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).     

Leukocyte, lymphocyte and platelet response to dynamic exercise. Duration or intensity effect?

The influence of work intensity and duration on the white blood cell (WBC), lymphocyte (L) and platelet (P) count response to exercise was studied in 16 trained subjects (22 +/- 5.4 years, means +/- SD). They performed three cyclo-ergospirometric protocols: A) 10 min at 150 W followed by a progressive test (30 W/3 min) till exhaustion; B) constant maximal work (VO2max); C) a 45 min Square-Wave Endurance Exercise Test (SWEET), (n = 5). Arterial blood samples were taken: at rest, submaximal and maximal exercise in A; maximal exercise in B; 15th, 30th and 45th min in the SWEET. Lactate, [H+], PaCO2, PaO2, [Hct], Hb, cortisol, ACTH, total platelet volume (TPV), total blood red cell (RBC), WBC, L and P were measured. At 150 W, WBC, L, P, and TPV increased. VO2max did not differ between A and B, but a difference was found in total exercise time (A = 25 +/- 3 min; B = 7 +/- 2 min, p less than 0.001). In A, at VO2max, the increase was very small for Hct, [Hb], and RBC (10%), in contrast with large changes for WBC (+93%), L (+137%), P (+32%), TPV (+35%), [H+] (+39%), lactate (+715%), and ACTH (+95%). At VO2max there were no differences in these variables between A and B. During the SWEET: WBC, L, P, TPV and ACTH increased at the 15th min as much as in VO2max, but no difference was observed between the 15th, 30th and 45th min, except for ACTH which continued to rise; the lactate increase during the SWEET was about half (+341%) the value observed at VO2max, and [H+] did not vary with respect to values at rest.(ABSTRACT TRUNCATED AT 250 WORDS)     

Phospholipid transfer protein activity is associated with inflammatory markers in patients with cardiovascular disease

Plasma phospholipid lipid transfer protein (PLTP) has several known key functions in lipoprotein metabolism. Recent studies suggest that it also may play a role in the inflammatory response. Inflammatory cell activity contributes to the development of atherosclerosis. To seek further evidence for the association of PLTP with inflammation, we studied the relationship between PLTP activity and five inflammatory markers [C-reactive protein (CRP), serum amyloid A (SAA), interleukin 6 (IL-6), white blood cells (WBC), and fibrinogen] in 93 patients with low HDL and cardiovascular disease (CVD). Plasma PLTP activity had the strongest correlation with CRP (r=0.332, P<0.001) followed by SAA (r=0.239, P=0.021). PLTP, CRP, and SAA were significantly associated with body mass index (BMI), insulin or glucose, apolipoprotein (apo) B, and/or apo E level (r=0.264-0.393, P<0.01). PLTP, SAA, and IL-6 also were associated with the concentration of HDL particles without apo A-II [Lp(A-I)](r=0.373-0.472, P<0.005, n=56), but not particles with apo A-II. Smoking was associated with increased PLTP activity, CRP, and WBC, and hypertension with increased PLTP activity. In linear models, CRP remained significantly associated with PLTP after adjustment of CVD risk factors and insulin resistance. Also, much of the variability of plasma PLTP activity was explained by CRP, BMI, Lp(A-I), smoking, glucose, and blood pressure. These findings show for the first time that plasma PLTP activity is associated positively with CRP in CVD, a state of chronic inflammation.     

No effect of short-term 17beta-estradiol supplementation in healthy men on systemic inflammatory responses to exercise

Sex-based differences in inflammatory responses to exercise may be mediated by estrogen through increased muscle membrane stability and/or inhibited cytokine production. In this study, in vivo effects of estrogen on systemic inflammation-related responses to exercise were assessed in healthy men. In a double-blind, placebo-controlled, crossover design, 11 men cycled for 90 min at 65% Vo2 max after 8 days of 17beta-estradiol supplementation (ES; 2 mg/day) or placebo (PL; glucose polymer). After a 2-wk washout, exercise was repeated after 8 days on the alternate treatment. Blood was collected pre- and postexercise to determine IL-6, soluble intercellular adhesion molecule-1 (sICAM-1), neutrophil counts, and cortisol. Preexercise serum was assayed for sex hormones. ES increased estradiol (133+/-71 to 840+/-633 pmol/l, P=0.005) and reduced testosterone (19.9+/-3.7 to 16.1+/-3.9 nmol/l, P=0.007). Exercise increased cortisol (P=0.02), IL-6 (P<0.001) and neutrophil counts (P<0.001) with no influence on sICAM-1 (P=0.34) and no effect of ES on these changes. Postexercise IL-6 and neutrophil counts were correlated (r=0.58, P=0.005); postexercise IL-6 and cortisol (r=0.18, P=0.43) and postexercise cortisol and neutrophil counts (r=0.06, P=0.78) were not. Postexercise sICAM-1 was not correlated with the above variables (P>or=0.79). In conclusion, 8 days of ES in healthy men did not influence systemic inflammation-related responses to acute exercise. Future studies should investigate 17beta-estradiol effects on IL-6 production and neutrophil infiltration within skeletal muscle during and after exercise.     

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.     

Predictors of sweat loss in man during prolonged exercise

Nineteen healthy male subjects, differing in training status and Vo2max (52 +/- 1 ml.min-1.kg-1, mean +/- SEM; 43-64 ml.min-1.kg-1, range), exercised for 1 h at an absolute workload of 192 +/- 8 W (140-265 W); this was equivalent to 70 +/- 1% Vo2max (66-74%). Each exercise test was performed on an electrically braked cycle ergometer at a constant ambient temperature (22.5 +/- 0.0 degrees C) and relative humidity (85 +/- 0%). Nude body weight was recorded prior to and after each exercise test. Absolute sweat loss (body weight loss corrected for respiratory weight loss) during each test was 910 +/- 82 g (426-1665 g); this was equivalent to 1.3 +/- 0.1% (0.7-2.2%) of pre-exercise body weight (relative sweat loss). Weighted mean skin temperature and rectal temperature increased after 5 min of exercise from 30.5 +/- 0.3 degrees C and 37.2 +/- 0.1 degrees C respectively to 32.5 +/- 0.2 degrees C and 38.8 +/- 0.1 degrees C respectively, recorded immediately prior to the end of exercise. Bivariate linear regression and Pearson's correlation demonstrated absolute sweat loss was related to Vo2max (r = 0.72, p less than 0.001), absolute exercise workload (r = 0.66, p less than 0.01), body surface area (r = 0.62, p less than 0.01), weight (r = 0.60, p less than 0.01) and height (r = 0.53, p less than 0.05). Relative sweat loss was related to VO2max (r = 0.77, P less than 0.001) and absolute exercise workload (R = 0.59, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

The respiratory Vco2/Vo2 exchange ratio during maximum exercise and its use as a predictor of maximum oxygen uptake

The purpose of this study was to define carefully the dynamic relationship between oxygen uptake (as % Vo2max) and the respiratory Vco2/Vo2 exchange ratio (R) during maximum progressive treadmill exercise in trained and untrained men, and to determine if this relationship could be used to predict Vo2max. Respiratory gases were continuously monitored and the %Vo2max/R time profile calculated at 15 sec intervals over the final 5 min of each test. Young sedentary men (controls, n = 122) and over-60y sedentary men (n = 30) shared the same %Vo2max/R relationship but the latter group had lower R values at Vo2max (1.06 +/- 0.03 vs 1.08 +/- 0.03, p less than 0.01) than controls. Endurance trained men (n = 45) had a lower %Vo2max/R relationship and higher R at Vo2max (1.11 +/- 0.02, p less than 0.001), team athletes (n = 98) had a lower %Vo2max/R relationship but lower R at Vo2max (1.06 +/- 0.03, p less than 0.001) and the weight trained (n = 19) had a higher %Vo2max/R relationship and lower R at Vo2max (1.01 +/- 0.02, p less than 0.001) all compared to controls. From the %Vo2max/R time profile, the following formulae were devised for the estimation of Vo2max (Vo2maxR): Young Sedentary, Vo2maxR = Vo2R (3.000-1.874 R); Over-60y Sedentary, Vo2maxR = Vo2R (3.457-2.345 R); Endurance Trained, Vo2max = Vo2R (1.980-0.912 R); Team Athletes, Vo2maxR = Vo2R (2.805-1.726 R); Weight Trained, Vo2maxR = Vo2R (4.236-3.191 R).(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in cardiorespiratory fitness and coronary heart disease risk factors following 24 wk of moderate- or high-intensity exercise of equal energy cost.

This study was designed to investigate the effect of exercise intensity on cardiorespiratory fitness and coronary heart disease risk factors. Maximum oxygen consumption (Vo(2 max)), lipid, lipoprotein, and fibrinogen concentrations were measured in 64 previously sedentary men before random allocation to a nonexercise control group, a moderate-intensity exercise group (three 400-kcal sessions per week at 60% of Vo(2 max)), or a high-intensity exercise group (three 400-kcal sessions per week at 80% of Vo(2 max)). Subjects were instructed to maintain their normal dietary habits, and training heart rates were represcribed after monthly fitness tests. Forty-two men finished the study. After 24 wk, Vo(2 max) increased by 0.38 +/- 0.14 l/min in the moderate-intensity group and by 0.55 +/- 0.27 l/min in the high-intensity group. Repeated-measures analysis of variance identified a significant interaction between monthly Vo(2 max) score and exercise group (F = 3.37, P < 0.05), indicating that Vo(2 max) responded differently to moderate- and high-intensity exercise. Trend analysis showed that total cholesterol, low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, and fibrinogen concentrations changed favorably across control, moderate-intensity, and high-intensity groups. However, significant changes in total cholesterol (-0.55 +/- 0.81 mmol/l), low-density lipoprotein cholesterol (-0.52 +/- 0.80 mmol/l), and non-high-density lipoprotein cholesterol (-0.54 +/- 0.86 mmol/l) were only observed in the high-intensity group (all P < 0.05 vs. controls). These data suggest that high-intensity training is more effective in improving cardiorespiratory fitness than moderate-intensity training of equal energy cost. These data also suggest that changes in coronary heart disease risk factors are influenced by exercise intensity.     

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.     

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.     

Influence of the IL-6 -572C>G polymorphism on inflammatory markers according to cigarette smoking in Korean healthy men

We investigated whether smoking would interact with the interleukin-6 (IL-6) polymorphisms (-174G>C and -572C>G, -597G>A and -1363G>T) in determining circulating levels of inflammatory markers and its consequence to oxidative stress. The G/G genotype (n=26) of the -572C>G in nonsmokers (n=376) was associated with higher IL-6 (P=0.028), fibrinogen (P=0.007) and ox-LDL (P=0.006) than those with C/C (n=209) or C/G (n=141). Results were similar for nonsmokers and smokers (n=268), but in smokers, the -572G/G genotype was associated with a greater difference in levels of IL-6 (P=0.031), fibrinogen (P=0.001), ox-LDL (P=0.037) and PGF(2alpha) (P=0.050). IL-6 had positive relations with CRP, fibrinogen, ox-LDL and PGF(2alpha). There was no evidence of an effect of -572C>G genotype on CRP levels in nonsmokers, however, this polymorphism was associated with a highly significant effect on CRP in smokers (P<0.001) (genotype-smoking interaction P=0.04, adjusted for age, BMI and IL-6). The C allele frequency at the -174 promoter region of IL-6 was very rare (<0.01) and -597G>A and -1363G>T were monomorphic in this study. Our results suggest that IL-6 -572C>G has a greater response over time to the inflammatory effects of smoking and this may result in smokers having higher oxidative stress in subjects with G/G compared to C/C or C/G.     

V(O2) max is unaffected by altering the temporal pattern of stimulation frequency in rat hindlimb in situ.

It might be anticipated that fatiguing contractions would impair the aerobic metabolic response in skeletal muscle if significant fatigue developed before full activation of aerobic metabolism. On the basis of this premise, we examined two groups of rats to test the hypothesis that a gradual increase in stimulation frequency would yield a higher maximal O2 uptake (Vo2 max) than beginning immediately with an intense stimulation frequency because of a slower progression of fatigue under the former conditions. In one group of animals, the distal hindlimb muscles were electrically stimulated at a frequency of 60 tetani/min for 4 min (F60; n = 6 rats); in the other group, the muscles were incrementally stimulated for 1 min at each of 7.5, 15, 30, and 60 tetani/min and for 2 min at 90 tetani/min (FInc; n = 5 rats). Despite large differences in rate of fatigue [time to 60% of initial force was 47 +/- 3 (SE) vs. 188 +/- 1 s in F60 and FInc, respectively] and the time at which Vo2 max occurred (120 +/- 15 vs. 264 +/- 6 s), Vo2 max was not different (419 +/- 24 vs. 381 +/- 44 micromol x min-1. 100 g-1). Furthermore, time x tension integral at Vo2 max (3.82 +/- 0.41 vs. 4.07 +/- 0.31 N. s) and peak lactate efflux (910 +/- 45 vs. 800 +/- 98 micromol x min-1. 100 g-1) were not different between groups. Thus our results show that the more rapid progression of fatigue in F60 did not compromise the aerobic metabolic response in electrically stimulated rat hindlimb muscles. However, in both groups, O2 uptake and lactate efflux declined after Vo2 max was attained in similar proportion to a further fall in force, suggesting that ongoing fatigue with intense contractions reduced ATP demand below that requiring maximal aerobic and glycolytic metabolic responses once Vo2 max was reached.     

HCY、CRP、Fib、WBC 水平在冠心病诊断中的临床价值

目的:探讨血清同型半胱氨酸(HCY)、C反应蛋白、纤维蛋白原(Fib)、白细胞(WBC)与冠心病(CHD)病变程度的相关性和作为检测指标的敏感性;检测BMI是否为CHD的独立风险因子。方法:测定102例不同类型冠心病患者和33例健康的HCY、CRP、Fib、WBC的水平,比较AMI.UAP.SAP组和对照组间各项指标的差异。结果:BMI24和BMI24两组中AMI、UAP、SPA和Control的构成比的差别,结果显示男性患者中两组构成有明显差异(P=0.011);女性患者中两组构成没有明显差异(P=0.28)。各组的HCY、CRP、Fib和WBC的水平为:AMI组大于UAP组大于SAP组大于对照组,AMI组与UAP组相比,差异有统计学意义(均为P0.01),UAP组与SAP组相比,差异有统计学意义(P0.05,P0.01)。CRP和WBC的诊断价值较好,HCY和Fib的诊断价值中等。结论:同型半胱氨酸、C反应蛋白、纤维蛋白原和白细胞水平变化与冠心病的发生、发展密切相关,它们的四个指标可作为区别冠心病类型和评价其病变严重程度的辅助性指标。     

Greater rate of decline in maximal aerobic capacity with age in endurance-trained than in sedentary men.

To determine the relation between habitual endurance exercise status and the age-associated decline in maximal aerobic capacity [i.e., maximal O(2) consumption (Vo(2 max))] in men, we performed a well-controlled cross-sectional laboratory study on 153 healthy men aged 20-75 yr: 64 sedentary and 89 endurance trained. Vo(2 max) (ml. kg(-1). min(-1)), measured by maximal treadmill exercise, was inversely related to age in the endurance-trained (r = -0.80) and sedentary (r = -0.74) men but was higher in the endurance-trained men at any age. The rate of decline in Vo(2 max) with age (ml. kg(-1). min(-1)) was greater (P < 0.001) in the endurance-trained than in the sedentary men. Whereas the relative rate of decline in Vo(2 max) (percent decrease per decade from baseline levels in young adulthood) was similar in the two groups, the absolute rate of decline in Vo(2 max) was -5.4 and -3.9 ml. kg(-1). min(-). decade(-1) in the endurance-trained and sedentary men, respectively. Vo(2 max) declined linearly across the age range in the sedentary men but was maintained in the endurance-trained men until approximately 50 yr of age. The accelerated decline in Vo(2 max) after 50 yr of age in the endurance-trained men was related to a decline in training volume (r = 0.46, P < 0.0001) and was associated with an increase in 10-km running time (r = -0.84, P < 0.0001). We conclude that the rate of decline in maximal aerobic capacity during middle and older age is greater in endurance-trained men than in their sedentary peers and is associated with a marked decline in O(2) pulse.     

Preexercise metabolic alkalosis induced via bicarbonate ingestion accelerates Vo2 kinetics at the onset of a high-power-output exercise in humans.

The present study investigated the effect of preexercise metabolic alkalosis on the primary component of oxygen uptake (Vo(2)) kinetics, characterized by tau(1). Seven healthy physically active nonsmoking men, aged 22.4 +/- 1.8 (mean +/- SD) yr, maximum Vo(2) (Vo(2 max)) 50.4 +/- 4 ml.min(-1).kg(-1), performed two bouts of cycling, corresponding to 40 and 87% of Vo(2 max), lasting 6 min each, separated by a 20-min pause, once as a control study and a few days later at approximately 90 min after ingestion of 3 mmol/kg body wt of NaHCO(3). Blood samples for measurements of bicarbonate concentration and hydrogen ion concentration were taken from antecubital vein via catheter. Pulmonary Vo(2) was measured continuously breath by breath. The values of tau(1) were calculated by using six various approaches published in the literature. Preexercise level of bicarbonate concentration after ingestion of NaHCO(3) was significantly elevated (P < 0.01) compared with the control study (28.96 +/- 2.11 vs. 24.84 +/- 1.18 mmol/l; P < 0.01), and [H(+)] was significantly (P < 0.01) reduced (42.79 +/- 3.38 nmol/l vs. 46.44 +/- 3.51 nmol/l). This shift (P < 0.01) was also present during both bouts of exercise. During cycling at 40% of Vo(2 max), no significant effect of the preexercise alkalosis on the magnitude of tau(1) was found. However, during cycling at 87% of Vo(2 max), the tau(1) calculated by all six approaches was significantly (P < 0.05) reduced, compared with the control study. The tau(1) calculated as in Borrani et al. (Borrani F, Candau R, Millet GY, Perrey S, Fuchsloscher J, and Rouillon JD. J Appl Physiol 90: 2212-2220, 2001) was reduced on average by 7.9 +/- 2.6 s, which was significantly different from zero with both the Student's t-test (P = 0.011) and the Wilcoxon's signed-ranks test (P = 0.014).     

Effects of exercise training on acclimatization to hypoxia: systemic O2 transport during maximal exercise.

Acclimatization to hypoxia has minimal effect on maximal O2 uptake (Vo2 max). Prolonged hypoxia shows reductions in cardiac output (Q), maximal heart rate (HR-max), myocardial beta-adrenoceptor (beta-AR) density, and chronotropic response to isoproterenol. This study tested the hypothesis that exercise training (ET), which attenuates beta-AR downregulation, would increase HRmax and Q of acclimatization and result in higher Vo2 max. After 3 wk of ET, rats lived at an inspired Po2 of 70 Torr for 10 days (acclimatized trained rats) or remained in normoxia, while both groups continued to train in normoxia. Controls were sedentary acclimatized and nonacclimatized rats. All rats exercised maximally in normoxia and hypoxia (inspired Po2 of 70 Torr). Myocardial beta-AR density and the chronotropic response to isoproterenol were reduced, and myocardial cholinergic receptor density was increased after acclimatization; all of these receptor changes were reversed by ET. Normoxic Vo2 max (in ml.min-1.kg-1) was 95.8 +/- 1.0 in acclimatized trained (n = 6), 87.7 +/- 1.7 in nonacclimatized trained (P < 0.05, n = 6), 74.2 +/- 1.4 in acclimatized sedentary (n = 6, P < 0.05), and 72.5 +/- 1.2 in nonacclimatized sedentary (n = 8; P > 0.05 acclimatized sedentary vs. nonacclimatized sedentary). A similar distribution of Vo2 max values occurred in hypoxic exercise. Q was highest in trained acclimatized and nonacclimatized, intermediate in nonacclimatized sedentary, and lowest in acclimatized sedentary groups. ET preserved Q in acclimatized rats thanks to maintenance of HRmax as well as of maximal stroke volume. Q preservation, coupled with a higher arterial O2 content, resulted in the acclimatized trained rats having the highest convective O2 transport and Vo2 max. These results show that ET attenuates beta-AR downregulation and preserves Q and Vo2 max after acclimatization, and support the idea that beta-AR downregulation partially contributes to the limitation of Vo2 max after acclimatization in rats.     

The effects of previous severe exercise upon the respiratory Vco2/Vo2 exchange ratio as a predictor of maximum oxygen uptake

The present study examined the effect of previous severe exercise upon (i) respiratory exchange during maximal exercise, and (ii) the respiratory Vco2/Vo2 exchange ratio (R) as a predictor of maximum oxygen uptake (Vo2max). Thirteen healthy males performed a progressive treadmill test to Vo2max: at rest (T1); after a 1 h run on the level treadmill at a speed corresponding 82.4 +/- 7.3% of their Vo2max (T2); after 1 h recovery (T3); and after 24 h recovery (T4). Respiratory gases were continuously monitored. No changes in average work Vo2, Vo2max or maximum heart rate were found between trials. Average work Vco2 was lower in T2 (2.055 +/- 0.093 1.min-1, p less than 0.001), T3 (2.080 +/- 0.087 1.min-1, p less than 0.001) and T4 (2.337 +/- 0.154 1.min-1, NS) compared with T1 (2.360 +/- 0.147 1.min-1). This resulted in lower average R values in T2 (0.81 +/- 0.02, p less than 0.001), T3 (0.83 +/- 0.02, p less than 0.001) and T4 (0.94 +/- 0.02, NS) in relation to T1 (0.95 +/- 0.02). Analysis of the %Vo2max/R relationship over the final 5 min of each test showed a shift to the left during T2 (p less than 0.001), T3 (p less than 0.001) and T4 (NS) compared with T1. As a result predictions of Vo2max based on R (Vo2max/R) were similar to recorded Vo2max in T1 (+ 0.6%) and T4 (+ 2.2%). But higher in T2 (+ 8.7%, p less than 0.001) and T3 (+ 6.9%, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Elevated white blood cell count, CRP and fibrinogen levels are not associated with increased anti-endothelial and anti-ox-LDL antibody, MCP-1, and RANTES levels in early onset occlusive carotid artery disease

BACKGROUND: Inflammatory processes have importance in atherosclerosis. We evaluated if subjects below 55 years of age with occlusive carotid artery disease have higher serum levels of antibodies against oxidized LDL and endothelial cells and the chemokines MCP-1 and RANTES than age matched subjects without atherosclerosis. METHODS AND RESULTS: Sixty patients with occlusive carotid artery disease (stenosis or occlusion) and 30 age-matched controls participated in the study. We measured the degree of carotid artery stenosis and intima-media thickness (IMT) by duplex ultrasound. White blood cell count (WBC), C-reactive protein (CRP), and fibrinogen levels were significantly higher in patients (means+/-SD: 7.5+/-1.8 vs. 6.1+/-1.1 G/L, p<0.001; 7.7+/-20.7 vs. 2.5+/-1.9 mg/L, p=0.015; and 3.7+/-0.9 vs. 3.1+/-0.5 g/L, p<0.001, respectively). Antibody levels against oxidized LDL and endothelial cells (21.1+/-22.9 and 19.9+/-15.3 EU/mL, p=0.6; and 19+/-15 vs. 20+/-9 U/mL, p=0.07) and RANTES and MCP-1 levels (72.4+/-32.3 vs. 73.8+/-27.3 ng/mL, p=0.7; and 468+/-1041 vs. 318+/-131 pg/mL, p=0.7) did not differ significantly between patients and controls and did not correlate with IMT. CONCLUSIONS: Higher levels of WBC, CRP, and fibrinogen suggest an ongoing inflammation in early-onset carotid atherosclerosis, but increased IMT is not associated by the elevation of serum levels of chemokines and antibodies evaluated in this study.     

Effect of high-intensity hypoxic training on sea-level swimming performances.

The objective of this study was to test the hypothesis that high-intensity hypoxic training improves sea-level performances more than equivalent training in normoxia. Sixteen well-trained collegiate and Masters swimmers (10 women, 6 men) completed a 5-wk training program, consisting of three high-intensity training sessions in a flume and supplemental low- or moderate-intensity sessions in a pool each week. Subjects were matched for gender, performance level, and training history, and they were assigned to either hypoxic [Hypo; inspired O2 fraction (Fi(O(2))) = 15.3%, equivalent to a simulated altitude of 2,500 m] or normoxic (Norm; Fi(O(2)) = 20.9%) interval training in a randomized, double-blind, placebo-controlled design. All pool training occurred under Norm conditions. The primary performance measures were 100- and 400-m freestyle time trials. Laboratory outcomes included maximal O(2) uptake (Vo(2 max)), anaerobic capacity (accumulated O(2) deficit), and swimming economy. Significant (P = 0.02 and <0.001 for 100- and 400-m trials, respectively) improvements were found in performance on both the 100- [Norm: -0.7 s (95% confidence limits: +0.2 to -1.7 s), -1.2%; Hypo: -0.8 s (95% confidence limits: -0.1 to -1.5 s), -1.1%] and 400-m freestyle [Norm: -3.6 s (-1.8 to -5.5 s), -1.2%; Hypo: -5.3 s (-2.3 to -8.3 s), -1.7%]. There was no significant difference between groups for either distance (ANOVA interaction, P = 0.91 and 0.36 for 100- and 400-m trials, respectively). Vo(2 max) was improved significantly (Norm: 0.16 +/- 0.23 l/min, 6.4 +/-8.1%; Hypo: 0.11 +/- 0.18 l/min, 4.2 +/- 7.0%). There was no significant difference between groups (P = 0.58). We conclude that 5 wk of high-intensity training in a flume improves sea-level swimming performances and Vo(2 max) in well-trained swimmers, with no additive effect of hypoxic training.     

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.