Live high:train low increases muscle buffer capacity and submaximal cycling efficiency

This study investigated whether hypoxic exposure increased muscle buffer capacity (βm) and mechanical efficiency during exercise in male athletes. A control (CON, n=7) and a live high:train low group (LHTL, n=6) trained at near sea level (600 m), with the LHTL group sleeping for 23 nights in simulated moderate altitude (3000 m). Whole body oxygen consumption (V˙O ₂) was measured under normoxia before, during and after 23 nights of sleeping in hypoxia, during cycle ergometry comprising 4×4‐min submaximal stages, 2‐min at 5.6 ± 0.4 W kg^–1, and 2‐min ‘all‐out’ to determine total work and V˙O _2peak. A vastus lateralis muscle biopsy was taken at rest and after a standardized 2‐min 5.6 ± 0.4 W kg^–1 bout, before and after LHTL, and analysed for βm and metabolites. After LHTL, βm was increased (18%, P < 0.05). Although work was maintained, V˙O _2peak fell after LHTL (7%, P < 0.05). Submaximal V˙O ₂ was reduced (4.4%, P < 0.05) and efficiency improved (0.8%, P < 0.05) after LHTL probably because of a shift in fuel utilization. This is the first study to show that hypoxic exposure, per se, increases muscle buffer capacity. Further, reduced V˙O ₂ during normoxic exercise after LHTL suggests that improved exercise efficiency is a fundamental adaptation to LHTL.     

Metabolic and hormonal responses during repeated bouts of brief and intense exercise: effects of pre-exercise glucose ingestion

We investigated metabolic and hormonal responses during repeated bouts of brief and intense exercise (a force-velocity test; Fv test) and examined the effect of glucose ingestion on these responses and on exercise performance. The test was performed twice by seven subjects [27 (2) years] according to a double-blind randomized crossover protocol. During the experimental trial (GLU), the subjects ingested 500 ml of glucose polymer solution containing 25 g glucose 15 min before starting the exercise. During the control trial (CON), the subjects received an equal volume of sweet placebo (aspartame). Exercise performance was assessed by calculating peak anaerobic power ( W˙ _an,peak). Venous plasma lactate concentration increased significantly during the Fv test (P P? W˙ _an,peak and for up to 10?min during the recovery period (P? W˙ _an,peak in GLU compared with CON (P?P? W˙ _an,peak (P? W˙ _an,peak was not significantly different between CON and GLU. In conclusion, blood glucose and insulin concentrations decreased during repeated bouts of brief and intense exercise, while blood lactate concentration increased markedly without any significant change in glucagon and epinephrine concentrations. Glucose ingestion altered metabolic and hormonal responses during the Fv test, but the performance as measured by W˙ _an,peak was not changed.     

Anaerobic contribution to the time to exhaustion at the minimal exercise intensity at which maximal oxygen uptake occurs in elite cyclists, kayakists and swimmers

Using 23 elite male athletes (8 cyclists, 7 kayakists, and 8 swimmers), the contribution of the anaerobic energy system to the time to exhaustion (t _lim) at the minimal exercise intensity (speed or power) at which maximal oxygen uptake (V˙O_{2 max}) occurs (I _{V˙O2 max}) was assessed by analysing the relationship between the t _lim and the accumulated oxygen deficit (AOD). After 10-min warming up at 60% of V˙O_{2 max}, the exercise intensity was increased so that each subject reached his I _V˙O2max in 30?s and then continued at that level until he was exhausted. Pre-tests included a continuous incremental test with 2?min steps for determining the I _V˙O2max and a series of 5-min submaximal intensities to collect the data that would allow the estimation of the energy expenditure at I _V˙O2max . The AOD for the t _lim exercise was calculated as the difference between the above estimation and the accumulated oxygen uptake. The mean percentage value of energy expenditure covered by anaerobic metabolism was 15.2 [(SD 6)%, range 8.9–24.1] with significant differences between swimmers and kayakists (16.8% vs 11.5%, P≤0.05) and cyclists and kayakists (16.4% vs 11.5%, P≤0.05). Absolute AOD values ranged from 26.4?ml?·?kg^?1 to 83.6?ml?·?kg^?1 with a mean value of 45.9 (SD 18)?ml?·?kg^?1. Considering all the subjects, the t _lim was found to have a positive and significant correlation with AOD (r?=?0.62, P≤0.05), and a negative and significant correlation with V˙O_{2 max} (r?=??0.46, P≤0.05). The data would suggest that the contribution of anaerobic processes during exercise performed at I _V˙O2max should not be ignored when t _lim is used as a supplementary parameter to evaluate specific adaptation of athletes.     

Change point in V˙CO2 during incremental exercise test: a new method for assessment of human exercise tolerance

The main purpose of this study was to present a new method to determine the level of power output (PO) at which V˙CO ₂ during incremental exercise test (IT) begins to rise non-linearly in relation to power output (PO) – the change point in V˙CO ₂ (CP-V˙CO ₂). Twenty-two healthy non-smoking men (mean ± SD: age 22.0 ± 0.9 years; body mass 74.5 ± 7.5 kg; height 181 ± 7 cm; V˙O _2max 3.753 ± 0.335 l min^–1) performed an IT on a cycloergometer. The IT started at a PO of 30 W, followed by gradual increases of 30 W every 3 min. Antecubital venous blood samples were taken at the end of each step and analysed for plasma lactate concentration [La]_pl, blood PO ₂, PCO ₂ [HCO₃^–]_b and [H⁺]_b. In the detection of the change-point V˙CO ₂ (CP-V˙CO ₂), a two-phase model was assumed for the ‘third-minute-data’ of each step of the test. In the first phase, a linear relationship between V˙CO ₂ and PO was assumed, whereas in the second, an additional increase in V˙CO ₂ was allowed, above the values expected from the linear model. The PO at which the first phase ends is called the change point in V˙CO ₂. The identification of the model consists of two steps: testing for the existence of the change point, and estimating its location. Both procedures are based on suitably normalized recursive residuals (see 32 . Eur J Appl Physiol 78 , 369–377). In the case of each of our subjects it was possible to detect the CP-V˙CO ₂ and the CP-V˙O ₂ as described in our model. The PO at the CP-V˙CO ₂ amounted to 134 ± 42 W. The CP- V˙O ₂ was detected at 136 ± 32 W, whereas the PO at the LT amounted to 128 ± 30 W and corresponded to 49 ± 11, 49 ± 8 and 47 ± 8.6% V˙O _2max, respectively, for the CP-V˙CO ₂, CP-V˙O ₂ and the LT. The [La]_pl at the CP-V˙CO ₂ (2.65 ± 0.76 mmol L^–1), at the CP-V˙O ₂ (2.53 ± 0.56 mmol L^–1) and at the LT (2.25 ± 0.49 mmol L^–1) were already significantly higher (P < 0.01, Students t-test) than the value reached at rest (1.86 ± 0.43 mmol L^–1). Our study illustrates that the CP-V˙CO ₂ and the CP-V˙O ₂ occur at a very similar power output as the LT. We therefore postulate that the CP-V˙CO ₂ and the CP-V˙O ₂ be applied as an additional criterion to assess human exercise tolerance.     

Effect of training intensity on insulin sensitivity as evaluated by insulin tolerance test

The purpose of this study was to evaluate the role of exercise intensity in the effect of physical training on insulin sensitivity. The insulin tolerance test (ITT) was applied to quantify insulin sensitivity. Eighteen healthy, young, untrained men and women participated in a 4-week, five times per week, 1-h per session bicycle-ergometer training program. Training consisted of 3-min bouts of cycling interspersed with 2?min at a lower exercise intensity. Intensities were 80 and 40% of pretraining maximal power output (W˙ _max) in the high-intensity (HI) and 40 and 20% W˙ _max in the low-intensity (LI) group. The insulin sensitivity index (IS_index) was similar in the HI and LI group before the training intervention [mean (SD) ?0.1898 (0.058) and ?0.1892 (0.045), respectively]. After training, the IS_index was ?0.2358 (0.051) (P?=?0.005 vs pretraining) in the HI group and ?0.2050 (0.035) (P?=?0.099 against pretraining) in the LI group. We conclude that improvements in insulin sensitivity are more pronounced with high-intensity training, when exercise frequency and duration are kept similar. We further conclude that the ITT is suitable for use in intervention studies.     

Intracellular hyperhydration induced by a 7-day endurance race

A group of 15 competitive male cyclists [mean peak oxygen uptake, V˙O_2peak 68.5 (SEM 1.5?ml?· kg^?1?·?min^?1)] exercised on a cycle ergometer in a protocol which began at an intensity of 150?W and was increased by 25?W every 2?min until the subject was exhausted. Blood samples were taken from the radial artery at the end of each exercise intensity to determine the partial pressures of blood gases and oxyhaemoglobin saturation (S _aO₂), with all values corrected for rectal temperature. The S _a O₂ was also monitored continuously by ear oximetry. A significant decrease in the partial pressure of oxygen in arterial blood (P _aO₂) was seen at the first exercise intensity (150?W, about 40% V˙O_2peak). A further significant decrease in P _aO₂ occurred at 200?W, whereafter it remained stable but still significantly below the values at rest, with the lowest value being measured at 350?W [87.0 (SEM 1.9) mmHg]. The partial pressure of carbon dioxide in arterial blood (P _aCO₂) was unchanged up to an exercise intensity of 250?W whereafter it exhibited a significant downward trend to reach its lowest value at an exercise intensity of 375?W [34.5 (SEM 0.5) mmHg]. During both the first (150?W) and final exercise intensities (V˙O_2peak) P _aO₂ was correlated significantly with both partial pressure of oxygen in alveolar gas (P _AO₂, r?=?0.81 and r?=?0.70, respectively) and alveolar-arterial difference in oxygen partial pressure (P _A?aO₂, r?=?0.63 and r?=?0.86, respectively) but not with P _aCO₂. At V˙O_2peak P _aO₂ was significantly correlated with the ventilatory equivalents for both oxygen uptake and carbon dioxide output (r?=?0.58 and r?=?0.53, respectively). When both P _AO₂ and P _A?aO₂ were combined in a multiple linear regression model, at least 95% of the variance in P _aO₂ could be explained at both 150?W and V˙O_2peak. A significant downward trend in S _aO₂ was seen with increasing exercise intensity with the lowest value at 375?W [94.6 (SEM 0.3)%]. Oximetry estimates of S _aO₂ were significantly higher than blood measurements at all times throughout exercise and no significant decrease from rest was seen until 350?W. The significant correlations between P _aO₂ and P _AO₂ with the first exercise intensity and at V˙O_2peak led to the conclusion that inadequatehyperventilation is a major contributor to exercise-induced hypoxaemia.     

Breathing pattern in highly competitive cyclists during incremental exercise

The purpose of our investigation was to analyse the breathing patterns of professional cyclists during incremental exercise from submaximal to maximal intensities. A group of 11 elite amateur male road cyclists [E, mean age 23 (SD 2) years, peak oxygen uptake (V˙O_2peak) 73.8 (SD 5.0) ml?·?kg^?1?·?min^?1] and 14 professional male road cyclists [P, mean age 26 (SD 2) years, (V˙O_2peak) 73.2 (SD 6.6) ml?·?kg^?1?·?min^?1] participated in this study. Each of the subjects performed an exercise test on a cycle ergometer following a ramp protocol (exercise intensity increases of 25?W?·?min^?1) until the subject was exhausted. For each subject, the following parameters were recorded during the tests: oxygen consumption (V˙O₂), carbon dioxide output (V˙CO₂), pulmonary ventilation (V˙ _E), tidal volume (V _T), breathing frequency (f _b), ventilatory equivalents for oxygen (V˙ _E·V˙O₂ ^?1) and carbon dioxide (V˙ _E·V˙CO₂ ^?1), end-tidal partial pressure of oxygen and partial pressure of carbon dioxide, inspiratory (t _I) and expiratory (t _E) times, inspiratory duty cycle (t _I/t _TOT, where t _TOT is the time for one respiratory cycle), and mean inspiratory flow rate (V _T/t _I). Mean values of V˙ _E were significantly higher in E at 300, 350 and 400?W (P?P?P?f _b was also higher in E in most moderate-to-maximal intensities. On the other hand, V _T showed a different pattern in both groups at near-to maximal intensities, since no plateau was observed in P. The response of t _I and t _E was also different. Finally, V _T/t _I and t _I/t _TOT showed a similar response in both P and E. It was concluded that the breathing pattern of the two groups differed mainly in two aspects: in the professional cyclists, V˙ _E increased at any exercise intensity as a result of increases in both V _T and f _b, with no evidence of tachypnoeic shift, and t _E was prolonged in this group at high exercise intensities. In contrast, neither the central drive nor the timing component of respiration seem to have been significantly altered by the training demands of professional cycling.     

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

The so-called velocity associated with V˙O_2max, defined as the minimal velocity which elicits V˙O_2max in an incremental exercise protocol (v _{V˙ O2max}), is currently used for training to improve V˙O_2max. However, it is well known that it is not the sole velocity which elicits V˙O_2max and it is possible to achieve V˙O_2max at velocities lower and higher than v _{V˙ O2max}. The goal of this study was to determine the velocity which allows exercise to be maintained the longest time at V˙O_2max. Using the relationship between time to exhaustion at V˙O_2max in the all-out runs at 90%, 100%, 120% and 140% of v _{V˙ O2max} and distance run at V˙O_2max, the velocity which elicits the longest time to exhaustion at V˙O_2max (CV′) was determined. For the six subjects tested (physical education students), this velocity was not significantly different from v _{V˙ O2max} (16.96?±?0.92?km?·?h^?1 vs 17.22?± 1.12?km?·?h^?1, P?=?0.2 for CV′ and v _{V˙ O2max}, respectively) and these two velocities were correlated (r?=?0.88, P?=?0.05).     

Hyperoxia does not increase peak muscle oxygen uptake in small muscle group exercise

We examined the influence of hyperoxia on peak oxygen uptake (V˙O _2peak) and peripheral gas exchange during exercise with the quadriceps femoris muscle. Young, trained men (n=5) and women (n=3) performed single-leg knee-extension exercise at 70% and 100% of maximum while inspiring normal air (NOX) or 60% O₂ (HiOX). Blood was sampled from the femoral vein of the exercising limb and from the contralateral artery. In comparison with NOX, hyperoxic arterial O₂ tension (P_aO ₂) increased from 13.5 ± 0.3 (x ± SE) to 41.6 ± 0.3 kPa, O₂ saturation (S_aO ₂) from 98 ± 0.1 to 100 ± 0.1%, and O₂ concentration (C_aO ₂) from 177 ± 4 to 186 ± 4 mL L^–1 (all P < 0.01). Peak exercise femoral venous PO ₂ (P_vO ₂) was also higher in HiOX (3.68 ± 0.06 vs. 3.39 ± 0.7 kPa; P < 0.05), indicating a higher O₂ diffusion driving pressure. HiOX femoral venous O₂ saturation averaged 36.8 ± 2.0% as opposed to 33.4 ± 1.5% in NOX (P < 0.05) and O₂ concentration 63 ± 6 vs. 55 ± 4 mL L^–1 (P < 0.05). Peak exercise quadriceps blood flow (Q˙_leg), measured by the thermo-dilution technique, was lower in HiOX than in NOX, 6.4 ± 0.5 vs. 7.3 ± 0.9 L min^–1 (P < 0.05); mean arterial blood pressure at inguinal height was similar in NOX and HiOX at 144 and 142 mmHg, respectively. O₂ delivery to the limb (Q˙_leq times C_aO ₂) was not significantly different in HiOX and NOX. V˙O _2peak of the exercising limb averaged 890 mL min^–1 in NOX and 801 mL min^–1 in HiOX (n.s.) corresponding to 365 and 330 mL min^–1 per kg active muscle, respectively. The V˙O _2peak-to-P_vO ₂ ratio was lower (P < 0.05) in HiOX than in NOX suggesting a lower O₂ conductance. We conclude that the similar V˙O _2peak values despite higher O₂ driving pressure in HiOX indicates a peripheral limitation for V˙O _2peak. This may relate to saturation of the rate of O₂ turnover in the mitochondria during exercise with a small muscle group but can also be caused by tissue diffusion limitation related to lower O₂ conductance.     

Water immersion delays the oxygen uptake response to sitting arm-cranking in humans

We investigated the effect of central hypervolaemia during water immersion up to the xiphoid process on the oxygen uptake (V˙O₂) and heart rate (HR) response to arm cranking. Seven men performed a 6-min arm-cranking exercise at an intensity requiring a V˙O₂ at 80% ventilatory threshold both in air [C trial, 29 (SD 9)?W] and immersed in water [WI trial, 29 (SD 11)?W] after 6 min of sitting. The V˙O₂ (phase 2) and HR responses to exercise were obtained from a mono-exponential fit [f(t)=baseline+gain·(1?e^{?( t ? TD )/})]. The response was evaluated by the mean response time [MRT; sum of time constant () and time delay (TD)]. No significant difference in V˙O₂ and HR gains between the C and WI trials was observed [V˙O₂ 0.78 (SD 0.1) vs 0.80 (SD 0.2) l?·?min^?1, HR 36 (SD 7) vs 37 (SD 8) beats?·?min^?1, respectively]. Although the HR MRT was not significantly different between the C and WI trials [17 (SD 3), 19 (SD 8)?s, respectively), V˙O₂ MRT was greater in the WI trial than in the C trial [40 (SD 6), 45 (SD 6)?s, respectively; P<0.05]. Assuming no difference in V˙O₂ in active muscle between the two trials, these results would indicate that an increased oxygen store and/or an altered response in muscle blood distribution delayed the V˙O₂ response to exercise.     

Modelling of aerobic and anaerobic energy production during exhaustive exercise on a cycle ergometer

An extension of the original hyperbolic model (Model-2) was proposed by using power output required to elicit maximal oxygen uptake (P _t). This study aimed to test this new model (Model-α) using mechanical work produced during cycle ergometry. Model α assumed that power exceeding a critical power (P _c) was met partly by the anaerobic metabolism. The parameter α was the proportion of the power exceeding P _c provided by anaerobic metabolism, while power exceeding P _t was exclusively met by anaerobic metabolism. Aerobic power was assumed to rise monoexponentially with a time constant τ. The exhaustion was assumed to be reached when the anaerobic work capacity W′ was entirely utilised. Twelve subjects performed one progressive ramp test to assess the power at ventilatory threshold (P _VT) and P _t and five constant-load exercise to exhaustion within 2–30 min, with one to estimate the maximal accumulated oxygen deficit (MAOD). Parameters from Model α were fitted with τ equal to 0, 10, 20 and 30 s. Results in goodness-of-fit was better than Model-2 whatever the value assumed for τ (P < 0.05). The value of τ did not affect much the estimates for P _c and α. P _c estimates were significantly correlated with P _c from Model-2 and with P _VT. W′ estimates, which were dependent on the value ascribed to τ, were not statistically different than MAOD. These two variables were, however, not significantly correlated. In conclusion, Model α could provide useful information on the critical power and the anaerobic contribution according to exercise intensity, whereas W′ estimates should be used with care because of the sensitivity to the assumption on aerobic power kinetics τ.     

Serum hormone and myocellular protein recovery after intermittent runs at the velocity associated with V˙O2max

The responses of serum myocellular proteins and hormones to exercise were studied in ten well-trained middle-distance runners [maximal oxygen consumption (V˙O_2max)?=?69.4?(5.1)?ml?·?kg^?1?·?min^?1] during 3 recovery days and compared to various measures of physical performance. The purpose was to establish the duration of recovery from typical intermittent middle-distance running exercises. The subjects performed, in random, order two 28-min treadmill running exercises at a velocity associated with V˙O_2max: 14 bouts of 60-s runs with 60?s of rest between each run (IR₆₀) and 7 bouts of 120-s runs with 120?s of rest between each run (IR₁₂₀). Before the exercises (pre- exercise), 2?h after, and 1, 2 and 3 days after the exercises, the same series of measurements were performed, including those for serum levels of the myocellular proteins creatine kinase, myoglobin and carbonic anhydrase III (S-CK, S-Mb and S-CA III, respectively), serum hormones testosterone, Luteinizing hormone, follicle-stimulating hormone and cortisol (S-testosterone, S-LH, S-FSH and S-cortisol, respectively) and various performance parameters: maximal vertical jump height (CMJ) and stride length, heart rate and ratings of perceived exertion during an 8-min run at 15?km?·?h^?1 (SL_15?km·h?1, HR_15?km?·?h?1 and RPE_15?km?·?h?1, respectively). Two hours after the end of both exercise bouts the concentration of each measured serum protein had increased significantly (P?15?km?·?h?1 or CMJ. During the recovery days only S-CK was significantly raised (P?P?15?km?·?h?1 (P?120 the post-exercise responses returned to their pre-exercise levels within the 3 days of recovery. The present findings suggest that a single 28-min intermittent middle-distance running exercise does not induce changes in serum hormones of well-trained runners during recovery over 3 days, while changes in S-CK, CMJ and RPE_15?km?·?h?1 indicate that 2–3 days of light training may be needed before the recovery at muscle level is complete.     

Regional differences in the effect of exercise intensity on thermoregulatory sweating and cutaneous vasodilation

To investigate regional body differences in the effect of exercise intensity on the thermoregulatory sweating response, nine healthy male subjects (23.2 ± 0.4 year) cycled at 35, 50 and 65% of their maximal O₂ uptake (V˙O _2max) for 30 min at an ambient temperature of 28.3 ± 0.2 °C and a relative humidity of 42.6 ± 2.4%. Local sweating rate ( m˙_sw) on the forehead, chest, back, forearm and thigh increased significantly with increases in the exercise intensity from 35 to 50% V˙O _2max and from 50 to 65% V˙O _2max (P < 0.05). The mean values for the density of activated sweat glands (ASG) at 50 and 65% V˙O _2max at the five sites were significantly greater than at 35% V˙O _2max. The mean value of the sweat output per gland (SGO) also increased significantly with the increase in exercise intensity (P < 0.05). The patterns of changes in ASG and SGO with an increase in exercise intensity differed from one region of the body to another. Although esophageal temperature (T_es) threshold for the onset of sweating at each site was not altered by exercise intensity, the sensitivity of the sweating response on the forehead increased significantly from 35 to 50 and 65% V˙O _2max (P < 0.05). The threshold for cutaneous vasodilation tend to increase with exercise intensity, although the exercise intensity did not affect the sensitivity (the slope in the relationship T_es vs. percentage of the maximal skin blood flow) at each site. T_es threshold for cutaneous vasodilation on the forearm was significantly higher at 65% V˙O _2max than at either 35 or 50% V˙O _2max, but this was not observed at the other sites, such as on the forehead and chest. These results suggest that the increase in m˙_sw seen with an increasing intensity of exercise depends first on ASG, and then on SGO, and the dependence of ASG and SGO on the increase in m˙_sw differs for different body sites. In addition, there are regional differences in the T_es threshold for vasodilation in response to an increase in exercise intensity.     

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.     

Changes in maximal exercise ventilation and breathing pattern in boys during growth: a mixed cross-sectional longitudinal study

The aim of this mixed cross-sectional longitudinal study covering a total age range of 11–17 years, i.e. the entire pubertal growth period, was (1) to specify the changes in maximal breathing pattern during incremental exercise; (2) to determine what parts of the changes are due to anthropometric characteristics, physical fitness and inspiratory or expiratory muscle strength; and (3) to determine if the role of these variables is identical before, during and after pubertal growth spurt. This study was conducted in 44 untrained schoolboys separated into three groups, with an initial age of 11.2 ± 0.2 years for group A, 12.9 ± 0.25 years for group B, and 14.9 ± 0.26 years for group C. These children were subsequently followed for 3 years, during the same time period each year. The maximal inspiratory and expiratory pressures (P_{I max} and P_{E max}) were used as an index of the respiratory muscle strength. During an incremental exercise test, maximal ventilation (V˙_{E max}), tidal volume (V_{T max}), breathing frequency (f_max), inspiratory and expiratory times (t_{I max} and t_{E max}) and mean inspiratory flow (V_T/t_{I max}) were measured at maximal oxygen uptake (V˙_O2max). Our study showed that there was a marked increase with age in V˙_{E max}, V_{T max}, and V_T/t_{I max} , and no significant changes in f_max, t_{I max} and t_{E max}. P_{I max} and P_{E max} showed a general trend towards an increase between 11 and 17 years. The study of the linear correlations between maximal breathing pattern and the anthropometric characteristics, physical fitness and inspiratory or expiratory muscle strength showed that, in the three groups of children, (1) lean body mass was the major determinant of V˙_{E max}, V_{T max} and V_T/t_{I max} and the relationships were significantly different before, during and after the pubertal growth spurt; (2) physical fitness was the main determinant of t_{I max}, t_{E max} and f_max before and after the pubertal growth spurt; and (3) maximal respiratory strength did not play a significant role. In conclusion, this mixed cross-sectional longitudinal study showed, at maximal exercise, a significant increase in V˙_{E max} during growth due only to a significant increase in V_{T max} and V_T/t_{I max}, and that the relationships of anthropometric characteristics and physical fitness with maximal breathing pattern change during growth.     

Oxygen cost of dynamic leg exercise on a cycle ergometer: effects of gravity acceleration

A model of the metabolic internal power (?_int) during cycling, which includes the gravity acceleration (a_g) as a variable, is presented. This model predicts that ?_int is minimal in microgravity (0 g; g=9.81 m s^–2), and increases linearly with a_g, whence the hypothesis that the oxygen uptake (V˙O ₂) during cycling depends on a_g. Repeated V˙O ₂ measurements during steady-state exercise at 50, 75 and 100 W on the cycle ergometer, performed in space (0 g) and on Earth (1 g) on two subjects, validated the model. V˙O ₂ was determined from the time course of decreasing O₂ fraction during rebreathing. The gas volume during rebreathing was determined by the dilution principle, using an insoluble inert gas (SF₆). Average V˙O ₂ for subject 1 at each power was 0.99, 1.21 and 1.52 L min^–1 at 1 g (n=3) and 0.91, 1.13 and 1.32 L min^–1 at 0 g (n=5). For subject 2 it was 0.90, 1.12 and 1.42 L min^–1 at 1 g, and 0.76, 0.98 and 1.21 L min^–1 at 0 g. These values corresponded to those predicted from the model. Although resting V˙O ₂ was lower at 0 g than at 1 g, the net (total minus resting) exercise V˙O ₂ was still smaller at 0 g than at 1 g. This difference reflects the lower ?_int at 0 g.     

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.     

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).