Pregnancy-induced changes in the maximal physiological responses during swimming.

The effect of pregnancy on peak O2 uptake (VO2 peak) during tethered swimming was evaluated in 10 women during their 25th and 35th wk of pregnancy, as well as 9-11 wk postpartum. The swim results were compared with cycle ergometry results obtained at similar times. The results indicated that exercise-induced maximal heart rates remained the same and were similar for the swim and cycle trials, approximately 184 +/- 4 beats/min. Cycling VO2 peak was not affected by pregnancy, averaging 1.94 +/- 0.11 l/min. Postpartum swim VO2 peak was similar to the cycle results; however, during pregnancy it was significantly lower than cycling VO2 peak (P less than 0.05; postpartum, 1.78 +/- 0.14 l/min; 25th wk, 1.64 +/- 0.12; 35th wk, 1.48 +/- 0.11). Hemoglobin concentrations and hematocrits were lower during pregnancy; however, changes in plasma volume (based on hematocrit and hemoglobin) were found to be significantly greater during cycling than during swimming and also greater during pregnancy for both modes of exercise. It was concluded that, unlike cycling, the VO2 peak of pregnant women during swimming is reduced. This reduction in VO2 peak was associated with a decreased peak ventilation (r = 0.864) but was not correlated to exercise-induced hemoconcentration (r = -0.29). Furthermore, pregnancy results in a greater-than-normal exercise-induced hemoconcentration, which may be related to pregnancy-induced changes in capillary dynamics.     

Validity of pulse oximetry during exercise in elite endurance athletes.

Eleven highly trained male cyclists [maximal aerobic power (VO2max) = 70.6 +/- 4.2 ml.kg-1.min-1] performed both high intensity constant load (90-95% VO2max) and incremental cycle exercise tests with arterial blood sampling to evaluate the accuracy of pulse oximeter estimates (%SpO2) of arterial oxyhemoglobin fraction of total hemoglobin (%HbO2). Three subjects also performed an incremental exercise test in hypoxic conditions (inspired partial pressure of O2 = 89, 93, or 100 Torr). Arterial %HbO2 was determined via CO-oximetry and ranged from 72 to 99%. Three Ohmeda 3740 pulse oximeters were used to estimate %HbO2, one on each ear lobe and a finger probe. The finger probe tended to provide the best estimate of %HbO2 during exercise: the mean %SpO2 - %HbO2 difference for 232 exercise observations was 0.52 +/- 1.36% (SD). Finger probe %SpO2 and %HbO2 were highly correlated [r = 0.98, standard error of the estimate (SEE) = 1.32%, P less than 0.0001]. The accuracy of pulse oximeters has been questioned during high-intensity exercise. When aerobic power was greater than 81% of VO2max (n = 75), the finger probe's mean error was -0.01 +/- 1.40%. Finger probe %SpO2 and %HbO2 were highly correlated (r = 0.97, SEE = 1.32%, P less than 0.0001). These results indicate that this pulse oximeter is a valid predictor of %HbO2 in elite athletes during cycle exercise.     

Supramaximal exercise after training-induced hypervolemia. I. Gas exchange and acid-base balance

The effect of an exercise-induced reduction in blood O2-carrying capacity on ventilatory gas exchange and acid-base balance during supramaximal exercise was studied in six males [peak O2 consumption (VO2peak), 3.98 +/- 0.49 l/min]. Three consecutive days of supramaximal exercise resulted in a preexercise reduction of hemoglobin concentration from 15.8 to 14.0 g/dl (P less than 0.05). During exercise (120% VO2peak) performed intermittently (1 min work to 4 min rest); a small but significant (P less than 0.05) increase was found for both O2 consumption (VO2) (l X min) and heart rate (beats/min) on day 2 of the training. On day 3, VO2 (l/min) was reduced 3.2% (P less than 0.05) over day 1 values. No changes were found in CO2 output and minute ventilation during exercise between training days. Similarly, short-term training failed to significantly alter the changes in arterialized blood PCO2, pH, and [HCO-3] observed during exercise. It is concluded that hypervolemia-induced reductions in O2-carrying capacity in the order of 10-11% cause minimal impairment to gas exchange and acid-base balance during supramaximal non-steady-state exercise.     

Circadian variations in plasma renin activity, catecholamines and aldosterone during exercise in women

Four women were studied at 0400 h and 1600 h to determine if their hormonal and hemodynamic responses to exercise varied with the circadian cycle. Esophageal temperature was measured during rest and exercise (60% peak VO2; 30 min) in a warm room (Ta = 35 degrees C; PH2O = 1.7 kPa). Venous blood samples were drawn during rest and exercise and hemoglobin concentration (Hb), hematocrit (Hct), plasma osmolality (Posm), plasma protein concentration (Pp), colloid osmotic pressure (COP), plasma renin activity (PRA), cortisol, aldosterone, norepinephrine (NE) and epinephrine (E) were determined. Changes in plasma volume (PV) were estimated from changes in Hb and Hct. The relative hemoconcentration (-11.2%) was similar at 0400 h and 1600 h, but the absolute PV was smaller at 1600 h than at 0400 h (p = 0.03). The responses of Posm, Pp and COP to exercise were unaffected by time of day. Although PRA was not different at the two times of day, PRA was 244% greater during exercise at 1600 h, but only 103% greater during exercise at 0400 h. The normal circadian rhythms in plasma aldosterone (p = 0.043) and plasma cortisol (p = 0.004) were observed. Plasma aldosterone was 57% greater during exercise, while plasma cortisol did not change. The change in E and NE was greater at 0400 h, but this was due to the lower resting values of the catecholamines at 0400 h. These data indicate that time of day generally did not affect the hormonal or hemodynamic responses to exercise, with the exception that PRA was markedly higher during exercise at 1600 h compared to 0400 h.     

Sex differences in endurance capacity and metabolic response to prolonged, heavy exercise

In order to test for possible sex differences in endurance capacity, groups of young, physically active women (n = 6) and men (n = 7) performed bicycle ergometer exercise at 80% and 90% of their maximal oxygen uptakes (VO2 max). The groups were matched for age and physical activity habits. At 80% VO2 max the women performed significantly longer (P less than 0.05), 53.8 +/- 12.7 min vs 36.8 +/- 12.2 min, respectively (means +/- SD). Mid-exercise and terminal respiratory exchange ratio (R) values were significantly lower in women, suggesting a later occurrence of muscle glycogen depletion as a factor in their enhanced endurance. At 90% VO2 max the endurance times were similar for men and women, 21.2 +/- 10.3 min and 22.0 +/- 5.0 min, respectively. The blood lactate levels reached in these experiments were only marginally lower (mean differences 1.5 to 2 mmol X l-1) than those obtained at VO2 max, suggesting high lactate levels as a factor in exhaustion. The changes in body weight during the 80% experiments and the degree of hemoconcentration were not significantly different between men and women.     

Day-to-day changes in oxygen uptake kinetics at the onset of exercise during strenuous endurance training.

The aim of this study was to assess the effect of strenuous endurance training on day-to-day changes in oxygen uptake (VO2) on-kinetics (time constant) at the onset of exercise. Four healthy men participated in strenuous training for 30 min.day-1, 6 days.week-1 for 3 weeks. The VO2 was measured breath-by-breath every day except Sunday at exercise intensities corresponding to the lactate threshold (LT) and the onset of blood lactate accumulation (OBLA) which were obtained before training. Furthermore, an incremental exercise test was performed to determine LT, OBLA and maximal oxygen uptake (VO2max) before and after the training period and every weekend. The 30-min heavy endurance training was performed on a cycle ergometer 5 days.week-1 for 3 weeks. Another six men served as the control group. After training, significant reductions of the VO2 time constant for exercise at the pretraining LT exercise intensity (P less than 0.05) and at OBLA exercise intensity (P less than 0.01) were observed, whereas the VO2 time constants in the control group did not change significantly. A high correlation between the decrease in the VO2 time constant and training day was observed in exercise at the pretraining LT exercise intensity (r = -0.76; P less than 0.001) as well as in the OBLA exercise intensity (r = -0.91; P less than 0.001). A significant reduction in the blood lactate concentration during submaximal exercise and in the heart rate on-kinetics was observed in the training group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Adaptations in skeletal muscle exercise metabolism to a sustained session of heavy intermittent exercise

The purpose of this study was to investigate the hypothesis that a single, extended session of heavy exercise would be effective in inducing adaptations in energy metabolism during exercise in the absence of increases in oxidative potential. Ten healthy males [maximal aerobic power (VO(2 peak)) = 43.4 +/- 2.2 (SE) ml x kg(-1) x min(-1)] participated in a 16-h training session involving cycling for 6 min each hour at approximately 90% of maximal oxygen consumption. Measurements of metabolic changes were made on tissue extracted from the vastus lateralis during a two-stage standardized submaximal cycle protocol before (Pre) and 36-48 h after (Post) the training session. At Pre, creatine phosphate (PCr) declined (P < 0.05) by 32% from 0 to 3 min and then remained stable until 20 min of exercise at 60% VO(2 peak) before declining (P < 0.05) by a further 35% during 20 min of exercise at 75% VO(2 peak). Muscle lactate (mmol/kg dry wt) progressively increased (P < 0.05) from 4.59 +/- 0.64 at 0 min to 17.8 +/- 2.7 and 30.9 +/- 5.3 at 3 and 40 min, respectively, whereas muscle glycogen (mmol glucosyl units/kg dry wt) declined (P < 0.05) from a rest value of 360 +/- 24 to 276 +/- 31 and 178 +/- 36 at similar time points. During exercise after the training session, PCr and glycogen were not as depressed (P < 0.05), and increases in muscle lactate were blunted (P < 0.05). All of these changes occurred in the absence of increases in oxidative potential as measured by the maximal activities of citrate synthase and malate dehydrogenase. These findings are consistent with other studies, namely, that muscle metabolic adaptations to regular exercise are an early adaptive event that occurs before increases in oxidative potential.     

Increases in submaximal cycling efficiency mediated by altitude acclimatization.

To investigate the hypothesis that respiratory gas exchange and, in particular, the O(2) consumption (VO(2)) response to exercise is altered after a 21-day expedition to 6,194 m, five male climbers (age 28.2 +/- 2 yr; weight 76.9 +/- 4.3 kg; means +/- SE) performed a progressive and prolonged two-step cycle test both before and 3-4 days after return to sea level. During both exercise tests, a depression (P < 0.05) in VO(2) (l/min) and an increase (P < 0.05) in minute ventilation (VE BTPS; l/min) and respiratory exchange ratio were observed after the expedition. These changes occurred in the absence of changes in CO(2) production (l/min). During steady-state submaximal exercise, net efficiency, calculated from the rates of the mechanical power output to the energy expended (VO(2)) above that measured at rest, increased (P < 0.05) from 25.9 +/- 1.6 to 31. 3 +/- 1.3% at the lighter power output and from 24.4 +/- 1.3 to 29.5 +/- 1.5% at the heavy power output. These changes were accompanied by a 4.5% reduction (P < 0.05) in peak VO(2) (3.99 +/- 0.17 vs. 3.81 +/- 0.18 l/min). After the expedition, an increase (P < 0.05) in hemoglobin concentration (15.0 +/- 0.49 vs. 15.8 +/- 0.41 g/100 ml) was found. It is concluded that, because resting VO(2) was unchanged, net efficiency is enhanced during submaximal exercise after a mountaineering expedition when the exercise is performed soon after return to sea level conditions.     

Role of hemoglobin P50 in O2 transport during normoxic and hypoxic exercise in the dog

High hemoglobin affinity for O2 [low PO2 at 50% saturation of hemoglobin (P50)] could degrade exercise performance in normoxia by lowering mean tissue PO2 but could enhance O2 transport in hypoxic exercise by increasing arterial O2 saturation. We measured O2 transport at rest and at graded levels of steady-state exercise in tracheostomized dogs with normal P50 (28.8 +/- 1.8 Torr) and again after P50 was lowered (19.5 +/- 0.7 Torr) by sodium cyanate infusions. Measurements were made during ventilation with room air (RA), 12% O2 in N2, or 10% O2 in N2. Cardiac output (QT) as a function of O2 consumption (VO2) was not altered by low P50 at any inspired O2 fraction (P greater than 0.05). With RA exercise, arterial content (CaO2) and O2 delivery (QT X CaO2) were unchanged at low P50, whereas mixed venous PO2 was reduced at each level of VO2. With exercise in hypoxia, CaO2 and O2 delivery were significantly improved at low P50 (P less than 0.05). Mixed venous PO2 was lower than control during 12% O2 (P less than 0.05) but not different from control during 10% O2 exercise at low P50. Despite a presumed decrease in tissue PO2 during RA and 12% O2 exercise, exercise performance and base excess decline were not significantly worse than control levels. We conclude that, in canine steady-state exercise, hemoglobin P50 is not an important determinant of tissue O2-extraction capacity during normoxia or moderate hypoxia. In extreme hypoxia, low P50 may help to maintain tissue PO2 by enhancing systemic O2 delivery at each level of QT.     

Effect of maternal weight gain during pregnancy on exercise performance

We examined the effect of maternal weight gain during pregnancy on exercise performance. Ten women performed submaximal cycle (up to 60 W) and treadmill (4 km/h, up to 10% grade) exercise tests at 34 +/- 1.5 (SD) wk gestation and 7.6 +/- 1.7 wk postpartum. Postpartum subjects wearing weighted belts designed to equal their body weight during the antepartum tests performed two additional treadmill tests. Absolute O2 uptake (VO2) at the same work load was higher during pregnancy than postpartum during cycle (1.04 +/- 0.08 vs. 0.95 +/- 0.09 l/min, P = 0.014), treadmill (1.45 +/- 0.19 vs. 1.27 +/- 0.20 l/min, P = 0.0002), and weighted treadmill (1.45 +/ 0.19 vs. 1.36 +/- 0.20 l/min, P = 0.04) exercise. None of these differences remained, however, when VO2 was expressed per kilogram of body weight. Maximal VO2 (VO2max) estimated from the individual heart rate-VO2 curves was the same during and after pregnancy during cycling (1.96 +/- 0.37 to 1.98 +/- 0.39 l/min), whereas estimated VO2max increased postpartum during treadmill (2.04 +/- 0.38 to 2.21 +/- 0.36 l/min, P = 0.03) and weighted treadmill (2.04 +/- 0.38 to 2.19 +/- 0.38 l/min, P = 0.03) exercise. We conclude that increased body weight during pregnancy compared with the postpartum period accounts for 75% of the increased VO2 during submaximal weight-bearing exertion in pregnancy and contributes to reduced exercise capacity. The postpartum increase in estimated VO2max during weight-bearing exercise is the result of consistently higher antepartum heart rates during all submaximal work loads.     

Kinetics of CO uptake and diffusing capacity in transition from rest to steady-state exercise.

In the transition from rest to steady-state exercise, O2 uptake from the lungs (VO2) depends on the product of pulmonary blood flow and pulmonary arteriovenous O2 content difference. The kinetics of pulmonary blood flow are believed to be somewhat faster than changes in pulmonary arteriovenous O2 content difference. We hypothesized that during CO breathing, the kinetics of CO uptake (VCO) and diffusing capacity for CO (DLCO) should be faster than VO2 because changes in pulmonary arteriovenous CO content difference should be relatively small. Six subjects went abruptly from rest to constant exercise (inspired CO fraction = 0.0005) at 40, 60, and 80% of their peak VO2, measured with an incremental test (VO2peak). At all exercise levels, DLCO and VCO rose faster than VO2 (P less than 0.001), and DLCO rose faster than VCO (P less than 0.001). For example, at 40% VO2peak, the time constant (tau) for DLCO in phase 2 was 19 +/- 5 (SD), 24 +/- 5 s for VCO, and 33 +/- 5 s for VO2. Both VCO and DLCO increased with exercise intensity but to a lesser degree than VO2 at all exercise intensities (P less than 0.001). In addition, no significant rise in DLCO was observed between 60 and 80% VO2peak. We conclude that the kinetics of VCO and DLCO are faster than VO2, suggesting that VCO and DLCO kinetics reflect, to a greater extent, changes in pulmonary blood flow and thus recruitment of alveolar-capillary surface area. However, other factors, such as the time course of ventilation, may also be involved.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of "priming" exercise on pulmonary O2 uptake and muscle deoxygenation kinetics during heavy-intensity cycle exercise in the supine and upright positions.

We hypothesized that the performance of prior heavy exercise would speed the phase 2 oxygen consumption (VO2) kinetics during subsequent heavy exercise in the supine position (where perfusion pressure might limit muscle O2 supply) but not in the upright position. Eight healthy men (mean +/- SD age 24 +/- 7 yr; body mass 75.0 +/- 5.8 kg) completed a double-step test protocol involving two bouts of 6 min of heavy cycle exercise, separated by a 10-min recovery period, on two occasions in each of the upright and supine positions. Pulmonary O2 uptake was measured breath by breath and muscle oxygenation was assessed using near-infrared spectroscopy (NIRS). The NIRS data indicated that the performance of prior exercise resulted in hyperemia in both body positions. In the upright position, prior exercise had no significant effect on the time constant tau of the VO2 response in phase 2 (bout 1: 29 +/- 10 vs. bout 2: 28 +/- 4 s; P = 0.91) but reduced the amplitude of the VO2 slow component (bout 1: 0.45 +/- 0.16 vs. bout 2: 0.22 +/- 0.14 l/min; P = 0.006) during subsequent heavy exercise. In contrast, in the supine position, prior exercise resulted in a significant reduction in the phase 2 tau (bout 1: 38 +/- 18 vs. bout 2: 24 +/- 9 s; P = 0.03) but did not alter the amplitude of the VO2 slow component (bout 1: 0.40 +/- 0.29 vs. bout 2: 0.41 +/- 0.20 l/min; P = 0.86). These results suggest that the performance of prior heavy exercise enables a speeding of phase 2 VO2 kinetics during heavy exercise in the supine position, presumably by negating an O2 delivery limitation that was extant in the control condition, but not during upright exercise, where muscle O2 supply was probably not limiting.     

Effects of incomplete pulmonary gas exchange on VO2 max

Recent evidence suggests that heavy exercise may lower the percentage of O2 bound to hemoglobin (%SaO2) by greater than or equal to 5% below resting values in some highly trained endurance athletes. We tested the hypothesis that pulmonary gas exchange limitations may restrict VO2max in highly trained athletes who exhibit exercise-induced hypoxemia. Twenty healthy male volunteers were divided into two groups according to their physical fitness status and the demonstration of exercise-induced reductions in %SaO2 less than or equal to 92%: 1) trained (T), mean VO2max = 56.5 ml.kg-1.min-1 (n = 13) and 2) highly trained (HT) with maximal exercise %SaO2 less than or equal to 92%, mean VO2max = 70.1 ml.kg-1.min-1 (n = 7). Subjects performed two incremental cycle ergometer exercise tests to determine VO2max at sea level under normoxic (21% O2) and mild hyperoxic conditions (26% O2). Mean %SaO2 during maximal exercise was significantly higher (P less than 0.05) during hyperoxia compared with normoxia in both the T group (94.1 vs. 96.1%) and the HT group (90.6 vs. 95.9%). Mean VO2max was significantly elevated (P less than 0.05) during hyperoxia compared with normoxia in the HT group (74.7 vs. 70.1 ml.kg-1.min-1). In contrast, in the T group, no mean difference (P less than 0.05) existed between treatments in VO2max (56.5 vs. 57.1 ml.kg-1.min-1). These data suggest that pulmonary gas exchange may contribute significantly to the limitation of VO2max in highly trained athletes who exhibit exercise-induced reductions in %SaO2 at sea level.(ABSTRACT TRUNCATED AT 250 WORDS)     

Impact of exercise training on insulin sensitivity, physical fitness, and muscle oxidative capacity in first-degree relatives of type 2 diabetic patients

First-degree relatives of type 2 diabetic patients (offspring) are often characterized by insulin resistance and reduced physical fitness (VO2 max). We determined the response of healthy first-degree relatives to a standardized 10-wk exercise program compared with an age-, sex-, and body mass index-matched control group. Improvements in VO2 max (14.1 +/- 11.3 and 16.1 +/- 14.2%; both P < 0.001) and insulin sensitivity (0.6 +/- 1.4 and 1.0 +/- 2.1 mg x kg(-1) x min(-1); both P < 0.05) were comparable in offspring and control subjects. However, VO2 max and insulin sensitivity in offspring were not related at baseline as in the controls (r = 0.009, P = 0.96 vs. r = 0.67, P = 0.002). Likewise, in offspring, exercise-induced changes in VO2 max did not correlate with changes in insulin sensitivity as opposed to controls (r = 0.06, P = 0.76 vs. r = 0.57, P = 0.01). Skeletal muscle oxidative capacity tended to be lower in offspring at baseline but improved equally in both offspring and controls in response to exercise training (delta citrate synthase enzyme activity 26 vs. 20%, and delta cyclooxygenase enzyme activity 25 vs. 23%. Skeletal muscle fiber morphology and capillary density were comparable between groups at baseline and did not change significantly with exercise training. In conclusion, this study shows that first-degree relatives of type 2 diabetic patients respond normally to endurance exercise in terms of changes in VO2 max and insulin sensitivity. However, the lack of a correlation between the VO2 max and insulin sensitivity in the first-degree relatives of type 2 diabetic patients indicates that skeletal muscle adaptations are dissociated from the improvement in VO2 max. This could indicate that, in first-degree relatives, improvement of insulin sensitivity is dissociated from muscle mitochondrial functions.     

A comparison of skeletal muscle oxygenation and fuel use in sustained continuous and intermittent exercise

In this study we compared substrate oxidation and muscle oxygen availability during sustained intermittent intense and continuous submaximal exercise with similar overall (i.e. work and recovery) oxygen consumption (VO2). Physically active subjects (n = 7) completed 90 min of an intermittent intense (12 s work:18 s recovery) and a continuous submaximal treadmill running protocol on separate days. In another experiment (n = 5) we compared oxygen availability in the vastus lateralis muscle between these two exercise protocols using near-infrared spectroscopy. Initially, overall VO(2) (i.e. work and recovery) was matched, and from 37.5 min to 67.5 min of exercise was similar, although slightly higher during continuous exercise (8%; P < 0.05). Energy expenditure was constant (22.5-90 min of exercise) and was not different in intermittent intense [0.81 (0.01) kJ x min(-1). kg(-1)] and continuous submaximal [0.85 (0.01) kJ x min(-1) x kg(-1)] exercise. Overall exercise intensity, represented as a proportion of peak aerobic power (VO2(peak)), was 68.1 (2.5)% VO2(peak) and 71.8 (1.8)% VO2(peak) for intermittent and continuous exercise protocols, respectively. Fat oxidation was almost 3 times lower (P < 0.05) and carbohydrate oxidation was approximately 1.2 times higher (P < 0.05) during intermittent compared to continuous exercise, despite the same overall energy expenditure. Capillary plasma lactate was constant from 15 to 90 min of exercise, and pyruvate was constant from 15 to 75 min, although both were higher (P < 0.0001, lactate; P < 0.001, pyruvate) during intermittent [5.05 (0.28) mM, 200 (7) microM, respectively] compared to continuous exercise [2.41 (0.10) mM, 114 (4) microM, respectively]. There was no difference between protocols for either plasma glycerol or non-esterified fatty acids. The decrease in muscle oxygenation during work periods of intermittent exercise resulted in a lower nadir oxygenation [54.62 (0.41)%] compared to continuous exercise [58.82 (0.21)%, P < 0.001]. The decline in oxygenation was correlated with treadmill speed (r = 0.72; P < 0.05). These results show a difference in substrate utilisation and muscle oxygen availability during sustained intermittent intense and continuous submaximal exercise, despite a similar overall VO(2) and identical energy expenditure.     

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   

Pulmonary diffusing capacity for nitric oxide during exercise in morbid obesity

Morbidly obese individuals may have altered pulmonary diffusion during exercise. The purpose of this study was to examine pulmonary diffusing capacity for nitric oxide (DLNO) and carbon monoxide (DLCO) during exercise in these subjects. Ten morbidly obese subjects (age = 38 +/- 9 years, BMI = 47 +/- 7 kg/m(2), peak oxygen consumption or VO(2peak) = 2.4 +/- 0.4 l/min) and nine nonobese controls (age = 41 +/- 9 years, BMI = 23 +/- 2 kg/m(2), VO(2peak) = 2.6 +/- 0.9 l/min) participated in two sessions: the first measured resting O(2) and VO(2peak) for determination of wattage equating to 40, 75, and 90% oxygen uptake reserve (VO(2)R). The second session measured pulmonary diffusion from single-breath maneuvers of 5 s each, as well as heart rate (HR) and VO(2) over three workloads. DLNO, DLCO, and pulmonary capillary blood volume were larger in obese compared to nonobese groups (P 0.10). The morbidly obese have increased pulmonary diffusion per unit increase in VA compared with nonobese controls which may be due to a lower rise in VA per unit increase in VO(2) in the obese during exercise.     

The effect of citrate loading on exercise performance, acid-base balance and metabolism

Nine subjects (VO2max 65 +/- 2 ml.kg-1.min-1, mean +/- SEM) were studied on two occasions following ingestion of 500 ml solution containing either sodium citrate (C, 0.300 g.kg-1 body mass) or a sodium chloride placebo (P, 0.045 g.kg-1 body mass). Exercise began 60 min later and consisted of cycle ergometer exercise performed continuously for 20 min each at power outputs corresponding to 33% and 66% VO2max, followed by exercise to exhaustion at 95% VO2max. Pre-exercise arterialized-venous [H+] was lower in C (36.2 +/- 0.5 nmol.l-1; pH 7.44) than P (39.4 +/- 0.4 nmol.l-1; pH 7.40); the plasma [H+] remained lower and [HCO3-] remained higher in C than P throughout exercise and recovery. Exercise time to exhaustion at 95% VO2max was similar in C (310 +/- 69 s) and P (313 +/- 74 s). Cardiorespiratory variables (ventilation, VO2, VCO2, heart rate) measured during exercise were similar in the two conditions. The plasma [citrate] was higher in C at rest (C, 195 +/- 19 mumol.l-1; P, 81 +/- 7 mumol.l-1) and throughout exercise and recovery. The plasma [lactate] and [free fatty acid] were not affected by citrate loading but the plasma [glycerol] was lower during exercise in C than P. In conclusion, sodium citrate ingestion had an alkalinizing effect in the plasma but did not improve endurance time during exercise at 95% VO2max. Furthermore, citrate loading may have prevented the stimulation of lipolysis normally observed with exercise and prevented the stimulation of glycolysis in muscle normally observed in bicarbonate-induced alkalosis.     

Plasma volume expansion does not increase maximal cardiac output or VO2 max in lowlanders acclimatized to altitude

With altitude acclimatization, blood hemoglobin concentration increases while plasma volume (PV) and maximal cardiac output (Qmax) decrease. This investigation aimed to determine whether reduction of Qmax at altitude is due to low circulating blood volume (BV). Eight Danish lowlanders (3 females, 5 males: age 24.0 +/- 0.6 yr; mean +/- SE) performed submaximal and maximal exercise on a cycle ergometer after 9 wk at 5,260 m altitude (Mt. Chacaltaya, Bolivia). This was done first with BV resulting from acclimatization (BV = 5.40 +/- 0.39 liters) and again 2-4 days later, 1 h after PV expansion with 1 liter of 6% dextran 70 (BV = 6.32 +/- 0.34 liters). PV expansion had no effect on Qmax, maximal O2 consumption (VO2), and exercise capacity. Despite maximal systemic O2 transport being reduced 19% due to hemodilution after PV expansion, whole body VO2 was maintained by greater systemic O2 extraction (P < 0.05). Leg blood flow was elevated (P < 0.05) in hypervolemic conditions, which compensated for hemodilution resulting in similar leg O2 delivery and leg VO2 during exercise regardless of PV. Pulmonary ventilation, gas exchange, and acid-base balance were essentially unaffected by PV expansion. Sea level Qmax and exercise capacity were restored with hyperoxia at altitude independently of BV. Low BV is not a primary cause for reduction of Qmax at altitude when acclimatized. Furthermore, hemodilution caused by PV expansion at altitude is compensated for by increased systemic O2 extraction with similar peak muscular O2 delivery, such that maximal exercise capacity is unaffected.