A novel cardiopulmonary exercise test protocol and criterion to determine maximal oxygen uptake in chronic heart failure

Cardiopulmonary exercise testing for peak oxygen uptake (Vo(2peak)) can evaluate prognosis in chronic heart failure (CHF) patients, with the peak respiratory exchange ratio (RER(peak)) commonly used to confirm maximal effort and maximal oxygen uptake (Vo(2max)). We determined the precision of RER(peak) in confirming Vo(2max), and whether a novel ramp-incremental (RI) step-exercise (SE) (RISE) test could better determine Vo(2max) in CHF. Male CHF patients (n = 24; NYHA class I-III) performed a symptom-limited RISE-95 cycle ergometer test in the format: RI (4-18 W/min; ～10 min); 5 min recovery (10 W); SE (95% peak RI work rate). Patients (n = 18) then performed RISE-95 tests using slow (3-8 W/min; ～15 min) and fast (10-30 W/min; ～6 min) ramp rates. Pulmonary gas exchange was measured breath-by-breath. Vo(2peak) was compared within patients by unpaired t-test of the highest 12 breaths during RI and SE phases to confirm Vo(2max) and its 95% confidence limits (CI(95)). RER(peak) was significantly influenced by ramp rate (fast, medium, slow: 1.21 ± 0.1 vs. 1.15 ± 0.1 vs. 1.09 ± 0.1; P = 0.001), unlike Vo(2peak) (mean n = 18; 14.4 ± 2.6 ml·kg(-1)·min(-1); P = 0.476). Group Vo(2peak) was similar between RI and SE (n = 24; 14.5 ± 3.0 vs. 14.7 ± 3.1 ml·kg(-1)·min(-1); P = 0.407); however, within-subject comparisons confirmed Vo(2max) in only 14 of 24 patients (CI(95) for Vo(2max) estimation averaged 1.4 ± 0.8 ml·kg(-1)·min(-1)). The RER(peak) in CHF was significantly influenced by ramp rate, suggesting its use to determine maximal effort and Vo(2max) be abandoned. In contrast, the RISE-95 test had high precision for Vo(2max) confirmation with patient-specific CI(95) (without secondary criteria), and showed that Vo(2max) is commonly underestimated in CHF. The RISE-95 test was well tolerated by CHF patients, supporting its use for Vo(2max) confirmation.     

Ascorbic acid does not affect the age-associated reduction in maximal cardiac output and oxygen consumption in healthy adults.

Maximal aerobic capacity (Vo(2max)) decreases progressively with age, primarily because of a reduction in maximal cardiac output (Q(max)). This age-associated decline in Vo(2max) may be partially mediated by the development of oxidative stress that can suppress beta-adrenergic-receptor responsiveness and, consequently, reduce Q(max). To test this hypothesis, Vo(2max) (indirect calorimetry) and Q(max) (open-circuit acetylene breathing) were determined in 12 young (23 +/- 1 yr, mean +/- SE) and 10 older (61 +/- 1 yr) adults following systemic infusion of either saline (control) and/or the powerful antioxidant ascorbic acid (acute: bolus 0.06; drip 0.02 g/kg fat-free mass) and following chronic 30-day oral administration of ascorbic acid (500 mg/day). Plasma ascorbic acid concentration was not different between young and older adults and was increased similarly, independent of age [change (Delta) acute = 1,055 +/- 117%; Delta chronic = 62 +/- 19%]. Oxidized low-density lipoprotein concentration was greater (P < 0.001) in older (57 +/- 5 U/l) compared with young (34 +/- 3 U/l) adults and was reduced in both groups (P < 0.02) following acute (Delta = -6 +/- 2%) but not chronic (P = 0.18) ascorbic acid administration. Control (baseline) Vo(2max) and Q(max) were positively related (r = 0.76, P < 0.001) and were lower (P < 0.05) in older (34 +/- 2 ml.kg(-1).min(-1); 16.1 +/- 1.1 l/min) compared with young (43 +/- 3 ml.kg(-1).min(-1); 20.2 +/- 0.9 l/min) adults. Following ascorbic acid administration, neither Vo(2max) (young acute = 41 +/- 2; young chronic = 42 +/- 2; older acute = 34 +/- 2; older chronic = 34 +/- 2 ml.kg(-1).min(-1)) nor Q(max) (young acute = 20.1 +/- 0.9; young chronic = 19.1 +/- 0.8; older acute = 16.2 +/- 1.1; older chronic = 16.6 +/- 1.4 l/min) was changed. These data suggest that ascorbic acid administration does not affect the age-associated reduction in Q(max) and Vo(2max).     

The accuracy of the American College of Sports Medicine metabolic equation for walking at altitude and higher-grade conditions

The purpose of this study was to examine the accuracy of the American College of Sports Medicine (ACSM) walking equation at low walking speeds, altitude (1,550 m), and higher grades. Twenty men and women (mean +/- SD, age, 28 +/- 6 years; height, 171 +/- 13 cm; weight, 67.8 +/- 18.1 kg) completed 2 randomized testing sessions under altitude (AL) (P(I)o(2) = 123.1 mm Hg [20.93%]) and sea level control (SLC) (P(I)o(2) = 147.3 mm Hg [25.00%]) conditions. Steady-state oxygen uptake (Vo(2)) was measured while subjects walked at 50 m.min(-1) at 8 separate grades (0, 5, 10, 15, 18, 21, 24, and 27%). Steady-state Vo(2) measurements from the last 2 minutes of each grade in AL and SLC were compared to the predicted Vo(2) of each grade according to the ACSM walking equation. Mean Vo(2) differences between predicted and AL values ranged from -0.5 to 1.4 ml.kg(-1).min(-1), averaged -0.1 ml.kg(-1).min(-1) across all grades, and were significant (p < 0.05) at 0 percent grade. Mean Vo(2) differences between predicted and SLC values ranged from 0.6 to 3.0 ml.kg(-1).min(-1), averaged 1.4 ml.kg(-1).min(-1) across all grades, and were statistically significant (p < 0.05) at 0 and 5 percent. The standard error of the estimate (SEE) for the prediction of Vo(2) under AL and SLC were 2.2 and 2.0 ml.kg(-1).min(-1), respectively. Total errors for the prediction of Vo(2)max under AL and SLC were 2.3 and 2.6 ml.kg(-1).min(-1), respectively. Overall, the findings indicate that the current ACSM prediction equation for walking is appropriate for application at low speeds, moderate altitude, and higher grades.     

Exercise hyperventilation, dyspnea sensation, and ergoreflex activation in lone atrial fibrillation

Lone atrial fibrillation may be associated with daily life disability and exercise limitation. The extracardiac pathophysiology of these effects is poorly explored. In 35 subjects with lone atrial fibrillation (mean age 67 +/- 7 yr), we investigated pulmonary function, symptom-limited cardiopulmonary exercise performance, muscle ergoreflex (handgrip exercise) contribution to ventilation, and brachial artery flow-mediated dilation (as a measure of endothelial function) before and after (average interval 20 +/- 5 days) restoring sinus rhythm with external cardioversion. Respiratory volumes and lung diffusing capacity at rest were within normal limits during both atrial fibrillation and after restoring sinus rhythm. Cardioversion was associated with the following changes: a decrease of the slope of exercise ventilation vs. CO2 production (from 35 +/- 5 to 29 +/- 3; P <0.01) and of dyspnea sensation (Borg score from 4 to 2) and an increase of peak oxygen uptake (Vo2; from 16 +/- 4 to 20 +/- 5 ml.min(-1).kg(-1); P <0.01), Vo2 at anaerobic threshold (from 11 +/- 2 to 13 +/- 2 ml.min(-1).kg(-1); P <0.05), and O2 pulse (from 8 +/- 3 to 11 +/- 3 ml/beat; P <0.01). After cardioversion, the observed improvement in ventilatory efficiency was accompanied by a significant peak end-tidal CO2 increase (from 33 +/- 2 to 37 +/- 2 mmHg; P <0.01) and no changes in dead space-to-tidal volume ratio (from 0.23 +/- 0.03 to 0.23 +/- 0.02; P=not significant). In addition, the ergoreflex contribution to ventilation was remarkably attenuated, and the brachial artery flow-mediated dilatation was significantly augmented (from 0.32 +/- 0.07 to 0.42 +/- 0.08 mm; P <0.01). Ten patients had atrial fibrillation relapse and, compared with values after restoration of regular sinus rhythm, invariably showed worsening of endothelial function, exercise ventilatory efficiency, and muscle ergoreflex contribution to ventilation. In subjects with lone atrial fibrillation, an impairment in ventilatory efficiency appears to be involved in the pathophysiology of exercise limitation, and to be primarily related with a demodulated peripheral control of ventilation.     

Three weeks of caloric restriction alters protein metabolism in normal-weight, young men

The effects of prolonged caloric restriction (CR) on protein kinetics in lean subjects has not been investigated previously. The purpose of this study was to test the hypotheses that 21 days of CR in lean subjects would 1) result in significant losses of lean mass despite a suppression in leucine turnover and oxidation and 2) negatively impact exercise performance. Nine young, normal-weight men [23 +/- 5 y, 78.6 +/- 5.7 kg, peak oxygen consumption (Vo2 peak) 45.2 +/- 7.3 ml.kg(-1).min(-1), mean +/- SD] were underfed by 40% of the calories required to maintain body weight for 21 days and lost 3.8 +/- 0.3 kg body wt and 2.0 +/- 0.4 kg lean mass. Protein intake was kept at 1.2 g.kg(-1).day(-1). Leucine kinetics were measured using alpha-ketoisocaproic acid reciprocal pool model in the postabsorptive state during rest and 50 min of exercise (EX) at 50% of Vo2 peak). Body composition, basal metabolic rate (BMR), and exercise performance were measured throughout the intervention. At rest, leucine flux (approximately 131 micromol.kg(-1).h(-1)) and oxidation (R(ox); approximately 19 micromol.kg(-1).h(-1)) did not differ pre- and post-CR. During EX, leucine flux (129 +/- 6 vs. 121 +/- 6) and R(ox) (54 +/- 6 vs. 46 +/- 8) were lower after CR than they were pre-CR. Nitrogen balance was negative throughout the intervention ( approximately 3.0 g N/day), and BMR declined from 1,898 +/- 262 to 1,670 +/- 203 kcal/day. Aerobic performance (Vo2 peak, endurance cycling) was not impacted by CR, but arm flexion endurance decreased by 20%. In conclusion, 3 wk of caloric restriction reduced leucine flux and R(ox) during exercise in normal-weight young men. However, despite negative nitrogen balance and loss of lean mass, whole body exercise performance was well maintained in response to CR.     

Six sessions of sprint interval training increases muscle oxidative potential and cycle endurance capacity in humans.

Parra et al. (Acta Physiol. Scand 169: 157-165, 2000) showed that 2 wk of daily sprint interval training (SIT) increased citrate synthase (CS) maximal activity but did not change "anaerobic" work capacity, possibly because of chronic fatigue induced by daily training. The effect of fewer SIT sessions on muscle oxidative potential is unknown, and aside from changes in peak oxygen uptake (Vo(2 peak)), no study has examined the effect of SIT on "aerobic" exercise capacity. We tested the hypothesis that six sessions of SIT, performed over 2 wk with 1-2 days rest between sessions to promote recovery, would increase CS maximal activity and endurance capacity during cycling at approximately 80% Vo(2 peak). Eight recreationally active subjects [age = 22 +/- 1 yr; Vo(2 peak) = 45 +/- 3 ml.kg(-1).min(-1) (mean +/- SE)] were studied before and 3 days after SIT. Each training session consisted of four to seven "all-out" 30-s Wingate tests with 4 min of recovery. After SIT, CS maximal activity increased by 38% (5.5 +/- 1.0 vs. 4.0 +/- 0.7 mmol.kg protein(-1).h(-1)) and resting muscle glycogen content increased by 26% (614 +/- 39 vs. 489 +/- 57 mmol/kg dry wt) (both P < 0.05). Most strikingly, cycle endurance capacity increased by 100% after SIT (51 +/- 11 vs. 26 +/- 5 min; P < 0.05), despite no change in Vo(2 peak). The coefficient of variation for the cycle test was 12.0%, and a control group (n = 8) showed no change in performance when tested approximately 2 wk apart without SIT. We conclude that short sprint interval training (approximately 15 min of intense exercise over 2 wk) increased muscle oxidative potential and doubled endurance capacity during intense aerobic cycling in recreationally active individuals.     

A single bout of exercise influences natural killer cells in elderly women, especially those who are habitually active

The purpose of our study was to examine the effects of a single exercise bout on the natural killer (NK) cell count and activity in physically active elderly people, sedentary elderly people, and sedentary young people. Eight elderly women who trained by walking (age, 64 +/- 1 years; Vo(2peak), 32.2 +/- 1.1 ml.kg(-1).min(-1)), 8 age-matched untrained women (63 +/- 1 years, 28.8 +/- 1.0 ml.kg(-1).min(-1)), and 8 young untrained women (25 +/- 1 years, 37.6 +/- 1.6 ml.kg(-1).min(-1)) were studied. Blood samples were taken before, immediately after, and 2 hours after a 30-minute bout of exercise at an intensity equivalent to 70-75% of Vo(2peak). Peripheral blood mononuclear cells were isolated and the NK cell count and activity were analyzed. The NK cell count of the elderly sedentary group immediately after exercise was significantly higher than those of the elderly women who walked and young sedentary women, whereas no significant interaction was detected in NK cell activity and NK cell activity per cell number among the 3 groups. Consequently, an intrinsic defect in the cytotoxic ability of NK cells appeared in sedentary elderly people but not in active elderly people who perform habitual exercise.     

Human lung density is not altered following normoxic and hypoxic moderate-intensity exercise: implications for transient edema.

The purpose of this study was to examine the effects of exercise on extravascular lung water as it may relate to pulmonary gas exchange. Ten male humans underwent measures of maximal oxygen uptake (Vo2 max) in two conditions: normoxia (N) and normobaric hypoxia of 15% O2 (H). Lung density was measured by quantified MRI before and 48.0 +/- 7.4 and 100.7 +/- 15.1 min following 60 min of cycling exercise in N (intensity = 61.6 +/- 9.5% Vo2 max) and 55.5 +/- 9.8 and 104.3 +/- 9.1 min following 60 min cycling exercise in H (intensity = 65.4 +/- 7.1% hypoxic Vo2 max), where Vo2 max = 65.0 +/- 7.5 ml x kg(-1) x min(-1) (N) and 54.1 +/- 7.0 ml x kg(-1) x min(-1) (H). Two subjects demonstrated mild exercise-induced arterial hypoxemia (EIAH) [minimum arterial oxygen saturation (SaO2 min) = 94.5% and 93.8%], and seven subjects demonstrated moderate EIAH (SaO2 min = 91.4 +/- 1.1%) as measured noninvasively during the Vo2 max test in N. Mean lung densities, measured once preexercise and twice postexercise, were 0.177 +/- 0.019, 0.181 +/- 0.019, and 0.173 +/- 0.019 g/ml (N) and 0.178 +/- 0.021, 0.174 +/- 0.022, and 0.176 +/- 0.019 g/ml (H), respectively. No significant differences (P > 0.05) were found in lung density following exercise in either condition or between conditions. Transient interstitial pulmonary edema did not occur following sustained steady-state cycling exercise in N or H, indicating that transient edema does not result from pulmonary capillary leakage during sustained submaximal exercise.     

Is running performance enhanced with creatine serum ingestion?

Runners Advantage (RA) creatine (Cr) serum has been marketed to increase running performance. To test this claim, cross-country runners completed baseline testing (BASE), an outdoor 5,000-m run followed by treadmill Vo(2)max testing on the same day. Subjects repeated testing after ingesting 5 ml of RA (n = 13) containing 2.5 g of Cr or placebo (n = 11). Heart rate (HR), rating of perceived exertion (RPE), and run time were recorded. With RA (56.48 +/- 8.93 ml.kg(-1.)min(-1)), Vo(2)max was higher (p = 0.01) vs. BASE (54.07 +/- 9.36 ml.kg(-1.)min(-1)), yet the magnitude of the increase was within the coefficient of variation of Vo(2)max. No effect of RA on maximal HR was exhibited, yet Vco(2)max and duration of incremental exercise were significantly higher (p < 0.025) vs. BASE. Vo(2)max was similar in PL (58.85 +/- 6.67 ml.kg(-1).min(-1)) and BASE (57.28 +/- 7.22 ml.kg(-1.)min(-1)). With RA, the 5,000-m time was unchanged, and RPE was lower (p < 0.025) vs. BASE. These data do not support the ergogenic claims of RA in its current form and dose.     

The relationship of the heart rate deflection point to the ventilatory threshold in trained cyclists

The purpose of this study was to assess the relationship of the heart rate deflection point (HRDP) to the ventilatory threshold (VT) in trained cyclists. Twenty-one endurance-trained cyclists (mean +/- SD: Vo(2)max = 67.6 +/- 4.7 ml x kg x min(-1)) completed a maximal cycle ergometer test of volitional fatigue using a ramped protocol. Ventilatory variables (Ve, Vo(2), Vco(2)) and power were measured online with averages reported every 20 seconds. Heart rate (HR) was recorded every 20 seconds using a Polar monitor. VT was calculated using the excess CO(2) elimination curve. The first derivative of a logistic growth curve fit to the HR-power data produced the HRDP. No significant differences (p > 0.01) existed between HR values at HRDP (171.7 +/- 9.6 b x min(-1)) and VT (169.8 +/- 9.9 b x min(-1)) or between Vo(2) values at HRDP (53.6 +/- 4.2 ml x kg x min(-1)) and VT (52.2 +/- 4.8 ml x kg x min(-1)). But power values at HRDP (318.7 +/- 30.7 W) were significantly different (p < 0.01) from those at VT (334.8 +/- 36.7 W). There were significant relationships between HRDP and VT for the physiological variables of HR (r = 0.92, p < 0.001), Vo(2) (r = 0.72, p < 0.001), and power (r = 0.77, p < 0.001). These findings indicate that HR and Vo(2) at HRDP are not significantly different from the values at VT in trained cyclists. HR values derived from HRDP may be used to set parameters for training intensity. Variability in the speed/power-HRDP relationship across detrained/trained states may be used to evaluate training programs.     

Heart rate deflection point as a strategy to defend stroke volume during incremental exercise.

The purpose of this study was to examine whether the heart rate (HR) deflection point (HRDP) in the HR-power relationship is concomitant with the maximal stroke volume (SV(max)) value achievement in endurance-trained subjects. Twenty-two international male cyclists (30.3 +/- 7.3 yr, 179.7 +/- 7.2 cm, 71.3 +/- 5.5 kg) undertook a graded cycling exercise (50 W every 3 min) in the upright position. Thoracic impedance was used to measure continuously the HR and stroke volume (SV) values. The HRDP was estimated by the third-order curvilinear regression method. As a result, 72.7% of the subjects (HRDP group, n = 16) presented a break point in their HR-work rate curve at 89.9 +/- 2.8% of their maximal HR value. The SV value increased until 78.0 +/- 9.3% of the power associated with maximal O(2) uptake (Vo(2 max)) in the HRDP group, whereas it increased until 94.4 +/- 8.6% of the power associated with Vo(2 max) in six other subjects (no-HRDP group, P = 0.004). Neither SV(max) (ml/beat or ml.beat(-1).m(-2)) nor Vo(2 max) (ml/min or ml.kg(-1).min(-1)) were different between both groups. However, SV significantly decreased before exhaustion in the HRDP group (153 +/- 44 vs. 144 +/- 40 ml/beat, P = 0.005). In the HRDP group, 62% of the variance in the power associated with the SV(max) could also be predicted by the power output at which HRDP appeared. In conclusion, in well-trained subjects, the power associated with the SV(max)-HRDP relationship supposed that the HR deflection coincided with the optimal cardiac work for which SV(max) was attained.     

Effects of progressive exercise and hypoxia on human muscle sarcoplasmic reticulum function.

This study examined the effects of progressive exercise to fatigue in normoxia (N) on muscle sarcoplasmic reticulum (SR) Ca(2+) cycling and whether alterations in SR Ca(2+) cycling are related to the blunted peak mechanical power output (PO(peak)) and peak oxygen consumption (Vo(2 peak)) observed during progressive exercise in hypoxia (H). Nine untrained men (20.7 +/- 0.42 yr) performed progressive cycle exercise to fatigue on two occasions, namely during N (inspired oxygen fraction = 0.21) and during H (inspired oxygen fraction = 0.14). Tissue extracted from the vastus lateralis before exercise and at power output corresponding to 50 and 70% of Vo(2 peak) (as determined during N) and at fatigue was used to investigate changes in homogenate SR Ca(2+)-cycling properties. Exercise in H compared with N resulted in a 19 and 21% lower (P < 0.05) PO(peak) and Vo(2 peak), respectively. During progressive exercise in N, Ca(2+)-ATPase kinetics, as determined by maximal activity, the Hill coefficient, and the Ca(2+) concentration at one-half maximal activity were not altered. However, reductions with exercise in N were noted in Ca(2+) uptake (before exercise = 357 +/- 29 micromol x min(-1) x g protein(-1); at fatigue = 306 +/- 26 micromol x min(-1) x g protein(-1); P < 0.05) when measured at free Ca(2+) concentration of 2 microM and in phase 2 Ca(2+) release (before exercise = 716 +/- 33 micromol x min(-1) x g protein(-1); at fatigue = 500 +/- 53 micromol x min(-1) x g protein(-1); P < 0.05) when measured in vitro in whole muscle homogenates. No differences were noted between N and H conditions at comparable power output or at fatigue. It is concluded that, although structural changes in SR Ca(2+)-cycling proteins may explain fatigue during progressive exercise in N, they cannot explain the lower PO(peak) and Vo(2 peak) observed during H.     

Physical fitness profile of Army ROTC cadets

One role of Army Reserved Officer's Training Corps (ROTC) programs is to physically prepare cadets for the demands of a military career. Cadets participate in physical training 3 days per week as part of their military science curriculum. Limited research has been conducted on the fitness level of ROTC cadets; therefore, the purpose of this study was to profile the physical fitness status of a cadre of ROTC cadets. Forty-three cadets (30 men and 13 women) performed Army Physical Fitness Test (APFT) assessments (2-mile run, 2-minute maximum push-ups and sit-ups) and clinical assessments of fitness (Bruce protocol Vo(2)max, underwater weighing, and 1 repetition maximum [1RM] bench press tests). Mean +/- standard deviations were calculated to provide the physical fitness profile for each parameter. Male cadets (21 +/- 2.2 years; height 177.4 +/- 6.6 cm; mass 79.2 +/- 9.4 kg) scored 49.6 +/- 6.1 ml.kg(-1).min(-1) for Vo(2)max, 14.8 +/- 4.2% fat, 86.5 +/- 24.9 kg 1RM bench press, 2-mile run of 13.97 +/- 1.4 minutes, 70.5 +/- 12.8 sit-ups, and 60.2 +/- 13.2 push-ups. Female cadets (20 +/- 2.4 years; height 165.1 +/- 8.0 cm; mass 63.5 +/- 10.0 kg) scored 40.8 +/- 3.9 ml.kg(-1).min(-1) for Vo(2) max, 23.9 +/- 3.8% fat, 35.3 +/- 8.2 kg 1RM bench press, 2-mile run of 17.0 +/- 1.6 minutes, 65.0 +/- 12.9 sit-ups, and 33.3 +/- 11.2 push-ups. The mean scores were above the 83rd percentile on all APFT items and average (percent fat) to above average (Vo(2)max and men's bench press scores) when compared with peer-age and sex-corrected norms. Only the women's bench press score was below average. With the exception of the women's bench press, these ROTC cadets possessed average to above average levels of fitness.     

A new non-exercise-based Vo2max prediction equation for aerobically trained men

The purposes of the present study were to (a) modify previously published Vo(2)max equations using the constant error (CE = mean difference between actual and predicted Vo(2)max) values from Malek et al. (28); (b) cross-validate the modified equations to determine their accuracy for estimating Vo(2)max in aerobically trained men; (c) derive a new non- exercise-based equation for estimating Vo(2)max in aerobically trained men if the modified equations are not found to be accurate; and (d) cross-validate the new Vo(2)max equation using the predicted residual sum of squares (PRESS) statistic and an independent sample of aerobically trained men. One hundred and fifty-two aerobically trained men (Vo(2)max mean +/- SD = 4,154 +/- 629 ml.min(-1)) performed a maximal incremental test on a cycle ergometer to determine actual Vo(2)max. An aerobically trained man was defined as someone who had participated in continuous aerobic exercise 3 or more sessions per week for a minimum of 1 hour per session for at least the past 18 months. Nine previously published Vo(2)max equations were modified for use with aerobically trained men. The predicted Vo(2)max values from the 9 modified equations were compared to actual Vo(2)max by examining the CE, standard error of estimate (SEE), validity coefficient (r), and total error (TE). Cross-validation of the modified non-exercise-based equations on a random subsample of 50 subjects resulted in a %TE > or = 13% of the mean of actual Vo(2)max. Therefore, the following non-exercise-based Vo(2)max equation was derived from a random subsample of 112 subjects: Vo(2)max (ml.min(-1)) = 27.387(weight in kg) + 26.634(height in cm) - 27.572(age in years) + 26.161(h.wk(-1) of training) + 114.904(intensity of training using the Borg 6-20 scale) + 506.752(natural log of years of training) - 4,609.791 (R = 0.82, R(2) adjusted = 0.65, and SEE = 378 ml.min(-1)). Cross-validation of this equation on the remaining sample of 40 subjects resulted in a %TE of 10%. Therefore, the non-exercise-based equation derived in the present study is recommended for estimating Vo(2)max in aerobically trained men.     

Effects of rate of decrease in power output in decrement-load exercise on oxygen uptake

The purpose of this study was to examine how oxygen uptake (Vo2) in decrement-load exercise (DLE) is affected by changing rate of decrease in power output. DLE was performed at three different rates of decrease in power output (10, 20 and 30 watts.min(-1): DLE10, DLE20 and DLE30, respectively) from power output corresponding to 90 % of peak Vo2. Vo2 exponentially increased and then decreased, and the rate of its decrease was reduced at low power output. The values of Vo2 in the three DLE tests were not different for the first 2 min despite the difference in power output. The relationship between Vo2 and power output below 50 watts was obtained as a slope to estimate excessive Vo2 (ex-Vo2) above 50 watts. The slopes were 10.0+/-0.9 for DLE10, 9.9+/-0.7 for DLE20 and 10.2+/-1.0 ml.min(-1).watt(-1) for DLE30. The difference between Vo2 estimated from the slope and measured Vo2 was defined as ex-Vo2. The peak value of ex-Vo2 for DLE10 (189+/-116 ml.min(-1)) was significantly greater than those for DLE20 and for DLE30 (93+/-97 and 88+/-34 ml.min(-1)). The difference between Vo2 in DLE and that in incremental-load exercise (ILE) below 50 watts (DeltaVo2) was greater in DLE30 and smallest in DLE10. There were significant differences in DeltaVo2 among the three DLE tests. The values of DeltaVo2 at 30 watts were 283+/-152 for DLE10, 413+/-136 for DLE20 and 483+/-187 ml.min(-1) for DLE30. Thus, a faster rate of decrease in power output resulted in no change of Vo2 at the onset of DLE, smaller ex-Vo2 and greater DeltaVo2. These results suggest that Vo2 is disposed in parallel in each motor unit released from power output or recruited in DLE.     

Effect of pedal rate on primary and slow-component oxygen uptake responses during heavy-cycle exercise.

We hypothesized that a higher pedal rate (assumed to result in a greater proportional contribution of type II motor units) would be associated with an increased amplitude of the O(2) uptake (Vo(2)) slow component during heavy-cycle exercise. Ten subjects (mean +/- SD, age 26 +/- 4 yr, body mass 71.5 +/- 7.9 kg) completed a series of square-wave transitions to heavy exercise at pedal rates of 35, 75, and 115 rpm. The exercise power output was set at 50% of the difference between the pedal rate-specific ventilatory threshold and peak Vo(2), and the baseline power output was adjusted to account for differences in the O(2) cost of unloaded pedaling. The gain of the Vo(2) primary component was significantly higher at 35 rpm compared with 75 and 115 rpm (mean +/- SE, 10.6 +/- 0.3, 9.5 +/- 0.2, and 8.9 +/- 0.4 ml. min(-1). W(-1), respectively; P < 0.05). The amplitude of the Vo(2) slow component was significantly greater at 115 rpm (328 +/- 29 ml/min) compared with 35 rpm (109 +/- 30 ml/min) and 75 rpm (202 +/- 38 ml/min) (P < 0.05). There were no significant differences in the time constants or time delays associated with the primary and slow components across the pedal rates. The change in blood lactate concentration was significantly greater at 115 rpm (3.7 +/- 0.2 mM) and 75 rpm (2.8 +/- 0.3 mM) compared with 35 rpm (1.7 +/- 0.4 mM) (P < 0.05). These data indicate that pedal rate influences Vo(2) kinetics during heavy exercise at the same relative intensity, presumably by altering motor unit recruitment patterns.     

Release of luteinizing hormone and growth hormone after recovery from maximal exercise

Pulsatile properties of luteinizing hormone (LH) and growth hormone (GH) release were evaluated in 19 eumenorrheic untrained females [mean age 31.1 +/- 1.1 yr, height 165.2 +/- 1.4 cm, weight 64.8 +/- 2.1 kg, peak oxygen uptake (Vo2) 41.6 +/- 1.4 (SE) ml.kg-1.min-1] during the early follicular phase of the menstrual cycle (days 3-4 after the onset of menses). Each subject was studied during two consecutive menstrual cycles under each of two conditions in random order: 1) no formal exercise for 72 h (C) and 2) 12-24 h after two maximal exercise bouts (peak Vo2/lactate threshold treadmill evaluation and a 3,200-m time-trial run or a maximal Vo2 inclined treadmill test) performed on consecutive days (EX). Blood sampling was performed every 10 min for 12 h. LH and GH pulsatile parameters were identified and characterized by the Cluster pulse detection algorithm. No significant differences were noted in the number of peaks, peak amplitude, interpeak interval, peak increment, or 12-h integrated concentrations between C and EX for LH or GH. We conclude that maximal exercise protocols typically used for exercise evaluation do not have an effect on the pulsatile characteristics of LH or GH release in untrained women during the early follicular phase of the menstrual cycle if 12-24 h of recovery are allowed before evaluation of the pulsatile secretion of gonadotropins or GH.     

Metabolism and thermoregulation during fasting in king penguins, Aptenodytes patagonicus, in air and water

We measured oxygen consumption rate (Vo(2)) and body temperatures in 10 king penguins in air and water. Vo(2) was measured during rest and at submaximal and maximal exercise before (fed) and after (fasted) an average fasting duration of 14.4 +/- 2.3 days (mean +/- 1 SD, range 10-19 days) in air and water. Concurrently, we measured subcutaneous temperature and temperature of the upper (heart and liver), middle (stomach) and lower (intestine) abdomen. The mean body mass (M(b)) was 13.8 +/- 1.2 kg in fed and 11.0 +/- 0.6 kg in fasted birds. After fasting, resting Vo(2) was 93% higher in water than in air (air: 86.9 +/- 8.8 ml/min; water: 167.3 +/- 36.7 ml/min, P < 0.01), while there was no difference in resting Vo(2) between air and water in fed animals (air: 117.1 +/- 20.0 ml O(2)/min; water: 114.8 +/- 32.7 ml O(2)/min, P > 0.6). In air, Vo(2) decreased with M(b), while it increased with M(b) in water. Body temperature did not change with fasting in air, whereas in water, there were complex changes in the peripheral body temperatures. These latter changes may, therefore, be indicative of a loss in body insulation and of variations in peripheral perfusion. Four animals were given a single meal after fasting and the temperature changes were partly reversed 24 h after refeeding in all body regions except the subcutaneous, indicating a rapid reversal to a prefasting state where body heat loss is minimal. The data emphasize the importance in considering nutritional status when studying king penguins and that the fasting-related physiological changes diverge in air and water.     

Lung density is not altered following intense normobaric hypoxic interval training in competitive female cyclists.

Noninvasive imaging techniques have been used to assess pulmonary edema following exercise but results remain equivocal. Most studies examining this phenomenon have used male subjects while the female response has received little attention. Some suggest that women, by virtue of their smaller lungs, airways, and diffusion surface areas may be more susceptible to pulmonary limitations during exercise. Accordingly, the purpose of this study was to determine if intense normobaric hypoxic exercise could induce pulmonary edema in women. Baseline lung density was obtained in eight highly trained female cyclists (mean +/- SD: age = 26 +/- 7 yr; height = 172.2 +/- 6.7 cm; mass = 64.1 +/- 6.7 kg; Vo(2max) = 52.2 +/- 2.2 ml.kg(-1).min(-1)) using computed tomography (CT). CT scans were obtained at the level of the aortic arch, the tracheal carina, and the superior end plate of the tenth thoracic vertebra. While breathing 15% O(2), subjects then performed five 2.5-km cycling intervals [mean power = 212 +/- 31 W; heart rate (HR) = 94.5 +/- 2.2%HRmax] separated by 5 min of recovery. Throughout the intervals, subjects desaturated to 82 +/- 4%, which was 13 +/- 2% below resting hypoxic levels. Scans were repeated 44 +/- 8 min following exercise. Mean lung density did not change from pre (0.138 +/- 0.014 g/ml)- to postexercise (0.137 +/- 0.011 g/ml). These findings suggest that pulmonary edema does not occur in highly trained females following intense normobaric hypoxic exercise.     

Splenic denervation worsens lipopolysaccharide-induced hypotension, hemoconcentration, and hypovolemia

During lipopolysaccharide (LPS)-induced endotoxemia, increased intrasplenic fluid efflux contributes to a reduction in plasma volume. We hypothesized that splenic sympathetic nerve activity (SSNA), which increases during endotoxemia, limits intrasplenic fluid efflux. We reasoned that splenic denervation would exaggerate LPS-induced intrasplenic fluid efflux and worsen the hypotension, hemoconcentration, and hypovolemia. A nonlethal dose of LPS (150 microg x kg(-1) x h(-1) for 18 h) was infused into conscious male rats bearing transit time flow probes on the splenic artery and vein. Fluid efflux was estimated from the difference in splenic arterial inflow and venous outflow (A-V). LPS significantly increased the (A-V) flow differential (fluid efflux) in intact rats (saline -0.01 +/- 0.02 ml/min, n = 8 vs. LPS +0.21 +/- 0.06 ml/min, n = 8); this was exaggerated in splenic denervated rats (saline -0.03 +/- 0.01 ml/min, n = 7 vs. LPS +0.41 +/- 0.08 ml/min, n = 8). Splenic denervation also exacerbated the LPS-induced hypotension, hemoconcentration, and hypovolemia (peak fall in mean arterial pressure: denervated 19 +/- 3 mmHg, n = 10 vs. intact 12 +/- 1 mmHg, n = 8; peak rise in hematocrit: denervated 6.7 +/- 0.3%, n = 8 vs. intact 5.0 +/- 0.3%, n = 8; decrease in plasma volume at 90-min post-LPS infusion: denervated 1.08 +/- 0.15 ml/100 g body wt, n = 7 vs. intact 0.54 +/- 0.08 ml/100 g body wt, n = 8). The exaggerated LPS-induced hypovolemia associated with splenic denervation was mirrored in the rise in plasma renin activity (90 min post-LPS: denervated 11.5 +/- 0.8 ng x ml(-1) x h(-1), n = 9 vs. intact 6.6 +/- 0.7 ng x ml(-1) x h(-1), n = 8). These results are consistent with our proposal that SSNA normally limits LPS-induced intrasplenic fluid efflux.