Oxygen cost of exercise hyperpnea: implications for performance.

We addressed two questions concerned with the metabolic cost and performance of respiratory muscles in healthy young subjects during exercise: 1) does exercise hyperpnea ever attain a "critical useful level"? and 2) is the work of breathing (WV) at maximum O2 uptake (VO2max) fatiguing to the respiratory muscles? During progressive exercise to maximum, we measured tidal expiratory flow-volume and transpulmonary pressure- (Ptp) volume loops. At rest, subjects mimicked their maximum and moderate exercise Ptp-volume loops, and we measured the O2 cost of the hyperpnea (VO2RM) and the length of time subjects could maintain reproduction of their maximum exercise loop. At maximum exercise, the O2 cost of ventilation (VE) averaged 10 +/- 0.7% of the VO2max. In subjects who used most of their maximum reserve for expiratory flow and for inspiratory muscle pressure development during maximum exercise, the VO2RM required 13-15% of VO2max. The O2 cost of increasing VE from one work rate to the next rose from 8% of the increase in total body VO2 (VO2T) during moderate exercise to 39 +/- 10% in the transition from heavy to maximum exercise; but in only one case of extreme hyperventilation, combined with a plateauing of the VO2T, did the increase in VO2RM equal the increase in VO2T. All subjects were able to voluntarily mimic maximum exercise WV for 3-10 times longer than the duration of the maximum exercise. We conclude that the O2 cost of exercise hyperpnea is a significant fraction of the total VO2max but is not sufficient to cause a critical level of "useful" hyperpnea to be achieved in healthy subjects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in the leucocyte count during and after brief intense exercise.

Twelve healthy male volunteers exercised at 200 W on a cycle ergometer for 8 min or until exhausted, if sooner. Retrospectively, subjects fell into two groups. During the last minute of exercise at 200 W, those in group 1 (n = 5) had a mean respiratory exchange ratio (R) of 1.06 (SD 0.01) and were working at a mean of 79% (SD 4%) of their maximum oxygen consumption (VO2max) as measured in a separate incremental load test. For subjects in group 2 (n = 7), R was 1.31 (SD 0.08) and their VO2 was maximal (mean 101%. SD 3%). Plasma lactate, and adrenaline concentrations rose to higher levels during exercise in subjects in group 2 than in those in group 1. At the finish of exercise, the leucocyte count and the plasma lactate concentration immediately began to fall in subjects in group 1 whereas in group 2 subjects both rose for several minutes before falling. Plasma catecholamine concentrations fell rapidly in both groups during recovery.     

Dexamethasone in resting and exercising men. I. Effects on bioenergetics, minerals, and related hormones.

A placebo and a low and a high dose of dexamethasone (Dex) were administered for 4.5 days, at 3-wk intervals, to 24 healthy men, following a double-blind, random-order, crossover procedure. After the last dose the subjects performed a maximal cycling exercise, during which respiratory exchanges, electrocardiogram, and blood pressures were monitored. Blood was sampled just before and after each exercise bout. Dex showed no significant effect on fitness, sleep, exhaustion during exercise, maximal O(2) consumption, ventilatory threshold, maximal blood lactate, or rest and exercise blood pressures. On the contrary, both doses of Dex significantly decreased heart rate at rest and during maximal exercise. Blood glucose at rest was higher after both doses of Dex than after placebo; the opposite was found during exercise. Blood levels of ACTH, beta-endorphin, cortisol, and cortisol-binding globulin were lowered by Dex at rest and after exercise. Dex stimulated the increase in atrial natriuretic factor during exercise and lowered rest and postexercise aldosterone. Finally, no difference between "fit or trained" and "less fit or untrained" subjects could be found with respect to Dex effects.     

Effect of mechanical loading on breathing patterns in women

First-breath ventilatory responses to graded inspiratory elastic and resistive loads were obtained from 80 women unfamiliar with respiratory experimentation. For each load 1) responses from different subjects ranged from a weak tidal volume defense coupled with an increased breathing frequency to a strong tidal volume defense coupled with a decreased frequency; 2) strong tidal volume defenders employed longer inspirations than did weak tidal volume defenders; and 3) individual respiratory frequency responses were mediated by changes in inspiratory and/or expiratory timing. Thus the group response was qualitatively the same as that reported for 80 men. Quantitatively, however, mean inspiratory airflow responses of women exceeded those of men by an amount attributable to women's higher intrinsic respiratory elastance. Tidal volume responses, on the other hand, did not differ significantly, suggesting that men and women produce different neural adjustments to loads. In support of this hypothesis, analysis of respiratory timing responses revealed that 1) men actively prolonged inspiration more than women during resistive loading; and 2) women actively shortened inspiration more than men during elastic loading. These findings indicate that the load-compensating behavior exhibited by men and women is similar but not identical.     

Short-term effect of tidal pleural pressure swings on pulmonary blood flow during rest and exercise

Because pleural pressure (Ppl) has important effects on venous return and left ventricular function, it is possible that the magnitude of respiratory fluctuations in Ppl importantly influences cardiac output (pulmonary blood flow, QL) during exercise. To examine this question, we increased (+15 cmH2O) and decreased (-11 cmH2O) the amplitude of fluctuations in Ppl by elastic loading and unloading, respectively, during steady-state exercise (50 W) and estimated the corresponding changes in QL from measurement of breath-by-breath alveolar O2 consumption [(Vo2)A] by a modification of the technique of Beaver et al. (J. Appl. Physiol. 51: 1662-1675, 1981). Load changes were applied for three breaths. Using oscilloscopic volume feedback, subjects maintained constant breathing pattern and end-expiratory volume during control and experimental breaths. This procedure minimized errors in computing (Vo2)A. Furthermore, because over the brief period of load change (especially the first 1 or 2 breaths) mixed venous and arterial O2 contents were not likely to have changed, changes in (Vo2)A reflected changes in QL according to the Fick principle. In six normal subjects, neither loading nor unloading had any effect on (Vo2)A in the first, second, or third breath (P greater than 0.5). Additional studies at rest produced equally negative results. We conclude that the magnitude of respiratory fluctuations in Ppl has no short-term effect on pulmonary blood flow at rest or during mild exercise.     

Sustained maximal ventilation after endurance exercise in athletes

Although impaired respiratory muscle performance that persists up to 5 min after exercise is stopped has been demonstrated during exhaustive exercise in normal young men, it is not known whether impaired respiratory muscle function follows endurance exercise to exhaustion in highly trained athletes. To study the effects of exercise on sustained maximal voluntary ventilation immediately after exercise, eight elite cross-country skiers performed a 4-min maximal sustained ventilation (MSV) test before and immediately after exhaustive exercise. Subjects were encouraged to maintain maximal ventilation (VE) throughout the MSV test. To encourage greater effort, rapid visual feedback of VE was provided on a computer terminal along with a target VE based on their 12-s maximum voluntary ventilation (MVV). The subjects (7 males, 1 female) were 18.5 +/- 0.9 yr old (mean +/- SD) and exercised for 62.5 +/- 16.7 min at 77 +/- 5% of their maximum oxygen consumption during which average VE was 106.7 +/- 24.2 l/min BTPS. The mean MVV was 196.0 +/- 29.9 l/min or 107% of their age- and height-predicted MVV. Before exercise the MSV was 86% of the MVV or 176.7 +/- 30.5 l/min, whereas after exercise the MSV was 90% of the MVV or 180.3 +/- 28.9 l/min (P = NS). The total volume of gas expired during the 4-min MSV was 706.7 +/- 121.9 liters before and 721.2 +/- 115.5 liters after exercise (P = NS). In this group of athletes, exhaustive exercise produced no deleterious effects on the ability to perform a 4-min MSV test immediately after exercise.     

Ventilatory control in hypercapnia and exercise: optimization hypothesis

A model of the respiratory control system incorporating both chemical and respiratory neuromechanical feedbacks is proposed to describe the steady-state ventilatory responses to CO2 inhalation and exercise. It is postulated that ventilatory output (VE) is set by the respiratory center to minimize a net operating cost representing the conflicting challenges of arterial chemical imbalance and respiratory-mechanical discomfort (intolerance of effort), given, respectively, by a quadratic function of arterial PCO2 and a logarithmic function of VE. In addition, the system is assumed to be mechanically limited at maximum VE (Vmax). The predicted responses in VE during moderate hypercapnia, exercise, and ventilatory loading closely mimic those normally observed, even though no separate signal unique to exercise is assumed. As a quantitative validation, the model yielded good fits to ventilatory response data obtained in eight healthy subjects during eucapnic and hypercapnic exercise; the predicted Vmax averaged approximately 77% of the maximum voluntary ventilation in all subjects. The results demonstrate the plausibility of the proposed optimization mechanism and suggest an important role for respiratory-mechanical factors in the control of VE.     

Pulmonary gas exchange during exercise in women: effects of exercise type and work increment.

Exercise-induced arterial hypoxemia (EIAH) has been reported in male athletes, particularly during fast-increment treadmill exercise protocols. Recent reports suggest a higher incidence in women. We hypothesized that 1-min incremental (fast) running (R) protocols would result in a lower arterial PO(2) (Pa(O(2))) than 5-min increment protocols (slow) or cycling exercise (C) and that women would experience greater EIAH than previously reported for men. Arterial blood gases, cardiac output, and metabolic data were obtained in 17 active women [mean maximal O(2) uptake (VO(2 max)) = 51 ml. kg(-1). min(-1)]. They were studied in random order (C or R), with a fast VO(2 max) protocol. After recovery, the women performed 5 min of exercise at 30, 60, and 90% of VO(2 max) (slow). One week later, the other exercise mode (R or C) was similarly studied. There were no significant differences in VO(2 max) between R and C. Pulmonary gas exchange was similar at rest, 30%, and 60% of VO(2 max). At 90% of VO(2 max), Pa(O(2)) was lower during R (mean +/- SE = 94 +/- 2 Torr) than during C (105 +/- 2 Torr, P < 0.0001), as was ventilation (85.2 +/- 3.8 vs. 98.2 +/- 4.4 l/min BTPS, P < 0.0001) and cardiac output (19.1 +/- 0.6 vs. 21.1 +/- 1.0 l/min, P < 0.001). Arterial PCO(2) (32.0 +/- 0.5 vs. 30.0 +/- 0.6 Torr, P < 0.001) and alveolar-arterial O(2) difference (A-aDO(2); 22 +/- 2 vs. 16 +/- 2 Torr, P < 0.0001) were greater during R. Pa(O(2)) and A-aDO(2) were similar between slow and fast. Nadir Pa(O(2)) was 相似文献   

Orthostatism and heat acclimation.

Three groups of subjects (6 subj in each group) underwent the following precedures: group A was given a 20-min head-up tilt at 21 degrees C followed by 4 h of exercise at 33.9 degrees C DB, 32.2 degrees C WB, and a repetition of tilting after exercise in heat; group B underwent the same procedure at 21 degrees C; group C was tilted at 21 degrees C, rested in heat for 4 h and was retilted in heat. The above procedures were repeated for 8 days, and on the last day groups B and C underwent the same treatment as group A. Group A showed the usual decreases in heart rate and rectal temperature and an increase in sweat rate on acclimation. This corresponded to marked improvements in heat-orthostatism. While five subjects in group A fainted during post-exposure tilting on the first exposure, none fainted on the last day. Resting in heat (group C) did not cause any acclimation to work in heat. This corresponded to poor heat-orthostatism after the work-heat procedure when five subjects fainted. Mild training at 21 degrees C (group B) resulted in minor improvements to work in heat as evident by some improvements in heart rate responses after the 1st and 2nd h of exposure. This corresponded to better heat-orthostatism and fewer men fainting than in group C. The results indicated that heat-orthostatism improves on acclimation to the same extent as exercise heart rate and rectal temperature.     

Physiological responses of young and elderly men to prolonged exercise at critical power

The critical power (CP) of a muscle group or individual may represent the highest rate of work which can be performed for an extended period. We investigated this concept in young (n = 13, 24.5 years) and elderly (n = 12, 70.7 years) active men by first determining CP and then comparing responses elicited by 24 min of cycle exercise at power outputs (omega) corresponding to CP. Values from the final 2 min of the 24-min ride were expressed relative to maximal values established in a ramp test. CP for the elderly was only 65% that for the young, but on a relative basis, it was significantly higher both in terms of omega (67 vs 62% of omega max) and oxygen consumption (VO2) (91.5 vs 85.2% of maximum oxygen consumption). There were no group differences in relative values for ventilation (VE), heart rate or respiratory exchange ratio (R). During the 24-min ride, VO2 and R achieved a plateau in both groups, while VE, blood lactate and arterial PCO2 continued to change in the young. It was concluded that CP can be determined in active elderly men, but that CP may not represent a true non-fatiguing work rate in either young or elderly men.     

Respiration during exercise in conscious laryngectomized humans

We compared respiratory patterning at rest and during steady cycle exercise at work rates of 30, 60, and 90 W in 7 male chronically laryngectomized subjects and 13 normal controls. Breathing was measured with a pneumotachograph and end-tidal PCO2 by mass spectrometer. Inspired air was humidified and enriched to 35% O2. Peak flow, volume, and times for the inspiratory and expiratory half cycles, time for expiratory flow, minute ventilation, and mean inspiratory flow were computer averaged over at least 40 breaths at rest and during the last 2 min of 5-min periods at each work rate. During the transition from rest to exercise and with increasing work rate in both groups, there was an increase in respiratory rate and depth with selective and progressive shortening of expiratory time; these responses were not significantly different between the two groups, but there was a suggestion that respiratory "drive" as quantitated by mean inspiratory flow may limit in the laryngectomized subjects at high work rates. Time for expiratory flow increased on transition from rest to exercise and then decreased in both groups as the work rate increased; it was shorter in the laryngectomy than control group at all levels. In the laryngectomized subjects there was significantly more breath-by-breath scatter in some variables at rest, but there was no difference during exercise. It is concluded that chronic removal of the larynx and upper airways in mildly hyperoxic conscious humans has only subtle and, therefore, functionally insignificant effects on breathing during moderate exercise. Evidence is provided that the upper airways can modulate expiratory flow but not expiratory time during exercise.     

Exercise responses following ozone exposure.

We have tested the response of 28 subjects to a three-stage ergometer test, with loads adjusted to 45, 60, and 75% of maximum aerobic power following ozone exposure. The subjects were exposed to one of 0.37, 0.50, or 0.75 ppm O3 for 2 h either at rest (R) or while exercising intermittently (IE) (15 min rest alternated with 15 min exercise at approximately 50 W. sufficient to increase VE by a factor of 2.5). Also, all subjects completed a mock exposure VE, respiratory frequency (fR), mixed expired PO2 and PCO2, and electrocardiogram were monitored continuously during the exercise test. Neither submaximal exercise oxygen consumption nor minute ventilation was significantly altered following any level of ozone exposure. The major response noted was an increase in respiratory frequency during exercise following ozone exposure. The increase in fR was closely correlated with the total dose of ozone (r = 0.98) and was accompanied by a decrease in tidal volume (r = 0.91) so that minute volume was unchanged. It is concluded that through its irritant properties, ozone modifies the normal ventilatory response to exercise, and that this effect is dose dependent.     

Exercise induced increase in plasma atrial natriuretic peptide and effect of sodium loading in normal man

Atrial tachyarrhythmias and atrial pacing are associated with increased cardiac secretion of atrial natriuretic peptide (ANP) in man. Using treadmill exercise to exhaustion, we have studied the effect of exercise induced tachycardia on plasma immunoreactive ANP (IR-ANP) and vasoactive hormones in 6 normal men before and after 6 days of sodium loading (salt supplements and 0.4 mg 9 alpha fludro hydrocortisone daily for 4 days). Similar increases in heart rate and plasma catecholamine levels occurred during exercise in both studies. Sodium loading increased resting supine plasma IR-ANP (P less than 0.037) and suppressed plasma renin and aldosterone, including the renin-aldosterone response to exercise. Plasma IR-ANP increased more than 3-fold during exercise to 48 +/- 7 before and 66 +/- 12 pmol/l after sodium loading (P greater than 0.1). When the response of individual subjects was examined, there was no significant correlation between change in plasma IR-ANP and change in heart rate or catecholamine levels in either exercise study. Exercise induces greater increments in plasma IR-ANP than either acute or chronic sodium loading in normal men and may be a useful and rapid means of assessing the heart's ability to secrete ANP.     

Cardiovascular responses to arm cranking and FNS-induced leg exercise in paraplegics

Twelve spinal cord-injured males performed arm-crank exercise (ACE) with and without concurrent functional neuromuscular stimulation (FNS) of paralyzed leg muscles to investigate the hypothesis that FNS would augment cardiovascular performance during submaximal ACE. Six men who exhibited vigorous isometric contractions of thigh and calf muscles were classed as "responders" to FNS (R), and the remaining subjects with poor or nonexistent contractions served as "nonresponder controls" (C). Steady-state heart rate and oxygen uptake during ACE at 30, 60, and 90 W were not appreciably different from the ACE + FNS condition. However, cardiac outputs in R were augmented by 30% during FNS at rest (from 4.9 to 6.4 l/min), by 18% during 30-W ACE + FNS (from 8.6 to 10.1 l/min), and by 28% during 90-W ACE + FNS (from 12.1 to 15.6 l/min). Similarly, resting stroke volumes were increased by 18% (9 ml) and by 23% (19 ml) at 60 W during FNS in the R group. Calculated total peripheral resistance was reduced at rest and during 90-W ACE + FNS by approximately 24%. In contrast, no alterations of circulatory hemodynamics were observed for C subjects. These data indicate that FNS-induced contractions of paralyzed leg muscles augment venous return to aid central cardiovascular control during upper-body submaximal exercise in paraplegics.     

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.     

Systemic arterial compliance, systemic vascular resistance, and effective arterial elastance during exercise in endurance-trained men

Systemic arterial compliance (C) and vascular resistance (R) regulate effective arterial elastance (Ea), an index of artery load. Increases in Ea during exercise are due primarily to reductions of C and maintain optimal ventricular-arterial coupling. Because C at rest and left ventricular functional reserve are greater in endurance-trained (ET) compared with sedentary control (SC) humans, we hypothesized that reductions of C and increases in Ea are greater in ET than SC individuals. The aim of this study was to investigate C, R, and Ea during exercise in ET and SC humans. C, R, Ea, and cardiac cycle length (T) were measured at rest and during exercise of 40, 60, and 80% maximal oxygen uptake using Doppler ultrasonography in 12 SC and 13 ET men. C decreased in an exercise intensity-dependent manner in both groups, but its reductions were greater in the ET than SC subjects. Consequently, although C at rest was greater in the ET than SC group, the intergroup difference in C disappeared during exercise. Exercise-related changes in R/T were relatively slight and R/T was lower in the ET than the SC group, both at rest and during exercise. Although Ea at rest was lower in the ET than SC group, there were no intergroup differences in Ea at 40, 60, or 80% maximal oxygen uptake. We conclude that the reductions of C from rest to exercise are more marked in ET than SC humans. This may be related to the exercise-associated disappearance of the difference in Ea between ET and SC humans.     

Gender differences in glucoregulatory responses to intense exercise.

We compared glucoregulatory responses to intense exercise (14 min at 88% maximum O(2) uptake) between genders (16 men, 12 women). Analysis of covariance of maximum O(2) uptake showed no gender effect, with 82% of variance due to fat-free mass (FFM). Glycemia rose comparably during exercise but was higher in women during recovery (P = 0.02). Glucose production [rate of appearance (R(a)); in mg/min] increased markedly in both; stepwise multiple regression and analysis of covariance of R(a) (peak and incremental area under the curve) showed no effect of gender, body weight, or FFM. Glucose uptake [rate of disappearance (R(d))] increased less than R(a) and slower in women. R(d) area under the curve related to FFM (P = 0.01) but not gender or body weight. Norepinephrine and epinephrine responses (13-18x baseline) were the same and correlated significantly with R(a). Exercise insulin and glucagon changes were slight, but postexercise hyperinsulinemia was greater in women (P = 0.018), along with higher R(d). Therefore, intense exercise glucoregulation is qualitatively similar between genders, with a "feed-forward" regulation of R(a) (consistent with catecholamine mediation). However, women have a lesser R(d) response, related to FFM. This combination leads to greater recovery-period hyperglycemia and hyperinsulinemia.     

Plasma FFA responses to prolonged walking in untrained men and women

Gender differences in plasma FFA responses to 90 min of treadmill walking at 35% VO2max were investigated in six men and six women following an overnight fast. The subjects represented average values for maximal oxygen uptake and body fat percentage for age and gender. Mean plasma FFA concentration at 45 and 90 min of exercise were significantly (P less than 0.05) higher for women (0.82 mmol X 1(-1), 0.88 mmol X 1(-1)) than men (0.42 mmol X 1(-1), 0.59 mmol X 1(-1)). Lower R values for women throughout the exercise period indicated a greater percentage fat in total metabolism than for men while the FFA/glycerol results supported greater lipolytic activity for women. The uniformity of percent fat in metabolism for women from rest to exercise showed that FFA release from adipose tissue increased rapidly with the onset of exercise which was not the case for men. Comparison of metabolic data as well as a statistical analysis (ANCOVA) controlling for the influence of VO2max and percentage body fat on FFA plasma concentration suggested that gender differences in FFA responses to prolonged submaximal exercise can be expected to occur in untrained subjects.     

Effects on energy expenditure of facial cooling during exercise.

Estimated energy expenditures for men during Arctic manhauling expeditions were 29-33 MJ day-1, higher than those documented for other hard-working groups and exceeding predicted energy costs for such activities. Although physiological effects from generalised cooling were unlikely, cold exposure of the face could have influenced exercise metabolism via autonomic stimulation. This hypothesis was examined by measuring oxygen consumption, energy expenditure, respiratory exchange ratio (R) and cardiovascular changes during rest and exercise, with and without exposure of the face to air at--20 degrees C. Measurements were made in five subjects during 15 min of rest followed by continuous exercise on a cycle ergometer consisting of 15-min periods at 75, 100, 125 and 150 W external work. The cold air caused a profound fall in facial temperatures and small falls in mean skin and rectal temperatures (P less than 0.001). These changes were associated with a small increase in the mean oxygen consumption over all levels of rest and exercise (0.86 l min-1 vs 0.82 l min-1, P less than 0.001) and a corresponding increase in mean energy expenditure (294 W vs 283 W, P less than 0.05). Cold air also caused an increase in mean resting R values (1.00 vs 0.88, P less than 0.01) but a decrease in the mean R value for all levels of exercise (0.85 vs 0.91, P less than 0.05). Pulse rates were unchanged but systolic and diastolic blood pressures were relatively elevated throughout the cold face experiments (P less than 0.001).