Detection of the change point in oxygen uptake during an incremental exercise test using recursive residuals: relationship to the plasma lactate accumulation and blood acid base balance

The purpose of this study was to develop a method to determine the power output at which oxygen uptake (V˙O₂) during an incremental exercise test begins to rise non-linearly. A group of 26 healthy non-smoking men [mean age 22.1?(SD 1.4)?years, body mass 73.6?(SD 7.4)?kg, height 179.4?(SD 7.5)?cm, maximal oxygen uptake (V˙O_2max) 3.726?(SD 0.363)?l?·?min^?1], experienced in laboratory tests, were the subjects in this study. They performed an incremental exercise test on a cycle ergometer at a pedalling rate of 70?rev?·?min^?1. The test started at a power output of 30?W, followed by increases amounting to 30?W every 3?min. At 5?min prior to the first exercise intensity, at the end of each stage of exercise protocol, blood samples (1?ml each) were taken from an antecubital vein. The samples were analysed for plasma lactate concentration [La]_pl, partial pressure of O₂ and CO₂ and hydrogen ion concentration [H⁺]_b. The lactate threshold (LT) in this study was defined as the highest power output above which [La^?]_pl showed a sustained increase of more than 0.5?mmol?·?l^?1?·?step^?1. The V˙O₂ was measured breath-by-breath. In the analysis of the change point (CP) of V˙O₂ during the incremental exercise test, a two-phase model was assumed for the 3rd-min-data of each step of the test: X _i =at _i +b+? _i for i=1,2,…,T, and E(X _i )>at _i +b for i =T+1,…,n, where X ₁, … , X _n are independent and ? _i ～N(0,σ²). In the first phase, a linear relationship between V˙O₂ and power output was assumed, whereas in the second phase an additional increase in V˙O₂ above the values expected from the linear model was allowed. The power output at which the first phase ended was called the change point in oxygen uptake (CP-V˙O₂). The identification of the model consisted of two steps: testing for the existence of CP and estimating its location. Both procedures were based on suitably normalised recursive residuals. We showed that in 25 out of 26 subjects it was possible to determine the CP- O₂ as described in our model. The power output at CP-V˙O₂ amounted to 136.8?(SD 31.3)?W. It was only 11?W – non significantly – higher than the power output corresponding to LT. The V˙O₂ at CP-V˙O₂ amounted to 1.828?(SD 0.356)?l?·?min^?1 was [48.9?(SD 7.9)% V˙O_{2 max} ]. The [La^?]_pl at CP-V˙O₂, amounting to 2.57?(SD 0.69)?mmol?·?l^?1 was significantly elevated (P<0.01) above the resting level [1.85?(SD 0.46)?mmol?·?l^?1], however the [H⁺]_b at CP-V˙O₂ amounting to 45.1 (SD 3.0)?nmol?·?l^?1, was not significantly different from the values at rest which amounted to 44.14?(SD 2.79)?nmol?·?l^?1. An increase of power output of 30?W above CP-V˙O₂ was accompanied by a significant increase in [H⁺]_b above the resting level (P=0.03).     

Decreased exercise blood lactate concentrations after respiratory endurance training in humans

For many years, it was believed that ventilation does not limit performance in healthy humans. Recently, however, it has been shown that inspiratory muscles can become fatigued during intense endurance exercise and decrease their exercise performance. Therefore, it is not surprising that respiratory endurance training can prolong intense constant-intensity cycling exercise. To investigate the effects of respiratory endurance training on blood lactate concentration and oxygen consumption (V˙O₂) during exercise and their relationship to performance, 20?healthy, active subjects underwent 30?min of voluntary, isocapnic hyperpnoea 5 days a week, for 4 weeks. Respiratory endurance tests, as well as incremental and constant-intensity exercise tests on a cycle ergometer, were performed before and after the 4-week period. Respiratory endurance increased from 4.6 (SD 2.5) to 29.1?(SD 4.0)?min (P?P?V˙O₂ did not change at any exercise intensity whereas blood lactate concentration was lower at the end of the incremental [10.4 (SD 2.1) vs 8.8?(SD 1.9)?mmol?·?l^?1, P??1, P?相似文献   

Substrate use during and following moderate- and low-intensity exercise: Implications for weight control

Substrate utilization during and after low- and moderate-intensity exercise of similar caloric expenditure was compared. Ten active males [age: 26.9?(4.8) years; height: 181.1?(4.8)?cm; Mass: 75.7?(8.8)?kg; maximum O₂ consumption (V˙O_{2 max} ): 51.2?(4.8)?ml?·?kg^?1?· min^?1] cycled at 33% and 66% V˙O_{2 max} on separate days for 90 and 45 min, respectively. After exercise, subjects rested in a recumbent position for 6?h. Two?h post-exercise, subjects ate a standard meal of 66% carbohydrate (CHO), 11% protein, and 23% fat. Near-continuous indirect calorimetry and measurement of urinary nitrogen excretion were used to determine substrate utilization. Total caloric expenditure was similar for the two trials; however, significantly (P<0.05) more fat [42.4?(3.6)?g versus 24.0?(12.2)?g] and less CHO [142.5?(28.5)?g versus 188.8?(45.2)?g] was utilized as a substrate during the low-intensity compared to the moderate-intensity trial. Protein utilization was similar for the two trials. The difference in substrate use can be attributed to the exercise period because over twice as much fat was utilized during low-intensity [30.0?(11.0)?g] compared to moderate-intensity exercise [13.6?(6.6)?g]. Significantly more (P<0.05) CHO was utilized during the moderate-intensity [106.0?(27.8)?g] compared to the low-intensity exercise [68.7?(20.0)?g]. Substrate use during the recovery period was not significantly different. We conclude that low-intensity, long-duration exercise results in a greater total fat oxidation than does moderate intensity exercise of similar caloric expenditure. Dietary-induced thermogenesis was not different for the two trials.     

Sex-related differences in thermoregulatory responses while wearing protective clothing

This study examined the thermoregulatory responses of men (group M) and women (group F) to uncompensable heat stress. In total, 13?M [mean (SD) age 31.8 (4.7) years, mass 82.7 (12.5)?kg, height?1.79?(0.06)?m, surface area to mass ratio 2.46?(0.18)?m²?·?kg^?1?·?10^?2, Dubois surface area 2.01 (0.16)?m², %body fatness 14.6 (3.9)%, V˙O_2peak 49.0?(4.8)?ml?·?kg^?1?·?min^?1] and 17 F [23.2 (4.2) years, 62.4 (7.7)?kg, 1.65 (0.07)?m, 2.71 (0.14)?m²?·?kg^?1?·?10^?2, 1.68 (0.13)?m², 20.2 (4.8)%, 43.2 (6.6)?ml?·?kg^?1?·?min^?1, respectively] performed light intermittent exercise (repeated intervals of 15?min of walking at 4.0?km?·?h^?1 followed by 15?min of seated rest) in the heat (40°C, 30% relative humidity) while wearing nuclear, biological, and chemical protective clothing (0.29?m²?·°C · W^?1 or 1.88 clo, Woodcock vapour permeability coefficient 0.33?i _m). Group F consisted of eight non-users and nine users of oral contraceptives tested during the early follicular phase of their menstrual cycle. Heart rates were higher for F throughout the session reaching 166.7 (15.9) beats?·?min^?1 at 105?min (n?=?13) compared with 145.1 (14.4)?beats?·?min^?1 for M. Sweat rates and evaporation rates from the clothing were lower and average skin temperature ( ) was higher for F. The increase in rectal temperature (T _re) was significantly faster for the F, increasing 1.52 (0.29)°C after 105?min compared with an increase of 1.37?(0.29)°C for M. Tolerance times were significantly longer for M [142.9?(24.5)?min] than for F [119.3?(17.3)?min]. Partitional calorimetric estimates of heat storage (S) revealed that although the rate of S was similar between genders [42.1?(6.6) and 46.1?(9.7) W?·?m^?2 for F and M, respectively], S expressed per unit of total mass was significantly lower for F [7.76?(1.44)?kJ?·?kg^?1] compared with M [9.45?(1.26) kJ?·?kg^?1]. When subjects were matched for body fatness (n?=?8?F and 8?M), tolerance times [124.5?(14.7) and 140.3?(27.4)?min for F and M, respectively] and S [8.67?(1.44) and 9.39?(1.05)?kJ?·?kg^?1 for F and M, respectively] were not different between the genders. It was concluded that females are at a thermoregulatory disadvantage compared with males when wearing protective clothing and exercising in a hot environment. This disadvantage can be attributed to the lower specific heat of adipose versus non-adipose tissue and a higher percentage body fatness.     

Effect of pedal cadence on the accumulated oxygen deficit, maximal aerobic power and blood lactate transition thresholds of high-performance junior endurance cyclists

In this study we investigated the effect of pedal cadence on the cycling economy, accumulated oxygen deficit (AOD), maximal oxygen consumption (V˙O_2max) and blood lactate transition thresholds of ten high-performance junior endurance cyclists [mean (SD): 17.4 (0.4) years; 183.8?(3.5)?cm, 71.56?(3.75)?kg]. Cycling economy was measured on three ergometers with the specific cadence requirements of: 90–100?rpm for the road dual chain ring (RDCR_90–100rpm) ergometer, 120–130?rpm for the track dual chain ring (TDCR_120–130rpm) ergometer, and 90–130?rpm for the track single chain ring (TSCR_90–130rpm) ergometer. AODs were then estimated using the regression of oxygen consumption (V˙O₂) on power output for each of these ergometers, in conjunction with the data from a 2-min supramaximal paced effort on the TSCR_90–130rpm ergometer. A regression of V˙O₂ on power output for each ergometer resulted in significant differences (P<0.001) between the slopes and intercepts that produced a lower AOD for the RDCR_90–100rpm [2.79 (0.43)?l] compared with those for the TDCR_120–130rpm [4.11?(0.78)?l] and TSCR_90–130rpm [4.06 (0.84)?l]. While there were no statistically significant V˙O_2max differences (P?=?0.153) between the three treatments [RDCR_90–100rpm: 5.31?(0.24)?l?·?min^?1; TDCR_120–130rpm; 5.33?(0.25)?l?·?min^?1; TSCR_90–130rpm: 5.44?(0.27)?l?·?min^?1], all pairwise comparisons of the power output at which V˙O_2max occurred were significantly different (P?90–100rpm and TDCR_120–130rpm tests for power output (P?=?0.003) and blood lactate (P?=?0.003) at the lactate threshold (Th_la?), and for power output (P?=?0.005) at the individual anaerobic threshold (Th_iat). Our findings emphasise that pedal cadence specificity is essential when assessing the cycling economy, AOD and blood lactate transition thresholds of high-performance junior endurance cyclists.     

Effects of 3 days of carbohydrate supplementation on muscle glycogen content and utilisation during a 1-h cycling performance

This study compared the effects of supplementing the normal diets of six trained cyclists [maximal oxygen uptake $(\dot {V}$ O_2max) 4.5 (0.36)l · min^?1; values are mean (SD)] with additional carbohydrate (CHO) on muscle glycogen utilisation during a 1-h cycle time-trial (TT). Using a randomised crossover design, subjects consumed either their normal diet (NORM) for 3 days, which consisted of 426 (137) g · day^?1 CHO [5.9 (1.4) g · kg^?1 body mass (BM)], or additional CHO (SUPP) to increase their intake to 661 (76) g · day^?1 [9.3 (0.7) g · kg^?1 BM]. The SUPP diet elevated muscle glycogen content from 459?(83) to 565?(62) mmol?·?kg^?1 dry weight (d.w.) (P < 0.05). However, despite the increased pre-exercise muscle glycogen stores, there was no difference in the distance cycled during the TT [40.41 (1.44) vs 40.18 (1.76)?km for NORM and SUPP, respectively]. With NORM, muscle glycogen declined from 459 (83) to 175?(64) mmol?·?kg^?1 d.w., whereas with SUPP the corresponding values were 565?(62) and 292?(113) mmol?·?kg^?1 d.w. Accordingly, both muscle glycogen utilisation [277?(64) vs 273?(114) mmol?·?kg^?1 d.w.] and total CHO oxidation [169 (20) vs 165?(30)?g?·?h^?1 for NORM and SUPP, respectively] were similar. Neither were there any differences in plasma glucose or lactate concentrations during the two experimental trials. Plasma glucose concentration averaged 5.5 (0.5) and 5.6 (0.6) mmol?·?l^?1, while plasma lactate concentration averaged 4.4 (1.9) and 4.4 (2.3) mmol?·?l^?1 for NORM and SUPP, respectively. The results of this study show that when well-trained subjects increase the CHO content of their diet for 3 days from 6 to 9 g?·?kg^?1 BM there is only a modest increase in muscle glycogen content. Since supplementary CHO did not improve TT performance, we conclude that additional CHO provides no benefit to performance for athletes who compete in intense, continuous events lasting 1?h. Furthermore, the substantial muscle CHO reserves observed at the termination of exercise indicate that whole-muscle glycogen depletion does not determine fatigue at this exercise intensity and duration.     

Oxygen uptake during moderate intensity running: response following a single bout of interval training

Eight male endurance runners [mean ± (SD): age 25 (6) years; height 1.79?(0.06)?m; body mass 70.5?(6.0)?kg; % body fat 12.5 (3.2); maximal oxygen consumption (V˙O_2max 62.9?(1.7)?ml?·?kg^?1?·?min^?1] performed an interval training session, preceded immediately by test 1, followed after 1?h by test 2, and after 72?h by test 3. The training session was six 800-m intervals at 1?km?·?h^?1 below the velocity achieved at V˙O_2max with 3?min of recovery between each interval. Tests 1, 2 and 3 were identical, and included collection of expired gas, measurement of ventilatory frequency (f _v ), heart rate (f _c), rate of perceived exertion (RPE), and blood lactate concentration ([La^?]_B) during the final 5?min of 15?min of running at 50% of the velocity achieved at V˙O_2max (50% ?V˙O_2max).?Oxygen uptake (V˙O₂), ventilation (V˙ _E ), and respiratory exchange ratio (R) were subsequently determined from duplicate expired gas collections. Body mass and plasma volume changes were measured preceding and immediately following the training session, and before tests 1–3. Subjects ingested water immediately following the training session, the volume of which was determined from the loss of body mass during the session. Repeated measures analysis of variance with multiple comparison (Tukey) was used to test differences between results. No significant differences in body mass or plasma volume existed between the three test stages, indicating that the differences recorded for the measured parameters could not be attributed to changes in body mass or plasma volume between tests, and that rehydration after the interval training session was successful. A significant (P?V˙O₂ [2.128?(0.147) to 2.200?(0.140)?1?·?min^?1], f _c [125 (17) to 132?(16)?beats?· min^?1], and RPE [9 (2) to 11 (2)]. A significant (P?R [0.89 (0.03) to 0.85 (0.04)]. These results suggest that alterations in V˙O₂ during moderate-intensity, constant-velocity running do occur following heavy-intensity endurance running training, and that this is due to factors in addition to changed substrate metabolism towards greater fat utilisation, which could explain only 31% of the increase in V˙O₂.     

The effect of a low-carbohydrate diet on performance, hormonal and metabolic responses to a 30-s bout of supramaximal exercise

The aim of this study was to find out whether a low-carbohydrate diet (L-CHO) affects: (1) the capacity for all-out anaerobic exercise, and (2) hormonal and metabolic responses to this type of exercise. To this purpose, eight healthy subjects underwent a 30-s bicycle Wingate test preceded by either 3 days of a controlled mixed diet (130?kJ/kg of body mass daily, 50% carbohydrate, 30% fat, 20% protein) or 3 days of an isoenergetic L-CHO diet (up to 5% carbohydrate, 50% fat, 45% protein) in a randomized order. Before and during 1?h after the exercise venous blood samples were taken for measurement of blood lactate (LA), β-hydroxybutyrate (β-HB), glucose, adrenaline (A), noradrenaline (NA) and insulin levels. Oxygen consumption (V˙O₂) was also determined. It was found that the L-CHO diet diminished the mean power output during the 30-s exercise bout [533 (7)?W vs 581 (7)?W, P??1, P??1, P??1, P??1] were lower. The 1-h post-exercise excess of V˙O₂ [9.1 (0.25)?vs 10.6 (0.25)?l, P??1, P??1 and 14.30 (1.41)?vs 8.20 (1.31)?nmol?·?l^?1, P?相似文献   

Significant changes in VLDL-Triacylglycerol and glucose tolerance in obese subjects following ten days of training

We characterized the effect of ten days of training on lipid metabolism in 6 [age 37.2 (2.3) years] sedentary, obese [BMI 34.4?(3.0)?kg?·?m^?2] males with normal glucose tolerance. An oral glucose tolerance test was performed prior to and at the end of the 10?d of training period. The duration of each daily exercise session was 40?min at an intensity equivalent to ?75% of the age predicted maximum heart rate. Blood measurements were performed after an overnight fast, before and at the end of the 10?d period. Plasma triacylglycerol was significantly (p??1). Very low density lipoprotein-triacylglycerol was also significantly?(p??1). No significant changes in high density lipoprotein-cholesterol were observed as a result of training. Following training fasting plasma glucose and fasting plasma insulin were significantly reduced [Glucose: 5.9 (0.2)?mmol?·?l^?1 vs.?5.3 (0.22)?mmol?·?l^?1 (p??1 vs. 200.9 (30.1) ρ?·?mol?·?l^?1, p?=?0.05]. The total area under the glucose curve during the OGTT decreased significantly (p?相似文献   

Oxygen uptake does not increase linearly at high power outputs during incremental exercise test in humans

A group of 12 healthy non-smoking men [mean age 22.3 (SD 1.1)?years], performed an incremental exercise test. The test started at 30?W, followed by increases in power output (P) of 30?W every 3 min, until exhaustion. Blood samples were taken from an antecubital vein for determination of plasma concentration lactate [La^?]_pl and acid-base balance variables. Below the lactate threshold (LT) defined in this study as the highest P above which a sustained increase in [La^?]_pl was observed (at least 0.5 mmol?·?l^?1 within 3 min), the pulmonary oxygen uptake (V˙O₂) measured breath-by-breath, showed a linear relationship with P. However, at P above LT [in this study 135 (SD 30)?W] there was an additional accumulating increase in V˙O₂ above that expected from the increase in P alone. The magnitude of this effect was illustrated by the difference in the final P observed at maximal oxygen uptake (V˙O_2max) during the incremental exercise test (P _max,obs at V˙O_2max) and the expected power output at V˙O_2max(P _max,exp at V˙O_2max) predicted from the linear V˙O₂-P relationship derived from the data collected below LT. The P _max,obs at V˙O_2max amounting to 270 (SD 19)?W was 65.1 (SD 35)?W (19%) lower (P<0.01) than the P _max,exp at V˙O_{2max .} The mean value of V˙O_2max reached at P _max,obs amounted to 3555 (SD 226)?ml?·?min^?1 which was 572 (SD 269)?ml?·?min^?1 higher (P<0.01) than the V˙O₂ expected at this P, calculated from the linear relationship between V˙O₂ and P derived from the data collected below LT. This fall in locomotory efficiency expressed by the additional increase in V˙O₂, amounting to 572 (SD 269) ml O₂?·?min^?1, was accompanied by a significant increase in [La^?]_pl amounting to 7.04 (SD 2.2)?mmol?·?l^?1, a significant increase in blood hydrogen ion concentration ([H⁺]_b) to 7.4 (SD 3)?nmol?·?l^?1 and a significant fall in blood bicarbonate concentration to 5.78 (SD 1.7)?mmol?·?l^?1, in relation to the values measured at the P of the LT. We also correlated the individual values of the additional V˙O₂ with the increases (Δ) in variables [La^?]_pl and Δ[H⁺]_b. The Δ values for [La^?]_pl and Δ[H⁺]_b were expressed as the differences between values reached at the P _max,obs at V˙O_2max and the values at LT. No significant correlations between the additional V˙O₂ and Δ[La^?]_pl on [H⁺]_b were found. In conclusion, when performing an incremental exercise test, exceeding P corresponding to LT was accompanied by a significant additional increase in V˙O₂ above that expected from the linear relationship between V˙O₂ and P occurring at lower P. However, the magnitude of the additional increase in V˙O₂ did not correlate with the magnitude of the increases in [La^?]_pl and [H⁺]_b reached in the final stages of the incremental test.     

Failure to obtain a unique threshold on the blood lactate concentration curve during exercise

The purpose of this study was to compare various methods and criteria used to identify the anaerobic threshold (AT), and to correlate the AT obtained with each other and with running performance. Furthermore, a number of additional points throughout the entire range of lactate concentrations [La^?] were obtained and correlated with performance. A group of 19 runners [mean age 33.7 (SD 9.6) years, height 173 (SD 6.3) cm, body mass 68.3 (SD 5.4)?kg, maximal O₂ uptake (V˙O_{2 max} ) 55.2 (SD 5.9)?ml?·?kg^?1?·?min^?1] performed a maximal multistage treadmill test (1?km?·?h^?1 every 3.5?min) with blood sampling at the end of each stage while running. All AT points selected (visual [La^?], 4?mmol?·?l^?1 [La^?], 1?mmol?·?l^?1 above baseline, log-log breakpoint, and 45° tangent to the exponential regression) were highly correlated one with another and with performance (r?>?0.90) even when there were many differences among the AT (P??1 [La^?], 1 to 6?mmol?·?l^?1 [La^?] above the baseline, and 30 to 70° tangent to the exponential curve of [La^?]) were also highly correlated with performance (r?>?0.90). These results failed to demonstrate a distinct AT because many points of the curve provided similar information. Intercorrelations and correlations between AT and performance were, however, reduced when AT were expressed as the percentage of maximal treadmill speed obtained at AT or percentage of V˙O_{2 max} . This would indicate that different attributes of aerobic performance (i.e. maximal aerobic power, running economy and endurance) are measured when manipulating units. Thus, coaches should be aware of these results when they prescribe an intensity for training and concentrate more on the physiological consequences of a chosen [La^?] rather than on a “threshold”.     

Effect of muscle glycogen availability on maximal exercise performance

This investigation determined the influence of pre-exercise muscle glycogen availability on performance during high intensity exercise. Nine trained male cyclists were studied during 75 s of all-out exercise on an air-braked cycle ergometer following muscle glycogen-lowering exercise and consumption of diets (energy content approximately 14 MJ) that were either high (HCHO – 80% CHO) or low (LCHO – 25% CHO) in carbohydrate content. The exercise-diet regimen was successful in producing differences in pre-exercise muscle glycogen contents [HCHO: 578(SEM?55) mmol?·?kg^?1 dry mass; LCHO: 364 (SEM 58) P??1 dry mass]. Despite this difference in muscle glycogen availability, there were no between trial differences for peak power [HCHO 1185 (SEM 50)W, LCHO 1179 (SEM?48)W], mean power [HCHO 547 (SEM?5)W, LCHO 554 (SEM ?8)W] and maximal accumulated oxygen deficit [HCHO 54.4 (SEM?2.3)?ml?·?kg^?1, LCHO 54.6 (SEM?2.0) ml?·?kg^?1]. Postexercise muscle lactate contents (HCHO 95.9 (SEM?4.6)?mmol?·?kg^?1 dry mass, LCHO 82.7 (SEM?12.3) mmol?·?kg^?1 dry mass, n?=?8] were no different between the two trials, nor were venous blood lactate concentrations immediately after and during recovery from exercise. These results would indicate that increased muscle glycogen availability has no direct effect on performance during all-out high intensity exercise.     

V˙O2peak and the gas-exchange anaerobic threshold during incremental arm cranking in able-bodied and paraplegic men

Resting energy expenditure, peak oxygen uptake (V˙O_2peak) and the gas-exchange anaerobic threshold (Th_an) were measured during incremental arm cranking (15?W?·?min^?1) in six able-bodied (AB) and six paraplegic (P) subjects. Only male subjects with traumatic spinal cord injuries in the area of the 10–12th thoracic segment were included in the P group. All AB and P subjects were physically active. Mean (SE) values for age and body mass were 28 (2)?years and 78.9 (3.9)?kg for the AB group and 32 (4)?years and 70.8 (7.9)?kg for the P group (P?>?0.05). Resting energy expenditure values were not found to be significantly different between AB [5.8 (0.2)?kJ?·?min^?1] and P [5.1 (0.3)?kJ?·?min^?1] subjects. Mean V˙O_2peak values were 29.3 (2.4)?ml?· kg^?1?· min^?1 and 29.6 (2.2)?ml?·?kg^?1?·?min^?1 for the AB and P groups, respectively (P?>?0.05). Absolute oxygen uptake values measured at two gas-exchange anaerobic threshold (Th_an) were not significantly different between the two groups. However, the Th_an occurred at a significantly higher percentage of V˙O_2peak in the P [58.9 (1.7)%] group than in the AB [50.0 (2.8)%] group (P?R) values obtained at the Th_an and at 15, 45, 60, 75 and 90?W of incremental exercise were significantly lower in the P group than in the AB group. Heart rates were significantly elevated at every submaximal work stage (15–120?W) in the P group compared to the AB group (P?R) during arm exercise. These local adaptations may be in part responsible for the significantly higher Th_an observed for arm exercise in P subjects, even though V˙O_2peak values were essentially the same for both groups.     

Plasma hypoxanthine and ammonia in humans during prolonged exercise

In this study we examined the time course of changes in the plasma concentration of oxypurines [hypoxanthine (Hx), xanthine and urate] during prolonged cycling to fatigue. Ten subjects with an estimated maximum oxygen uptake (V˙O_2max) of 54 (range 47–67) ml?·?kg^?1?·?min^?1 cycled at [mean?(SEM)] 74?(2)% of V˙O_2max until fatigue [79?(8) min]. Plasma levels of oxypurines increased during exercise, but the magnitude and the time course varied considerably between subjects. The plasma concentration of Hx ([Hx]) was 1.3?(0.3)?μmol/l at rest and increased eight fold at fatigue. After 60?min of exercise plasma [Hx] was >10?μmol/l in four subjects, whereas in the remaining five subjects it was <5?μmol/l. The muscle contents of total adenine nucleotides (TAN?=?ATP+ADP+AMP) and inosine monophosphate (IMP) were measured before and after exercise in five subjects. Subjects with a high plasma [Hx] at fatigue also demonstrated a pronounced decrease in muscle TAN and increase in IMP. Plasma [Hx] after 60?min of exercise correlated significantly with plasma concentration of ammonia ([NH₃], r?=?0.90) and blood lactate (r?=?0.66). Endurance, measured as time to fatigue, was inversely correlated to plasma [Hx] at 60?min (r?=??0.68, P?3] or blood lactate. It is concluded that during moderate-intensity exercise, plasma [Hx] increases, but to a variable extent between subjects. The present data suggest that plasma [Hx] is a marker of adenine nucleotide degradation and energetic stress during exercise. The potential use of plasma [Hx] to assess training status and to identify overtraining deserves further attention.     

Cerebral blood flow velocity responses to hypoxia in subjects who are susceptible to high-altitude pulmonary oedema

Cerebral blood flow increases on exposure to high altitude, and perhaps more so in subjects who develop acute mountain sickness. We determined cerebral blood flow by transcranial Doppler ultrasound of the middle cerebral artery at sea level, in normoxia (fraction of inspired O₂, F _IO₂ 0.21), and during 15-min periods of either hypoxic (F _IO₂ 0.125) or hyperoxic (F _IO₂ 1.0) breathing, in 7 subjects with previous high-altitude pulmonary oedema, 6 climbers who had previously tolerated altitudes between 6000?m and 8150?m, and in 20 unselected controls. Hypoxia increased mean middle cerebral artery flow velocity from 69 (3) to 83 (4) cm?·?s^?1 (P??1 (P??1 (P??1 (P??1 (P??1 (P?相似文献   

Relationship between maximal oxygen uptake on different ergometers, lean arm volume and strength in paraplegic subjects

The present experiment was designed to study the importance of strength and muscle mass as factors limiting maximal oxygen uptake (V˙O_{2 max} ) in wheelchair subjects. Thirteen paraplegic subjects [mean age 29.8 (8.7) years] were studied during continuous incremental exercises until exhaustion on an arm-cranking ergometer (AC), a wheelchair ergometer (WE) and motor-driven treadmill (TM). Lean arm volume (LAV) was estimated using an anthropometric method based upon the measurement of various circumferences of the arm and forearm. Maximal strength (MVF) was measured while pushing on the rim of the wheelchair for three positions of the hand on the rim (?30°, 0° and +30°). The results indicate that paraplegic subjects reached a similar V˙O_{2 max} [1.23 (0.34) l?·?min^?1, 1.25 (0.38) l?·?min^?1, 1.22?(0.18) l?·?min^?1 for AC, TM and WE, respectively] and V˙O_{2 max} /body mass [19.7?(5.2)?ml?·?min^?1?·?kg^?1, 19.5 (6.14) ml?·?min^?1?·?kg^?1, 19.18 (4.27) ml?·?min^?1?·?kg^?1 for AC, TM and WE, respectively on the three ergometers. Maximal heart rate f _{c max} during the last minute of AC (173 (17) beats?·?min^?1], TM [168 (14) beats?·?min^?1], and WE [165 (16) beats?·?min^?1], were correlated, but f _{c max} was significantly higher for AC than for TM (P<0.03). There were significant correlations between MVF and LAV (P<0.001) and between the MVF data obtained at different angles of the hand on the rim [311.9 (90.1) N, 313.2 (81.2) N, 257.1 (71) N, at ?30°, 0° and +30°, respectively]. There was no correlation between V˙O_{2 max} and LAV or MVF. The relatively low values of f _{c max} suggest that V˙O_{2 max} was, at least in part, limited by local aerobic factors instead of central cardiovascular factors. On the other hand, the lack of a significant correlation between V˙O_{2 max} and MVF or muscle mass was not in favour of muscle strength being the main factor limiting V˙O_{2 max} in our subjects.     

Effect of work and recovery duration on skeletal muscle oxygenation and fuel use during sustained intermittent exercise

The purpose of this study was to compare rates of substrate oxidation in two protocols of intermittent exercise, with identical treadmill speed and total work duration, to reduce the effect of differences in factors such as muscle fibre type activation, hormonal responses, muscle glucose uptake and non-esterified fatty acid (NEFA) availability on the comparison of substrate utilisation. Subjects (n?=?7) completed 40?min of intermittent intense running requiring a work:recovery ratio of either 6?s:9?s (short-interval exercise, SE) or 24?s:36?s (long-interval exercise, LE), on separate days. Another experiment compared O₂ availability in the vastus lateralis muscle across SE (10?min) and LE (10?min) exercise using near-infrared spectroscopy (RunMan, NIM. Philadelphia, USA). Overall (i.e. work and recovery) O₂ consumption (V˙O₂) and energy expenditure were lower during LE (P?P?V˙O_2peak), was [mean (SEM)] 64.9?(2.7)% V˙O_2peak (LE) and 71.4?(2.4)% V˙O_2peak (SE). Fat oxidation was three times lower (P?P?P?P?P?n?=?4) or plasma noradrenaline and adrenaline. Muscle oxygenation declined in both protocols (P?P?r?=?0.68; P?n?=?12). Lower levels of fat oxidation occurred concurrent with accelerated carbohydrate metabolism, increases in lactate and pyruvate and reduced muscle O₂ availability. These changes were associated with proportionately longer work and recovery periods, despite identical treadmill speed and total work duration. The proposal that a metabolic regulatory factor within the muscle fibre retards fat oxidation under these conditions is supported by the current findings.     

A comparison of skeletal muscle oxygenation and fuel use in sustained continuous and intermittent exercise

In this study we compared substrate oxidation and muscle oxygen availability during sustained intermittent intense and continuous submaximal exercise with similar overall (i.e. work and recovery) oxygen consumption (V˙O₂). Physically active subjects (n?=?7) completed 90?min of an intermittent intense (12?s work:18?s recovery) and a continuous submaximal treadmill running protocol on separate days. In another experiment (n?=?5) we compared oxygen availability in the vastus lateralis muscle between these two exercise protocols using near-infrared spectroscopy. Initially, overall V˙O₂ (i.e. work and recovery) was matched, and from 37.5?min to 67.5?min of exercise was similar, although slightly higher during continuous exercise (8%; P??1?·?kg^?1] and continuous submaximal [0.85 (0.01)?kJ?·?min^?1?·?kg^?1] exercise. Overall exercise intensity, represented as a proportion of peak aerobic power (V˙O_2peak), was 68.1 (2.5)% V˙O_2peak and 71.8 (1.8)% V˙O_2peak for intermittent and continuous exercise protocols, respectively. Fat oxidation was almost 3 times lower (P?P?P?P?P?r?=?0.72; P?V˙O₂ and identical energy expenditure.     

Comparison of cardiopulmonary responses to two types of dry-land upper-body exercise testing modes in competitive swimmers

In this study we compared cardiopulmonary responses to upper-body exercise in 12 swimmers, using simulation of the front-crawl arm-pulling action on a computer-interfaced isokinetic swim bench and arm cranking on a modified cycle ergometer. Subjects adopted a prone posture; exercise was initially set at 20?W and subsequently increased by 10?W?·?min^?1. The tests were performed in a randomised order at the same time of day, within 72?h. The highest (peak) oxygen consumption (V˙O_2peak), heart rate (HR_peak), blood lactate ([la^?]_peak) and exercise intensity (EI_peak) were recorded at exhaustion. Mean (SEM) peak responses to simulated swimming were higher than those to arm cranking for V˙O_2peak [2.9 (0.2) vs 2.4 (0.1) l?·?min^?1; P?=?0.01], HR_peak [174 (2) vs 161 (2) beats?·?min^?1; P?=?0.03], and EI_peak [122 (6) vs 102 (5) W; P?=?0.02]. However, there were no significant differences in [la^?]_peak [9.6 (0.6) vs 8.2 (0.6) mmol?·?l^?1; P?=?0.08]. Thus simulated swimming is the preferred form of dry-land ergometry for the assessment of swimmers.     

Vascular endothelial growth factor in exercising humans under different environmental conditions

It was the aim of this study to investigate the time course of changes in the serum concentrations of vascular endothelial growth factor (VEGF) during a regular survival training programme combined with food and fluid deprivation and during a high altitude marathon run. We studied soldiers of the Austrian Special Forces performing survival training at sea-level and marathon runners of the Posta Atletica who crossed the border between Chile and Argentina at altitudes up to 4722?m. Baseline data collected before the 1-week of survival training showed that the soldiers had normal VEGF [n=8, 246.7?(SD 118.5)?pg?·?ml^?1] serum concentrations which remained unchanged during the course of the study. Before the high altitude marathon the subjects showed normal VEGF serum concentrations [178?(SD 84.5)?pg?·?ml^?1]. After the run VEGF concentrations were found to be significantly decreased [41.0?(SD 41.6)?pg?·?ml^?1, P?相似文献