Energy demands in taekwondo athletes during combat simulation

The purpose of this study was to investigate energy system contributions and energy costs in combat situations. The sample consisted of 10 male taekwondo athletes (age: 21 ± 6 years old; height: 176.2 ± 5.3 cm; body mass: 67.2 ± 8.9 kg) who compete at the national or international level. To estimate the energy contributions, and total energy cost of the fights, athletes performed a simulated competition consisting of three 2 min rounds with a 1 min recovery between each round. The combats were filmed to quantify the actual time spent fighting in each round. The contribution of the aerobic (W _AER), anaerobic alactic (W _PCR), and anaerobic lactic (W _[La^-]) (W_{ [{\rm La}^-]}) energy systems was estimated through the measurement of oxygen consumption during the activity, the fast component of excess post-exercise oxygen consumption, and the change in blood lactate concentration in each round, respectively. The mean ratio of high intensity actions to moments of low intensity (steps and pauses) was ~1:7. The W _AER, W _PCR and (W _[La^-]) (W_{ [{\rm La}^-]}) system contributions were estimated as 120 ± 22 kJ (66 ± 6%), 54 ± 21 kJ (30 ± 6%), 8.5 kJ (4 ± 2%), respectively. Thus, training sessions should be directed mainly to the improvement of the anaerobic alactic system (responsible by the high-intensity actions), and of the aerobic system (responsible by the recovery process between high-intensity actions).     

Energy systems contributions in 2,000 m race simulation: a comparison among rowing ergometers and water

This study investigated the energy system contributions of rowers in three different conditions: rowing on an ergometer without and with the slide and rowing in the water. For this purpose, eight rowers were submitted to 2,000 m race simulations in each of the situations defined above. The fractions of the aerobic (W _AER), anaerobic alactic (W _PCR) and anaerobic lactic (W _[La−_]) systems were calculated based on the oxygen uptake, the fast component of excess post-exercise oxygen uptake and changes in net blood lactate, respectively. In the water, the metabolic work was significantly higher [(851 (82) kJ] than during both ergometer [674 (60) kJ] and ergometer with slide [663 (65) kJ] (P ≤ 0.05). The time in the water [515 (11) s] was higher (P < 0.001) than in the ergometers with [398 (10) s] and without the slide [402 (15) s], resulting in no difference when relative energy expenditure was considered: in the water [99 (9) kJ min⁻¹], ergometer without the slide [99.6 (9) kJ min⁻¹] and ergometer with the slide [100.2 (9.6) kJ min⁻¹]. The respective contributions of the W _AER, W _PCR and W _[La−_] systems were water = 87 (2), 7 (2) and 6 (2)%, ergometer = 84 (2), 7 (2) and 9 (2)%, and ergometer with the slide = 84 (2), 7 (2) and 9 (1)%. [(V)\dot]\textO ₂ \dot{V}{\text{O}}_{ 2} , HR and lactate were not different among conditions. These results seem to indicate that the ergometer braking system simulates conditions of a bigger and faster boat and not a single scull. Probably, a 2,500 m test should be used to properly simulate in the water single-scull race.     

Anaerobic performance and metabolism in boys and male adolescents

Short-term maximum intensity performance, absolute and related to body mass, is lower in children than adolescents. The underlying mechanisms are not clear. We analysed Wingate Anaerobic Test (WAnT) performance and metabolism in ten boys (mean (SD); age 11.8 (0.5) years, height 1.51 (0.05) m, body mass 36.9 (2.5) kg, muscle mass 13.0 (1.0) kg) and 10 adolescents (16.3 (0.7) years, 1.81 (0.05) m, 67.3 (4.1) kg, 28.2 (1.7) kg). Related to body mass, power of flywheel acceleration (6.0 (1.6) vs. 8.1 (1.1) W kg⁻¹), peak power (10.8 (0.7) vs. 11.5 (0.6) W kg⁻¹), average power (7.9 (0.5) vs. 8.9 (0.7) W kg⁻¹), minimum power (6.1 (0.7) vs. 6.9 (0.9) W kg⁻¹) and anaerobic lactic energy (687.6 (75.6) vs. 798.2 (43.0) J kg⁻¹) were lower (P < 0.05) in boys than in adolescents. Related to muscle mass the change in lactate (0.69 (0.08) vs. 0.69 (0.04) mmol kg_MM⁻¹ s⁻¹) and PCr (0.60 (0.17) vs. 0.52 (0.10) mmol kg_MM⁻¹ s⁻¹) were not different. The corresponding oxygen uptake (1.34 (0.13) vs. 1.09 (0.13) ml kg_MM⁻¹ s⁻¹), total metabolic rate (132.4 (12.6) vs. 119.7 (8.5) W kg_MM⁻¹) and PP (30.5 (2.6) vs. 27.5 (1.7 W) kg_MM⁻¹) were higher (P < 0.01) in boys than in adolescents. The results reflect a lower relative muscle mass combined with no differences in muscular anaerobic but fascilitated aerobic metabolism in boys. Compared with adolescents, boys’ performance seemed to be significantly impaired by flywheel inertia but supported by identical brake force related to body mass.     

Influence of recovery manipulation after hyperlactemia induction on the lactate minimum intensity

This study analyzed the influence of recovery phase manipulation after hyperlactemia induction on the lactate minimum intensity during treadmill running. Twelve male runners (24.6 ± 6.3 years; 172 ± 8.0 cm and 62.6 ± 6.1 kg) performed three lactate minimum tests involving passive (LMT_P) and active recoveries at 30%vVO_2max (LMT_A30) and 50%vVO_2max (LMT_A50) in the 8-min period following initial sprints. During subsequent graded exercise, lactate minimum speed and VO₂ in LMT_A50 (12.8 ± 1.5 km h⁻¹ and 40.3 ± 5.1 ml kg⁻¹ min⁻¹) were significantly lower (P < 0.05) than those in LMT_A30 (13.3 ± 1.6 km h⁻¹ and 42.9 ± 5.3 ml kg⁻¹ min⁻¹) and LMT_P (13.8 ± 1.6 km h⁻¹ and 43.6 ± 6.1 ml kg⁻¹ min⁻¹). In addition, lactate minimum speed in LMT_A30 was significantly lower (P < 0.05) than that in LMT_P. These results suggest that lactate minimum intensity is lowered by active recovery after hyperlactemia induction in an intensity-dependent manner compared to passive recovery.     

Energy system contributions in indoor rock climbing

The present study cross-sectionally investigated the influence of training status, route difficulty and upper body aerobic and anaerobic performance of climbers on the energetics of indoor rock climbing. Six elite climbers (EC) and seven recreational climbers (RC) were submitted to the following laboratory tests: (a) anthropometry, (b) upper body aerobic power, and (c) upper body Wingate test. On another occasion, EC subjects climbed an easy, a moderate, and a difficult route, whereas RC subjects climbed only the easy route. The fractions of the aerobic (W _AER), anaerobic alactic (W _PCR) and anaerobic lactic systems were calculated based on oxygen uptake, the fast component of excess post-exercise oxygen uptake, and changes in net blood lactate, respectively. On the easy route, the metabolic cost was significantly lower in EC [40.3 (6.5) kJ] than in RC [60.1 (8.8) kJ] (P < 0.05). The respective contributions of the W _AER, W _PCR, and systems in EC were: easy route = 41.5 (8.1), 41.1 (11.4) and 17.4% (5.4), moderate route = 45.8 (8.4), 34.6 (7.1) and 21.9% (6.3), and difficult route = 41.9 (7.4), 35.8 (6.7) and 22.3% (7.2). The contributions of the W _AER, W _PCR, and systems in RC subjects climbing an easy route were 39.7 (5.0), 34.0 (5.8), and 26.3% (3.8), respectively. These results indicate that the main energy systems required during indoor rock climbing are the aerobic and anaerobic alactic systems. In addition, climbing economy seems to be more important for the performance of these athletes than improved energy metabolism.     

Skin microvascular reactivity in trained adolescents

Whilst endothelial dysfunction is associated with a sedentary lifestyle, enhanced endothelial function has been documented in the skin of trained individuals. The purpose of this study was to investigate whether highly trained adolescent males possess enhanced skin microvascular endothelial function compared to their untrained peers. Seventeen highly and predominantly soccer trained boys ( [(V)\dot]\textO_2 \textpeak \dot{V}{\text{O}}_{{2\,{\text{peak}}}} : 55 ± 6 mL kg⁻¹ min⁻¹) and nine age- and maturation-matched untrained controls ( [(V)\dot]\textO_2 \textpeak \dot{V}{\text{O}}_{{2\,{\text{peak}}}} : 43 ± 5 mL kg⁻¹ min⁻¹) aged 13–15 years had skin microvascular endothelial function assessed using laser Doppler flowmetry. Baseline and maximal thermally stimulated skin blood flow (SkBF) responses were higher in forearms of trained subjects compared to untrained participants [baseline SkBF: 11 ± 4 vs. 9 ± 3 perfusion units (PU), p < 0.05; SkBF_max: 282 ± 120 vs. 204 ± 68 PU, p < 0.05]. Similarly, cutaneous vascular conductance (CVC) during local heating was superior in the forearm skin of trained versus untrained individuals (CVC_max: 3 ± 1 vs. 2 ± 1 PU mmHg⁻¹, p < 0.05). Peak hyperaemia following arterial occlusion and area under the reactive hyperaemia curve were also greater in forearm skin of the trained group (peak hyperaemia: 51 ± 21 vs. 35 ± 15 PU, p < 0.05; area under curve: 1596 ± 739 vs. 962 ± 796 PUs, p < 0.05). These results suggest that chronic exercise training in adolescents is associated with enhanced microvascular endothelial vasodilation in non-glabrous skin.     

Myocardial function and aerobic fitness in adolescent females

A recent report indicated that variations in myocardial functional (systolic and diastolic) responses to exercise do not contribute to inter-individual differences in aerobic fitness (peak VO₂) among young males. This study was designed to investigate the same question among adolescent females. Thirteen highly fit adolescent football (soccer) players (peak VO₂ 43.5 ± 3.4 ml kg⁻¹ min⁻¹) and nine untrained girls (peak VO₂ 36.0 ± 5.1 ml kg⁻¹ min⁻¹) matched for age underwent a progressive cycle exercise test to exhaustion. Cardiac variables were measured by standard echocardiographic techniques. Maximal stroke index was greater in the high-fit group (50 ± 5 vs. 41 ± 4 ml m⁻²), but no significant group differences were observed in maximal heart rate or arterial venous oxygen difference. Increases in markers of both systolic (ejection rate, tissue Doppler S′) and diastolic (tissue Doppler E′, mitral E velocity) myocardial functions at rest and during the acute bout of exercise were similar in the two groups. This study suggests that among healthy adolescent females, like young males, myocardial systolic and diastolic functional capacities do not contribute to inter-individual variability in physiologic aerobic fitness.     

Fibrinolytic markers and vasodilatory capacity following acute exercise among men of differing training status

We evaluated the effect of differing physical activity patterns on fibrinolysis and vasodilatory capacity using a cross-sectional design with 16 endurance-trained (ET) (mean ± SE) (28 ± 6 years), 14 resistance-trained (RT) (28 ± 7 years), and 10 untrained (UT) (26 ± 7 years) men. t-PA and PAI-1 activity and t-PA antigen were measured before and after a maximal treadmill test (VO_2peak). Vasodilatory capacity was assessed using strain-gauge plethysmography on the forearm following reactive hyperemia (RH) before and after the treadmill test. The ET group had a smaller body mass index (BMI) (22.8 ± 0.5 ET, 26.4 ± 0.4 RT, 25.1 ± 0.8 UT kg m⁻²) (P < 0.05) and a greater VO_2peak (57 ± 1 ET, 42 ± 2 RT, 45 ± 2 UT mL min⁻¹ kg⁻¹) (P < 0.05). Peak vasodilatory capacity (29.7 ± 2 ET, 32.0 ± 2 RT, 27.4 ± 2 UT mL min⁻¹ 100 mL of tissue) was similar between groups before and after exercise. Area under the curve for forearm blood flow was greater following acute exercise (212 vs. 122, P < 0.05), again with no differences between groups. t-PA activity and antigen increased following maximal exercise in all groups (P < 0.0001), with no group differences. PAI-1 activity decreased the least in RT after exercise (70% decrease vs. 86% ET and 82% UT; P < 0.05). The change in t-PA activity with exercise was not related to exercise-induced change in overall vasodilatory capacity. These findings demonstrate that in healthy young men different physical activity patterns do not appear to impact the exercise-induced changes in fibrinolysis or vasodilatory capacity.     

The effect of 48?weeks of aerobic exercise training on cutaneous vasodilator function in post-menopausal females

Skin blood flow (SkBF) and endothelial-dependent vasodilatation decline with ageing and can be reversed with exercise training. We tested whether 48 weeks of training could improve SkBF and endothelial function in post-menopausal females; 20 post-menopausal subjects completed the study. SkBF was measured by laser-Doppler flowmetry (LDF). Cutaneous vascular conductance (CVC) was calculated as LDF/blood pressure. Resting CVC was measured at 32°C and peak CVC at 42°C. Cutaneous endothelial-dependent and -independent vasodilatations were determined by the iontophoresis of acetylcholine (ACh) and sodium nitroprusside (SNP), respectively. All assessments described were performed at entry (week 0), and after 6, 12, 24, 36, and 48 weeks of training. Resting CVC measures did not change (P > 0.05) throughout the study. Peak CVC increased (P < 0.05) after 24 weeks (7.2 ± 1.2 vs. 11.6 ± 1.4 AU mmHg⁻¹) and at the 36- and 48-week assessments (13.0 ± 1.7 and 14.9 ± 2.1 AU mmHg⁻¹, respectively). Responses to ACh also increased (P < 0.05) at the 24-week assessment (5.1 ± 2.1 vs. 8.55 ± 2.3 AU mmHg⁻¹) and increased further at the 36 and 48-week assessments (11.6 ± 3.7 and 13.2 ± 3.9 AU mmHg⁻¹, respectively). Cutaneous responses to SNP increased (P < 0.05) after 36 weeks (8.7 ± 2.1 vs. 13.02 ± 2.23 AU mmHg⁻¹ at 36 weeks). VO_2max increased after 12 weeks (23.5 ± 0.7 vs. 25.4 ± 0.9 ml kg⁻¹ min⁻¹) and improved (P < 0.05) further throughout the study (31.6 ± 1.8 ml kg⁻¹ min⁻¹ at week 48). Aerobic exercise produces positive adaptations in the cutaneous vasodilator function to local heating as well as in cutaneous endothelial and endothelial-independent vasodilator mechanisms. Aerobic capacity was also significantly improved. These adaptations were further enhanced with progressive increases in exercise intensity.     

Exercise intensity and oxygen uptake kinetics in African-American and Caucasian women

The effect of exercise intensity on the on- and off-transient kinetics of oxygen uptake (VO₂) was investigated in African American (AA) and Caucasian (C) women. African American (n = 7) and Caucasian (n = 6) women of similar age, body mass index and weight, performed an incremental test and bouts of square-wave exercise at moderate, heavy and very heavy intensities on a cycle ergometer. Gas exchange threshold (LT_GE) was lower in AA (13.6 ± 2.3 mL kg⁻¹ min⁻¹) than C (18.6 ± 5.6 mL kg⁻¹ min⁻¹). The dynamic exercise and recovery VO₂ responses were characterized by mathematical models. There were no significant differences in (1) peak oxygen uptake (VO_2peak) between AA (28.5 ± 5 mL kg⁻¹ min⁻¹) and C (31.1 ± 6.6 mL kg⁻¹ min⁻¹) and (2) VO₂ kinetics at any exercise intensity. At moderate exercise, the on- and off- VO₂ kinetics was described by a monoexponential function with similar time constants τ _1,on (39.4 ± 12.5; 38.8 ± 15 s) and τ _1,off (52.7 ± 10.1; 40.7 ± 4.4 s) for AA and C, respectively. At heavy and very heavy exercise, the VO₂ kinetics was described by a double-exponential function. The parameter values for heavy and very heavy exercise in the AA group were, respectively: τ _1,on (47.0 ± 10.8; 44.3 ± 10 s), τ _2,on (289 ± 63; 219 ± 90 s), τ _1,off (45.9 ± 6.2; 50.7 ± 10 s), τ _2,off (259 ± 120; 243 ± 93 s) while in the C group were, respectively: τ _1,on (41 ± 12; 43.2 ± 15 s); τ _{2, on} (277 ± 81; 215 ± 36 s), τ _1,off (40.2 ± 3.4; 42.3 ± 7.2 s), τ _2,off (215 ± 133; 228 ± 64 s). The on- and off-transients were symmetrical with respect to model order and dependent on exercise intensity regardless of race. Despite similar VO₂ kinetics, LT_GE and gain of the VO₂ on-kinetics at moderate intensity were lower in AA than C. However, generalization to the African American and Caucasian populations is constrained by the small subject numbers.     

The effect of acute aerobic exercise on pulse wave velocity and oxidative stress following postprandial hypertriglyceridemia in healthy men

Oxidative stress is postulated to be responsible for the postprandial impairments in vascular function. The purpose of this study was to measure pulse wave velocity (PWV) and markers of postprandial oxidative stress before and after an acute bout of moderate exercise. Ten trained male subjects (age 21.5 ± 2.5 years, VO₂ max 58.5 ± 7.1 ml kg⁻¹ min⁻¹) participated in a randomised crossover design: (1) high-fat meal alone (2) high-fat meal followed 2 h later by a bout of 1 h moderate (60% max HR) exercise. PWV was examined at baseline, 1, 2, 3, and 4 h postprandially. Blood Lipid hydroperoxides (LOOHs), Superoxide dismutase (SOD) and other biochemical markers were measured. PWV increased at 1 h (6.49 ± 2.1 m s⁻¹), 2 h (6.94 ± 2.4 m s⁻¹), 3 h (7.25 ± 2.1 m s⁻¹) and 4 h (7.41 ± 2.5 m s⁻¹) respectively, in the control trial (P < 0.05). There was no change in PWV at 3 h (5.36 ± 1.1 m s⁻¹) or 4 h (5.95 ± 2.3 m s⁻¹) post ingestion in the exercise trial (P > 0.05). LOOH levels decreased at 3 h post ingestion in the exercise trial compared to levels at 3 h (P < 0.05) in the control trial. SOD levels were lower at 3 h post ingestion in the control trial compared to 3 h in the exercise trial (0.52 ± 0.05 vs. 0.41 ± 0.1 units μl⁻¹; P < 0.05). These findings suggest that a single session of aerobic exercise can ameliorate the postprandial impairments in arterial function by possibly reducing oxidative stress levels.     

Effects of athletes’ muscle mass on urinary markers of hydration status

To determine if athletes’ muscle mass affects the usefulness of urine specific gravity (U _sg) as a hydration index. Nine rugby players and nine endurance runners differing in the amount of muscle mass (42 ± 6 vs. 32 ± 3 kg, respectively; P = 0.0002) were recruited. At waking during six consecutive days, urine was collected for U _sg analysis, urine osmolality (U _osm), electrolytes ( \mathop U\nolimits_{[\textNa ⁺ ]} {\mathop U\nolimits_{[{\text{Na}}^{ + } ]} }, \mathop U\nolimits_{[\textK ⁺ ]} {\mathop U\nolimits_{[{\text{K}}^{ + } ]} } and \mathop U\nolimits_{[\textCl ^- ]} {\mathop U\nolimits_{[{\text{Cl}}^{ - } ]} }) and protein metabolites (U _[Creatinine], U _[Urea] and U _{[Uric acid]}) concentrations. In addition, fasting blood serum osmolality (S _osm) was measured on the sixth day. As averaged during 6 days, U _sg (1.021 ± 0.002 vs. 1.016 ± 0.001), U _osm (702 ± 56 vs. 554 ± 41 mOsmol kg⁻¹ H₂O), U _[Urea] (405 ± 36 vs. 302 ± 23 mmol L⁻¹) and U _{[Uric acid]} (2.7 ± 0.3 vs. 1.7 ± 0.2 mmol L⁻¹) were higher in rugby players than runners (P < 0.05). However, urine electrolyte concentrations were not different between groups. A higher percentage of rugby players than runners (56 vs. 11%; P = 0.03) could be cataloged as hypohydrated by U _sg (i.e., >1.020) despite S _osm being below 290 mOsmol kg⁻¹ H₂O in all participants. A positive correlation was found between muscle mass and urine protein metabolites (r = 0.47; P = 0.04) and between urine protein metabolites and U _sg (r = 0.92; P < 0.0001). In summary, U _sg specificity to detect hypohydration was reduced in athletes with large muscle mass. Our data suggest that athletes with large muscle mass (i.e., rugby players) are prone to be incorrectly classified as hypohydrated based on U _sg.     

Is the balance between skeletal muscular metabolic capacity and oxygen supply capacity the same in endurance trained and untrained subjects?

We attempted to test whether the balance between muscular metabolic capacity and oxygen supply capacity in endurance-trained athletes (ET) differs from that in a control group of normal physically active subjects by using exercises with different muscle masses. We compared maximal exercise in nine ET subjects [Maximal oxygen uptake (VO₂max) 64 ml kg⁻¹ min⁻¹ ± SD 4] and eight controls (VO₂max 46 ± 4 ml kg⁻¹ min⁻¹) during one-legged knee extensions (1-KE), two-legged knee extensions (2-KE) and bicycling. Maximal values for power output (P), VO₂max, concentration of blood lactate ([La⁻]), ventilation (VE), heart rate (HR), and arterial oxygen saturation of haemoglobin (SpO₂) were registered. P was 43 (2), 89 (3) and 298 (7) W (mean ± SE); and VO₂max: 1,387 (80), 2,234 (113) and 4,115 (150) ml min⁻¹) for controls in 1-KE, 2-KE and bicycling, respectively. The ET subjects achieved 126, 121 and 126% of the P of controls (p < 0.05) and 127, 124, and 117% of their VO₂max (p < 0.05). HR and [La⁻] were similar for both groups during all modes of exercise, while VE in ET was 147 and 114% of controls during 1-KE and bicycling, respectively. For mass-specific VO₂max (VO₂max divided by the calculated active muscle mass) during the different exercises, ET achieved 148, 141, and 150% of the controls’ values, respectively (p < 0.05). During bicycling, both groups achieved 37% of their mass-specific VO₂ during 1-KE. Finally we conclude that ET subjects have the same utilization of the muscular metabolic capacity during whole body exercise as active control subjects.     

Impaired glomerular permselectivity for albumin in chemically medullectomized WKY rats

Chemical renal medullectomy with 2-bromo-ethylamine hydrobromide (BEA) has been used to study the importance of the renal medulla in blood pressure regulation. However, conclusive evidence as to whether BEA treatment affects the glomerular barrier is lacking. In the present study, the effects of BEA upon glomerular permselectivity for albumin were studied using isolated kidneys (IPK) perfused at a low temperature (8 °C) to inhibit tubular reabsorption of proteins. Sixteen WKY rats (W_B) received an i.v. injection of BEA (150 mg kg^-1) while 10 rats served as controls (W_C). Volume balance, urinary osmolality and creatinine clearance (GFR) were measured in metabolic cages. Acute paired experiments (n=9) were performed 5–7 weeks after BEA. The rats were anaesthetized and the total in vivo albumin excretion was recorded. The kidneys were then isolated and perfused for measurements of inulin clearance (GFR) and fractional albumin clearance without tubular reabsorption of protein. The nine BEA treated rats showed polyuria and hypoosmotic urine. In vivo GFR was lower in the BEA treated groups when measured with creatinine clearance (459±22 vs. 213±41 μL min^-1 100 g^-1 body wt, P<0.001), while GFR was not significantly changed in the IPK (W_C=135±27, W_B=92±14 μL min^-1 100 g^-1 body wt, n.s.) when perfused at identical pressures. The fractional albumin clearance was increased three times in the BEA group (W_B=9.6±3.4J, P<0.05). Moreover, albumin excretion in vivo was similar in the two groups despite low GFR in the BEA group. We conclude that BEA treatment affects glomerular permselectivity for albumin.     

Walking economy in male adults with Down syndrome

The purpose of this study was to investigate walking economy in response to steady-state locomotion in adult males with Down syndrome (DS) and in healthy controls. Twelve participants with DS (34.5 ± 7.0 years) and 11 non-disabled controls (34.3 ± 8.7 years) performed submaximal (0% grade, 2.5 km h⁻¹ for 8 min) and maximal treadmill tests with metabolic and heart-rate measurements. For submaximal walking, submaximal oxygen uptake (VO₂) (9.1 vs. 9.5 mL kg⁻¹ min⁻¹), net VO₂ (5.9 vs. 5.4 mL kg⁻¹ min⁻¹) were not different between the groups (P > 0.05). However, oxygen-pulse (6.6 vs. 8.6 mL/beat) was lower and relative work intensity (44.6 vs. 19.9% of max) was higher in individuals with DS compared to controls (P < 0.05). Findings indicate similar walking economy between groups. Nevertheless, participants with DS exercised at lower submaximal oxygen-pulse and higher percentage of VO_2peak. Therefore, despite similar walking economy, participants with DS have lower cardiorespiratory function than controls for a given steady-state treadmill speed.     

Power output during women’s World Cup road cycle racing

Little information exists on the power output demands of competitive women’s road cycle racing. The purpose of our investigation was to document the power output generated by elite female road cyclists who achieved success in FLAT and HILLY World Cup races. Power output data were collected from 27 top-20 World Cup finishes (19 FLAT and 8 HILLY) achieved by 15 nationally ranked cyclists (mean ± SD; age: 24.1±4.0 years; body mass: 57.9±3.6 kg; height: 168.7±5.6 cm; 63.6±2.4 mL kg⁻¹ min⁻¹; peak power during graded exercise test (GXT_{peak power}): 310±25 W). The GXT determined GXT_{peak power}, lactate threshold (LT) and anaerobic threshold (AT). Bicycles were fitted with SRM powermeters, which recorded power (W), cadence (rpm), distance (km) and speed (km h⁻¹). Racing data were analysed to establish time in power output and metabolic threshold bands and maximal mean power (MMP) over different durations. When compared to HILLY, FLAT were raced at a similar cadence (75±8 vs. 75±4 rpm, P=0.93) but higher speed (37.6±2.6 vs. 33.9±2.7 km h⁻¹, P=0.008) and power output (192±21 vs. 169±17 W, P=0.04; 3.3±0.3 vs. 3.0±0.4 W kg⁻¹, P=0.04). During FLAT races, riders spent significantly more time above 500 W, while greater race time was spent between 100 and 300 W (LT-AT) for HILLY races, with higher MMPs for 180–300 s. Racing terrain influenced the power output profiles of our internationally competitive female road cyclists. These data are the first to define the unique power output requirements associated with placing well in both flat and hilly women’s World Cup cycling events.     

Evidence of break-points in breathing pattern at the gas-exchange thresholds during incremental cycling in young, healthy subjects

The present study investigated whether ‘break-points’ in breathing pattern correspond to the first ( G_\textEX1 G_{{{\text{EX}}_{1} }} ) and second gas-exchange thresholds ( G_{\textEX 2} G_{{{\text{EX}}_{ 2} }} ) during incremental cycling. We used polynomial spline smoothing to detect accelerations and decelerations in pulmonary gas-exchange data, which provided an objective means of ‘break-point’ detection without assumption of the number and shape of said ‘break-points’. Twenty-eight recreational cyclists completed the study, with five individuals excluded from analyses due to low signal-to-noise ratios and/or high risk of ‘pseudo-threshold’ detection. In the remaining participants (n = 23), two separate and distinct accelerations in respiratory frequency (f _R) during incremental work were observed, both of which demonstrated trivial biases and reasonably small ±95% limits of agreement (LOA) for the G_\textEX1 G_{{{\text{EX}}_{1} }} (0.2 ± 3.0 ml O₂ kg⁻¹ min⁻¹) and G_{\textEX 2} G_{{{\text{EX}}_{ 2} }} (0.0 ± 2.4 ml O₂ kg⁻¹ min⁻¹), respectively. A plateau in tidal volume (V _T) data near the G_\textEX1 G_{{{\text{EX}}_{1} }} was identified in only 14 individuals, and yielded the most unsatisfactory mean bias ±LOA of all comparisons made (−0.4 ± 5.3 ml O₂ kg⁻¹ min⁻¹). Conversely, 18 individuals displayed V _T-plateau in close proximity to the G_{\textEX 2} G_{{{\text{EX}}_{ 2} }} evidenced by a mean bias ± LOA of 0.1 ± 3.1 ml O₂ kg⁻¹ min⁻¹. Our findings suggest that both accelerations in f _R correspond to the gas-exchange thresholds, and a plateau (or decline) in V _T at the G_{\textEX 2} G_{{{\text{EX}}_{ 2} }} is a common (but not universal) feature of the breathing pattern response to incremental cycling.     

Indirect measures of human vagal withdrawal during head-up tilt with and without a respiratory acidosis

Human ECG records were analyzed during supine (SUP) rest and whole body 80° head-up tilt (HUT), with a respiratory acidosis (5%CO₂) and breathing room air (RA). HUT increased heart rate in both conditions (RA_SUP 60 ± 13 vs. RA_HUT 79 ± 16; 5%CO_2SUP 63 ± 12 vs. 5%CO_2HUT 79 ± 14 beats min⁻¹) and decreased mean R–R interval, with no changes in the R–R interval standard deviation. When corrected for changes in frequency spectrum total power (NU), the high frequency (0.15–0.4 Hz) component (HF_NU) of heart rate variability decreased (RA_SUP 44.01 ± 21.57 vs. RA_HUT 24.05 ± 13.09; 5%CO_2SUP 69.23 ± 15.37 vs. 5%CO_2HUT 47.64 ± 21.11) without accompanying changes in the low frequency (0.04–0.15 Hz) component (LF_NU) (RA_SUP 52.36 ± 21.93 vs. RA_HUT 66.58 ± 19.49; 5%CO_2SUP 22.97 ± 11.54 vs. 5%CO_2HUT 40.45 ± 21.41). Positive linear relations between the tilt-induced changes (Δ) in HF_NU and R–R interval were recorded for RA (ΔHF_NU = 0.0787(ΔR−R) − 11.3, R ² = 0.79, P < 0.05), and for 5%CO₂ (ΔHF_NU = 0.0334(ΔR−R) + 1.1, R ² = 0.82, P < 0.05). The decreased HF component suggested withdrawal of vagal activity during HUT. For both RA and 5%CO₂, the positive linear relations between ΔHF_NU and ΔR−R suggested that the greater the increase in heart rate with HUT, the greater the vagal withdrawal. However, a reduced range of ΔHF during HUT with respiratory acidosis suggested vagal withdrawal was lower with a respiratory acidosis.     

Computationally Managed Bradycardia Improved Cardiac Energetics While Restoring Normal Hemodynamics in Heart Failure

In acute heart failure, systemic arterial pressure (AP), cardiac output (CO), and left atrial pressure (P _LA) have to be controlled within acceptable ranges. Under this condition, cardiac energetic efficiency should also be improved. Theoretically, if heart rate (HR) is reduced while AP, CO, and P _LA are maintained by preserving the functional slope of left ventricular (LV) Starling’s curve (S _L) with precisely increased LV end-systolic elastance (E _es), it is possible to improve cardiac energetic efficiency and reduce LV oxygen consumption per minute (MVO ₂). We investigated whether this hemodynamics can be accomplished in acute heart failure using an automated hemodynamic regulator that we developed previously. In seven anesthetized dogs with acute heart failure (CO < 70 mL min⁻¹ kg⁻¹, P _LA > 15 mmHg), the regulator simultaneously controlled S _L with dobutamine, systemic vascular resistance with nitroprusside and stressed blood volume with dextran or furosemide, thereby controlling AP, CO, and P _LA. Normal hemodynamics were restored and maintained (CO; 88 ± 3 mL min⁻¹ kg⁻¹, P _LA; 10.9 ± 0.4 mmHg), even when zatebradine significantly reduced HR (−27 ± 3%). Following HR reduction, E _es increased (+34 ± 14%), LV mechanical efficiency (stroke work/oxygen consumption) increased (+22 ± 6%), and MVO ₂ decreased (−17 ± 4%) significantly. In conclusion, in a canine acute heart failure model, computationally managed bradycardia improved cardiac energetic efficiency while restoring normal hemodynamic conditions.