Ventilation and respiratory mechanics during exercise in younger subjects breathing CO2 or HeO2

To determine if ventilation (VE) during maximal exercise would be increased as much by 3% CO2 loading as by resistive unloading of the airways, we studied seven subjects (39 +/- 5 years; mean +/- S.D.) during graded-cycle ergometry to exhaustion while breathing: (1) room air (RA); (2) 3% CO2, 21% O2, and 76% N2; or (3) 79% He and 21% O2). VE and respiratory mechanics were measured during each 1-min increment (20 or 30 W) in work rate. VE during maximal exercise was increased 21 +/- 17% when breathing 3% CO2 and 23 +/- 16% when breathing HeO2 (P < 0.01). Further, the ventilatory response to exercise above ventilatory threshold (VTh) was increased (P < 0.05) when breathing HeO2 (0.89 +/- 0.26 L/min/W) as compared with breathing RA (0.65 +/- 0.12). When breathing HeO2, end-expiratory lung volume (% total lung capacity, TLC) was lower during maximal exercise (46 +/- 7) when compared with RA (53 +/- 6, P < 0.01). In conclusion, VE during maximal exercise can be augmented equally by 3% CO2 loading as by resistive unloading of the airways in younger subjects. This suggests that in younger subjects with normal lung function there are minimal mechanical ventilatory constraints on VE during maximal exercise.     

Relationship between nitric oxide and prostaglandins in carrageenin pleurisy

PURPOSE: To examine the effects of repeated bouts of exercise on the blood lactate [HLa]-ratings of perceived exertion (RPE) relation. METHODS: Six moderately trained males were studied on two occasions: a sequential exercise bouts day (SEB: 1000 h, 1130 h, and 1300 h) and a delayed exercise bouts day (DEB: 1000 h, 1400 h, and 1800 h). Each of the three exercise bouts within a given condition were 30 min in duration at the power output (PO) associated with 70% of VO2peak on a cycle ergometer. A standardized meal was provided at 0600 h. VO2, PO, HR, and RER were recorded every min during exercise and blood [HLa] and RPE were measured every 5 min during exercise. RESULTS: A 2 x 3 analysis of variance with repeated measures revealed that blood [HLa] decreased significantly with each repeated exercise bout (X +/- SEM: bout 1: SEB = 3.5 (0.3), DEB = 3.8 (0.4); bout 2: SEB = 2.6 (0.3), DEB = 2.8 (0.3); bout 3: SEB = 2.0 (0.2), DEB = 2.1 (0.4); mM). No differences were observed in the blood [HLa] response to repeated bouts of exercise between SEB and DEB. RPE-peripheral (legs, RPE-L) was higher during bout 3 compared with bout 1 (P <0.05) (bout 1: SEB = 11.8 (0.8), DEB = 12.3 (0.2); bout 2: SEB = 12.3 (0.5), DEB = 13.3 (0.4); bout 3: SEB = 13.5 (0.8), DEB = 14.0 (0.7); RPE-central (chest and breathing, RPE-C) was not affected by repeated bouts of exercise, whereas RPE-Overall (RPE-O) was higher during bout 3 compared with bouts 1 and 2 (P < 0.05) (bout 1: SEB = 12.5 (0.2), DEB = 12.3 (0.4); bout 2: SEB = 12.8 (0.4), DEB = 12.7 (0.4); bout 3: SEB = 13.7 (0.7), DEB = 13.2 (0.3)). No interaction for RPE x condition was observed. HR increased with repeated bouts of exercise with HR during exercise bout 3 being higher than HR during exercise bout 1 (164 vs. 156 bpm, P < 0.05). There was also a strong trend for HR during exercise bout 3 to be higher than HR during exercise bout 2 (P < 0.06). A trend for a reduction in VO2 with repeated exercise was observed (P < 0.07), with the reduction apparently related to the SEB condition (P < 0.12 for VO2 x condition). PO and kcal.min-1 were not affected by repeated bouts of exercise. RER decreased significantly with each repeated bout of exercise (from RER = 0.96 to RER = 0.89, P < 0.05) with no difference observed between SEB and DEB. CONCLUSIONS: We conclude that the blood [HLa]-RPE relation is altered by repeated bouts of exercise and that this alteration does not appear to be affected by recovery time between exercise bouts (up to 3.5 h of recovery). These data suggest that, after the first exercise bout, RPE should not be used to produce a specific blood [HLa] on subsequent exercise bouts.     

Effect of acute bicarbonate administration on exercise responses of COPD patients

Patients with severe chronic obstructive pulmonary disease (COPD) are limited in their exercise tolerance by the level of ventilation (VE) they can sustain. We determined whether acutely increasing blood bicarbonate levels decreased acid stimulation to the respiratory chemoreceptors during exercise, thereby improving exercise tolerance. Responses were compared with those obtained during 100% O2 breathing (known to reduce VE in these patients) and to the responses of healthy young subjects. Participants were six patients with severe COPD (forced expired volume in 1 s = 31 +/- 11% predicted) but without chronic CO2 retention and 5 healthy young subjects. Each subject performed three incremental cycle ergometer exercise tests: 1) control, 2) after ingestion of 0.3 g.kg-1 of sodium bicarbonate and 3) while breathing 100% O2. During these tests VE was measured continuously and arterialized venous blood (patients) or arterial blood (healthy subjects) was sampled serially to assess acid base variables. Bicarbonate loading increased standard bicarbonate by 4-6 mmol.L-1 and this elevation persisted during exercise. In both groups, bicarbonate loading resulted in a substantially higher arterial pH; arterial PCO2 was either unchanged (healthy subjects) or mildly (averaging 5 torr) higher (COPD patients). However, in neither group did bicarbonate loading result in an altered VE response to exercise or an increase in exercise tolerance. In contrast, superimposing hyperoxia on bicarbonate ingestion yielded, on average, 24% reduction in VE and 50% increase in peak work rate in the patients (but not in the healthy young subjects). We conclude that acute bicarbonate loading is not an ergogenic aid in patients with severe COPD.     

Reliability of peak-lactate, heart rate, and plasma volume following the Wingate test

PURPOSE: The 30-s Wingate Anaerobic Test (WAnT) has been used to assess anaerobic performance capacity and to evaluate physiological responses to supramaximal exercise. Blood lactate concentration ([La]) following supramaximal exercise is often used in the field and in the laboratory to assess the glycolytic contribution to exercise. Although the reliability of the performance in the WAnT has been established, this has not been the case with the WAnT's [La] response. Thus, the main purpose of this research was to study the test-retest reliability of peak [La] following the WAnT. Additionally, the test-retest reliability of the heart rate (HR) and plasma volume changes (deltaPV) response was also evaluated. METHODS: Twenty-nine subjects (15 male, 14 female) of diverse training levels as well as physical characteristics (mean +/- SD: 23.3+/-7.0 yr, 62.5+/-12.0 kg, 170.8+/-9.7 cm, and 16.3+/-6.2% fat) performed two WAnTs within 1 wk. Capillary blood was sampled from a prewarmed fingertip at rest, just before the WAnT and at 3, 5, 7, and 9 min following it. HR was also measured during these times. RESULTS: Mean-power (MP) (+/-SE) in test 1 and test 2 was 8.4+/-0.2 and 8.3+/-0.2 W X kg(-1) body mass, respectively. Peak [La] was attained 5-7 min following the WAnTs and was not significantly different between test 1 and test 2 (9.7+/-0.3 vs 9.8+/-0.3 mM, respectively). Peak HR occurred within 5 s post-WAnT and was not different between tests (170.8+/-2.2 and 171.3+/-2.2 beats X min(-1), in test 1 and test 2, respectively). Peak deltaPV was not different between tests (-12.0+/-3.4 and -11.1+/-3.2%, in test 1 and test 2, respectively). The intraclass reliability coefficients for peak [La]. peak HR and deltaPV were 0.926, 0.941, and 0.878, respectively, whereas the corresponding value for MP was 0.982. CONCLUSIONS: We conclude that peak [La], peak HR, and deltaPV following the WAnT are reliable measures.     

The influence of PaO2, pH and SaO2 on maximal oxygen uptake

Influence of arterial oxygen pressure (PaO2) and pH on haemoglobin saturation (SaO2) and in turn on O2 uptake (VO2) was evaluated during ergometer rowing (156, 276 and 376 W; VO2max, 5.0 L min-1; n = 11). During low intensity exercise, neither pH nor SaO2 were affected significantly. In response to the higher work intensities, ventilations (VE) of 129 +/- 10 and 155 +/- 8 L min-1 enhanced the end tidal PO2 (PETO2) to the same extent (117 +/- 2 mmHg), but PaO2 became reduced (from 102 +/- 2 to 78 +/- 2 and 81 +/- 3 mmHg, respectively). As pH decreased during maximal exercise (7.14 +/- 0.02 vs. 7.30 +/- 0.02), SaO2 also became lower (92.9 +/- 0.7 vs. 95.1 +/- 0.1%) and arterial O2 content (CaO2) was 202 +/- 3 mL L-1. An inspired O2 fraction (F1O2) of 0.30 (n = 8) did not affect VE, but increased PETO2 and PaO2 to 175 +/- 4 and 164 +/- 5 mmHg and the PETO2-PaO2 difference was reduced (21 +/- 4 vs. 36 +/- 4 mmHg). pH did not change when compared with normoxia and SaO2 remained within 1% of the level at rest in hyperoxia (99 +/- 0.1%). Thus, CaO2 and VO2max increased to 212 +/- 3 mL L-1 and 5.7 +/- 0.2 L min-1, respectively. The reduced PaO2 became of importance for SaO2 when a low pH inhibited the affinity of O2 to haemoglobin. An increased F1O2 reduced the gradient over the alveolar-arterial membrane, maintained haemoglobin saturation despite the reduction in pH and resulted in increases of the arterial oxygen content and uptake.     

Gas exchange kinetics during functional electrical stimulation in subjects with spinal cord injury

We examined the kinetics of VO2, VCO2, and VE following the onset of unloaded leg cycling, and in recovery, in six patients with spinal cord injury (SCI). Exercise was produced by functional electrical stimulation (FES) of the quadriceps, hamstrings, and gluteal muscles. End-exercise VO2 (1.03 +/- 0.16 l.min-1), VCO2 (1.20 +/- 0.22 l.min-1) and VE (41 +/- 10 l.min-1) were elevated compared to values typically seen in healthy ambulatory subjects performing similar unloaded cycling. Mean response times for the on transients (MRTon) were both long and variable across subjects for VO2 (165 +/- 62 s), VCO2 (173 +/- 58 s), and VE (202 +/- 61 s). Recovery kinetics showed much less intersubject variability, and for five of six subjects were faster than the equivalent exercise MRT for all three variables (MRToff for VO2 of 103 +/- 28 s, VCO2 136 +/- 20 s, and VE 144 +/- 34 s), but P > 0.05 for all three. Size of the O2 deficit (1.96 +/- 0.90 l) and end-exercise lactate (7.05 +/- 1.65 mmol.l-1) were similar to values reported for healthy sedentary subjects performing maximal voluntary exercise, but the end-exercise heart rate (102 +/- 16 bpm) was lower than expected for this intensity of exercise. In conclusion, FES-induced unloaded cycling leads to exaggerated responses of pulmonary gas exchange and long time constants in patients with SCI. The delayed kinetics may be due in part to a blunted increase in heart rate in addition to severe deconditioning.     

Post-exercise changes in blood pressure, heart rate and rate pressure product at different exercise intensities in normotensive humans

To evaluate the effect of exercise intensity on post-exercise cardiovascular responses, 12 young normotensive subjects performed in a randomized order three cycle ergometer exercise bouts of 45 min at 30, 50 and 80% of VO2peak, and 12 subjects rested for 45 min in a non-exercise control trial. Blood pressure (BP) and heart rate (HR) were measured for 20 min prior to exercise (baseline) and at intervals of 5 to 30 (R5-30), 35 to 60 (R35-60) and 65 to 90 (R65-90) min after exercise. Systolic, mean, and diastolic BP after exercise were significantly lower than baseline, and there was no difference between the three exercise intensities. After exercise at 30% of VO2peak, HR was significantly decreased at R35-60 and R65-90. In contrast, after exercise at 50 and 80% of VO2peak, HR was significantly increased at R5-30 and R35-60, respectively. Exercise at 30% of VO2peak significantly decreased rate pressure (RP) product (RP = HR x systolic BP) during the entire recovery period (baseline = 7930 +/- 314 vs R5-30 = 7150 +/- 326, R35-60 = 6794 +/- 349, and R65-90 = 6628 +/- 311, P < 0.05), while exercise at 50% of VO2peak caused no change, and exercise at 80% of VO2peak produced a significant increase at R5-30 (7468 +/- 267 vs 9818 +/- 366, P < 0.05) and no change at R35-60 or R65-90. Cardiovascular responses were not altered during the control trial. In conclusion, varying exercise intensity from 30 to 80% of VO2peak in young normotensive humans did not influence the magnitude of post-exercise hypotension. However, in contrast to exercise at 50 and 80% of VO2peak, exercise at 30% of VO2peak decreased post-exercise HR and RP.     

O2 uptake kinetics after acetazolamide administration during moderate- and heavy-intensity exercise

Inhibition of carbonic anhydrase (CA) is associated with a lower plasma lactate concentration ([La-]pl) during fatiguing exercise. We hypothesized that a lower [La-]pl may be associated with faster O2 uptake (V(O2)) kinetics during constant-load exercise. Seven men performed cycle ergometer exercise during control (Con) and acute CA inhibition with acetazolamide (Acz, 10 mg/kg body wt iv). On 6 separate days, each subject performed 6-min step transitions in work rate from 0 to 100 W (below ventilatory threshold, VE(T). Gas exchange was measured breath by breath. Trials were interpolated at 1-s intervals and ensemble averaged to yield a single response. The mean response time (MRT, i.e., time to 63% of total exponential increase) for on- and off-transients was determined using a two- (VE(T)). Arterialized venous blood was sampled from a dorsal hand vein and analyzed for [La-]pl. MRT was similar during Con (31.2 +/- 2.6 and 32.7 +/- 1.2 s for on and off, respectively) and Acz (30.9 +/- 3.0 and 31.4 +/- 1.5 s for on and off, respectively) for work rates VE(T), MRT was similar between Con (69.1 +/- 6.1 and 50.4 +/- 3.5 s for on and off, respectively) and Acz (69.7 +/- 5.9 and 53.8 +/- 3.8 s for on and off, respectively). On- and off-MRTs were slower for >VE(T) than for VE(T) exercise but was lower at the end of the transition during Acz (1.4 +/- 0.2 and 7.1 +/- 0.5 mmol/l for VE(T) respectively) than during Con (2.0 +/- 0.2 and 9.8 +/- 0.9 mmol/l for VE(T), respectively). CA inhibition does not affect O2 utilization at the onset of VE(T) exercise, suggesting that the contribution of oxidative phosphorylation to the energy demand is not affected by acute CA inhibition with Acz.     

ANP gene expression in rat hearts during hypoxia

The relationships between muscle capillarization, estimated O2 diffusion distance from capillary to mitochondria, and O2 uptake (VO2) kinetics were studied in 11 young (mean age, 25.9 yr) and 9 old (mean age, 66.0 yr) adults. VO2 kinetics were determined by calculating the time constants (tau) for the phase 2 VO2 adjustment to and recovery from the average of 12 repeats of a 6-min, moderate-intensity plantar flexion exercise. Muscle capillarization was determined from cross sections of biopsy material taken from lateral gastrocnemius. Young and old groups had similar VO2 kinetics (tau VO2-on = 44 vs. 48 s; tau VO2-off = 33 vs. 44 s, for young and old, respectively), muscle capillarization, and estimated O2 diffusion distances. Muscle capillarization, expressed as capillary density or average number of capillary contacts per fiber/average fiber area, and the estimates of diffusion distance were significantly correlated to VO2-off kinetics in the young (r = -0.68 to -0.83; P < 0.05). We conclude that 1) capillarization and VO2 kinetics during exercise of a muscle group accustomed to everyday activity (e.g., walking) are well maintained in old individuals, and 2) in the young, recovery of VO2 after exercise is faster, with a greater capillary supply over a given muscle fiber area or shorter O2 diffusion distances.     

Smaller lungs in women affect exercise hyperpnea

We subjected 29 healthy young women (age: 27 +/- 1 yr) with a wide range of fitness levels [maximal oxygen uptake (VO2 max): 57 +/- 6 ml . kg-1 . min-1; 35-70 ml . kg-1 . min-1] to a progressive treadmill running test. Our subjects had significantly smaller lung volumes and lower maximal expiratory flow rates, irrespective of fitness level, compared with predicted values for age- and height-matched men. The higher maximal workload in highly fit (VO2 max > 57 ml . kg-1 . min-1, n = 14) vs. less-fit (VO2 max < 56 ml . kg-1 . min-1, n = 15) women caused a higher maximal ventilation (VE) with increased tidal volume (VT) and breathing frequency (fb) at comparable maximal VT/vital capacity (VC). More expiratory flow limitation (EFL; 22 +/- 4% of VT) was also observed during heavy exercise in highly fit vs. less-fit women, causing higher end-expiratory and end-inspiratory lung volumes and greater usage of their maximum available ventilatory reserves. HeO2 (79% He-21% O2) vs. room air exercise trials were compared (with screens added to equalize external apparatus resistance). HeO2 increased maximal expiratory flow rates (20-38%) throughout the range of VC, which significantly reduced EFL during heavy exercise. When EFL was reduced with HeO2, VT, fb, and VE (+16 +/- 2 l/min) were significantly increased during maximal exercise. However, in the absence of EFL (during room air exercise), HeO2 had no effect on VE. We conclude that smaller lung volumes and maximal flow rates for women in general, and especially highly fit women, caused increased prevalence of EFL during heavy exercise, a relative hyperinflation, an increased reliance on fb, and a greater encroachment on the ventilatory "reserve." Consequently, VT and VE are mechanically constrained during maximal exercise in many fit women because the demand for high expiratory flow rates encroaches on the airways' maximum flow-volume envelope.     

The effects of changing intracellular pH on calcium and potassium currents in smooth muscle cells from the guinea-pig ureter

Effect of weight training exercise and treadmill exercise on postexercise oxygen consumption. Med. Sci. Sports Exerc., Vol. 30, No. 4, pp. 518-522, 1998. To compare the effect of weight training (WT) and treadmill (TM) exercise on postexercise oxygen consumption (VO2), 15 males (mean +/- SD) age = 22.7 +/- 1.6 yr; height = 175.0 +/- 6.2 cm; mass = 82.0 +/- 14.3 kg) performed a 27-min bout of WT and a 27-min bout of TM exercise at matched rates of VO2. WT consisted of performing two circuits of eight exercises at 60% of each subject's one repetition maximum with a work/rest ratio of 45 s/60 s. Approximately 5 d after WT each subject walked or jogged on the TM at a pace that elicited an average VO2 matched with his mean value during WT. VO2 was measured continuously during exercise and the first 30 min into recovery and at 60 and 90 min into recovery. VO2 during WT (1.58 L.min-1) and TM exercise (1.55 L.min-1) were not significantly (P > 0.05) different; thus the two activities were matched for VO2. Total oxygen consumption during the first 30 min of recovery was significantly higher (P < 0.05) as a result of WT (19.0 L) compared with that during TM exercise (12.7 L). However, VO2 values at 60 (0.32 vs 0.29 L.min-1), and 90 min (0.33 vs 0.30 L.min-1) were not significantly different (P > 0.05) between WT and TM exercise, respectively. The results suggest that, during the first 30 min following exercise. WT elicits a greater elevated postexercise VO2 than TM exercise when the two activities are performed at matched VO2 and equal durations. Therefore, total energy expenditure as a consequence of WT will be underestimated if based on exercise VO2 only.     

Microvascular permeability of the non-heart-beating rabbit lung after warm ischemia and reperfusion: role of neutrophil elastase

STUDY OBJECTIVES: Criteria used to define the respective roles of pulmonary mechanics and cardiovascular disease in limiting exercise performance are usually obtained at peak exercise, but are dependent on maximal patient effort. To differentiate heart from lung disease during a less effort-dependent domain of exercise, the predictive value of the breathing reserve index (BRI=minute ventilation [VE]/maximal voluntary ventilation [MVV]) at the lactate threshold (LT) was evaluated. DESIGN: Thirty-two patients with COPD and a pulmonary mechanical limit (PML) to exercise defined by classic criteria at maximum oxygen uptake (VO2max) were compared with 29 patients with a cardiovascular limit (CVL) and 12 normal control subjects. Expired gases and VE were measured breath by breath using a commercially available metabolic cart (Model 2001; MedGraphics Corp; St. Paul, Minn). Arterial blood gases, pH, and lactate were sampled each minute during exercise, and cardiac output (Q) was measured by first-pass radionuclide ventriculography (System 77; Baird Corp; Bedford, Mass) at rest and peak exercise. RESULTS: For all patients, the BRI at lactate threshold (BRILT) correlated with the BRI at VO2max (BRIMAX) (r=0.85, p<0.0001). The BRILT was higher for PML (0.73+/-0.03, mean+/-SEM) vs CVL (0.27+/-0.02, p<0.0001), and vs control subjects (0.24+/-0.03, p<0.0001). A BRILT > or = 0.42 predicted a PML at maximum exercise, with a sensitivity of 96.9%, a specificity of 95.1%, a positive predictive value of 93.9%, and a negative predictive value of 97.5%. CONCLUSIONS: The BRILT, a variable measured during the submaximal realm of exercise, can distinguish a PML from CVL.     

Can the ventilatory equivalent for carbon dioxide predict the severity of functional impairment in patients with cardiac insufficiency?

OBJECTIVE: To evaluate whether the changes in the ventilatory equivalent for carbon dioxide (VE/VCO2), during the early stages of cardiopulmonary exercise testing, can predict maximal oxygen consumption (VO2max) in patients with chronic heart failure. METHODS: We studied 38 patients (30 males, mean age 56 +/- 11 years) with chronic heart failure. All patients performed maximal symptom limited, treadmill exercise test with breath-by-breath respiratory gas analysis. They were divided in two groups according to their maximal oxygen consumption (group I-VO2max above 14 ml/kg/min and group II-VO2max below 14 ml/kg/min). In both groups, we analysed VE/VCO2 at rest, at the anaerobic threshold (AT) and at peak exercise, and the percentage of VE/VCO2 reduction from rest to AT. RESULTS: Eleven patients had a VO2max below 14 ml/kg/min (group II). At rest VE/VCO2 = 53 +/- 13 in group II versus 47 +/- 10 in group I (p = 0.048), at the AT VE/VCO2 = 46 +/- 12 in group II versus 36 +/- 7 in group I (p = 0.001) and at peak exercise VE/VCO2 = 46.2 +/- 13 in group II versus 36.2 +/- 6 in group I (p = 0.0002). There was a 24% reduction in the VE/VCO2, from rest to AT in group I, compared to a 16% reduction in group II (p = 0.004). A reduction in the VE/VCO2 from rest to AT less than 16% predicted a VO2max below 14 ml/kg/min with a sensitivity of 60% and a specificity of 93%. CONCLUSIONS: Patients with severe functional impairment have higher values of VE/VCO2 in all exercise stages. A reduction of VE/VCO2 from rest to anaerobic threshold of less than 16% is a high specific predictor of a VO2max below 14 ml/kg/min.     

Analysis of impaired exercise capacity in patients with cirrhosis

Exercise limitation in cirrhosis is typically attributed to a cirrhotic myopathy (without impaired oxygen utilization) and/or a cardiac chronotropic dysfunction. We performed symptom-limited cardiopulmonary exercise testing in 19 cirrhotics without confounding variables (cardiopulmonary disease, beta blockade, anemia, smoking). Twelve concurrently exercised patients without cirrhosis and with normal resting pulmonary function were controls. Oxygen consumption (VO2) at peak exercise, at anaerobic threshold (VO2-AT), work rate (WR), and heart rate (HR) were measured. Cirrhotics had significantly lower peak WR (73+/-4 vs 107+/-7% predicted, p < 0.001), VO2 (72+/-4 vs 98+/-5% predicted, P < 0.001), VO2-AT (53+/-4 vs 71+/-5% predicted peak VO2, P < 0.01), HR (83+/-2 vs 91+/-2% predicted, P < 0.01) and were more likely to have chronotropic dysfunction (peak HR < 85% predicted). Six cirrhotics had normal aerobic capacity (peak VO2 > 80% predicted), while 13 were abnormal. The abnormals had an earlier AT (46+/-2 vs 67+/-3% predicted peak VO2, P < 0.05) but no difference in peak HR percent predicted was found. In conclusion, two thirds of cirrhotics, without confounding factors, have significantly reduced aerobic capacity. Cirrhotic myopathy (without impaired O2 utilization) and cardiac chronotropic dysfunction do not adequately account for the observed decrease in aerobic capacity.     

Perceived exertion associated with breathing hyperoxic mixtures during submaximal work

The effect of an enriched inspired oxygen concentration on perceived exertion (RPE) was investigated while running at two submaximal treadmill loads. Twelve males (VO2 max = 49.3 ml/kg-min) worked at 50% and 80% VO2 max, breathing either air or 80% O2-20% N2 in random order using a single blind technique. Subjects were evaluated while running for 10 min and during a 20 min recovery. Heart rate (HR), ventilation (VE), respiration rate (RR), tidal volume (VT) and RPE were measured before, during and after work. Blood lactate was measured 1 min after work. Oxygen concentration did not statistically affect HR, VE, RR or VT during exercise or recovery. At both loads, RPE at the end of exercise was significantly reduced breathing the hyperoxic mixture. At 50% VO2 max, mean RPE decreased from 11.2 breathing room air to 9.6 breathing 80% O2 and, 80% VO2 max, from 13.8 to 11.7 (P less than 0.01). Blood lactates were significantly reduced breathing 80% O2; from 23.4 mg to 13.3 at 50% VO2 max and from 55.5 to 36.5 at 80% VO2 max (P less than 0.01). The RPE correlated with lactate (r=0.64) at the end of work. Results indicate that during moderate and heavy work RPE is significantly affected by the inspired O2 concentration and there is a significant relationship between RPE and blood lactate.     

Evaluation of right ventricular systolic pressure during incremental exercise by Doppler echocardiography in adults with atrial septal defect

STUDY OBJECTIVES: Pulmonary hypertension is the most important complication in patients with atrial septal defect (ASD), but its role in limiting exercise has not been examined. This study sought to evaluate exercise performance in adults with ASD and determine the contribution of elevated pulmonary artery pressure in limiting exercise capacity. DESIGN: We used Doppler echocardiography during exercise in 10 adults (aged 34 to 70 years) with isolated ASD (New York Heart Association class I, II) and an equal number of matched control subjects. Incremental exercise was performed on an electrically braked upright cycle ergometer. Expired gases and VE were measured breath-by-breath. Two-dimensional and Doppler echocardiographic images were obtained at rest prior to exercise to determine ASD size, stroke volume (SV), shunt ratio (Qp:Qs), right ventricular outflow tract (RVOT) size, and right ventricular systolic pressure at rest (RVSPr). Doppler echocardiography was repeated at peak exercise to measure right ventricular systolic pressure during exercise (RVSPex). RESULTS: Resting echocardiography revealed that RVOT was larger (21+/-4 vs 35+/-8 mm, mean+/-SD; p=0.0009) and RVSPr tended to be higher (17+/-8 vs 31+/-8 mm Hg; p=0.08) in ASD; however, left ventricular SV was not different (64+/-23 vs 58+/-23 mL; p>0.05), compared with control subjects. Despite normal resting left ventricular function, ASD patients had a significant reduction in maximum oxygen uptake (VO2max) (22.9+/-5.4 vs 17.3+/-4.2 mL/kg/min; p=0.005). RVSPex was higher (19+/-8 vs 51+/-10 mm Hg; p=0.001) and the mean RVSP-VO2 slope (1+/-2 vs 18+/-3 mm Hg/L/min; p=0.003) and intercept (17+/-4 vs 27+/-4 mm Hg; p=0.05) were higher in the ASD group. VO2max correlated inversely with both RVSPr (r=-0.69; p=0.007) and RVSPex (r=-0.67; p=0.01). CONCLUSION: These findings suggest that adults with ASD have reduced exercise performance, which may be associated with an abnormal increase in pulmonary artery pressure during exercise.     

Does acute exercise affect the susceptibility of low density lipoprotein to oxidation?

This study describes the effect of an acute exercise bout on the susceptibility of isolated low density lipoprotein (LDL) to in vitro oxidation. LDL was isolated from 23 subjects (exercisers, n = 11; sedentary, n = 12) immediately before and after a single bout of exercise (30 min of treadmill work at 55% & 70% peak oxygen consumption (VO2 peak) for exercisers and sedentary, respectively). A statistically significant decrease in lag time for LDL oxidation was observed following exercise compared to baseline (96.1+/-23.5 min vs. 92.1+/-23.3 minutes; n = 23, p < or = .03) using a 5 microM copper system. There was a statistically significant increase in plasma myeloperoxidase (MPO) levels following exercise compared to baseline values ( 1.58+/-.91 ng/dl versus 2.08+/-1.2 ng/dl; n = 12, p < or = .03). These results suggest that the 30 min exercise bout at a moderate intensity and duration was a sufficient oxidative stress to increase the susceptibility of LDL to in vitro oxidation. Additionally, the exercise bout appeared to activate neutrophils, subsequently releasing MPO protein.     

Skeletal muscle chemoreflex and pHi in exercise ventilatory control

To determine whether skeletal muscle hydrogen ion mediates ventilatory drive in humans during exercise, 12 healthy subjects performed three bouts of isotonic submaximal quadriceps exercise on each of 2 days in a 1.5-T magnet for 31P-magnetic resonance spectroscopy (31P-MRS). Bilateral lower extremity positive pressure cuffs were inflated to 45 Torr during exercise (BLPPex) or recovery (BLPPrec) in a randomized order to accentuate a muscle chemoreflex. Simultaneous measurements were made of breath-by-breath expired gases and minute ventilation, arterialized venous blood, and by 31P-MRS of the vastus medialis, acquired from the average of 12 radio-frequency pulses at a repetition time of 2.5 s. With BLPPex, end-exercise minute ventilation was higher (53.3 +/- 3.8 vs. 37.3 +/- 2.2 l/min; P < 0.0001), arterialized PCO2 lower (33 +/- 1 vs. 36 +/- 1 Torr; P = 0.0009), and quadriceps intracellular pH (pHi) more acid (6.44 +/- 0.07 vs. 6.62 +/- 0.07; P = 0.004), compared with BLPPrec. Blood lactate was modestly increased with BLPPex but without a change in arterialized pH. For each subject, pHi was linearly related to minute ventilation during exercise but not to arterialized pH. These data suggest that skeletal muscle hydrogen ion contributes to the exercise ventilatory response.     

Effects of a single bout of exercise on glucose effectiveness

The effects of a single bout of exercise on glucose effectiveness (SG) and insulin sensitivity (SI) in 22 sedentary subjects were estimated with a minimal model approach. The intravenous glucose tolerance test (IVGTT) was performed 1) 11 h after an exercise bout on a cycle ergometer at the lactate threshold level (mild exercise) for 60 min, 2) 11 h after an exercise bout at the 4 mM lactate level (hard exercise) for 36 +/- 1 min, 3) 11 h after an exhaustive-exercise bout (exhaustive exercise) for 96 +/- 7 min, or 4) without any prior exercise (control). Only the exhaustive exercise increased the glucose disappearance constant (2.69 +/- 0.28 vs. 2.05 +/- 0.13%/min; P < 0.05) and SI (15.0 +/- 2.0 vs. 10.3 +/- 0.9 x 10(-5) min/pM: P < 0.05) in comparison with the control condition. The SG and SG at zero insulin (GEZI) were not affected by any exercise condition. However, a marked individual difference in GEZI emerged after the exhaustive exercise and could be divided into two subgroups: one decreased in GEZI (0.014 +/- 0.001 vs. 0.007 +/- 0.001 min-1) and the other increased in GEZI (0.014 +/- 0.001 vs. 0.021 +/- 0.003 min-1). The former subgroup was accompanied by elevated levels of plasma creatine kinase (100 +/- 16 vs. 598 +/- 315 IU/l; P < 0.05) and myoglobin (Mb; 46 +/- 4 vs. 126 +/- 47 ng/ml; P < 0.05), whereas the latter subgroup showed no significant change in creatinine kinase (99 +/- 10 vs. 128 +/- 9 IU/l; P > 0.05) and Mb (50 +/- 7 vs. 51 +/- 4 ng/ml; P > 0.05). In both subgroups, SI was similarly increased after the exhaustive exercise. These results thus suggest that a single bout of exercise that results in muscle damage or changes in muscle permeability, as reflected in the increased creatine kinase and Mb levels, decreases GEZI, whereas exhaustive exercise without such alterations increases GEZI.     

Restrained and nonrestrained eaters'' orienting responses to food and nonfood odors

This study attempted to induce a major shift in the utilization of endogenous substrates during exercise in men by the use of a potent inhibitor of adipose tissue lipolysis, Acipimox, and to see to what extent this affects the 13C/12C ratio in expired air CO2. Six healthy volunteers exercised for 3 h on a treadmill at approximately 45% of their maximum O2 uptake, 75 min after having ingested either a placebo or 250 mg Acipimox. The rise in plasma free fatty acids and glycerol was almost totally prevented by Acipimox, and no significant rise in the utilization of lipids, evaluated by indirect calorimetry, was observed. Total carbohydrate oxidation averaged 128 +/- 17 (placebo) and 182 +/- 21 g/3 h (Acipimox). Conversely, total lipid oxidation was 84 +/- 5 (placebo) and 57 +/- 6 g/3 h (Acipimox; P < 0.01). Under placebo, changes in expired air CO2 delta 13C were minimal, with only a 0.49/1000 significant rise at 30 min. In contrast, under Acipimox, the rise in expired air CO2 delta 13C averaged 1/1000 and was significant throughout the 3-h exercise bout; in these conditions calculation of a "pseudooxidation" of an exogenous sugar naturally or artificially enriched in 13C, but not ingested, would have given an erroneous value of 19.8 +/- 2.6 g/3 h. Thus under conditions of extreme changes in endogenous substrate utilization, an appropriate control experiment is mandatory when studying exogenous substrate oxidation by 13C-labeled substrates and isotope-ratio mass spectrometry measurements on expired air CO2.