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.     

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.     

Intensity-dependent tolerance to exercise after attaining V(O2) max in humans.

The tolerable duration of high-intensity, constant-load cycle ergometry is a hyperbolic function of power, with an asymptote termed critical power (CP) and a curvature constant (W') with units of work. It has been suggested that continued exercise after exhaustion may only be performed below CP, where predominantly aerobic energy transfer can occur and W' can be partially replenished. To test this hypothesis, six volunteers each performed cycle-ergometer exercise with breath-by-breath determination of ventilatory and pulmonary gas exchange variables. Initially, four exercise tests to exhaustion were made: 1). a ramp-incremental and 2). three high-intensity constant-load bouts at different work rates, to estimate lactate (theta(L)) and CP thresholds, W', and maximum oxygen uptake (Vo2 max). Subsequently, subjects cycled to the limit of tolerance (for approximately 360 s) on three occasions, each followed by a work rate reduction to 1). 110% CP, 2). 90% CP, and 3). 80% theta(L) for a 20-min target. W' averaged 20.9 +/- 2.35 kJ or 246 +/- 30 J/kg. After initial fatigue, 110% CP was tolerated for only 30 +/- 12 s. Each subject completed 20 min at 80% theta(L), but only two sustained 20 min at 90% CP; the remaining four subjects fatigued at 577 +/- 306 s, with oxygen consumption at 89 +/- 8% Vo2 max. The results support the suggestion that replenishing W' after fatigue necessitates a sub-CP work rate. The variation in subjects' responses during 90% CP was unexpected but consistent with mechanisms such as reduced CP consequent to prior high-intensity exercise, variation in lactate handling, and/or regional depletion of energy substrates, e.g., muscle glycogen.     

Pulmonary O2 uptake kinetics as a determinant of high-intensity exercise tolerance in humans

Tolerance to high-intensity constant-power (P) exercise is well described by a hyperbola with two parameters: a curvature constant (W') and power asymptote termed "critical power" (CP). Since the ability to sustain exercise is closely related to the ability to meet the ATP demand in a steady state, we reasoned that pulmonary O(2) uptake (Vo(2)) kinetics would relate to the P-tolerable duration (t(lim)) parameters. We hypothesized that 1) the fundamental time constant (τVo(2)) would relate inversely to CP; and 2) the slow-component magnitude (ΔVo(2sc)) would relate directly to W'. Fourteen healthy men performed cycle ergometry protocols to the limit of tolerance: 1) an incremental ramp test; 2) a series of constant-P tests to determine Vo(2max), CP, and W'; and 3) repeated constant-P tests (WR(6)) normalized to a 6 min t(lim) for τVo(2) and ΔVo(2sc) estimation. The WR(6) t(lim) averaged 365 ± 16 s, and Vo(2max) (4.18 ± 0.49 l/min) was achieved in every case. CP (range: 171-294 W) was inversely correlated with τVo(2) (18-38 s; R(2) = 0.90), and W' (12.8-29.9 kJ) was directly correlated with ΔVo(2sc) (0.42-0.96 l/min; R(2) = 0.76). These findings support the notions that 1) rapid Vo(2) adaptation at exercise onset allows a steady state to be achieved at higher work rates compared with when Vo(2) kinetics are slower; and 2) exercise exceeding this limit initiates a "fatigue cascade" linking W' to a progressive increase in the O(2) cost of power production (Vo(2sc)), which, if continued, results in attainment of Vo(2max) and exercise intolerance. Collectively, these data implicate Vo(2) kinetics as a key determinant of high-intensity exercise tolerance in humans.     

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)     

高原青少年最大有氧能力的研究

采用自行车递增负荷运动试验,对青海西宁地区(海拔2260m)86名13～16岁男女中学生的最大摄氧量,无氧阈以及血氧饱和度等指标进行了测定。结果表明,高原青少年的最大摄氧量较低,而无氧阈则较高。血氧饱和度随负荷增加逐渐降低,在接近极限负荷时迅速下降,提示高原低氧是限制最大运动能力的主要因素。无氧阈较高说明高原青少年组织细胞利用氧的能力提高,这是对高原低氧环境长期适应的结果。     

Regional hemodynamics during postexercise hypotension. II. Cutaneous circulation.

After an acute bout of exercise, there is an unexplained elevation in systemic vascular conductance that is not completely offset by an increase in cardiac output, resulting in a postexercise hypotension. The contributions of the splanchnic and renal circulations are examined in a companion paper (Pricher MP, Holowatz LA, Williams JT, Lockwood JM, and Halliwill JR. J Appl Physiol 97: 2065-2070, 2004). The purpose of this study was to determine the contribution of the cutaneous circulation in postexercise hypotension under thermoneutral conditions (approximately 23 degrees C). Arterial blood pressure was measured via an automated sphygmomanometer, internal temperature was measured via an ingestible pill, and skin temperature was measured with eight thermocouples. Red blood cell flux (laser-Doppler flowmetry) was monitored at four skin sites (chest, forearm, thigh, and leg), and cutaneous vascular conductance (CVC) was calculated (red blood cell flux/mean arterial pressure) and scaled as percent maximal CVC (local heating to 43 degrees C). Ten subjects [6 men and 4 women; age 23 +/- 1 yr; peak O(2) uptake (Vo(2 peak)) 45.8 +/- 2.0 ml.kg(-1).min(-1)] volunteered for this study. After supine rest (30 min), subjects exercised on a bicycle ergometer for 1 h at 60% of their Vo(2 peak) and were then positioned supine for 90 min. Exercise elicited a postexercise hypotension reaching a nadir at 46.0 +/- 4.5 min postexercise (77 +/- 1 vs. 82 +/- 2 mmHg preexercise; P < 0.05). Internal temperature increased (38.0 +/- 0.1 vs. 36.7 +/- 0.1 degrees C preexercise; P < 0.05), remaining elevated at 90 min postexercise (36.9 +/- 0.1 degrees C vs. preexercise; P < 0.05). CVC at all four skin sites was elevated by the exercise bout (P < 0.05), returning to preexercise values within 50 min postexercise (P > 0.05). Therefore, although transient changes in CVC occur postexercise, they do not appear to play an obligatory role in mediating postexercise hypotension under thermoneutral conditions.     

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).     

Lymphocyte proliferation responses after exercise in men: fitness, intensity, and duration effects

This study investigated the effects of intensity and duration of exercise on lymphocyte proliferation as a measure of immunologic function in men of defined fitness. Three fitness groups--low [maximal O2 uptake (VO2max) = 44.9 +/- 1.5 ml O2.kg-1.min-1 and sedentary], moderate (VO2max = 55.2 +/- 1.6 ml O2.kg-1.min-1 and recreationally active), and high (VO2max = 63.3 +/- 1.8 ml O2.kg-1.min-1 and endurance trained)--and a mixed control group (VO2max = 52.4 +/- 2.3 ml O2.kg-1.min-1) participated in the study. Subjects completed four randomly ordered cycle ergometer rides: ride 1, 30 min at 65% VO2max; ride 2, 60 min at 30% VO2max; ride 3, 60 min at 75% VO2max; and ride 4, 120 min at 65% VO2max. Blood samples were obtained at various times before and after the exercise sessions. Lymphocyte responses to the T cell mitogen concanavalin A were determined at each sample time through the incorporation of radiolabeled thymidine [( 3H]TdR). Despite differences in resting levels of [3H]TdR uptake, a consistent depression in mitogenesis was present 2 h after an exercise bout in all fitness groups. The magnitude of the reduction in T cell mitogenesis was not affected by an increase in exercise duration. A trend toward greater reduction was present in the highly fit group when exercise intensity was increased. The reduction in lymphocyte proliferation to the concanavalin A mitogen after exercise was a short-term phenomenon with recovery to resting (preexercise) values 24 h after cessation of the work bout. These data suggest that single sessions of submaximal exercise transiently reduce lymphocyte function in men and that this effect occurs irrespective of subject fitness level.     

Visfatin mRNA expression in human subcutaneous adipose tissue is regulated by exercise

Visfatin [pre-beta-cell colony-enhancing factor (PBEF)] is a novel adipokine that is produced by adipose tissue, skeletal muscle, and liver and has insulin-mimetic actions. Regular exercise enhances insulin sensitivity. In the present study, we therefore examined visfatin mRNA expression in abdominal subcutaneous adipose tissue and skeletal muscle biopsies obtained from healthy young men at time points 0, 3, 4.5, 6, 9, and 24 h in relation to either 3 h of ergometer cycle exercise at 60% of Vo(2 max) or rest. Adipose tissue visfatin mRNA expression increased threefold at the time points 3, 4.5, and 6 h in response to exercise (n = 8) compared with preexercise samples and compared with the resting control group (n = 7, P = 0.001). Visfatin mRNA expression in skeletal muscle was not influenced by exercise. The exercise-induced increase in adipose tissue visfatin was, however, not accompanied by elevated levels of plasma visfatin. Recombinant human IL-6 infusion to mimic the exercise-induced IL-6 response (n = 6) had no effect on visfatin mRNA expression in adipose tissue compared with the effect of placebo infusion (n = 6). The finding that exercise enhances subcutaneous adipose tissue visfatin mRNA expression suggests that visfatin has a local metabolic role in the recovery period following exercise.     

Blood lactate in trained cyclists during cycle ergometry at critical power

The purposes of this investigation were to determine the validity of critical power (CP) as a measure of the work rate that can be maintained for a very long time without fatigue and to determine whether this corresponded with the maximal lactate steady-state (lass,max). Eight highly trained endurance cyclists (maximal oxygen uptake 74.1 ml.kg-1.min-1, SD 5.3) completed four cycle ergometer tests to exhaustion at pre-determined work rates (360, 425, 480 and 520 W). From these four co-ordinates of work and time to fatigue the regression of work limit on time limit was calculated for each individual (CP). The cyclists were then asked to exercise at their CP for 30 min. If CP could not be maintained, the resistance was reduced minimally to allow the subject to complete the test and maintain a blood lactate plateau. Capillary blood was sampled at 0,5,10,20 and 30 min into exercise for the analysis of lactate. Six of the eight cyclists were unable to maintain CP for 30 min without fatigue. In these subjects, the mean power attained was 6.4% below that estimated by CP. Mean blood lactates (n = 8) reached a steady-state (8.9 mmol.l-1 SD 1.6) during the last 20 min of exercise indicating that CP slightly overestimated lass,max, Individual blood lactates during the last 20 min of exercise were more closely related to the gamma-intercept of the CP curve (r = 0.78, P less than 0.05) than either CP (0.34, NS) or mean power output (r = 0.42, NS).     

Oxygen consumption following exercise of moderate intensity and duration.

To study the effects of exercise intensity and duration on excess postexercise oxygen consumption (EPOC), 8 men [age = 27.6 (SD 3.8) years, VO2max = 46.1 (SD 8.5) ml min-1 kg-1] performed four randomly assigned cycle-ergometer tests (20 min at 60% VO2max, 40 min at 60% VO2max, 20 min at 70% VO2max, and 40 min at 70% VO2max). O2 uptake, heart rate and rectal temperature were measured before, during, and for 1 h following the exercise tests. Blood for plasma lactate measurements was obtained via cannulae before, and at selected times, during and following exercise. VO2 rapidly declined to preexercise levels following each of the four testing sessions, and there were no differences in EPOC between the sessions. Blood lactate and rectal temperature increased (P < 0.05) with exercise, but had returned to preexercise levels by 40 min of recovery. The results indicate that VO2 returned to resting levels within 40 min after the end of exercise, regardless of the intensity (60% and 70% VO2max) or duration (20 min and 40 min) of the exercise, in men with a moderate aerobic fitness level.     

Energy expenditure during simulated rowing

Metabolic function was measured by open-circuit spirometry for 310 competitive oarsmen during and following a 6-min maximal rowing ergometer exercise. Aerobic and anaerobic energy contributions to exercise were estimated by calculating exercise O2 cost and O2 debt.O2 debt was measured for 30 min of recovery using oxygen consumption (Vo2) during light rowing as the base line. Venous blood lactates were analyzed at rest and at 5 and 30 min of recovery. Maximal ventilation volumes ranged from 175 to 22l 1/min while Vo2 max values averaged 5,950 ml/min and 67.6 ml/kg min. Maximal venous blood lactates ranged from 126 to 240 mg/100 ml. Average O2 debt equaled 13.4 liters. The total energy cost for simulated rowing was calculated at 221.5 kcal assuming 5 kcal/l O2 with aerobic metabolism contributing 70% to the total energy released and anaerobiosis providing the remaining 30%. Vo2 values for each minute of exercise reflect a severe steady state since oarsmen work at 96-98% of maximal aerobic capacity. O2 debt and lactate measurements attest to the severity of exercise and dominance of anaerobic metabolism during early stages of work.     

训练专一性对无氧阈测定的影响

本文对以上肢训练为主的15名优秀皮划艇运动员和以下肢训练为主的14名优秀中长跑运动员在两种常规负荷方式下的无氧阈及最大吸氧量进行了测定分析,以探讨训练专一性对无氧阈测定的影响。采用踏车式功量计和活动平板方式逐级递增负荷,通过与Apple Ⅱ_E辅助联机的Jaeger EOS自动分析系统,以通气和气体交换指标的变化,无创性地测定无氧阈和最大吸氧量。结果表明,训练专一性会影响无氧阈测定结果。欲测得最高的无氧阈值,实验室测试手段就应当尽量模拟训练时的运动形式。此外,能敏感地反映出运动训练专一性适应的是无氧阈时的吸氧量绝对值(1/min),而不是无氧阈的相对值(％Vo_2max)。     

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.     

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)     

Thigh muscle activation distribution and pulmonary VO2 kinetics during moderate, heavy, and very heavy intensity cycling exercise in humans

The mechanisms underlying the oxygen uptake (Vo(2)) slow component during supra-lactate threshold (supra-LT) exercise are poorly understood. Evidence suggests that the Vo(2) slow component may be caused by progressive muscle recruitment during exercise. We therefore examined whether leg muscle activation patterns [from the transverse relaxation time (T2) of magnetic resonance images] were associated with supra-LT Vo(2) kinetic parameters. Eleven subjects performed 6-min cycle ergometry at moderate (80% LT), heavy (70% between LT and critical power; CP), and very heavy (7% above CP) intensities with breath-by-breath pulmonary Vo(2) measurement. T2 in 10 leg muscles was evaluated at rest and after 3 and 6 min of exercise. During moderate exercise, nine muscles achieved a steady-state T2 by 3 min; only in the vastus medialis did T2 increase further after 6 min. During heavy exercise, T2 in the entire vastus group increased between minutes 3 and 6, and additional increases in T2 were seen in adductor magnus and gracilis during this period of very heavy exercise. The Vo(2) slow component increased with increasing exercise intensity (being functionally zero during moderate exercise). The distribution of T2 was more diverse as supra-LT exercise progressed: T2 variance (ms) increased from 3.6 +/- 0.2 to 6.5 +/- 1.7 between 3 and 6 min of heavy exercise and from 5.5 +/- 0.8 to 12.3 +/- 5.4 in very heavy exercise (rest = 3.1 +/- 0.6). The T2 distribution was significantly correlated with the magnitude of the Vo(2) slow component (P < 0.05). These data are consistent with the notion that the Vo(2) slow component is an expression of progressive muscle recruitment during supra-LT exercise.     

Carbohydrate feedings before, during, or in combination improve cycling endurance performance.

This study examined the effects of no carbohydrate (PP), preexercise carbohydrate feeding (CP), carbohydrate feedings during exercise (PC), and the combination of carbohydrate feedings before and during exercise (CC) on the metabolic responses during exercise and on exercise performance. Nine well-trained cyclists exercised at 70% of maximal O2 uptake until exhaustion. Blood glucose peaked 30 min after the preexercise carbohydrate feeding and at the start of exercise was 25% below the prefeeding concentration (4.76 mM). At exhaustion, glucose had declined to 3.8 (PP), 4.0 (CP), 4.6 (PC), and 5.0 mM (CC). Insulin was 300% above basal (7 microU/ml) at the start of exercise for CC and CP and returned to baseline by 120 min of exercise. When carbohydrates were consumed, the rate of carbohydrate oxidation was significantly higher throughout exercise than during PP. Total work produced during exercise was 19-46% (P less than 0.05) higher when carbohydrates were consumed. Time to exhaustion was 44% (CC), 32% (PC), and 18% (CP) greater than PP (201 min; P less than 0.05). Performance was improved by ingestion of carbohydrates before and/or during exercise; performance was further improved by their combination. This is probably the result of enhanced carbohydrate oxidation, especially during the later stages of exercise.     

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.     

Step ergometry: is it task-specific training?

Maximal exercise responses were measured before and after 10 weeks of training in two groups of men, one trained on a treadmill (n = 12) and the other on a step ergometer (n = 9); the groups were pre- and post-tested on both machines to examine the specificity of the training modes. Training for both groups consisted of 3 days week-1, 30 min day-1, progressing to 50 min day-1, at an intensity of 75%-80% heart rate maximum reserve. Pre-training maximal oxygen uptake (VO2max) was significantly higher on the treadmill for both groups (X = 8.5%). VO2max increased 6.9% on the treadmill (P less than 0.05) and 6.9% (P greater than 0.05) on the step ergometer after treadmill training. The small increases may be attributed to the specificity of the testing protocols used to elicit VO2max. Significant (P less than 0.01) increases in VO2max were found for both modalities after step-ergometry training (treadmill = 11.8%; step ergometer = 23.2%). These increases resulted in equal post-test VO2max values (4.05 l min-1; 51 ml kg-1 min-1) on the step ergometer and treadmill. The significant increases in VO2max found for both modalities after step-ergometry training shows that (1) step ergometry is an effective training modality, and (2) its effects can be measured on the treadmill and therefore it is not task-specific training.