Determination of the velocity associated with the longest time to exhaustion at maximal oxygen uptake

The so-called velocity associated with VO2max, defined as the minimal velocity which elicits VO2max in an incremental exercise protocol (v(VO2max)), is currently used for training to improve VO2max. However, it is well known that it is not the sole velocity which elicits VO2max and it is possible to achieve VO2max at velocities lower and higher than v(VO2max). The goal of this study was to determine the velocity which allows exercise to be maintained the longest time at v(VO2max). Using the relationship between time to exhaustion at VO2max in the all-out runs at 90%, 100%, 120% and 140% of v(VO2max) and distance run at VO2max, the velocity which elicits the longest time to exhaustion at VO2max (CV') was determined. For the six subjects tested (physical education students), this velocity was not significantly different from v(VO2max) (16.96+/-0.92 km x h(-1) vs 17.22+/-1.12 km x h(-1), P = 0.2 for CV' and v(VO2max), respectively) and these two velocities were correlated (r = 0.88, P = 0.05).     

Development of a submaximal test to predict elliptical cross-trainer VO2max

The purpose of this study was to develop an equation to predict VO2max from a submaximal elliptical cross-trainer test. Fifty-four apparently healthy subjects (25 men and 29 women, mean +/- SD age: 29.5 +/- 7.1 years, height: 173.3 +/- 12.6 cm, weight: 72.3 +/- 7.9 kg, percent body fat: 17.3 +/- 5.0%, and elliptical cross-trainer VO2max: 43.9 +/- 7.2 ml x kg(-1) x min(-1)) participated in the study and were randomly assigned to an original sample group (n = 40) and a cross-validation group (n = 14). Each subject completed an elliptical cross-trainer submaximal (3 5-minute submaximal stages) and a VO2max test on the same day, with a 15-minute rest period in between. Stepwise multiple regression analyses were used to develop an equation for estimating elliptical cross-trainer VO2max from the data of the original sample group. The accuracy of the equation was tested by using data from the cross-validation group. Because there was no shrinkage in R2 between the original sample group and the cross-validation group, data were combined in the final prediction equation (R2 = 0.732, standard error of the estimate = 3.91 ml x kg(-1) x min(-1), p < 0.05): VO2max = 73.676 + 7.383(gender) - 0.317(weight) + 0.003957(age x cadence) - 0.006452(age x heart rate at stage 2). The correlation coefficient between the predicted and measured VO2max values was r = 0.86. Dependent t-tests resulted in no significant differences (p > 0.05) between predicted (43.8 ml x kg(-1) x min(-1)) and measured (43.9 ml x kg(-1) x min(-1)) VO2max measurements. Results indicate that the protocol and equation developed in the current study can be used by exercise professionals to provide acceptably accurate estimates of VO2max in non-laboratory-based settings.     

Monitoring VO2max during fourteen weeks of endurance training using the CardioCoach

This study evaluated the validity of the desktop CardioCoach metabolic system to measure VO2max and VEmax. Sixteen subjects (mean age = 19.5 +/- 3.2 years) completed 2 maximal graded exercise tests following the same protocol before and after 7 and 14 weeks of endurance training. Subjects' VO2max and VEmax were measured by either the CardioCoach or the ParvoMedics TrueOne 2400 metabolic measurement system (TrueOne). An alpha level of significance of p < 0.05 was maintained for all statistical analyses. The time to test completion and the final treadmill grade of the exercise tests performed by both the CardioCoach and the TrueOne increased over the 3 testing periods, confirming an improvement in cardiorespiratory fitness resulting from the 14 weeks of training. A linear growth curve analysis indicated that there were statistically significant differences between VO2max (ml x kg(-1) x min(-1)) as measured by the TrueOne and the CardioCoach before (44.4 +/- 5.0 and 49.3 +/- 5.4) and after 7 weeks (46.0 +/- 5.2 and 48.2 +/- 5.4) of training but not after 14 weeks of training (47.8 +/- 5.6 and 48.4 +/- 5.2). Significant differences also existed in VEmax (L x min(-1)) as measured by the TrueOne and the CardioCoach before (76.8 +/- 17.7 and 71.9 +/- 13.7), after 7 weeks (81.4 +/- 16.2 and 72.8 +/- 14.1), and after 14 weeks (86.8 +/- 19.4 and 74.2 +/- 13.1) of training. Although significant growth of VO2max (0.24 ml x kg(-1) x min(-1) x wk(-1)) and VEmax (0.71 L x min(-1) x wk(-1)) was measured by the TrueOne over 14 weeks of training, the CardioCoach was unable to detect growth in VO2max (-0.02 ml x kg(-1) x min(-1) x wk(-1)) or VEmax (0.17 L x min(-1) x wk(-1)). This study indicates that the CardioCoach did not accurately measure or monitor changes in VO2max or VEmax resulting from training.     

Predicting maximal aerobic capacity (VO2max) from the critical velocity test in female collegiate rowers

The objective of this study was to examine the relationship between the critical velocity (CV) test and maximal oxygen consumption (VO2max) and develop a regression equation to predict VO2max based on the CV test in female collegiate rowers. Thirty-five female (mean ± SD; age, 19.38 ± 1.3 years; height, 170.27 ± 6.07 cm; body mass, 69.58 ± 0.3 1 kg) collegiate rowers performed 2 incremental VO2max tests to volitional exhaustion on a Concept II Model D rowing ergometer to determine VO2max. After a 72-hour rest period, each rower completed 4 time trials at varying distances for the determination of CV and anaerobic rowing capacity (ARC). A positive correlation was observed between CV and absolute VO2max (r = 0.775, p < 0.001) and ARC and absolute VO2max (r = 0.414, p = 0.040). Based on the significant correlation analysis, a linear regression equation was developed to predict the absolute VO2max from CV and ARC (absolute VO2max = 1.579[CV] + 0.008[ARC] - 3.838; standard error of the estimate [SEE] = 0.192 L·min(-1)). Cross validation analyses were performed using an independent sample of 10 rowers. There was no significant difference between the mean predicted VO2max (3.02 L·min(-1)) and the observed VO2max (3.10 L·min(-1)). The constant error, SEE and validity coefficient (r) were 0.076 L·min(-1), 0.144 L·min(-1), and 0.72, respectively. The total error value was 0.155 L·min(-1). The positive relationship between CV, ARC, and VO2max suggests that the CV test may be a practical alternative to measuring the maximal oxygen uptake in the absence of a metabolic cart. Additional studies are needed to validate the regression equation using a larger sample size and different populations (junior- and senior-level female rowers) and to determine the accuracy of the equation in tracking changes after a training intervention.     

Effect of creatine supplementation on cycle ergometer exercise in a hyperthermic environment

In order to examine thermoregulatory response to creatine (CR) supplementation, competitive male cyclists and triathletes (n = 7, VO2max = 50.6 +/- 0.8 ml x kg(-1) x min(-1)) completed three 1-hour hyperthermic (ambient temperature = 38.7 +/- 1.0 degrees C, relative humidity = 33 +/- 4%) exercise sessions at 181 +/- 12 W (50% of Wmax, approximately 66% of VO2max). Subjects completed a baseline (BL) session, then 2 sessions following 5 days of CR (20 g x d(-1)) and placebo (PL, 20 g x d(-1)) administered in a double-blind counterbalanced crossover manner with > or = 28-day washout. Pre-exercise BL, CR, and PL body mass were unchanged, with similar decreases in postexercise mass among the three conditions. Tympanic temperature, heart rate, systolic blood pressure, perceived exertion, and lactate, cortisol, and aldosterone concentrations increased similarly during BL, CR, and PL exercise. A greater (p = 0.013) estimated decrease in plasma volume occurred following BL (-16.5 +/- 2.0%) and PL (-17.6 +/- 1.7%) exercise compared to CR (-13.5 +/- 2.1%). Creatine supplementation reduces plasma volume loss during 1 hour of hyperthermic exercise but does not appear to otherwise change thermoregulatory response to hyperthermic exercise.     

Relative vs. absolute physiological measures as predictors of mountain bike cross-country race performance

The aims of this study were to document the effect terrain has on the physiological responses and work demands (power output) of riding a typical mountain bike cross-country course under race conditions. We were particularly interested in determining whether physiological measures relative to mass were better predictors of race performance than absolute measures. Eleven A-grade male cross-country mountain bike riders (VO2max 67.1 +/- 3.6 ml x kg(-1) x min(-1)) performed 2 tests: a laboratory-based maximum progressive exercise test, and a 15.5-km (six 2.58-km laps) mountain bike cross-country time trial. There were significant differences among the speed, cadence, and power output measured in each of 8 different terrain types found in the cross-country time trial course. The highest average speed was measured during the 10-15% downhill section (22.7 +/- 2.6 km x h(-1)), whereas the cadence was highest in the posttechnical flat sections (74.3 +/- 5.6 rpm) and lowest on the 15-20% downhill sections (6.4 +/- 12.1 rpm). The highest mean heart rate (HR) was obtained during the steepest (15-20% incline) section of the course (179 +/- 8 b x min(-1)), when the power output was greatest (419.8 +/- 39.7 W). However, HR remained elevated relative to power output in the downhill sections of the course. Physiological measures relative to total rider mass correlated more strongly to average course speed than did absolute measures (peak power relative to mass r = 0.93, p < 0.01, vs. peak power r = 0.64, p < 0.05; relative VO2max r = 0.80, p < 0.05, vs. VO2max r = 0.66, p < 0.05; power at anaerobic threshold relative to mass r = 0.78, p < 0.05, vs. power at anaerobic threshold r = 0.5, p < 0.05). This suggests that mountain bike cross-country training programs should focus upon improving relative physiological values rather than focusing upon maximizing absolute values to improve performance.     

Exercise-induced prostacyclin release positively correlates with VO(2max) in young healthy men

In this study we have evaluated the effect of maximal incremental cycling exercise (IE) on the systemic release of prostacyclin (PGI(2)), assessed as plasma 6-keto-PGF(1alpha) concentration in young healthy men. Eleven physically active - untrained men (mean +/- S.D.) aged 22.7 +/- 2.1 years; body mass 76.3 +/- 9.1 kg; BMI 23.30 +/- 2.18 kg . m(-2); maximal oxygen uptake (VO(2max)) 46.5 +/- 3.9 ml . kg(-1) . min(-1), performed an IE test until exhaustion. Plasma concentrations of 6-keto-PGF(1alpha), lactate, and cytokines were measured in venous blood samples taken prior to the exercise and at the exhaustion. The net exercise-induced increase in 6-keto-PGF(1alpha) concentration, expressed as the difference between the end-exercise minus pre-exercise concentration positively correlated with VO(2max) (r=0.78, p=0.004) as well as with the net VO(2) increase at exhaustion (r=0.81, p=0.003), but not with other respiratory, cardiac, metabolic or inflammatory parameters of the exercise (minute ventilation, heart rate, plasma lactate, IL-6 or TNF-alpha concentrations). The exercise-induced increase in 6-keto-PGF(1alpha) concentration?? was significantly higher (p=0.008) in a group of subjects (n=5) with the highest VO(2max) when compared to the group of subjects with the lowest VO(2max), in which no increase in 6-keto-PGF(1alpha) concentration was found. In conclusion, we demonstrated, to our knowledge for the first time, that exercise-induced release of PGI(2) in young healthy men correlates with VO(2max), suggesting that vascular capacity to release PGI(2) in response to physical exercise represents an important factor characterizing exercise tolerance. Moreover, we postulate that the impairment of exercise-induced release of PGI(2) leads to the increased cardiovascular hazard of vigorous exercise.     

Effects of prior exercise on muscle metabolism during sprint exercise in horses.

The effect of warm-up exercise on energy metabolism and muscle glycogenolysis during sprint exercise (Spr) was examined in six fit Standardbred horses exercised at 115% of maximal O(2) consumption (VO(2 max)) until fatigued, 5 min after each of three protocols: 1) no warm-up (NWU); 2) 10 min at 50% of VO(2 max) [low-intensity warm-up (LWU)]; and 3) 7 min at 50% VO(2 max) followed by 45-s intervals at 80, 90, and 100% VO(2 max) [high-intensity warm-up (HWU)]. Warm-up increased (P < 0.0001) muscle temperature (T(m)) at the onset of Spr in LWU (38.3 +/- 0.2 degrees C) and HWU (40.0 +/- 0. 3 degrees C) compared with NWU (36.6 +/- 0.2 degrees C), and the rate of rise in T(m) during Spr was greater in NWU than in LWU and HWU (P < 0.01). Peak VO(2) was higher and O(2) deficit lower (P < 0. 05) when Spr was preceded by warm-up. Rates of muscle glycogenolysis were lower (P < 0.05) in LWU, and rates of blood and muscle lactate accumulation and anaerobic ATP provision during Spr were lower in LWU and HWU compared with NWU. Mean runtime (s) in LWU (173 +/- 10 s) was greater than HWU (142 +/- 11 s) and NWU (124 +/- 4 s) (P < 0. 01). Warm-up was associated with augmentation of aerobic energy contribution to total energy expenditure, decreased glycogenolysis, and longer run time to fatigue during subsequent sprint exercise, with no additional benefit from HWU vs. LWU.     

Influence of inhaled nitric oxide on gas exchange during normoxic and hypoxic exercise in highly trained cyclists.

This study tested the effects of inhaled nitric oxide [NO; 20 parts per million (ppm)] during normoxic and hypoxic (fraction of inspired O(2) = 14%) exercise on gas exchange in athletes with exercise-induced hypoxemia. Trained male cyclists (n = 7) performed two cycle tests to exhaustion to determine maximal O(2) consumption (VO(2 max)) and arterial oxyhemoglobin saturation (Sa(O(2)), Ohmeda Biox ear oximeter) under normoxic (VO(2 max) = 4.88 +/- 0.43 l/min and Sa(O(2)) = 90.2 +/- 0.9, means +/- SD) and hypoxic (VO(2 max) = 4.24 +/- 0.49 l/min and Sa(O(2)) = 75.5 +/- 4.5) conditions. On a third occasion, subjects performed four 5-min cycle tests, each separated by 1 h at their respective VO(2 max), under randomly assigned conditions: normoxia (N), normoxia + NO (N/NO), hypoxia (H), and hypoxia + NO (H/NO). Gas exchange, heart rate, and metabolic parameters were determined during each condition. Arterial blood was drawn at rest and at each minute of the 5-min test. Arterial PO(2) (Pa(O(2))), arterial PCO(2), and Sa(O(2)) were determined, and the alveolar-arterial difference for PO(2) (A-aDO(2)) was calculated. Measurements of Pa(O(2)) and Sa(O(2)) were significantly lower and A-aDO(2) was widened during exercise compared with rest for all conditions (P < 0.05). No significant differences were detected between N and N/NO or between H and H/NO for Pa(O(2)), Sa(O(2)) and A-aDO(2) (P > 0.05). We conclude that inhalation of 20 ppm NO during normoxic and hypoxic exercise has no effect on gas exchange in highly trained cyclists.     

Living and training in moderate hypoxia does not improve VO2 max more than living and training in normoxia.

The objective of these experiments was to determine whether living and training in moderate hypoxia (MHx) confers an advantage on maximal normoxic exercise capacity compared with living and training in normoxia. Rats were acclimatized to and trained in MHx [inspired PO2 (PI(O2)) = 110 Torr] for 10 wk (HTH). Rats living in normoxia trained under normoxic conditions (NTN) at the same absolute work rate: 30 m/min on a 10 degrees incline, 1 h/day, 5 days/wk. At the end of training, rats exercised maximally in normoxia. Training increased maximal O2 consumption (VO2 max) in NTN and HTH above normoxic (NS) and hypoxic (HS) sedentary controls. However, VO2 max and O2 transport variables were not significantly different between NTN and HTH: VO2 max 86.6 +/- 1.5 vs. 86.8 +/- 1.1 ml x min(-1) x kg(-1); maximal cardiac output 456 +/- 7 vs. 443 +/- 12 ml x min(-1) x kg(-1); tissue blood O2 delivery (cardiac output x arterial O2 content) 95 +/- 2 vs. 96 +/- 2 ml x min(-1) x kg(-1); and O2 extraction ratio (arteriovenous O2 content difference/arterial O2 content) 0.91 +/- 0.01 vs. 0.90 +/- 0.01. Mean pulmonary arterial pressure (Ppa, mmHg) was significantly higher in HS vs. NS (P < 0.05) at rest (24.5 +/- 0.8 vs. 18.1 +/- 0.8) and during maximal exercise (32.0 +/- 0.9 vs. 23.8 +/- 0.6). Training in MHx significantly attenuated the degree of pulmonary hypertension, with Ppa being significantly lower at rest (19.3 +/- 0.8) and during maximal exercise (29.2 +/- 0.5) in HTH vs. HS. These data indicate that, despite maintaining equal absolute training intensity levels, acclimatization to and training in MHx does not confer significant advantages over normoxic training. On the other hand, the pulmonary hypertension associated with acclimatization to hypoxia is reduced with hypoxic exercise training.     

Oxidative metabolism and anaerobic glycolysis during repeated exercise

The purpose of the present study was to examine aerobic and muscle anaerobic energy production during supramaximal repeated exercise. Eight subjects performed three 2-min bouts of cycling (EX1-EX3) at an intensity corresponding to about 125 % of VO2 max separated by 15 min of rest. Ventilatory variables were measured breath by breath during the exercise and a muscle biopsy was taken before and after each exercise bout. Blood samples were collected before and after each cycling period and during the recovery periods. Total work in the first 2 min bout of cycling, EX1, [46.3 +/- 2.1 KJ] was greater than in the second, EX2, (p < 0.01) and in the third, EX3, (p < 0.05). The ATP utilization [4.0 +/- 1.4 mmol x (kg dry weight)(-1), EX1] during the three exercise bouts was the same. The decrement in muscle phosphocreatine (PCr) [46.8 +/- 8.5 mmol x (kg dry weight)(-1), EX1] was also similar for the three exercise bouts. Muscle lactate accumulation was greater (p < 0.05) during EX1 compared to EX2 and EX3. The total oxygen consumption was the same for the three exercise bouts, but when it is corrected for the total work performed, oxygen uptake during EX2 (153 +/- 9 ml x KJ(-1)) and EX3 (150 +/- 9 ml x KJ(-1)) was higher (p < 0.01 and p < 0.05, respectively) than during EX1 (139 +/- 8 ml x KJ(-1)). The present data suggest that oxidative metabolism does not compensate for the reduction of anaerobic glycolysis during repeated fatiguing exercise.     

Pulmonary gas exchange during exercise in women: effects of exercise type and work increment.

Exercise-induced arterial hypoxemia (EIAH) has been reported in male athletes, particularly during fast-increment treadmill exercise protocols. Recent reports suggest a higher incidence in women. We hypothesized that 1-min incremental (fast) running (R) protocols would result in a lower arterial PO(2) (Pa(O(2))) than 5-min increment protocols (slow) or cycling exercise (C) and that women would experience greater EIAH than previously reported for men. Arterial blood gases, cardiac output, and metabolic data were obtained in 17 active women [mean maximal O(2) uptake (VO(2 max)) = 51 ml. kg(-1). min(-1)]. They were studied in random order (C or R), with a fast VO(2 max) protocol. After recovery, the women performed 5 min of exercise at 30, 60, and 90% of VO(2 max) (slow). One week later, the other exercise mode (R or C) was similarly studied. There were no significant differences in VO(2 max) between R and C. Pulmonary gas exchange was similar at rest, 30%, and 60% of VO(2 max). At 90% of VO(2 max), Pa(O(2)) was lower during R (mean +/- SE = 94 +/- 2 Torr) than during C (105 +/- 2 Torr, P < 0.0001), as was ventilation (85.2 +/- 3.8 vs. 98.2 +/- 4.4 l/min BTPS, P < 0.0001) and cardiac output (19.1 +/- 0.6 vs. 21.1 +/- 1.0 l/min, P < 0.001). Arterial PCO(2) (32.0 +/- 0.5 vs. 30.0 +/- 0.6 Torr, P < 0.001) and alveolar-arterial O(2) difference (A-aDO(2); 22 +/- 2 vs. 16 +/- 2 Torr, P < 0.0001) were greater during R. Pa(O(2)) and A-aDO(2) were similar between slow and fast. Nadir Pa(O(2)) was 相似文献   

Pro- and macroglycogenolysis: relationship with exercise intensity and duration.

We examined the net catabolism of two pools of glycogen, proglycogen (PG) and macroglycogen (MG), in human skeletal muscle during exercise. Male subjects (n = 21) were assigned to one of three groups. Group 1 exercised 45 min at 70% maximal O(2) uptake (VO(2 max)) and had muscle biopsies at rest, 15 min, and 45 min. Group 2 exercised at 85% VO(2 max) to exhaustion (45.4 +/- 3.4 min) and had biopsies at rest, 10 min, and exhaustion. Group 3 performed three 3-min bouts of exercise at 100% VO(2 max) separated by 6 min of rest. Biopsies were taken at rest and after each bout. Group 1 had small MG and PG net glycogenolysis rates (ranging from 3.8 +/- 1.0 to 2.4 +/- 0.6 mmol glucosyl units. kg(-1). min(-1)) that did not change over time. In group 2, the MG glycogenolysis rate remained low and unchanged over time, whereas the PG rate was initially elevated (11.3 +/- 2.3 mmol glucosyl units. kg(-1). min(-1)) and declined (P < or = 0.05) with time. During the first 10 min, PG concentration ([PG]) declined (P < or = 0.05), whereas MG concentration ([MG]) did not. Similarly, in group 3, in both the first and the second bouts of exercise [PG] declined (P < or = 0.05) and [MG] did not, although by the end of the second exercise period the [MG] was lower (P < or = 0.05) than the rest level. The net catabolic rates for PG in the first two exercises were 22.6 +/- 6.8 and 21.8 +/- 8.2 mmol glucosyl units. kg(-1). min(-1), whereas the corresponding values for MG were 17.6 +/- 6.0 and 10.8 +/- 5.6. The MG pool appeared to be more resistant to mobilization, and, when activated, its catabolism was inhibited more rapidly than that of PG. This suggests that the metabolic regulation of the two pools must be different.     

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.     

Epinephrine infusion during moderate intensity exercise increases glucose production and uptake

The glucoregulatory response to intense exercise [IE, >80% maximum O(2) uptake (VO(2 max))] comprises a marked increment in glucose production (R(a)) and a lesser increment in glucose uptake (R(d)), resulting in hyperglycemia. The R(a) correlates with plasma catecholamines but not with the glucagon-to-insulin (IRG/IRI) ratio. If epinephrine (Epi) infusion during moderate exercise were able to markedly stimulate R(a), this would support an important role for the catecholamines' response in IE. Seven fit male subjects (26 +/- 2 yr, body mass index 23 +/- 0.5 kg/m(2), VO(2 max) 65 +/- 5 ml x kg(-1) x min(-1)) underwent 40 min of postabsorptive cycle ergometer exercise (145 +/- 14 W) once without [control (CON)] and once with Epi infusion [EPI (0.1 microg x kg(-1) x min(-1))] from 30 to 40 min. Epi levels reached 9.4 +/- 0.8 nM (20x rest, 10x CON). R(a) increased approximately 70% to 3.75 +/- 0.53 in CON but to 8.57 +/- 0.58 mg x kg(-1) x min(-1) in EPI (P < 0.001). Increments in R(a) and Epi correlated (r(2) = 0.923, P 相似文献   

Mechanistic basis for the gas exchange threshold in Thoroughbred horses.

The exercising Thoroughbred horse (TB) is capable of exceptional cardiopulmonary performance. However, because the ventilatory equivalent for O2 (VE/VO2) does not increase above the gas exchange threshold (Tge), hypercapnia and hypoxemia accompany intense exercise in the TB compared with humans, in whom VE/VO2 increases during supra-Tge work, which both removes the CO2 produced by the HCO buffering of lactic acid and prevents arterial partial pressure of CO2 (PaCO2) from rising. We used breath-by-breath techniques to analyze the relationship between CO2 output (VCO2) and VO2 [V-slope lactate threshold (LT) estimation] during an incremental test to fatigue (7 to approximately 15 m/s; 1 m x s(-1) x min(-1)) in six TB. Peak blood lactate increased to 29.2 +/- 1.9 mM/l. However, as neither VE/VO2 nor VE/VCO2 increased, PaCO2 increased to 56.6 +/- 2.3 Torr at peak VO2 (VO2 max). Despite the presence of a relative hypoventilation (i.e., no increase in VE/VO2 or VE/VCO2), a distinct Tge was evidenced at 62.6 +/- 2.7% VO2 max. Tge occurred at a significantly higher (P < 0.05) percentage of VO2 max than the lactate (45.1 +/- 5.0%) or pH (47.4 +/- 6.6%) but not the bicarbonate (65.3 +/- 6.6%) threshold. In addition, PaCO2 was elevated significantly only at a workload > Tge. Thus, in marked contrast to healthy humans, pronounced V-slope (increase VCO2/VO2) behavior occurs in TB concomitant with elevated PaCO2 and without evidence of a ventilatory threshold.     

Metabolic equivalents during scooter exercise

The purpose of this study was to determine the metabolic equivalents (METs) for scooter exercise (riding a scooter, scootering) and to examine the energy expenditure and the heart rate response, so that the results can be used in health promotion activities. Eighteen young adults (10 males and 8 females) participated in scootering on a treadmill at three different speeds for six minutes each. Before, during, and after the exercise, pulmonary ventilation, oxygen uptake (VO(2)), carbon dioxide product, respiratory exchange ratio (R), and heart rate (HR) were measured. These measurements kept steady states from the 3rd to 6th minute of each different speed session. The MET values acquired during scootering at 80 m.min(-1), 110 m.min(-1), and 140 m.min(-1) were 3.9, 4.3, and 5.0, respectively. Calculated using VO(2) (ml.kg(-1).min(-1))x[4.0+R], the energy consumption for scootering at each speed was 67.0+/-10.6, 73.3+/-10.2, and 84.8+/-7.9 cal.kg(-1).min(-1), respectively. The regression equation between scootering speed (X, m.min(-1)) and VO(2) (Y, ml.kg(-1).min(-1)) is Y=0.062X+8.655, and the regression equation between HR (X, beats.min(-1)) and VO(2)reserve (Y, %) is Y=0.458X-11.264. These equations can be applied to both females and males. Thus, scootering at 80 to 140 m.min(-1) might not be sufficient to improve the cardiorespiratory fitness of young male adults similar to the participants, but it may contribute many healthy benefits to most female adults and even male adults, and improve their health and fitness at the faster speeds.     

Comparison of heart rate deflection and ventilatory threshold during a field cross-country roller-skiing test

This study was to assess whether the point of deflection from linearity of heart rate (HRd) could be an accurate predictor of ventilatory threshold (VT2) during a specific cross-country roller-skiing (RS) test. Ten well-trained cross-country skiers performed a maximal and incremental RS test in the field and a standardized maximal and incremental treadmill running (TR) test in the laboratory. Values of oxygen uptake (VO2) and heart rate (HR) were continuously recorded during all exercises by a portable breath-by-breath gas exchange measurement system and a wireless Polar monitoring system, respectively. The VT2 and HRd points were individually determined by visual analysis during RS. Maximal VO2 (VO2 max) and HR were higher (p < 0.05) during TR (67.1 +/- 7.3 ml x min(-1) x kg(-1) and 196.0 +/- 14.1 bpm, respectively) compared with RS (64.2 +/- 7.3 ml x min(-1) x kg(-1) and 191.5 +/- 13.1 bpm, respectively). However, a high correlation (r = 0.94, p < 0.01) between TR and VO2 max was observed. Paired t-tests showed no significant differences in HR (183.6 +/- 15.1 vs. 185.2 +/- 13.9 bpm) and VO2 (55.5 +/- 7.1 vs. 55.8 +/- 6.1 ml x min(-1) x kg(-1)) at intensities corresponding to HRd and VT2 during the RS test, respectively; Pearson product-moment correlation coefficients demonstrated significant relationships for HR at the HRd and VT2 points (r = 0.99, p < 0.001) as well as for VO2 (r = 0.95, p < 0.001). Our results indicate that the specific incremental RS test is effective in eliciting HRd in the field for all skiers and is an accurate predictor of VT2. These findings give very interesting practical applications to cross-country coaches and skiers to evaluate and control specific aerobic training loads.     

Exercise training in normobaric hypoxia in endurance runners. I. Improvement in aerobic performance capacity.

This study investigates whether a 6-wk intermittent hypoxia training (IHT), designed to avoid reductions in training loads and intensities, improves the endurance performance capacity of competitive distance runners. Eighteen athletes were randomly assigned to train in normoxia [Nor group; n = 9; maximal oxygen uptake (VO2 max) = 61.5 +/- 1.1 ml x kg(-1) x min(-1)] or intermittently in hypoxia (Hyp group; n = 9; VO2 max = 64.2 +/- 1.2 ml x kg(-1) x min(-1)). Into their usual normoxic training schedule, athletes included two weekly high-intensity (second ventilatory threshold) and moderate-duration (24-40 min) training sessions, performed either in normoxia [inspired O2 fraction (FiO2) = 20.9%] or in normobaric hypoxia (FiO2) = 14.5%). Before and after training, all athletes realized 1) a normoxic and hypoxic incremental test to determine VO2 max and ventilatory thresholds (first and second ventilatory threshold), and 2) an all-out test at the pretraining minimal velocity eliciting VO2 max to determine their time to exhaustion (T(lim)) and the parameters of O2 uptake (VO2) kinetics. Only the Hyp group significantly improved VO2 max (+5% at both FiO2, P < 0.05), without changes in blood O2-carrying capacity. Moreover, T(lim) lengthened in the Hyp group only (+35%, P < 0.001), without significant modifications of VO2 kinetics. Despite similar training load, the Nor group displayed no such improvements, with unchanged VO2 max (+1%, nonsignificant), T(lim) (+10%, nonsignificant), and VO2 kinetics. In addition, T(lim) improvements in the Hyp group were not correlated with concomitant modifications of other parameters, including VO2 max or VO2 kinetics. The present IHT model, involving specific high-intensity and moderate-duration hypoxic sessions, may potentialize the metabolic stimuli of training in already trained athletes and elicit peripheral muscle adaptations, resulting in increased endurance performance capacity.     

Electromyographic data do not support a progressive recruitment of muscle fibers during exercise exhibiting a VO2 slow component

The origin of the slow component (SC) of oxygen uptake kinetics, presenting during exercise above the ventilatory threshold (VT), remains unclear. Possible physiologic mechanisms include a progressive recruitment of type II muscle fibers. The purpose of this study was to examine alterations in muscle activity through electromyography (EMG) and mean power frequency (MPF) analysis during heavy cycling exercise. Eight trained cyclists (mean +/- S.E.; age = 30 +/- 3 years, height = 1771 +/- 4 cm, weight = 73.8 +/- 6.5 kg, VO2max = 4.33 +/- 0.28 l min(-1)) completed transitions from 20W to a workload equaling 50% of the difference between V(T) and VO2max. VO2 was monitored using a breath-by-breath measurement system, and EMG data were gathered from surface electrodes placed on the gastrocnemius lateralis and vastus lateralis oblique. Breath-by-breath data were time aligned, averaged, interpolated to 1-s intervals, and modeled with non-linear regression. Mean power frequency (MPF) and RMS EMG values were calculated for each minute during the exercise bout. Additionally, MPF was determined using both isolated EMG bursts and complete pedal revolutions. All subjects exhibited a VO2 SC (mean amplitude = 0.98 +/- 0.16 l min(-1)), yet no significant differences were observed during the exercise bout in MPF or RMS EMG data (p > 0.05) using either analysis technique. While it is possible that the sensitivity of EMG may be insufficient to identify changes in muscle activity theorized to affect the VO2 SC, the data indicated no relationship between MPF/EMG and the SC during heavy cycling.