Reduced exercise arteriovenous O2 difference in Type 2 diabetes.

Maximal O(2) consumption (Vo(2 max)) is lower in individuals with Type 2 diabetes than in sedentary nondiabetic individuals. This study aimed to determine whether the lower Vo(2 max) in diabetic patients was due to a reduction in maximal cardiac output (Q(max)) and/or peripheral O(2) extraction. After 11 Type 2 diabetic patients and 12 nondiabetic subjects, matched for age and body composition, who had not exercised for 2 yr, performed a bicycle ergometer exercise test to determine Vo(2 max), submaximal cardiac output, Q(max), and arterial-mixed venous O(2) (a-v O(2)) difference were assessed. Maximal workload, Vo(2 max), and maximal a-v O(2) difference were lower in Type 2 diabetic patients (P < 0.05). Q(max) was low in both groups but not significantly different: 11.2 and 10.0 l/min for controls and diabetic patients, respectively (P > 0.05). Submaximal O(2) uptake and heart rate were lower at several workloads in diabetic patients; respiratory exchange ratio was similar between groups at all workloads. Vo(2 max) was linearly correlated with a-v O(2) difference, but not Q(max) in diabetic patients. These data suggest that a reduction in maximal a-v O(2) difference contributes to a decreased Vo(2 max) in Type 2 diabetic patients.     

Retention of intravenously infused [13C]bicarbonate is transiently increased during recovery from hard exercise.

The effects of exercise on energy substrate metabolism persist into the postexercise recovery period. We sought to derive bicarbonate retention factors (k) to correct for carbon tracer oxidized, but retained from pulmonary excretion before, during, and after exercise. Ten men and nine women received a primed-continuous infusion of [(13)C]bicarbonate (sodium salt) under three different conditions: 1) before, during, and 3 h after 90 min of exercise at 45% peak oxygen consumption (Vo(2peak)); 2) before, during, and 3 h after 60 min of exercise at 65% Vo(2peak); and 3) during a time-matched resting control trial, with breath samples collected for determination of (13)CO(2) excretion rates. Throughout the resting control trial, k was stable and averaged 0.83 in men and women. During exercise, average k in men was 0.93 at 45% Vo(2peak) and 0.94 at 65% Vo(2peak), and in women k was 0.91 at 45% Vo(2peak) and 0.92 at 65% Vo(2peak), with no significant differences between intensities or sexes. After exercise at 45% Vo(2peak), k returned rapidly to control values in men and women, but following exercise at 65% Vo(2peak), k was significantly less than control at 30 and 60 min postexercise in men (0.74 and 0.72, respectively, P < 0.05) and women (0.75 and 0.76, respectively, P < 0.05) with no significant postexercise differences between men and women. We conclude that bicarbonate/CO(2) retention is transiently increased in men and women for the first hour of postexercise recovery following endurance exercise bouts of hard but not moderate intensity.     

Inspiratory muscle training lowers the oxygen cost of voluntary hyperpnea

The purpose of this study was to determine if inspiratory muscle training (IMT) alters the oxygen cost of breathing (Vo(2RM)) during voluntary hyperpnea. Sixteen male cyclists completed 6 wk of IMT using an inspiratory load of 50% (IMT) or 15% placebo (CON) of maximal inspiratory pressure (Pi(max)). Prior to training, a maximal incremental cycle ergometer test was performed to determine Vo(2) and ventilation (V(E)) at multiple workloads. Pre- and post-training, subjects performed three separate 4-min bouts of voluntary eucapnic hyperpnea (mimic), matching V(E) that occurred at 50, 75, and 100% of Vo(2 max). Pi(max) was significantly increased (P < 0.05) by 22.5 ± 8.7% from pre- to post-IMT and remained unchanged in the CON group. The Vo(2RM) required during the mimic trial corresponded to 5.1 ± 2.5, 5.7 ± 1.4, and 11.7% ± 2.5% of the total Vo(2) (Vo(2T)) at ventilatory workloads equivalent to 50, 75, and 100% of Vo(2 max), respectively. Following IMT, the Vo(2RM) requirement significantly decreased (P < 0.05) by 1.5% (4.2 ± 1.4% of Vo(2T)) at 75% Vo(2 max) and 3.4% (8.1 ± 3.5% of Vo(2T)) at 100% Vo(2 max). No significant changes were shown in the CON group. IMT significantly reduced the O(2) cost of voluntary hyperpnea, which suggests that a reduction in the O(2) requirement of the respiratory muscles following a period of IMT may facilitate increased O(2) availability to the active muscles during exercise. These data suggest that IMT may reduce the O(2) cost of ventilation during exercise, providing an insight into mechanism(s) underpinning the reported improvements in whole body endurance performance; however, this awaits further investigation.     

Gluconeogenesis in humans with induced hyperlactatemia during low-intensity exercise

We studied the role of lactate in gluconeogenesis (GNG) during exercise in untrained fasting humans. During the final hour of a 4-h cycle exercise at 33-34% maximal O(2) uptake, seven subjects received, in random order, either a sodium lactate infusion (60 micromol x kg(-1) x min(-1)) or an isomolar sodium bicarbonate infusion. The contribution of lactate to gluconeogenic glucose was quantified by measuring (2)H incorporation into glucose after body water was labeled with deuterium oxide, and glucose rate of appearance (R(a)) was measured by [6,6-(2)H(2)]glucose dilution. Infusion of lactate increased lactate concentration to 4.4 +/- 0.6 mM (mean +/- SE). Exercise induced a decrease in blood glucose concentration from 5.0 +/- 0.2 to 4.2 +/- 0.3 mM (P < 0.05); lactate infusion abolished this decrease (5.0 +/- 0.3 mM; P < 0.001) and increased glucose R(a) compared with bicarbonate infusion (P < 0.05). Lactate infusion increased both GNG from lactate (29 +/- 4 to 46 +/- 4% of glucose R(a), P < 0.001) and total GNG. We conclude that lactate infusion during low-intensity exercise in fasting humans 1). increased GNG from lactate and 2). increased glucose production, thus increasing the blood glucose concentration. These results indicate that GNG capacity is available in humans after an overnight fast and can be used to sustain blood glucose levels during low-intensity exercise when lactate, a known precursor of GNG, is available at elevated plasma levels.     

Relationship between resting ventilatory chemosensitivity and maximal oxygen uptake in moderate hypobaric hypoxia.

This study tested the hypothesis that the extent of the decrement in (.)Vo(2max) and the respiratory response seen during maximal exercise in moderate hypobaric hypoxia (H; simulated 2,500 m) is affected by the hypoxia ventilatory and hypercapnia ventilatory responses (HVR and HCVR, respectively). Twenty men (5 untrained subjects, 7 long distance runners, 8 middle distance runners) performed incremental exhaustive running tests in H and normobaric normoxia (N) condition. During the running test, (.)Vo(2), pulmonary ventilation (Ve) and arterial oxyhemoglobin saturation (Sa(O(2))) were measured, and in two ventilatory response tests performed during N, a rebreathing method was used to evaluate HVR and HCVR. Mean HVR and HCVR were 0.36 +/- 0.04 and 2.11 +/- 0.2 l.min(-1).mmHg(-1), respectively. HVR correlated significantly with the percent decrements in (.)Vo(2max) (%d(.)Vo(2max)), Sa(O(2)) [%dSa(O(2)) = (N-H).N(-1).100], and (.)Ve/(.)Vo(2) seen during H condition. By contrast, HCVR did not correlate with any of the variables tested. The increment in maximal Ve between H and N significantly correlated with %d(.)Vo(2max). Our findings suggest that O(2) chemosensitivity plays a significant role in determining the level of exercise hyperventilation during moderate hypoxia; thus, a higher O(2) chemosensitivity was associated with a smaller drop in (.)Vo(2max) and Sa(O(2)) under those conditions.     

Muscle glycogen oxidation during prolonged exercise measured with oral [13C]glucose: comparison with changes in muscle glycogen content.

Plasma glucose and muscle glycogen oxidation during prolonged exercise [75-min at 48 and 76% maximal O(2) uptake (Vo(2 max))] were measured in eight well-trained male subjects [Vo(2 max) = 4.50 l/min (SD 0.63)] using a simplified tracer technique in which a small amount of glucose highly enriched in (13)C was ingested: plasma glucose oxidation was computed from (13)C/(12)C in plasma glucose (which was stable beginning at minute 30 and minute 15 during exercise at 48 and 76% Vo(2 max), respectively) and (13)CO(2) production, and muscle glycogen oxidation was estimated by subtracting plasma glucose oxidation from total carbohydrate oxidation. Consistent data from the literature suggest that this small dose of exogenous glucose does not modify muscle glycogen oxidation and has little effect, if any, on plasma glucose oxidation. The percent contributions of plasma glucose and muscle glycogen oxidation to the energy yield at 48% Vo(2 max) [15.1% (SD 3.8) and 45.9% (SD 5.8)] and at 76% Vo(2 max) [15.4% (SD 3.6) and 59.8% (SD 9.2)] were well in line with data previously reported for similar work loads and exercise durations using conventional tracer techniques. The significant reduction in glycogen concentration measured from pre- and postexercise vastus lateralis muscle biopsies paralleled muscle glycogen oxidation calculated using the tracer technique and was larger at 76% than at 48% Vo(2 max). However, the correlation coefficients between these two estimates of muscle glycogen utilization were not different from zero at each of the two work loads. The simplified tracer technique used in the present experiment appears to be a valid alternative approach to the traditional tracer techniques for computing plasma glucose and muscle glycogen oxidation during prolonged exercise.     

Effect of naloxone on perceived exertion and exercise capacity during maximal cycle ergometry.

We assessed the effects of naloxone, an opioid antagonist, on exercise capacity in 13 men and 5 women (mean age = 30.1 yr, range = 21-35 yr) during a 25 W/min incremental cycle ergometer test to exhaustion on different days during familiarization trial and then after 30 mg (iv bolus) of naloxone or placebo (Pl) in a double-blind, crossover design. Minute ventilation (Ve), O(2) consumption (Vo(2)), CO(2) production, and heart rate (HR) were monitored. Perceived exertion rating (0-10 scale) and venous samples for lactate were obtained each minute. Lactate and ventilatory thresholds were derived from lactate and gas-exchange data. Blood pressure was obtained before exercise, 5 min postinfusion, at maximum exercise, and 5 min postexercise. There were no control-Pl differences. The naloxone trial demonstrated decreased exercise time (96% Pl; P < 0.01), total cumulative work (96% Pl; P < 0.002), peak Vo(2) (94% Pl; P < 0.02), and HR (96% Pl; P < 0.01). Other variables were unchanged. HR and Ve were the same at the final common workload, but perceived exertion was higher (8.1 +/- 0.5 vs. 7.1 +/- 0.5) after naloxone than Pl (P < 0.01). The threshold for effort perception amplification occurred at approximately 60 +/- 4% of Pl peak Vo(2). Thus we conclude that peak work capacity was limited by perceived exertion, which can be attenuated by endogenous opioids rather than by physiological limits.     

Ventilatory dynamics and control of blood gases after maximal exercise in the Thoroughbred horse.

Despite enormous rates of minute ventilation (Ve) in the galloping Thoroughbred (TB) horse, the energetic demands of exercise conspire to raise arterial Pco(2) (i.e., induce hypercapnia). If locomotory-respiratory coupling (LRC) is an obligatory facilitator of high Ve in the horse such as those found during galloping (Bramble and Carrier. Science 219: 251-256, 1983), Ve should drop precipitously when LRC ceases at the galloptrot transition, thus exacerbating the hypercapnia. TB horses (n = 5) were run to volitional fatigue on a motor-driven treadmill (1 m/s increments; 14-15 m/s) to study the dynamic control of breath-by-breath Ve, O(2) uptake, and CO(2) output at the transition from maximal exercise to active recovery (i.e., trotting at 3 m/s for 800 m). At the transition from the gallop to the trot, Ve did not drop instantaneously. Rather, Ve remained at the peak exercising levels (1,391 +/- 88 l/min) for approximately 13 s via the combination of an increased tidal volume (12.6 +/- 1.2 liters at gallop; 13.9 +/- 1.6 liters over 13 s of trotting recovery; P < 0.05) and a reduced breathing frequency [113.8 +/- 5.2 breaths/min (at gallop); 97.7 +/- 5.9 breaths/min over 13 s of trotting recovery (P < 0.05)]. Subsequently, Ve declined in a biphasic fashion with a slower mean response time (85.4 +/- 9.0 s) than that of the monoexponential decline of CO(2) output (39.9 +/- 4.7 s; P < 0.05), which rapidly reversed the postexercise arterial hypercapnia (arterial Pco(2) at gallop: 52.8 +/- 3.2 Torr; at 2 min of recovery: 25.0 +/- 1.4 Torr; P < 0.05). We conclude that LRC is not a prerequisite for achievement of Ve commensurate with maximal exercise or the pronounced hyperventilation during recovery.     

Evaluation of physiological responses during recovery following three resistance exercise programs

The present study was conducted to examine (a) whether there is an association between maximal oxygen uptake (Vo(2)max) and reduction in postexercise heart rate (HR) and blood lactate concentrations ([La]) following resistance exercise and (b) how intensity and Volume of resistance exercise affect postexercise Vo(2). Eleven regularly weight-trained males (20.8 +/- 1.3 years; 96.2 +/- 14.4 kg, 182.4 +/- 7.3 cm) underwent 4 sets of squat exercise on 3 separate occasions that differed in both exercise intensity and volume. During each testing session, subjects performed either 15 repetitions.set(-1) at 60% of 1 repetition maximum (1RM) (L), 10 repetitions.set(-1) at 75% of 1RM (M), or 4 repetitions.set(-1) at 90% of 1RM (H). During each exercise, Vo(2) and HR were measured before (PRE), immediately post (IP), and at 10 (10P), 20 (20P) 30 (30P), and 40 (40P) minutes postexercise. The [La] was measured at PRE, IP, 20P, and 40P. Decrease in HR (DeltaHR) was determined by subtracting HR at 10P from that at IP, whereas decrease in [La] (Delta[La]) was computed by subtracting [La] at 20P from that at IP. A significant correlation (p < 0.05) was found between Vo(2)max and DeltaHR in all exercise conditions. A significant correlation (p < 0.05) was also found between Vo(2)max and Delta[La] in L and M but not in H. The Vo(2) was higher (p < 0.05) during M than H at IP and 10P, while no difference was seen between L and M and between L and H. These results indicate that those with greater aerobic capacity tend to have a greater reduction in HR and [La] during recovery from resistance exercise. In addition, an exercise routine performed at low to moderate intensity coupled with a moderate to high exercise volume is most effective in maximizing caloric expenditure following resistance exercise.     

Endothelial dysfunction and exercise performance in lone atrial fibrillation or associated with hypertension or diabetes: different results with cardioversion

Endothelial dysfunction and underperfusion of exercising muscle contribute to exercise intolerance, hyperventilation, and breathlessness in atrial fibrillation (AF). Cardioversion (CV) improves endothelial function and exercise performance. We examined whether CV is equally beneficial in diabetes and hypertension, diseases that cause endothelial dysfunction and are often associated with AF. Cardiopulmonary exercise and pulmonary and endothelial (brachial artery flow-mediated dilation) function were tested before and after CV in patients with AF alone (n = 18, group 1) or AF with hypertension (n = 19, group 2) or diabetes (n = 19, group 3). Compared with group 1, peak exercise workload, O2 consumption (Vo2), O2 pulse, aerobic efficiency (Delta Vo2/Delta WR), and ratio of brachial diameter changes to flow changes (Delta D/Delta F) were reduced in group 2 and, to a greater extent, in group 3; exercise ventilation efficiency (Ve/Vco2 slope) and dead space-to-tidal volume ratio (Vd/Vt) were similar among groups. CV had less effect on peak workload (+7% vs. +18%), peak Vo2 (+12% vs. +17%), O2 pulse (+33% vs. +50%), Delta Vo2/Delta WR (+7% vs. +12%), Ve/Vco2 slope (-6% vs. -12%), Delta D/Delta F (+7% vs. +10%), and breathlessness (Borg scale) in group 2 than in group 1 and was ineffective in group 3. The antioxidant vitamin C, tested in eight additional patients in each cohort, improved flow-mediated dilation in groups 1 and 2 before, but not after, CV and was ineffective in group 3, suggesting that the oxidative injury is least in lone AF, greater in hypertension with AF, and greater still in diabetes with AF. Comorbidities that impair endothelial activity worsen endothelial dysfunction and exercise intolerance in AF. The advantages of CV appear to be inversely related to the extent of the underlying oxidative injury.     

Contributions of working muscle to whole body lipid metabolism are altered by exercise intensity and training

To evaluate the contribution of working muscle to whole body lipid oxidation, we examined the effects of exercise intensity and endurance training (9 wk, 5 days/wk, 1 h, 75% Vo(2 peak)) on whole body and leg free fatty acid (FFA) kinetics in eight male subjects (26 +/- 1 yr, means +/- SE). Two pretraining trials [45 and 65% Vo(2 max) (45UT, 65UT)] and two posttraining trials [65% of pretraining Vo(2 peak) (ABT), and 65% of posttraining Vo(2 peak) (RLT)] were performed using [1-(13)C]palmitate infusion and femoral arteriovenous sampling. Training increased Vo(2 peak) by 15% (45.2 +/- 1.2 to 52.0 +/- 1.8 ml.kg(-1).min(-1), P < 0.05). Muscle FFA fractional extraction was lower during exercise (EX) compared with rest regardless of workload or training status ( approximately 20 vs. 48%, P < 0.05). Two-leg net FFA balance increased from net release at rest ( approximately -36 micromol/min) to net uptake during EX for 45UT (179 +/- 75), ABT (236 +/- 63), and RLT (136 +/- 110) (P < 0.05), but not 65UT (51 +/- 127). Leg FFA tracer measured uptake was higher during EX than rest for all trials and greater during posttraining in RLT (716 +/- 173 micromol/min) compared with pretraining (45UT 450 +/- 80, 65UT 461 +/- 72, P < 0.05). Leg muscle lipid oxidation increased with training in ABT (730 +/- 163 micromol/min) vs. 65UT (187 +/- 94, P < 0.05). Leg muscle lipid oxidation represented approximately 62 and 30% of whole body lipid oxidation at lower and higher relative intensities, respectively. In summary, training can increase working muscle tracer measured FFA uptake and lipid oxidation for a given power output, but both before and after training the association between whole body and leg lipid metabolism is reduced as exercise intensity increases.     

Sex differences in the perceived intensity of breathlessness during exercise with advancing age.

The prevalence of activity-related breathlessness increases with age, particularly in women, but the specific underlying mechanisms have not been studied. This novel cross-sectional study was undertaken to examine the effects of age and sex, and their interaction, on the perceptual and ventilatory responses to incremental treadmill exercise in 73 healthy participants (age range 40-80 yr old) with normal pulmonary function. Age-related changes at a standardized oxygen uptake (Vo(2)) during exercise included significant increases in breathlessness ratings (Borg scale), ventilation (Ve), ventilatory equivalent for carbon dioxide, and the ratio of tidal volume (Vt) to dynamic inspiratory capacity (IC) (all P < 0.05). These changes were quantitatively similar in women (n = 39) and in men (n = 34). For the group as a whole, exertional breathlessness ratings increased as resting static inspiratory muscle strength diminished (P = 0.05), as exercise ventilation increased relative to capacity (P = 0.013) and as the Vt/IC ratio increased (P = 0.003) during exercise. Older women (60-80 yr old, n = 23) reported greater (P < 0.05) intensity of exertional breathlessness at a standardized Vo(2) and Ve than age-matched men (n = 16), despite similar age-related changes in ventilatory demand and dynamic ventilatory mechanics. These increases in breathlessness ratings in older women disappeared when sex differences in baseline maximal ventilatory capacity were accounted for. In conclusion, although increased exertional breathlessness with advancing age is multifactorial, contributory factors included higher ventilatory requirements during exercise, progressive inspiratory muscle weakness, and restrictive mechanical constraints on Vt expansion related to reduced IC. The sensory consequences of this age-related respiratory impairment were more pronounced in women, who, by nature, have relatively reduced maximal ventilatory reserve.     

Bicarbonate attenuates arterial desaturation during maximal exercise in humans.

The contribution of pH to exercise-induced arterial O2 desaturation was evaluated by intravenous infusion of sodium bicarbonate (Bic, 1 M; 200-350 ml) or an equal volume of saline (Sal; 1 M) at a constant infusion rate during a "2,000-m" maximal ergometer row in five male oarsmen. Blood-gas variables were corrected to the increase in blood temperature from 36.5 +/- 0.3 to 38.9 +/- 0.1 degrees C (P < 0.05; means +/- SE), which was established in a pilot study. During Sal exercise, pH decreased from 7.42 +/- 0.01 at rest to 7.07 +/- 0.02 but only to 7.34 +/- 0.02 (P < 0.05) during the Bic trial. Arterial PO2 was reduced from 103.1 +/- 0.7 to 88.2 +/- 1.3 Torr during exercise with Sal, and this reduction was not significantly affected by Bic. Arterial O2 saturation was 97.5 +/- 0.2% at rest and decreased to 89.0 +/- 0.7% during Sal exercise but only to 94.1 +/- 1% with Bic (P < 0.05). Arterial PCO2 was not significantly changed from resting values in the last minute of Sal exercise, but in the Bic trial it increased from 40.5 +/- 0.5 to 45.9 +/- 2.0 Torr (P < 0.05). Pulmonary ventilation was lowered during exercise with Bic (155 +/- 14 vs. 142 +/- 13 l/min; P < 0.05), but the exercise-induced increase in the difference between the end-tidal O2 pressure and arterial PO2 was similar in the two trials. Also, pulmonary O2 uptake and changes in muscle oxygenation as determined by near-infrared spectrophotometry during exercise were similar. The enlarged blood-buffering capacity after infusion of Bic attenuated acidosis and in turn arterial desaturation during maximal exercise.     

Single bouts of exercise affect albumin redox state and carbonyl groups on plasma protein of trained men in a workload-dependent manner.

The purpose of this study was to investigate the effect of single bouts of exercise at three different intensities on the redox state of human serum albumin (HSA) and on carbonyl groups on protein (CP) concentrations in plasma. Trained men [n = 44, maximal oxygen consumption (Vo(2max)): 55 +/- 5 ml.kg(-1).min(-1), nonsmokers, 34 +/- 5 years of age] from a homogenous population, volunteers from a police special forces unit, were randomly assigned to perform on a cycle ergometer either at 70% (n = 14), 75% (n = 14), or 80% (n = 16) of Vo(2max) for 40 min. Blood was collected before exercise, immediately after the exercise test (IE), and 30 min after each test (30M) and 30 h after each test (30H). The reduced fraction of HSA, human mercaptalbumin (HMA), decreased at all three exercise intensities IE and 30M, returning to preexercise values by 30H (P < 0.05). HMA was primarily oxidized to its reversible fraction human nonmercaptalbumin 1 (HNA1). CP concentrations increased at 75% of Vo(2max) IE and 30M with a tendency (P < 0.1) and at 80% Vo(2max) IE and 30M significantly, returning to preexercise concentrations by 30H (P < 0.01). These results indicate that the HSA redox system in plasma is activated after a single bout of cycle ergometer exercise at 70% Vo(2max) and 40 min duration. The extent of the HSA modification increased with exercise intensity. Oxidative protein damage, as indicated by CP, was only significantly increased at 80% Vo(2max) intensity in this homogenous cohort of trained men.     

Exercise response after rapid intravenous infusion of saline in healthy humans.

Patients with chronic heart failure have an abnormal pattern of exercise ventilation (Ve), characterized by small tidal volumes (Vt), increased alveolar ventilation, and elevated physiological dead space (Vd/Vt). To investigate whether increased lung water in isolation could reproduce this pattern of exercise ventilation, 30 ml/kg of saline were rapidly infused into nine normal subjects, immediately before a symptom-limited incremental exercise test. Saline infusion significantly reduced forced vital capacity, 1-s forced expiratory volume, and alveolar volume (P < 0.01 for all). After saline, exercise ventilation assessed by the Ve/Vco(2) slope increased from 24.9 +/- 2.4 to 28.0 +/- 2.9 l/l, (P < 0.0002), associated with a small decrease in arterial Pco(2), but without changes in Vt, Vd/Vt, or alveolar-arterial O(2) difference. A reduction in maximal O(2) uptake of 175 +/- 184 ml/min (P < 0.02) was observed in the postsaline infusion exercise studies, associated with a consistent reduction in maximal exercise heart rate (8.1 +/- 5.9 beats/min, P < 0.01), but without a change in the O(2) pulse. Therefore, infusion of saline to normal subjects before exercise failed to reproduce either the increase in Vd/Vt or the smaller exercise Vt described in heart failure patients. The observed increase in Ve can be attributed to dilution acidosis from infusion of the bicarbonate-free fluid and/or to afferent signals from lung and exercising muscles. The reduction in maximal power output, maximal O(2) uptake, and heart rate after saline infusion may be linked to accumulation of edema fluid in exercising muscle, impairing the diffusion of O(2) to muscle mitochondria.     

Effect of heliox on lung dynamic hyperinflation, dyspnea, and exercise endurance capacity in COPD patients.

We tested the hypothesis that heliox breathing, by reducing lung dynamic hyperinflation (DH) and dyspnea (Dys) sensation, may significantly improve exercise endurance capacity in patients with chronic obstructive pulmonary disease [n = 12, forced expiratory volume in 1 s = 1.15 (SD 0.32) liters]. Each subject underwent two cycle ergometer high-intensity constant work rate exercises to exhaustion, one on room air and one on heliox (79% He-21% O2). Minute ventilation (VE), carbon dioxide output, heart rate, inspiratory capacity (IC), Dys, and arterial partial pressure of CO2 were measured. Exercise endurance time increased significantly with heliox [9.0 (SD 4.5) vs. 4.2 (SD 2.0) min; P < 0.001]. This was associated with a significant reduction in lung DH at isotime (Iso), as reflected by the increase in IC [1.97 (SD 0.40) vs. 1.77 (SD 0.41) liters; P < 0.001] and a decrease in Dys [6 (SD 1) vs. 8 (SD 1) score; P < 0.001]. Heliox induced a state of relative hyperventilation, as reflected by the increase in VE [38.3 (SD 7.7) vs. 35.5 (SD 8.8) l/min; P < 0.01] and VE/carbon dioxide output [36.3 (SD 6.0) vs. 33.9 (SD 5.6); P < 0.01] at peak exercise and by the reduction in arterial partial pressure of CO2 at Iso [44 (SD 6) vs. 48 (SD 6) Torr; P < 0.05] and at peak exercise [46 (SD 6) vs. 48 (SD 6) Torr; P < 0.05]. The reduction in Dys at Iso correlated significantly (R = -0.75; P < 0.01) with the increase in IC induced by heliox. The increment induced by heliox in exercise endurance time correlated significantly with resting increment in resting forced expiratory in 1 s (R = 0.88; P < 0.01), increase in IC at Iso (R = 0.70; P < 0.02), and reduction in Dys at Iso (R = -0.71; P < 0.01). In chronic obstructive pulmonary disease, heliox breathing improves high-intensity exercise endurance capacity by increasing maximal ventilatory capacity and by reducing lung DH and Dys.     

The role of exercise intensity in the bone metabolic response to an acute bout of weight-bearing exercise

We compared the effects of exercise intensity (EI) on bone metabolism during and for 4 days after acute, weight-bearing endurance exercise. Ten males [mean ± SD maximum oxygen uptake (Vo(2max)): 56.2 ± 8.1 ml·min(-1)·kg(-1)] completed three counterbalanced 8-day trials. Following three control days, on day 4, subjects completed 60 min of running at 55%, 65%, and 75% Vo(2max). Markers of bone resorption [COOH-terminal telopeptide region of collagen type 1 (β-CTX)] and formation [NH(2)-terminal propeptides of procollagen type 1 (P1NP), osteocalcin (OC), bone-alkaline phosphatase (ALP)], osteoprotegerin (OPG), parathyroid hormone (PTH), albumin-adjusted calcium (ACa), phosphate (PO(4)), and cortisol were measured during and for 3 h after exercise and on four follow-up days (FU1-FU4). At 75% Vo(2max), β-CTX was not significantly increased from baseline by exercise but was higher compared with 55% (17-19%, P < 0.01) and 65% (11-13%, P < 0.05) Vo(2max) in the first hour postexercise. Concentrations were decreased from baseline in all three groups by 39-42% (P < 0.001) at 3 h postexercise but not thereafter. P1NP increased (P < 0.001) during exercise only, while bone-ALP was increased (P < 0.01) at FU3 and FU4, but neither were affected by EI. PTH and cortisol increased (P < 0.001) with exercise at 75% Vo(2max) only and were higher (P < 0.05) than at 55% and 65% Vo(2max) during and immediately after exercise. The increases (P < 0.001) in OPG, ACa, and PO(4) with exercise were not affected by EI. Increasing EI from 55% to 75% Vo(2max) during 60 min of running resulted in higher β-CTX concentrations in the first hour postexercise but had no effect on bone formation markers. Increased bone-ALP concentrations at 3 and 4 days postexercise suggest a beneficial effect of this type of exercise on bone mineralization. The increase in OPG was not influenced by exercise intensity, whereas PTH was increased at 75% Vo(2max) only, which cannot be fully explained by changes in serum calcium or PO(4) concentrations.     

Plasma atrial natriuretic peptide during brief upright and supine exercise in humans

The factors associated with the exercise-induced increase in plasma atrial natriuretic peptide (ANP) have not been clearly established. Thus the purpose of the study was to further document the stimulus for the exercise-induced release of ANP and to examine the role of ANP in the control of hydromineral balance during exercise. Eight healthy male volunteers (25.1 +/- 4.5 yr) were submitted to a graded cycling exercise in both the upright and supine positions. Venous blood was sampled at rest and at the end of each 5-min work load at 40, 60, and 80% maximal oxygen uptake (Vo2max), at maximal exercise, and during recovery through an indwelling catheter for the determination of plasma vasopressin, aldosterone, catecholamines, plasma renin activity, and ANP concentrations. Results indicate a significant increase in ANP (pg/ml) from rest to maximal exercise in the upright position [rest, 21.9 +/- 10.2; 40%, 24.7 +/- 12.6; 60%, 32.4 +/- 17*; 80%, 47.8 +/- 27.7*; 100% Vo2max, 65.9 +/- 34.5* (*P less than or equal to 0.05)]. Supine concentrations were significantly higher than upright at 40 (37.9 +/- 15.2), 60 (54.0 +/- 18.8), and 80% Vo2max (68.9 +/- 16.6). Plasma ANP during maximal exercise was similar in both positions. Plasma vasopressin, aldosterone, renin activity, and catecholamines increased with increasing exercise intensity in both positions, although lower values were systematically observed in the supine position. The association of higher plasma ANP and blunted plasma vasopressin, plasma renin activity, and norepinephrine concentrations during supine exercise suggests that ANP may exert modulatory effects on the control of the hydromineral hormonal system during exercise.     

Effects of dichloroacetate on VO2 and intramuscular 31P metabolite kinetics during high-intensity exercise in humans.

Traditional control theories of muscle O2 consumption are based on an "inertial" feedback system operating through features of the ATP splitting (e.g., [ADP] feedback, where brackets denote concentration). More recently, however, it has been suggested that feedforward mechanisms (with respect to ATP utilization) may play an important role by controlling the rate of substrate provision to the electron transport chain. This has been achieved by activation of the pyruvate dehydrogenase complex via dichloroacetate (DCA) infusion before exercise. To investigate these suggestions, six men performed repeated, high-intensity, constant-load quadriceps exercise in the bore of an magnetic resonance spectrometer with each of prior DCA or saline control intravenous infusions. O2 uptake (Vo2) was measured breath by breath (by use of a turbine and mass spectrometer) simultaneously with intramuscular phosphocreatine (PCr) concentration ([PCr]), [Pi], [ATP], and pH (by 31P-MRS) and arterialized-venous blood sampling. DCA had no effect on the time constant (tau) of either Vo2 increase or PCr breakdown [tauVo2 45.5 +/- 7.9 vs. 44.3 +/- 8.2 s (means +/- SD; control vs. DCA); tauPCr 44.8 +/- 6.6 vs. 46.4 +/- 7.5 s; with 95% confidence intervals averaging < +/-2 s]. DCA, however, resulted in significant (P < 0.05) reductions in 1). end-exercise [lactate] (-1.0 +/- 0.9 mM), intramuscular acidification (pH, +0.08 +/- 0.06 units), and [Pi] (-1.7 +/- 2.1 mM); 2). the amplitude of the fundamental components for [PCr] (-1.9 +/- 1.6 mM) and Vo2 (-0.1 +/- 0.07 l/min, or 8%); and 3). the amplitude of the Vo2 slow component. Thus, although the DCA infusion lessened the buildup of potential fatigue metabolites and reduced both the aerobic and anaerobic components of the energy transfer during exercise, it did not enhance either tauVo2 or tau[PCr], suggesting that feedback, rather than feedforward, control mechanisms dominate during high-intensity exercise.     

Longitudinal changes in aerobic power in older men and women.

The purpose of this study was to describe the longitudinal (10 yr) decline in aerobic power [maximal O(2) uptake (Vo(2 max))] and anaerobic threshold [ventilatory threshold (T(Ve))] of older adults living independently in the community. Ten years after initial testing, 62 subjects (34 men, mean age 73.5 +/- 6.4 yr; 28 women, 72.1 +/- 5.3 yr) achieved Vo(2 max) criteria during treadmill walking tests to the limit of tolerance, with T(Ve) determined in a subset of 45. Vo(2 max) in men showed a rate of decline of -0.43 ml.kg(-1).min(-1).yr(-1), and the decline in Vo(2 max) was consequent to a lowered maximal heart rate with no change in the maximum O(2) pulse. The women showed a slower rate of decline of Vo(2 max) of -0.19.ml.kg(-1).min(-1).yr(-1) (P < 0.05), again with a lowered HR(max) and unchanged O(2) pulse. In this sample, lean body mass was not changed over the 10-yr period. Changes in Vo(2 max) were not significantly related to physical activity scores. T(Ve) showed a nonsignificant decline in both men and women. Groupings of young-old (65-72 yr at follow-up) vs. old-old (73-90 yr at follow-up) were examined. In men, there were no differences in the rate of Vo(2 max) decline. The young-old women showed a significant decline in Vo(2 max), whereas old-old women, initially at a Vo(2 max) of 19.4 +/- 3.1 ml.kg(-1).min(-1), showed no loss in Vo(2 max). The longitudinal data, vs. cross-sectional analysis, showed a greater decline for men but similar estimates of the rates of change in women. Thus the 10-yr longitudinal study of the cohort of community-dwelling older adults who remained healthy, ambulatory, and independent showed a 14% decline in Vo(2 max) in men, and a smaller decline of 7% in women, with the oldest women showing little change over the 10-yr period.