovery period an increase in VO(2musc) above end-exercise values. During moderate exercise, O(2) supply met requirements, but with heavy forearm exercise, inadequate O(2) supply during exercise caused accumulation of a large O(2) deficit that was repaid during recovery.     

Oxygen uptake kinetics in trained athletes differing in VO2max

Previous work has shown that when VO2 kinetics are compared for endurance trained athletes and untrained subjects, the highly trained athletes have a faster response time. However, it remains to be determined whether the more rapid adjustment of VO2 toward steady state in athletes is due to VO2max differences or training adaptation alone. One approach to this problem is to study the time course of VO2 kinetics at the onset of work in athletes who differ in VO2max but have similar training habits. Therefore, the purpose of these experiments was to compare the time course of VO2 kinetics at the onset of exercise in athletes with similar training routines but who differ in VO2max. Ten subjects (VO2max range 50-70 ml . kg-1 . min-1) performed 6-minutes of cycle ergometer exercise at approximately 50% VO2max. Ventilation and gas exchange were monitored by open circuit techniques. The data were modeled with a single component exponential function incorporating a time delay, (TD); delta VO2t = delta VO2ss (1-e-t-TD/tau), where tau is the time constant delta VO2t is the increase in VO2 at time t and delta VO2ss is the steady-rate increment above resting VO2. Kinetic analysis revealed a range of VO2 half times from 21.6 to 36.0 s across subjects with a correlation coefficient of r = -0.80 (p less than 0.05) between VO2max and VO2 half time. These data suggest that in highly trained individuals with similar training habits, those with a higher VO2max achieve a more rapid VO2 adjustment at the onset of work.     

V˙O2peak and the gas-exchange anaerobic threshold during incremental arm cranking in able-bodied and paraplegic men

Resting energy expenditure, peak oxygen uptake (VO2peak) and the gas-exchange anaerobic threshold (Than) were measured during incremental arm cranking (15 W x min(-1)) in six able-bodied (AB) and six paraplegic (P) subjects. Only male subjects with traumatic spinal cord injuries in the area of the 10-12th thoracic segment were included in the P group. All AB and P subjects were physically active. Mean (SE) values for age and body mass were 28 (2) years and 78.9 (3.9) kg for the AB group and 32 (4) years and 70.8 (7.9) kg for the P group (P>0.05). Resting energy expenditure values were not found to be significantly different between AB [5.8 (0.2) kJ x min(-1)] and P [5.1 (0.3) kJ min(-1)] subjects. Mean VO2peak values were 29.3 (2.4) ml x kg(-1) min(-1) and 29.6 (2.2) ml x kg(-1) x min(-1) for the AB and P groups, respectively (P>0.05). Absolute oxygen uptake values measured at two gas-exchange anaerobic threshold (Than) were not significantly different between the two groups. However, the Than occurred at a significantly higher percentage of VO2peak in the P [58.9 (1.7)%] group than in the AB [50.0 (2.8)%] group (P<0.05). Moreover, respiratory exchange ratio (R) values obtained at the Than and at 15, 45, 60, 75 and 90 W of incremental exercise were significantly lower in the P group than in the AB group. Heart rates were significantly elevated at every submaximal work stage (15-120 W) in the P group compared to the AB group (P<0.05). These findings suggest that chronic daily wheelchair activity produces local adaptations in the functional upper-body musculature, which reduce glycogenolysis and increase the rate of lipid utilization (lower R) during arm exercise. These local adaptations may be in part responsible for the significantly higher Than observed for arm exercise in P subjects, even though VO2peak values were essentially the same for both groups.     

Gastric emptying during walking and running: effects of varied exercise intensity

Gastric emptying is increased during running (50%-70% maximal aerobic uptake, VO2max) as compared to rest. Whether this increase varies as a function of mode (i.e. walking vs running) and intensity of treadmill exercise is unknown. To examine the gastric emptying characteristics of water during treadmill exercise performed over a wide range of intensities relative to resting conditions, 10 men ingested 400 ml of water prior to each of six 15 min exercise bouts or 15 min of seated rest. Three bouts of walking exercise (1.57 m.s-1) were performed at increasing grades eliciting approximately 28%, 41% or 56% of VO2max. On a separate day, three bouts of running (2.68 ms-1) exercise were performed at grades eliciting approximately 57%, 65% or 75% of VO2max. Gastric emptying was increased during treadmill exercise at all intensities excluding 75% VO2max as compared to rest. Gastric emptying was similar for all intensities during walking and at 57% and 65% VO2max during running. However, running at 74% VO2max decreased the volume of original drink emptied as compared to all lower exercise intensities. Stomach secretions were markedly less during running as compared to walking and rest. These data demonstrate that gastric emptying is similarly increased during both moderate intensity (approximately 28%-65% VO2max) walking or running exercise as compared to resting conditions. However, gastric emptying decreases during high intensity exercise. Increases in gastric emptying during moderate intensity treadmill exercise may be related to increases in intragastric pressure brought about by contractile activity of the abdominal muscles.     

Frequency domain analysis of ventilation and gas exchange kinetics in hypoxic exercise.

The kinetics of O2 up-take (VO2), CO2 output (VCO2), ventilation (VE), and heart rate (HR) were studied during exercise in normoxia and hypoxia [inspired O2 fraction (FIO2) 0.14]. Eight male subjects each completed 6 on- and off-step transitions in work rate (WR) from low (25 W) to moderate (100-125 W) levels and a pseudorandom binary sequence (PRBS) exercise test in which WR was varied between the same WRs. Breath-by-breath data were linearly interpolated to yield 1-s values. After the first PRBS cycle had been omitted as a warm-up, five cycles were ensemble-averaged before frequency domain analysis by standard Fourier methods. The step data were fit by a two-component (three for HR) exponential model to estimate kinetic parameters. In the steady state of low and moderate WRs, each value of VO2, VCO2, VE, and HR was significantly greater during hypoxic than normoxic exercise (P less than 0.05) with the exception of VCO2 (low WR). Hypoxia slowed the kinetics of VO2 and HR in on- and off-step transitions and speeded up the kinetics of VCO2 and VE in the on-transition and of VE in the off-transition. Frequency domain analysis confined to the range of 0.003-0.019 Hz for the PRBS tests indicated reductions in amplitude and greater phase shifts in the hypoxic tests for VO2 and HR at specific frequencies, whereas amplitude tended to be greater with little change in phase shift for VCO2 and VE during hypoxic tests.(ABSTRACT TRUNCATED AT 250 WORDS)     

VO(2) kinetics reveal a central limitation at the onset of subthreshold exercise in heart transplant recipients.

Because the cardiocirculatory response of heart transplant recipients (HTR) to exercise is delayed, we hypothesized that their O(2) uptake (VO(2)) kinetics at the onset of subthreshold exercise are slowed because of an impaired early "cardiodynamic" phase 1, rather than an abnormal subsequent "metabolic" phase 2. Thus we compared the VO(2) kinetics in 10 HTR submitted to six identical 10-min square-wave exercises set at 75% (36 +/- 5 W) of the load at their ventilatory threshold (VT) to those of 10 controls (C) similarly exercising at the same absolute (40 W; C40W group) and relative load (67 +/- 14 W; C67W group). Time-averaged heart rate, breath-by-breath VO(2), and O(2) pulse (O(2)p) data yielded monoexponential time constants of the VO(2) (s) and O(2)p increase. Separating phase 1 and 2 data permitted assessment of the phase 1 duration and phase 2 VO(2) time constant (). The VO(2) time constant was higher in HTR (38.4 +/- 7.5) than in C40W (22.9 +/- 9.6; P < or = 0. 002) or C67W (30.8 +/- 8.2; P < or = 0.05), as was the O(2)p time constant, resulting from a lower phase 1 VO(2) increase (287 +/- 59 vs. 349 +/- 66 ml/min; P < or = 0.05), O(2)p increase (2.8 +/- 0.6 vs. 3.6 +/- 1.0 ml/beat; P < or = 0.0001), and a longer phase 1 duration (36.7 +/- 12.3 vs. 26.8 +/- 6.0 s; P < or = 0.05), whereas the was similar in HTR and C (31.4 +/- 9.6 vs. 29.9 +/- 5.6 s; P = 0.85). Thus the HTR have slower subthreshold VO(2) kinetics due to an abnormal phase 1, suggesting that the heart is unable to increase its output abruptly when exercise begins. We expected a faster in HTR because of their prolonged phase 1 duration. Because this was not the case, their muscular metabolism may also be impaired at the onset of subthreshold exercise.     

Oxygen uptake during high-intensity running: response following a single bout of interval training

Elevated oxygen uptake (VO2) during moderate-intensity running following a bout of interval running training has been studied previously. To further investigate this phenomenon, the VO2 response to high-intensity exercise was examined following a bout of interval running. Well-trained endurance runners were split into an experimental group [maximum oxygen uptake, VO2max 4.73 (0.39)l x min(-1)] and a reliability group [VO2max 4.77 (0.26)l x min(-1)]. The experimental group completed a training session (4 x 800 m at 1 km x h(-1) below speed at VO2max, with 3 min rest between each 800-m interval). Five minutes prior to, and 1 h following the training session, subjects completed 6 min 30 s of constant speed, high-intensity running designed to elicit 40% delta (where delta is the difference between VO2 at ventilatory threshold and VO2max; tests 1 and 2, respectively). The slow component of VO2 kinetics was quantified as the difference between the VO2 at 6 min and the VO2 at 3 min of exercise, i.e. deltaVO2(6-3). The deltaVO2(-3) was the same in two identical conditions in the reliability group [mean (SD): 0.30 (0.10)l x min(-1) vs 0.32 (0.13)l x min(-1)]. In the experimental group, the magnitude of the slow component of VO2 kinetics was increased in test 2 compared with test 1 by 24.9% [0.27 (0.14)l x min(-1) vs 0.34 (0.08)l x min(-1), P < 0.05]. The increase in deltaVO2(6-3) in the experimental group was observed in the absence of any significant change in body mass, core temperature or blood lactate concentration, either at the start or end of tests 1 or 2. It is concluded that similar mechanisms may be responsible for the slow component of VO2 kinetics and for the fatigue following the training session. It has been suggested previously that this mechanism may be linked primarily to changes within the active limb, with the recruitment of alternative and/or additional less efficient fibres.     

Effect of fitness on arm vascular and metabolic responses to upper body exercise

We investigated arm perfusion and metabolism during upper body exercise. Eight average, fit subjects and seven rowers, mean +/- SE maximal oxygen uptake (VO2 max) 157 +/- 7 and 223 +/- 14 ml O2. kg(-0.73).min(-1), respectively, performed incremental arm cranking to exhaustion. Arm blood flow (ABF) was measured with thermodilution and arm muscle mass was estimated by dual-energy X-ray absorptiometry. During maximal arm cranking, pulmonary VO2 was approximately 45% higher in the rowers compared with the untrained subjects and peak ABF was 6.44 +/- 0.40 and 4.55 +/- 0.26 l/min, respectively (P < 0.05). The arm muscle mass for the rowers and the untrained subjects was 3.5 +/- 0.4 and 3.3 +/- 0.1 kg, i.e., arm perfusion was 1.9 +/- 0.2 and 1.4 +/- 0.1 l blood.kg(-1).min(-1), respectively (P < 0.05). The arteriovenous O2 difference was 156 +/- 7 and 120 +/- 8 ml/l, respectively, and arm VO2 was 0.98 +/- 0.08 and 0.60 +/- 0.04 l/min corresponding with 281 +/- 22 and 181 +/- 12 ml/kg, while arm O(2) diffusional conductance was 49.9 +/- 4.3 and 18.6 +/- 3.2 ml.min(-1).mmHg(-1), respectively (P < 0.05). Also, lactate release in the rowers was almost three times higher than in the untrained subjects (26.4 +/- 1.1 vs. 9.5 +/- 0.4 mmol/min, P < 0.05). The energy requirement of an approximately 50% larger arm work capacity after long-term arm endurance training is covered by an approximately 60% increase in aerobic metabolism and an almost tripling of the anaerobic capacity.