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.     

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   

Cycling efficiency and pedalling frequency in road cyclists

The purpose of this study was to determine the influence of pedalling rate on cycling efficiency in road cyclists. Seven competitive road cyclists participated in the study. Four separate experimental sessions were used to determine oxygen uptake (V˙O₂) and carbon dioxide output (V˙CO₂) at six exercise intensities that elicited a V˙O₂ equivalent to 54, 63, 73, 80, 87 and 93% of maximum V˙O₂ (V˙O_2max). Exercise intensities were administered in random order, separated by rest periods of 3–5?min; four pedalling frequencies (60, 80, 100 and 120?rpm) were randomly tested per intensity. The oxygen cost of cycling was always lower when the exercise was performed at 60?rpm. At each exercise intensity, V˙O₂ showed a parabolic dependence on pedalling rate (r = 0.99–1, all P?r = 0.94–1, all P?P?P?r = 0.98, n = 6, P?r = 0.98, P?P?V˙O₂ (P?V˙O₂. These results may help us to understand why competitive cyclists often pedal at cadences of 90–105?rpm to sustain a high power output during prolonged exercise.     

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).     

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.     

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.     

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.     

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.     

Impact of three different types of exercise on components of the inflammatory response

It was hypothesized that muscle injury would be greater with eccentric than with all-out or prolonged exercise, and that immune changes might provide an indication that supplements the information provided by traditional markers such as creatine kinase (CK) or delayed-onset muscle soreness. Eight healthy males [mean (SE): age?=?24.9?(2.3) years, maximum oxygen consumption (V˙O_2max)=43.0?(3.1)?ml?·?kg^?1?·?min^?1] were each assigned to four experimental conditions, one at a time, using a randomized-block design: 5?min of cycle ergometer exercise at 90% V˙O_2max (AO), a standard circuit-training routine (CT), 2?h cycle ergometer exercise at 60% V˙O_2max (Long), or remained seated for 5?h. Blood samples were analyzed for CK, natural killer (NK) cell counts (CD3^?/CD16⁺56⁺), cytolytic activity and plasma levels of the cytokines interleukin (IL)-6, IL-10, and tissue necrosis factor α (TNF-α). CK levels were only elevated significantly 72?h following CT. NK cell counts increased significantly during all three types of exercise, but returned to pre-exercise baseline values within 3?h of recovery. Cytolytic activity per NK cell was not significantly modified by any type of exercise. Prolonged exercise induced significant increases in plasma IL-6 and TNF-α. We conclude that the lack of correlation between traditional markers of muscle injury (plasma CK concentrations and muscle soreness rankings) and immune markers of the inflammatory response suggests that, for the types and intensities of exercise examined in this study, the exercise-induced inflammatory response is modified by humoral and cardiovascular correlates of exercise.     

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.     

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.     

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.     

Relationship between isocapnic buffering and maximal aerobic capacity in athletes

This study was performed to clarify the relationship between isocapnic buffering and maximal aerobic capacity (V˙O_{2 max} ) in athletes. A group of 15 trained athletes aged 21.1 (SD 2.6) years was studied. Incremental treadmill exercise was performed using a modified version of Bruce's protocol for determination of the anaerobic threshold (AT) and the respiratory compensation point (RC). Ventilatory and gas exchange responses were measured with an aeromonitor and expressed per unit of body mass. Heart rate and ratings of perceived exertion were recorded continuously during exercise. The mean V˙O_{2 max} , oxygen uptake (V˙O₂) at AT and RC were 58.2 (SD 5.8)?ml?·?kg^?1?·?min^?1, 28.0 (SD 3.3)?ml?·?kg^?1?·?min^?1 and 52.4 (SD 6.7)?ml?· kg^?1?·?min^?1, respectively. The mean values of AT and RC, expressed as percentages of V˙O_{2 max} , were 48.3 (SD 4.2)% and 90.0 (SD 5.2)%, respectively. The mean range of isocapnic buffering defined as V˙O₂ between AT and RC was 24.4 (SD 4.5) ml?·?kg^?1?·?min^?1, and the mean range of hypocapnic hyperventilation (HHV) defined as V˙O₂ between RC and the end of exercise was 5.8 (SD 3.0)?ml?·?kg^?1?·?min^?1. The V˙O_{2 max} per unit mass was significantly correlated with AT (r?=?0.683, P?V˙O_{2 max} /mass was closely correlated with both the range of isocapnic buffering (r?=?0.803, P?r?=?0.878, P?V˙O_{2 max} per unit mass and the range of HHV (r?=?0.011, NS.). These findings would suggest that the prominence of isocapnic buffering, in addition to the anaerobic threshold, may have been related to V˙O_{2 max} of the athletes. The precise mechanisms underlying this proposed relationship remain to be elucidated.     

Aerobic and anaerobic energy during a 2-km race simulation in female rowers

The maximal aerobic power (V˙O_2max) and maximal anaerobic capacity (AOD_max) of 16 female rowers were compared to their peak aerobic power (V˙O_2peak) and peak anaerobic capacity (AOD_peak, respectively) during a simulated 2-km race on a rowing ergometer. Each subject completed three tests, which included a 2-min maximal effort bout to determine the AOD_max, a series of four, 4-min submaximal stages with subsequent progression to V˙O_2max and a simulated 2-km race. Aerobic power was determined using an open-circuit system, and the accumulated oxygen deficit method was used to calculate anaerobic capacities from recorded mechanical power on a rowing ergometer. The average V˙O_2peak (3.58?l?·?min^?1), which usually occurred during the last minute of the race simulation, was not significantly different (P?>?0.05) from the V˙O_2max (3.55?l?· min^?1). In addition, the rowers' AOD_max (3.40?l) was not significantly different (P?>?0.05) from their AOD_peak (3.50?l). The average time taken for the rowers to complete the 2-km race simulation was 7.5?min, and the anaerobic system (AOD_peak) accounted for 12% of the rowers' total energy production during the race.     

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.     

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.     

Gender comparison of peak oxygen uptake: repetitive box lifting versus treadmill running

The gender differences in peak oxygen uptake (V˙O_2peak) for various modes of exercise have been examined previously; however, no direct gender comparisons have been made during repetitive lifting (RL). In the present study the V˙O_2peak between RL and treadmill running (TR) was compared between 20 men [mean (SD) age, height, body mass and body fat: 21 (3) years, 1.79 (0.06)?m, 81 (9)?kg, 19 (6)%, respectively] and 20 women [mean (SD) age, height, body mass and body fat: 21 (3) years, 1.63 (0.05)?m, 60 (7)?kg, 27 (6)%, respectively]. V˙O_2peak (l?·?min^?1), defined as the highest value obtained during exercise to volitional fatigue, was determined using discontinuous protocols with treadmill grade or box mass incremented to increase exercise intensity. For RL V˙O_2peak, a pneumatically driven shelf was used to lower a loaded box to the floor, and subjects then lifted the box, at a rate of 15 lifts?·?min^?1. V˙O_2peak (l?·?min^?1 and ml?·?kg^?1?·?min^?1) and minute ventilation (V˙ _E, l?·?min^?1) were determined using an on-line gas analysis system. A two-way repeated measures analysis of variance revealed significant gender effects, with men having higher values for V˙O_2peak (l?·?min^?1 and ml?·?kg^?1?·?min^?1) and V˙ _E, but women having higher values of the ventilatory equivalent for oxygen (V˙ _E/V˙O₂). There were also mode of exercise effects, with TR values being higher for V˙O_2peak (l?·?min^?1 and ml?·?kg^?1?·?min^?1) and V˙ _E and an interaction effect for V˙O_2peak {1?·?min^?1 and ml?·?kg^?1?·?min^?1) and V˙ _E/V˙O₂. The women obtained a greater percentage (≈84%) of their TR V˙O_2peak during RL than did the men (≈79%). There was a marginal tendency for women to decrease and men to increase their V˙ _E/V˙O₂ when comparing TR with RL. The magnitude of the gender differences between the two exercise modalities appeared to be similar for heart rate, V˙ _E and R, but differed for V˙O_2peak (1?·?min^?1 and ml?·?kg^?1?·?min^?1). Lifting to an absolute height (1.32?m for the RL protocol) may present a different physical challenge to men and women with respect to the degree of involvement of the muscle groups used during lifting and ventilation.     

Energetics of kayaking at submaximal and maximal speeds

The energy cost of kayaking per unit distance (C_k, kJ?·?m^?1) was assessed in eight middle- to high-class athletes (three males and five females; 45–76?kg body mass; 1.50–1.88?m height; 15–32 years of age) at submaximal and maximal speeds. At submaximal speeds, C_k was measured by dividing the steady-state oxygen consumption (V˙O₂, l?·?s^?1) by the speed (v, m?·?s^?1), assuming an energy equivalent of 20.9?kJ?·?l O^?1 ₂. At maximal speeds, C_k was calculated from the ratio of the total metabolic energy expenditure (E, kJ) to the distance (d, m). E was assumed to be the sum of three terms, as originally proposed by Wilkie (1980): E?=?AnS?+?αV˙O_2max?·?t?αV˙O_2max?·?τ(1?e ^?t·τ?1), were α is the energy equivalent of O₂ (20.9?kJ?·?l?O₂ ^?1), τ is the time constant with which V˙O_2max is attained at the onset of exercise at the muscular level, AnS is the amount of energy derived from anaerobic energy utilization, t is the performance time, and V˙O_2max is the net maximal V˙O₂. Individual V˙O_2max was obtained from the V˙O₂ measured during the last minute of the 1000-m or 2000-m maximal run. The average metabolic power output (E˙, kW) amounted to 141% and 102% of the individual maximal aerobic power (V˙O_2max) from the shortest (250?m) to the longest (2000?m) distance, respectively. The average (SD) power provided by oxidative processes increased with the distance covered [from 0.64 (0.14) kW at 250?m to 1.02 (0.31) kW at 2000?m], whereas that provided by anaerobic sources showed the opposite trend. The net C_k was a continuous power function of the speed over the entire range of velocities from 2.88 to 4.45?m?·?s^?1: C _k ?=?0.02?·?v ^2.26 (r?=?0.937, n?=?32).     

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