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.     

Comparison of cardiopulmonary responses to two types of dry-land upper-body exercise testing modes in competitive swimmers

In this study we compared cardiopulmonary responses to upper-body exercise in 12 swimmers, using simulation of the front-crawl arm-pulling action on a computer-interfaced isokinetic swim bench and arm cranking on a modified cycle ergometer. Subjects adopted a prone posture; exercise was initially set at 20 W and subsequently increased by 10 W. min(-1). The tests were performed in a randomised order at the same time of day, within 72 h. The highest (peak) oxygen consumption (VO(2peak)), heart rate (HR(peak)), blood lactate ([la(-)](peak)) and exercise intensity (EI(peak)) were recorded at exhaustion. Mean (SEM) peak responses to simulated swimming were higher than those to arm cranking for VO(2peak) [2.9 (0.2) vs 2.4 (0.1) l x min(-1); P = 0.01], HR(peak) [174 (2) vs 161 (2) beats x min(-1); P = 0.03], and EI(peak) [122 (6) vs 102 (5) W; P = 0.02]. However, there were no significant differences in [la(-)](peak) [9.6 (0.6) vs 8.2 (0.6) mmol x l(-1); P = 0.08]. Thus simulated swimming is the preferred form of dry-land ergometry for the assessment of swimmers.     

VCO2 and VE kinetics during moderate- and heavy-intensity exercise after acetazolamide administration.

The effect of carbonic anhydrase inhibition with acetazolamide (Acz) on CO2 output (VCO2) and ventilation (VE) kinetics was examined during moderate- and heavy-intensity exercise. Seven men [24 +/- 1 (SE) yr] performed cycling exercise during control (Con) and Acz (10 mg/kg body wt iv) sessions. Each subject performed step transitions (6 min) in work rate from 0 to 100 W [below ventilatory threshold (VET)]. VE and gas exchange were measured breath by breath. The time constant (tau) was determined for exercise VET by using a three-component model (fit from the start of exercise). VCO2 kinetics were slower in Acz (VET, MRT = 75 +/- 10 s) than Con (VET, MRT = 54 +/- 7 s). During VET kinetics were faster in Acz (MRT = 85 +/- 17 s) than Con (MRT = 106 +/- 16 s). Carbonic anhydrase inhibition slowed VCO2 kinetics during both moderate- and heavy-intensity exercise, demonstrating impaired CO2 elimination in the nonsteady state of exercise. The slowed VE kinetics in Acz during exercise 相似文献   

Cardiovascular response to punching tempo

Eighteen trained volunteers (12 men and 6 women: age = 22.0 +/- 2.8 years, height = 170.79 +/- 7.67 cm, weight = 71.54 +/- 12.63 kg) participated in 2-minute, randomized fitness boxing trials, wearing 0.34-kg punching gloves, at various tempos (60, 72, 84, 96, 108, and 120 b.min(-1)). During each trial, oxygen uptake (VO(2)), heart rate (HR), and ventilation (VE) were measured continuously. A rating of perceived exertion (RPE) was attained at the conclusion of each trial. Subjects were able to attain VO(2) values ranging from 26.83 to 29.75 ml.kg(-1).min(-1), which correspond to 67.7-72.5% of VO(2)max. The HR responses yielded results ranging from 167.4 to 182.2 b.min(-1), or 85 to 93% of HRmax. No significant difference (p > 0.05) was seen with VO(2) between trials, although a significant difference (p < 0.05) was observed with HR, VE, and RPE. It appears that boxing speed is associated with increased VE, HR response, and perceived effort but not with VO(2). Energy expenditure values ranged from 9.8 to 11.2 kcal.min(-1) for the boxing trials. These results suggest that fitness boxing programs compare favorably with other exercise modalities in cardiovascular response and caloric expenditure.     

Oxygen uptake kinetics for moderate exercise are speeded in older humans by prior heavy exercise.

This study examined the effect of heavy-intensity warm-up exercise on O(2) uptake (VO(2)) kinetics at the onset of moderate-intensity (80% ventilation threshold), constant-work rate exercise in eight older (65 +/- 2 yr) and seven younger adults (26 +/- 1 yr). Step increases in work rate from loadless cycling to moderate exercise (Mod(1)), heavy exercise, and moderate exercise (Mod(2)) were performed. Each exercise bout was 6 min in duration and separated by 6 min of loadless cycling. VO(2) kinetics were modeled from the onset of exercise by use of a two-component exponential model. Heart rate (HR) kinetics were modeled from the onset of exercise using a single exponential model. During Mod(1), the time constant (tau) for the predominant rise in VO(2) (tau VO(2)) was slower (P < 0.05) in the older adults (50 +/- 10 s) than in young adults (19 +/- 5 s). The older adults demonstrated a speeding (P < 0.05) of VO(2) kinetics when moderate-intensity exercise (Mod(2)) was preceded by high-intensity warm-up exercise (tau VO(2), 27 +/- 3 s), whereas young adults showed no speeding of VO(2) kinetics (tau VO(2), 17 +/- 3 s). In the older and younger adults, baseline HR preceding Mod(2) was elevated compared with Mod(1), but the tau for HR kinetics was slowed (P < 0.05) in Mod(2) only for the older adults. Prior heavy-intensity exercise in old, but not young, adults speeded VO(2) kinetics during Mod(2). Despite slowed HR kinetics in Mod(2) in the older adults, an elevated baseline HR before the onset of Mod(2) may have led to sufficient muscle perfusion and O(2) delivery. These results suggest that, when muscle blood flow and O(2) delivery are adequate, muscle O(2) consumption in both old and young adults is limited by intracellular processes within the exercising muscle.     

Metabolic and cardioventilatory responses during a graded exercise test before and 24 h after a triathlon

Previous studies have reported respiratory, cardiac and muscle changes at rest in triathletes 24 h after completion of the event. To examine the effects of these changes on metabolic and cardioventilatory variables during exercise, eight male triathletes of mean age 21.1 (SD 2.5) years (range 17-26 years) performed an incremental cycle exercise test (IET) before (pre) and the day after (post) an official classic triathlon (1.5-km swimming, 40-km cycling and 10-km running). The IET was performed using an electromagnetic cycle ergometer. Ventilatory data were collected every minute using a breath-by-breath automated system and included minute ventilation (V(E)), oxygen uptake (VO2), carbon dioxide production (VCO2), respiratory exchange ratio, ventilatory equivalent for oxygen (V(E)/VO2) and for carbon dioxide (V(E)/VCO2), breathing frequency and tidal volume. Heart rate (HR) was monitored using an electrocardiogram. The oxygen pulse was calculated as VO2/HR. Arterialized blood was collected every 2 min throughout IET and the recovery period, and lactate concentration was measured using an enzymatic method. Maximal oxygen uptake (VO2max) was determined using conventional criteria. Ventilatory threshold (VT) was determined using the V-slope method formulated earlier. Cardioventilatory variables were studied during the test, at the point when the subject felt exhausted and during recovery. Results indicated no significant differences (P > 0.05) in VO2max [62.6 (SD 5.9) vs 64.6 (SD 4.8) ml x kg(-1) x min(-1)], VT [2368 (SD 258) vs 2477 (SD 352) ml x min(-1)] and time courses of VO2 between the pre- versus post-triathlon sessions. In contrast, the time courses of HR and blood lactate concentration reached significantly higher values (P < 0.05) in the pre-triathlon session. We concluded that these triathletes when tested 24 h after a classic triathlon displayed their pre-event aerobic exercise capacity, bud did not recover pretriathlon time courses in HR or blood lactate concentration.     

Ventilatory and gas exchange kinetics during exercise in chronic airways obstruction

The influence of chronic obstructive pulmonary disease (COPD) on exercise ventilatory and gas exchange kinetics was assessed in nine patients with stable airway obstruction (forced expired volume at 1 s = 1.1 +/- 0.33 liters) and compared with that in six normal men. Minute ventilation (VE), CO2 output (VCO2), and O2 uptake (VO2) were determined breath-by-breath at rest and after the onset of constant-load subanaerobic threshold exercise. The initial increase in VE, VCO2, and VO2 from rest (phase I), the subsequent slow exponential rise (phase II), and the steady-state (phase III) responses were analyzed. The COPD group had a significantly smaller phase I increase in VE (3.4 +/- 0.89 vs. 6.8 +/- 1.05 liters/min), VCO2 (0.10 +/- 0.03 vs. 0.22 +/- 0.03 liters/min), VO2 (0.10 +/- 0.03 vs. 0.24 +/- 0.04 liters/min), heart rate (HR) (6 +/- 0.9 vs. 16 +/- 1.4 beats/min), and O2 pulse (0.93 +/- 0.21 vs. 2.2 +/- 0.45 ml/beat) than the controls. Phase I increase in VE was significantly correlated with phase I increase in VO2 (r = 0.88) and HR (r = 0.78) in the COPD group. Most patients also had markedly slower phase II kinetics, i.e., longer time constants (tau) for VE (87 +/- 7 vs. 65 +/- 2 s), VCO2 (79 +/- 6 vs. 63 +/- 3 s), and VO2 (56 +/- 5 vs. 39 +/- 2 s) and longer half times for HR (68 +/- 9 vs. 32 +/- 2 s) and O2 pulse (42 +/- 3 vs. 31 +/- 2 s) compared with controls. However, tau VO2/tau VE and tau VCO2/tau VE were similar in both groups. The significant correlations of the phase I VE increase with HR and VO2 are consistent with the concept that the immediate exercise hyperpnea has a cardiodynamic basis. The slow ventilatory kinetics during phase II in the COPD group appeared to be more closely related to a slowed cardiovascular response rather than to any index of respiratory function. O2 breathing did not affect the phase I increase in VE but did slow phase II kinetics in most subjects. This confirms that the role attributed to the carotid bodies in ventilatory control during exercise in normal subjects also operates in patients with COPD.     

Oxygen cost and oxygen uptake dynamics and recovery with 1 min of exercise in children and adults.

To test the hypothesis that O2 uptake (VO2) dynamics are different in adults and children, we examined the response to and recovery from short bursts of exercise in 10 children (7-11 yr) and 13 adults (26-42 yr). Each subject performed 1 min of cycle ergometer exercise at 50% of the anaerobic threshold (AT), 80% AT, and 50% of the difference between the AT and the maximal O2 uptake (VO2max) and 100 and 125% VO2max. Gas exchange was measured breath by breath. The cumulative O2 cost [the integral of VO2 (over baseline) through exercise and 10 min of recovery (ml O2/J)] was independent of work intensity in both children and adults. In above-AT exercise, O2 cost was significantly higher in children [0.25 +/- 0.05 (SD) ml/J] than in adults (0.18 +/- 0.02 ml/J, P less than 0.01). Recovery dynamics of VO2 in above-AT exercise [measured as the time constant (tau VO2) of the best-fit single exponential] were independent of work intensity in children and adults. Recovery tau VO2 was the same in both groups except at 125% VO2max, where tau VO2 was significantly smaller in children (35.5 +/- 5.9 s) than in adults (46.3 +/- 4 s, P less than 0.001). VO2 responses (i.e., time course, kinetics) to short bursts of exercise are, surprisingly, largely independent of work rate (power output) in both adults and children. In children, certain features of the VO2 response to high-intensity exercise are, to a small but significant degree, different from those in adults, indicating an underlying process of physiological maturation.     

Delayed kinetics of respiratory gas exchange in the transition from prior exercise

The kinetics of oxygen uptake (VO2), carbon dioxide output (VCO2), and expired ventilation (VE) in the transition from rest or from prior exercise were studied in response to step increases in power output (PO). The data were modeled with a single-component exponential function incorporating a time delay (TD). Each subject exercised on four occasions. Test 1 was an incremental test for determination of ventilatory anaerobic threshold (AT). Step increase tests were rest to 80% of PO at AT (test 2), rest-40% AT (3a), 40-80% AT (3b), rest-40% AT (4a), and 40-120% AT (4b). Respiratory gas exchange was monitored by open-circuit techniques. The VO2 kinetics showed the time constant (tau) to be longer in the transitions from prior exercise [tests 3b and 4b were 60.6 +/- 10.8 (SD) and 79.2 +/- 17.4 s] than from rest (tests 2, 3a, and 4a were 37.8 +/- 7.2, 30.0 +/- 7.8, and 39.6 +/- 17.4 s). The mean response time (MRT = tau + TD) was also longer for these tests. Kinetic analysis for VCO2 showed a tendency for tau to be shorter for the tests from prior exercise, but neither tau nor tau + TD were significantly different between tests. In contrast to VCO2, VE kinetics showed a significantly longer tau + TD for test 3b (P less than 0.05) and test 4b (P less than 0.01). This study has shown the VO2 kinetics to be delayed when a given increment in PO occurred from prior exercise, whether the final PO was below or above the AT. Further, the dissociation of VCO2 and VE kinetics does not support a direct link between these two variables as the sole control factor in exercise hyperpnea.     

Breathing pattern in highly competitive cyclists during incremental exercise

The purpose of our investigation was to analyse the breathing patterns of professional cyclists during incremental exercise from submaximal to maximal intensities. A group of 11 elite amateur male road cyclists [E, mean age 23 (SD 2) years, peak oxygen uptake (VO2peak) 73.8 (SD 5.0) ml kg(-1) min(-1)] and 14 professional male road cyclists [P, mean age 26 (SD 2) years, (VO2peak) 73.2 (SD 6.6) ml kg(-1) min(-1)] participated in this study. Each of the subjects performed an exercise test on a cycle ergometer following a ramp protocol (exercise intensity increases of 25 W x min(-1)) until the subject was exhausted. For each subject, the following parameters were recorded during the tests: oxygen consumption (VO2), carbon dioxide output (VCO2), pulmonary ventilation (VE), tidal volume (VT), breathing frequency (fb), ventilatory equivalents for oxygen (VE x VO2(-1)) and carbon dioxide (VE x VCO2(-1)), end-tidal partial pressure of oxygen and partial pressure of carbon dioxide, inspiratory (tI) and expiratory (tE) times, inspiratory duty cycle (tI/tTOT, where tTOT is the time for one respiratory cycle), and mean inspiratory flow rate (VT/tI). Mean values of VE were significantly higher in E at 300, 350 and 400 W (P < 0.05, P < 0.05 and P < 0.01, respectively); fb was also higher in E in most moderate-to-maximal intensities. On the other hand, VT showed a different pattern in both groups at near-to maximal intensities, since no plateau was observed in P. The response of tI and tE was also different. Finally, VT/tI and tI/tTOT showed a similar response in both P and E. It was concluded that the breathing pattern of the two groups differed mainly in two aspects: in the professional cyclists, VE increased at any exercise intensity as a result of increases in both VT and fb, with no evidence of tachypnoeic shift, and tE was prolonged in this group at high exercise intensities. In contrast, neither the central drive nor the timing component of respiration seem to have been significantly altered by the training demands of professional cycling.     

The physiological effects of caffeine in women during treadmill walking

Although the effects of caffeine ingestion on athletic performance in men have been studied extensively, there is limited previous research examining caffeine's effects on women of average fitness levels participating in common modes of physical activity. The purpose of this study was to determine the effect of 2 levels of caffeine dosage on the metabolic and cardiorespiratory responses to treadmill walking in women. Subjects were 20 women (19-28 years of age) of average fitness, not habituated to caffeine. Each subject was assigned randomly a 3-mg x kg(-1) dose of caffeine, 6-mg x kg(-1) dose of caffeine, and placebo for 3 trials of moderate steady-state treadmill walking at 94 m x min(-1) (3.5 mph). Steady-state rating of perceived exertion (RPE), heart rate (HR), respiratory exchange ratio (RER), weight-relative VO2, %VO2max reserve (%VO2R), and rate of energy expenditure (REE) were measured during each trial. Repeated measures analysis of variance revealed that a 6-mg x kg(-1), but not a 3-mg x kg(-1) dose of caffeine increased VO2 (p = 0.04), REE (p = 0.03), and %VO2R (p = 0.03), when compared to the placebo. Caffeine had no effect on RPE, HR, or RER. No significant differences were observed between the placebo trials and the 3-mg x kg(-1) dose trials. Although a 6-mg x kg(-1) dose of caffeine significantly increased REE during exercise, the observed increase (approximately 0.23 kcal x min(-1)) would not noticeably affect weight loss. Because caffeine had no effect on RPE, it would not be prudent for a trainer to recommend caffeine in order to increase a woman's energy expenditure or to decrease perception of effort during mild exercise. These data also demonstrate that caffeine intake should not interfere with monitoring walking intensity by tracking exercise heart rate in women.     

Effect of exercise modality on oxygen uptake kinetics during heavy exercise

The mechanisms responsible for the oxygen uptake (VO2) slow component during high-intensity exercise have yet to be established. In order to explore the possibility that the VO2 slow component is related to the muscle contraction regimen used, we examined the pulmonary VO2 kinetics during constant-load treadmill and cycle exercise at an exercise intensity that produced the same level of lactacidaemia for both exercise modes. Eight healthy subjects, aged 22-37 years, completed incremental exercise tests to exhaustion on both a cycle ergometer and a treadmill for the determination of the ventilatory threshold (defined as the lactate threshold, Th1a) and maximum VO2 (VO2max). Subsequently, the subjects completed two "square-wave" transitions from rest to a running speed or power output that required a VO2 that was halfway between the mode-specific Th1a and VO2max. Arterialised blood lactate concentration was determined immediately before and after each transition. The VO2 responses to the two transitions for each exercise mode were time-aligned and averaged. The increase in blood lactate concentration produced by the transitions was not significantly different between cycling [mean (SD) 5.9 (1.5) mM] and running [5.5 (1.6) mM]. The increase in VO2 between 3 and 6 min of exercise; (i.e. the slow component) was significantly greater in cycling than in running, both in absolute terms [290 (102) vs 200 (45) ml x min(-1); P<0.05] and as a proportion of the total VO2 response above baseline [10 (3)% vs 6 (1)%; P < 0.05]. These data indicate that: (a) a VO2 slow component does exist for high-intensity treadmill running, and (b) the magnitude of the slow component is less for running than for cycling at equivalent levels of lactacidaemia. The greater slow component observed in cycling compared to running may be related to differences in the muscle contraction regimen that is required for the two exercise modes.     

Exercise-induced hypoxaemia in highly trained cyclists at 40% peak oxygen uptake

A group of 15 competitive male cyclists [mean peak oxygen uptake, VO2peak 68.5 (SEM 1.5 ml x kg(-1) x min(-1))] exercised on a cycle ergometer in a protocol which began at an intensity of 150 W and was increased by 25 W every 2 min until the subject was exhausted. Blood samples were taken from the radial artery at the end of each exercise intensity to determine the partial pressures of blood gases and oxyhaemoglobin saturation (SaO2), with all values corrected for rectal temperature. The SaO2 was also monitored continuously by ear oximetry. A significant decrease in the partial pressure of oxygen in arterial blood (PaO2) was seen at the first exercise intensity (150 W, about 40% VO2peak). A further significant decrease in PaO2 occurred at 200 W, whereafter it remained stable but still significantly below the values at rest, with the lowest value being measured at 350 W [87.0 (SEM 1.9) mmHg]. The partial pressure of carbon dioxide in arterial blood (PaCO2) was unchanged up to an exercise intensity of 250 W whereafter it exhibited a significant downward trend to reach its lowest value at an exercise intensity of 375 W [34.5 (SEM 0.5) mmHg]. During both the first (150 W) and final exercise intensities (VO2peak) PaO2 was correlated significantly with both partial pressure of oxygen in alveolar gas (P(A)O2, r = 0.81 and r = 0.70, respectively) and alveolar-arterial difference in oxygen partial pressure (P(A-a)O2, r = 0.63 and r = 0.86, respectively) but not with PaCO2. At VO2peak PaO2 was significantly correlated with the ventilatory equivalents for both oxygen uptake and carbon dioxide output (r = 0.58 and r = 0.53, respectively). When both P(A)O2 and P(A-a)O2 were combined in a multiple linear regression model, at least 95% of the variance in PaO2 could be explained at both 150 W and VO2peak. A significant downward trend in SaO2 was seen with increasing exercise intensity with the lowest value at 375 W [94.6 (SEM 0.3)%]. Oximetry estimates of SaO2 were significantly higher than blood measurements at all times throughout exercise and no significant decrease from rest was seen until 350 W. The significant correlations between PaO2 and P(A)O2 with the first exercise intensity and at VO2peak led to the conclusion that inadequate hyperventilation is a major contributor to exercise-induced hypoxaemia.     

Effect of pre-cooling, with and without thigh cooling, on strain and endurance exercise performance in the heat

Body cooling before exercise (i.e. pre-cooling) reduces physiological strain in humans during endurance exercise in temperate and warm environments, usually improving performance. This study examined the effectiveness of pre-cooling humans by ice-vest and cold (3 degrees C) air, with (LC) and without (LW) leg cooling, in reducing heat strain and improving endurance performance in the heat (35 degrees C, 60% RH). Nine habitually-active males completed three trials, involving pre-cooling (LC and LW) or no pre-cooling (CON: 34 degrees C air) before 35-min cycle exercise: 20 min at approximately 65% VO2peak then a 15-min work-performance trial. At exercise onset, mean core (Tc, from oesophagus and rectum) and skin temperatures, forearm blood flow (FBF), heart rate (HR), and ratings of exertion, body temperature and thermal discomfort were lower in LW and LC than CON (P<0.05). They remained lower at 20 min [e.g. Tc: CON 38.4+/-0.2 (+/-S.E.), LW 37.9+/-0.1, and LC 37.8+/-0.1 degrees C; HR: 177+/-3, 163+/-3 and 167+/-3 b.p.m.), except that FBF was equivalent (P=0.10) between CON (15.5+/-1.6) and LW (13.6+/-1.0 ml.100 ml tissue(-1) x min(-1)). Subsequent power output was higher in LW (2.95+/-0.24) and LC (2.91+/-0.25) than in CON (2.52+/-0.28 W kg(-1), P=0.00, N=8), yet final Tc remained lower. Pre-cooling by ice-vest and cold air effectively reduced physiological and psychophysical strain and improved endurance performance in the heat, irrespective of whether thighs were warmed or cooled.     

Physiological demands of cyclists during an ultra-endurance relay race: a field study report

This study was to describe and compare the physiological demands of ultra-endurance cyclists during a 24 h cycling relay race. Eleven male athletes (means +/- SD: 34.8 +/- 5.6 years; 71.6 +/- 4.9 kg; 174.6 +/- 7.3 cm; BMI 23.5 +/- 0.5 kg/m2; VO2 max: 66.0 +/- 6.4 ml/kg/min) participated in the study; eight in teams with a format of four riders (4C) and three in teams with six riders (6C). To investigate exercise intensity, heart rate (HR) was recorded while cycling using portable telemetric monitors. Three different exercise intensities were defined according to the reference HR values obtained during a pre race laboratory incremental VO2 max test: Zone I (< anaerobic threshold [AT]), Zone II (between AT and the respiratory compensation point [RCP]), Zone III (> RCP). Total volume and intensity were integrated as a single variable (training impulse: TRIMP). The score for TRIMP in each zone was computed by multiplying the accumulated duration in this zone by a multiplier for this particular zone of exercise intensity. The average intensity did not differ between cyclists in 4C (means +/- SD; 4C: 87 +/- 3 HRmax) and 6C (87 +/- 1% of HRmax), despite the higher volume performed by 4C (means +/- SD; 4C: 361 +/- 65; 6C: 242 +/- 25 per min; P = 0.012). These differences in total exercise volume significantly affected the values TRIMP accumulated (means +/- SD; 4C: 801 +/- 98, confidence interval [CI] 95%: 719 - 884; 6C: 513 +/- 25, CI 95%: 451 - 575; P = 0.012). The ultra-endurance threshold of 4C and 6C athletes lies at about 87% of HRmax for both. Although the intensity profile was similar, the TRIMP values differed significantly as a consequence of the higher volume performed by the 4C cyclists.     

Plasma norepinephrine and heart rate dynamics during recovery from submaximal exercise in man

The time course of heart rate (HR) and venous blood norepinephrine concentration [NE], as an expression of the sympathetic nervous activity (SNA), was studied in six sedentary young men during recovery from three periods of cycle ergometer exercise at 21% +/- 2.8%, 43% +/- 2.1% and 65% +/- 2.3% of VO2max respectively (mean +/- SE). The HR decreased mono-exponentially with tau values of 13.6 +/- 1.6 s, 32.7 +/- 5.6 s and 55.8 +/- 8.1 s respectively in the three periods of exercise. At the low exercise level no change in [NE] was found. At medium and high exercise intensity: (a) [NE] increased significantly at the 5th min of exercise (delta [NE] = 207.7 +/- 22.5 pg.ml-1 and 521.3 +/- 58.3 pg.ml-1 respectively); (b) after a time lag of 1 min [NE] decreased exponentially (tau = 87 s and 101 s respectively); (c) in the 1st min HR decreased about 35 beats.min-1; (d) from the 2nd to 5th min of recovery HR and [NE] were linearly related (100 pg.ml-1 delta [NE] congruent to 5 beats.min-1). In the 1st min of recovery, independent of the exercise intensity, the adjustment of HR appears to have been due mainly to the prompt restoration of vagal tone. The further decrease in HR toward the resting value could then be attributed to the return of SNA to the pre-exercise level.     

Varied and repeated atropine dosages and exercise-heat stress

Comparisons of physiological responses to 0, 0.5, 1, and 2 mg atropine (IM) were made in seven males (X +/- SD: age, 24 +/- 3 years; ht, 174 +/- 12 cm; wt, 76 +/- 3 kg) while they exercised (approximately 390 W) in a hot-dry (40 degrees C, 20% rh) environment. Responses to 4 mg, as well as repeatability of responses to 2 mg, were studied in two and six of these subjects, respectively. On 8 test days an intramuscular injection of atropine or saline control was administered 20 min before subjects walked on a treadmill for two 50-min bouts. Heart rate (HR) during exercise did not change in the control trial but by min 50 increased during all atropine trials (P less than 0.01). Rectal temperature (Tre) increased (P less than 0.01) in all trials by min 50 and continued increasing (P less than 0.01) in the 2-mg trial during the second exercise bout. For the two subjects tested with all dosages (0.5 - 4 mg atropine), the change in HR and Tre between the atropine and control trials at 50 min of exercise was regressed against the various atropine dosages. The relationship (r = 0.92) for HR was curvilinear while the relationship (r = 0.99) for Tre was linear. Mean weighted skin temperature (Tsk) was relatively constant during exercise and was warmer (P less than 0.05) with increasing atropine dosage. In a repeat 2 mg trial, HR was 6 bt . min-1 lower (P less than 0.05) on the second exposure but Tre was the same (P greater than 0.05) on both days. For subjects walking in the heat, three new observations were: 1) 0.5 mg of atropine resulted in increased HR and Tsk compared to control values; 2) HR was elevated but the magnitude of change decreased with increasing dosage, while the elevation in Tre was consistent with increasing dosage; and 3) rectal temperatures (in trials with and without atropine) were unaffected by previous days of atropine administration.     

Physiological responses during prolonged exercise at the power output corresponding to the blood lactate threshold

Heart rate (HR) and oxygen uptake (VO2) at the mechanical power (W) corresponding to the capillary blood lactate ([la]cap) of 4 mmol.l-1 (Wlt) were measured in 34 healthy male subjects during incremental exercise (Winc). On the basis of these measurements, the subjects were asked to cycle at Wlt for 60 min (steady-state exercise, Wss). Twenty subjects could not reach the target time (mean exhaustion time, te, 38.2 min, SD 5.3), while 6 of the 14 remaining subjects declared themselves exhausted at the end of exercise. The final [la]cap if the two groups of exhausted subjects were 5.3 mmol.l-1, SD 2.3 and 4.3 mmol.l-1, SD 1.1, respectively. At the end of Wss, [la]cap and HR were significantly lower in the 8 unexhausted subjects than in the other subjects. This group also had a lower HR at Wlt during Winc. The HR and VO2 appeared to be higher during Wss than during Winc. When all subjects were ranked according to their te during Wss, Wlt (expressed per kilogram of body mass) was found to be negatively related to te. In conclusion, during Winc, measurements of physiological variables at fixed [la]cap give a poor prediction of their trends during Wss and of the relative te; at the same work load [la]cap can be quite different in the two experimental conditions. Furthermore, resistance to exercise fatigue at Wlt seems lower in the fitter subjects.     

Leukocyte, lymphocyte and platelet response to dynamic exercise. Duration or intensity effect?

The influence of work intensity and duration on the white blood cell (WBC), lymphocyte (L) and platelet (P) count response to exercise was studied in 16 trained subjects (22 +/- 5.4 years, means +/- SD). They performed three cyclo-ergospirometric protocols: A) 10 min at 150 W followed by a progressive test (30 W/3 min) till exhaustion; B) constant maximal work (VO2max); C) a 45 min Square-Wave Endurance Exercise Test (SWEET), (n = 5). Arterial blood samples were taken: at rest, submaximal and maximal exercise in A; maximal exercise in B; 15th, 30th and 45th min in the SWEET. Lactate, [H+], PaCO2, PaO2, [Hct], Hb, cortisol, ACTH, total platelet volume (TPV), total blood red cell (RBC), WBC, L and P were measured. At 150 W, WBC, L, P, and TPV increased. VO2max did not differ between A and B, but a difference was found in total exercise time (A = 25 +/- 3 min; B = 7 +/- 2 min, p less than 0.001). In A, at VO2max, the increase was very small for Hct, [Hb], and RBC (10%), in contrast with large changes for WBC (+93%), L (+137%), P (+32%), TPV (+35%), [H+] (+39%), lactate (+715%), and ACTH (+95%). At VO2max there were no differences in these variables between A and B. During the SWEET: WBC, L, P, TPV and ACTH increased at the 15th min as much as in VO2max, but no difference was observed between the 15th, 30th and 45th min, except for ACTH which continued to rise; the lactate increase during the SWEET was about half (+341%) the value observed at VO2max, and [H+] did not vary with respect to values at rest.(ABSTRACT TRUNCATED AT 250 WORDS)