Effect of internal power on muscular efficiency during cycling exercise

The purpose of this study was to investigate the muscular efficiency during cycling exercise under certain total power output (P _tot) or external power output (P _ext) experimental conditions that required a large range of pedal rates from 40 to 120 rpm. Muscular efficiency estimated as a ratio of P _tot, which is sum of internal power output (P _int) and P _ext, to rate of energy expenditure above a resting level was investigated in two experiments that featured different conditions on a cycle ergometer, which were carried out at the same levels of P _tot (Exp. 1) and P _ext (Exp. 2). Each experiment consisted of three exercise tests with three levels of pedal rates (40, 80 and 120 rpm) lasting for 2–3 min of unloaded cycling followed by 4–5 min of loaded cycling. during unloaded cycling (∼430 ml min⁻¹ for 40 rpm, ∼640 ml min⁻¹ for 80 rpm, ∼1,600 ml min⁻¹ for 120 rpm) and the P _int (∼3 W for 40 rpm, ∼25 W for 80 rpm, ∼90 W for 120 rpm) in the two experiments were markedly increased with increasing pedal rates. The highest muscular efficiency was found at 80 rpm in the two experiments, whereas a remarkable reduction (19%) in muscular efficiency obtained at 120 rpm could be attributable to greater O₂ cost due to higher levels of P _int accompanying the increased pedal rates. We concluded that muscular efficiency could be affected by the differences in O₂ cost and P _int during cycling under the large range of pedal rates employed in this study.     

Maximal lactate steady state concentration independent of pedal cadence in active individuals

The maximal lactate steady state (MLSS) is defined as the highest blood lactate concentration that can be maintained over time without a continual blood lactate accumulation. The objective of the present study was to analyze the effects of pedal cadence (50 vs. 100 rev min⁻¹) on MLSS and the exercise workload at MLSS (MLSS_workload) during cycling. Nine recreationally active males (20.9±2.9 years, 73.9±6.5 kg, 1.79±0.09 m) performed an incremental maximal load test (50 and 100 rev min⁻¹) to determine anaerobic threshold (AT) and peak workload (PW), and between two and four constant submaximal load tests (50 and 100 rev min⁻¹) on a mechanically braked cycle ergometer to determine MLSS_workload and MLSS. MLSS_workload was defined as the highest workload at which blood lactate concentration did not increase by more than 1 mM between minutes 10 and 30 of the constant workload. The maximal lactate steady state intensity (MLSS_intensity) was defined as the ratio between MLSS_workload and PW. MLSS_workload (186.1±21.2 W vs. 148.2±15.5 W) and MLSS_intensity (70.5±5.7% vs. 61.4±5.1%) were significantly higher during cycling at 50 rev min⁻¹ than at 100 rev min⁻¹, respectively. However, there was no significant difference in MLSS between 50 rev min⁻¹ (4.8±1.6 mM) and 100 rev min⁻¹ (4.7±0.8 mM). We conclude that MLSS_workload and MLSS_intensity are dependent on pedal cadence (50 vs. 100 rev min⁻¹) in recreationally active individuals. However, this study showed that MLSS is not influenced by the different pedal cadences analyzed.     

Cardiac function and arteriovenous oxygen difference during exercise in obese adults

The purpose of this study was to assess cardiac function and arteriovenous oxygen difference (a-vO₂ difference) at rest and during exercise in young, normal-weight (n = 20), and obese (n = 12) men and women who were matched for age and fitness level. Participants were assessed for body composition, peak oxygen consumption (VO_2peak), and cardiac variables (thoracic bioimpedance)—cardiac index (CI), cardiac output (Q), stroke volume (SV), heart rate (HR), and ejection fraction (EF)—at rest and during cycling exercise at 65% of VO_2peak. Differences between groups were assessed with multivariate ANOVA and mixed-model ANOVA with repeated measures controlling for sex. Absolute VO_2peak and VO_2peak relative to fat-free mass (FFM) were similar between normal-weight and obese groups (Mean ± SEE 2.7 ± 0.2 vs. 3.3 ± 0.3 l min⁻¹, p = 0.084 and 52.4 ± 1.5 vs. 50.9 ± 2.3 ml kg FFM⁻¹ min⁻¹, p = 0.583, respectively). In the obese group, resting Q and SV were higher (6.7 ± 0.4 vs. 4.9 ± 0.1 l min⁻¹, p < 0.001 and 86.8 ± 4.3 vs. 65.8 ± 1.9 ml min⁻¹, p < 0.001, respectively) and EF lower (56.4 ± 2.2 vs. 65.5 ± 2.2%, p = 0.003, respectively) when compared with the normal-weight group. During submaximal exercise, the obese group demonstrated higher mean CI (8.8 ± 0.3 vs. 7.7 ± 0.2 l min⁻¹ m⁻², p = 0.007, respectively), Q (19.2 ± 0.9 vs. 13.1 ± 0.3 l min⁻¹, p < 0.001, respectively), and SV (123.0 ± 5.6 vs. 88.9 ± 4.1 ml min⁻¹, p < 0.001, respectively) and a lower a-vO₂ difference (10.4 ± 1.0 vs. 14.0 ± 0.7 ml l00 ml⁻¹, p = 0.002, respectively) compared with controls. Our study suggests that the ability to extract oxygen during exercise may be impaired in obese individuals.     

The validity of two Omron pedometers during treadmill walking is speed dependent

The purpose of this study was to examine the effects of walking speed on the accuracy of measurement of steps, distance, and energy expenditure of two commercially available Omron pedometers [HJ-720IT-E2 (HJ-720) and HJ-113-E (HJ-113)]. Twenty-four untrained males (age, 22.7 ± 2.8 years; BMI, 24.38 ± 2.19 kg m⁻²; body fat (%), 16 ± 2.2; VO_2max, 40.2 ± 6.5 ml kg⁻¹ min⁻¹) and 18 females (age, 22.4 ± 2.9 years; BMI, 21.68 ± 2.43 kg m⁻²; body fat (%), 23% ± 1.8; VO_2max, 35.9 ± 2.8 ml kg⁻¹ min⁻¹) walked at five different velocities (54, 67, 80, 94 and 107 m min⁻¹) on a treadmill in 5-min stages while wearing three types of pedometers: (a) HJ-720, (b) HJ-113, and (c) Yamax Digi-Walker SW-200 (YAM). Step-count for each pedometer was recorded at the end of each stage and compared with the value of a hand counter. Additionally, Omron pedometers were evaluated on their distance and energy expenditure (against VO₂ measurement with a gas-exchange analyzer) accuracy during each stage. HJ-720 and HJ-113 demonstrated high accuracy (r = 0.80–0.99) at all speeds. YAM underestimated step-count only at 54 m min⁻¹ (r = 0.46). HJ-720 and HJ-113 overestimated distance at slower speeds and underestimated distance at faster speeds, providing mean distance values that where to within 1.5–4% at 80 m min⁻¹. HJ-720 and HJ-113 underestimated energy expenditure (gross kilocalories) by 28%, when compared to indirect calorimetry. These results suggest that although the Omron HJ-720 and HJ-113 pedometers are accurate in the measurement of step-count, they demonstrate limited accuracy in the assessment of traveled distance and energy expenditure in a speed-dependent manner.     

Induction and decay of short-term heat acclimation

The purpose of this work was to investigate adaptation and decay from short-term (5-day) heat acclimation (STHA). Ten moderately trained males (mean ± SD age 28 ± 7 years; body mass 74.6 ± 4.4 kg; [(V)\dot]_{\textO 2\textpeak} \dot{V}_{{{\text{O}}_{ 2{\text{peak}}} }} 4.26 ± 0.37 l min⁻¹) underwent heat acclimation (Acc) for 90-min on 5-days consecutively (T _a = 39.5°C, 60% RH), under controlled hyperthermia (rectal temperature 38.5°C). Participants completed a heat stress test (HST) 1 week before acclimation (Acc), then on the 2nd and 8th day (1 week) following Acc (T _a = 35°C, 60% RH). Seven participants completed HSTs 2 and 3 weeks after Acc. HST consisted of 90-min cycling at 40% peak power output before an incremental performance test. Rectal temperature at rest (37.1 ± 0.4°C) was not lowered by Acc (95% CI −0.3 to 0.2°C), after 90-min exercise (38.6 ± 0.5°C) it reduced 0.3°C (−0.5 to −0.1°C) and remained at this level 1 week later (−0.5 to −0.1°C), but not two (0.1°C −0.4 to 0.5°C; n = 7) or 3 weeks. Similarly, heart rate after 90-min exercise (146 ± 21 b min⁻¹) was reduced (−13: −6 to −20 b min⁻¹) and remained at this level after 1 week (−13: −6 to −20 b min⁻¹) but not two (−9: 6 to −23 b min⁻¹; n = 7) or 3 weeks. Performance (746 s) increased 106 s: 59 to 152 s after Acc and remained higher after one (76 s: 31 to 122) but not two (15 s: −88 to 142 s; n = 7) or 3 weeks. Therefore, STHA (5-day) induced adaptations permitting increased heat loss and this persisted 1 week but not 2 weeks following Acc.     

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.     

Carbohydrate intake reduces fat oxidation during exercise in obese boys

The recent surge in childhood obesity has renewed interest in studying exercise as a therapeutic means of metabolizing fat. However, carbohydrate (CHO) intake attenuates whole body fat oxidation during exercise in healthy children and may suppress fat metabolism in obese youth. To determine the impact of CHO intake on substrate utilization during submaximal exercise in obese boys, seven obese boys (mean age: 11.4 ± 1.0 year; % body fat: 35.8 ± 3.9%) performed 60 min of exercise at an intensity that approximated maximal fat oxidation. A CHO drink (CARB) or a placebo drink (CONT) was consumed in a double-blinded, counterbalanced manner. Rates of total fat, total CHO, and exogenous CHO (CHO_exo) oxidation were calculated for the last 20 min of exercise. During CONT, fat oxidation rate was 3.9 ± 2.4 mg × kg fat-free mass (FFM)⁻¹ × min⁻¹, representing 43.1 ± 22.9% of total energy expenditure (EE). During CARB, fat oxidation was lowered (p = 0.02) to 1.7 ± 0.6 mg × kg FFM⁻¹ × min⁻¹, contributing to 19.8 ± 4.9% EE. Total CHO oxidation rate was 17.2 ± 3.1 mg × kg FFM⁻¹ × min⁻¹ and 13.2 ± 6.1 mg × kg FFM⁻¹ × min⁻¹ during CARB and CONT, respectively (p = 0.06). In CARB, CHO_exo oxidation contributed to 23.3 ± 4.2% of total EE. CHO intake markedly suppresses fat oxidation during exercise in obese boys.     

Physiological costs and temporo-spatial parameters of walking on a treadmill vary with body weight unloading and speed in both healthy young and older women

Walking on a treadmill with Body Weight Unloading (BWU), which has been successfully used on patients with neurological conditions, may also be used as a training tool to increase walking speed in healthy individuals. We hypothesised that BWU enables individuals to walk at a faster speed on a treadmill than they would do in normal gravity conditions without increasing their effort and with an increase in both stride length (SL) and stride frequency (SF). Oxygen uptake, heart rate (HR), SL and SF of six older women (mean ± SD; 70 ± 4 years) and six young women (26 ± 3 years) were measured during treadmill walking at three self-selected speeds (comfortable, slow and fast) and three different percentages of BWU (0, 20 and 40%). No significant differences were found between the groups in any self-selected walking speeds and any of the other variables. The combined data of the two groups showed that walking energy cost per unit of time (WECt) and HR at fast speed with 40% of BWU (258 ± 60 J kg⁻¹ min⁻¹ and 95 ± 15 beats min⁻¹, respectively) were similar to those measured at comfortable speed with no BWU (273 ± 47 J kg⁻¹ min⁻¹ and 101 ± 16 beats min⁻¹, respectively). Also SL and SF increased significantly with speed (P < 0.017) at any given percentage of BWU. The results suggest that 40% of BWU enables both young and older women to walk at a faster speed on a treadmill without increasing their effort and with an increase in both SL and SF.     

Maximal voluntary hyperpnoea increases blood lactate concentration during exercise

Ventilatory work during heavy endurance exercise has not been thought to influence systemic lactate concentration. We evaluated the effect of maximal isocapnic volitional hyperpnoea upon arterialised venous blood lactate concentration ([lac⁻]_B) during leg cycling exercise at maximum lactate steady state (MLSS). Seven healthy males performed a lactate minimum test to estimate MLSS, which was then resolved using separate 30 min constant power tests (MLSS=207±8 W, mean ± SEM). Thereafter, a 30 min control trial at MLSS was performed. In a further experimental trial, the control trial was mimicked except that from 20 to 28 min maximal isocapnic volitional hyperpnoea was superimposed on exercise. Over 20–28 min minute ventilation, oxygen uptake, and heart rate during the control and experimental trials were 87.3±2.4 and 168.3±7.0 l min⁻¹ (P<0.01), the latter being comparable to that achieved in the maximal phase of the lactate minimum test (171.9±6.8 l min⁻¹), 3.46±0.20 and 3.83 ± 0.20 l min⁻¹ (P<0.01), and 158.5±2.7 and 166.8±2.7 beats min⁻¹ (P<0.05), respectively. From 20 to 30 min of the experimental trial [lac⁻]_B increased from 3.7±0.2 to 4.7±0.3 mmol l⁻¹ (P<0.05). The partial pressure of carbon dioxide in arterialised venous blood increased approximately 3 mmHg during volitional hyperpnoea, which may have attenuated the [lac⁻]_B increase. These results show that, during heavy exercise, respiratory muscle work may affect [lac⁻]_B. We speculate that the changes observed were related to the altered lactate turnover in respiratory muscles, locomotor muscles, or both.     

Muscle sympathetic nerve activity at rest compared to exercise tolerance

Cardiovascular autonomic function is associated with physical performance and exercise training adaptation. The association between physical performance and sympathetic regulation is not well known. We hypothesized that sympathetic nervous system activity is associated with physical performance among male runners. The study population included 26 healthy male club runners [age 33 ± 5 years, body mass index (BMI) 24 ± 1 kg/m², VO_2max 58 ± 5 ml kg⁻¹ min⁻¹; mean ± SD]. Muscle sympathetic nerve activity (MSNA) was assessed from the peroneal nerve by the microneurography technique during 5 min of supine rest. Physical performance was assessed by time to exhaustion during treadmill running. The mean resting MSNA was 20 ± 6 bursts min⁻¹ (range 6–34). The mean time to exhaustion was 1,005 ± 136 s (range 720–1260). When the study group was divided into tertiles according to their running performance (866 ± 69, 994 ± 30 and 1154 ± 71 s in time to exhaustion, P < 0.0001 between the groups), MSNA was lower (P = 0.032) in the group with the best running performance (16 ± 5 bursts min⁻¹) compared to those with the worst running performance (23 ± 7 bursts min⁻¹). In conclusion, baseline sympathetic activity, measured by a microneurography at rest, may be associated with the maximal running performance of healthy subjects.     

Prefrontal cortex oxygenation and neuromuscular responses to exhaustive exercise

Near-infrared spectroscopy (NIRS) allows non-invasive monitoring of central and peripheral changes in oxygenation during exercise and may provide valuable insight into the factors affecting fatigue. This study aimed to explore the changes in oxygenation of prefrontal cortex and active muscle tissue as limiting factors of incremental exercise performance in trained cyclists. Thirteen trained healthy subjects (mean ± SE: age 24.9 ± 1.5 years, body mass 70.1 ± 1.2 kg, training 6.1 ± 0.9 h week⁻¹) performed a progressive maximal exercise to exhaustion on a cycling ergometer. Prefrontal cortex (Cox) and vastus lateralis muscle (Mox) oxygenation were measured simultaneously by NIRS throughout the exercise. Maximal voluntary isometric knee torques and quadriceps neuromuscular fatigue (M-wave properties and voluntary activation ratio) were evaluated before and after exercise. Maximal power output and oxygen consumption were 380.8 ± 7.9 W and 75.0 ± 2.2 ml min⁻¹ kg⁻¹, respectively. Mox decreased significantly throughout exercise while Cox increased in the first minutes of exercise but decreased markedly from the workload corresponding to the second ventilatory threshold up to exhaustion (P < 0.05). No significant difference was noted 6 min after maximal exercise in either the voluntary activation ratio or the M-wave properties. These findings are compatible with the notion that supraspinal modulation of motor output precedes exhaustion. An erratum to this article can be found at     

Resetting of tubuloglomerular feedback in acute volume expansion in rats

Loss of sensitivity or “resetting” of tubuloglomerular feedback has been reported after both acute and chronic volume expansion in rats. In chronic volume expansion due to dietary salt loading, resetting was found to result from the appearance of an inhibitory factor in tubular fluid. The aim of the present study was to test the possibility that resetting after acute isooncotic volume expansion may also be due to such an inhibitor. Rats were acutely volume expanded (4.5% of body weight) by infusion of a solution of fresh plasma and Ringer's solution. Tubuloglomerular feedback activity was assessed in expanded and control animals by measuring early proximal flow (EPF) rate during perfusion of the loop of Henle at varying rates with proximal tubular fluid harvested from the control (control TF) and expanded animals (AVE TF). When loops of Henle in control animals were perfused with control TF at 10, 20 or 40 nl min⁻¹, EPF fell from (mean ±SD) 29.8±5.6 at zero loop flow to 27.5±7.5, 21.1±4.2 and 15.5±4.5 nl min⁻¹ gKW⁻¹ respectively. Perfusion at the same rates with control TF in expanded animals reduced EPF from 39.5±9.6 (at zero loop flow) to 35.9±11.3, 31.6±4.3 and 22.9±6.8 nl min⁻¹ gKW⁻¹ respectively. When loops of Henle in control animals were perfused with AVE TF, EPF fell from 28.6±9.5 (zero loop flow) to 23.5±8.6, 19.9±8.2 and 15.6±6.5 nl min⁻¹ gKW⁻¹ respectively. Perfusion at these rates with AVE TF in the expanded animals depressed EPF from 36.7±7.8 (at zero loop flow) to 33.6±7.3, 28.6±7.6 and 22.7±8.0 nl min⁻¹ gKW⁻¹ respectively. Since the responses to the two perfusion fluids were the same in each group, it is concluded that there is no inhibitory factor present in AVE TF. Although EPF at each perfusion rate was significantly higher in the expanded animals than in control, the change in EPF per unit change in loop perfusion rate was the same in both groups from which it is concluded that no resetting of tubuloglomerular feedback occurred in the present study. Some of the work described here was presented to the German Physiological Society at its 59th Meeting, Dortmund, March 26–30, 1984 and to the 17th Congress of the Gesellschaft für Nephrologie, Mainz, Sept. 22–25, 1985 and appears in abstract form in Pflügers Arch 400:R21 (1984), and Kidney Int 29:1253 (1986) respectively     

Stroke volume equation for impedance cardiography

The study's goal was to determine if cardiac output (CO), obtained by impedance cardiography (ICG), would be improved by a new equation N, implementing a square root transformation for dZ/dt_max/Z₀, and a variable magnitude, mass-based volume conductor V_c. Pulmonary artery catheterisation was performed on 106 cardiac surgery patients pre-operatively. Post-operatively, thermodilution cardiac output (TDCO) was simultaneously compared with ICG CO. dZ/dt_max/Z₀ and Z₀ were obtained from a proprietary bioimpedance device. The impedance variables, in addition to left ventricular ejection time T_LVE and patient height and weight, were input using four stroke volume (SV) equations: Kubicek (K), Sramek (S), Sramek-Bernstein (SB), and a new equation N. CO was calculated as SV × heart rate. Data are presented as mean ± SD. One way repeated measures of ANOVA followed by the Tukey test were used for inter-group comparisons. Bland-Altman methods were used to assess bias, precision and limits of agreement. P<0.05 was considered statistically significant. CO implementing N (6.06±1.48 l min⁻¹) was not different from TDCO (5.97±1.41 l min⁻¹). By contrast, CO calculated using K (3.70±1.53 l min⁻¹), S (4.16±1.83 l min⁻¹) and SB (4.37±1.82 l min⁻¹) was significantly less than TDCO. Bland-Altman analysis showed poor agreement between TDCO and K, S and SB, but not between TDCO and N. Compared with TDCO, equation N, using a square-root transformation for dZ/dt_max/Z₀, and a mass-based V_C was superior to existing transthoracic impedance techniques for SV and CO determination.     

The effect of acute metabolic alkalosis on bicarbonate transport along the loop of Henle. The role of active transport processes and passive paracellular backflux

The loop of Henle (LOH) reabsorbs approximately 15% of filtered HCO ₃ ⁻ via a luminal Na⁺-H⁺ exchanger and H⁺ATPase. During acute metabolic alkalosis (AMA) induced by i.v. HCO ₃ ⁻ infusion, we have observed previously inhibition of LOH net HCO ₃ ⁻ reabsorption , which contributes to urinary elimination of the HCO ₃ ⁻ load and correction of the systemic alkalosis. To determine whether the activities of the Na⁺-H⁺ exchanger and/or H⁺-ATPase are reduced during AMA, two inhibitors believed to be sufficiently specific for each transporter were delivered by in vivo LOH microperfusion during AMA. AMA reduced LOH from 205.0±0.8 to 96.2±11.8 pmol · min⁻¹ (P<0.001). Luminal perfusion with bafilomycin A₁ (10⁻⁴ mol · l⁻¹) caused a further reduction in by 83% and ethylisopropylamiloride (EIPA; 5.10⁻⁴ mol · l⁻¹) completely abolished net HCO ₃ ⁻ reabsorption. The combination of bafilomycin A₁ and EIPA in the luminal perfusate was additive, resulting in net HCO ₃ ⁻ secretion (−66.6±20.8 pmol · min⁻¹;P<0.001) and abolished net fluid reabsorption (from 5.0±0.6 during AMA to 0.2±1.1 nl · min⁻¹;P<0.001). To establish whether HCO ₃ ⁻ secretion via luminal stilbenesensitive transport mechanism participates in LOH adaptation to AMA, we added diisothiocyanato-2,2′-stilbenedisulphonate (DIDS; 10⁻⁴ mol · l⁻¹) to the perfusate. No effect was found. However, when the same LOH were exposed to luminal DIDS for more than 10 min, the direction of net HCO ₃ ⁻ movement was reversed and net HCO ₃ ⁻ secretion occurred: changed from 90.6±8.8 to −91.9±34.1 pmol · min⁻¹;P<0.01, an effect that was not observed in the control state (undisturbed acid-base balance). Thus, during AMA, neither the luminal Na⁺-H⁺ exchanger nor the H⁺-ATPase are noticeably suppressed. However, pharmacological elimination of both transporters, as well as prolonged exposure of the tubular lumen to DIDS, induced net HCO ₃ ⁻ secretion. This secretory flux may reflect paracellular backflux due to the steeper blood to lumen HCO ₃ ⁻ concentration gradient that presumably prevails in AMA.     

High-intensity exercise and carbohydrate-reduced energy-restricted diet in obese individuals

Continuous high glycemic load and inactivity challenge glucose homeostasis and fat oxidation. Hyperglycemia and high intramuscular glucose levels mediate insulin resistance, a precursor state of type 2 diabetes. The aim was to investigate whether a carbohydrate (CHO)-reduced diet combined with high-intensity interval training (HIIT) enhances the beneficial effects of the diet alone on insulin sensitivity and fat oxidation in obese individuals. Nineteen obese subjects underwent 14 days of CHO-reduced and energy-restricted diet. Ten of them combined the diet with HIIT (4 min bouts at 90% VO_2peak up to 10 times, 3 times a week). Oral glucose insulin sensitivity (OGIS) increased significantly in both groups; [diet–exercise (DE) group: pre 377 ± 70, post 396 ± 68 mL min⁻¹ m⁻²; diet (D) group: pre 365 ± 91, post 404 ± 87 mL min⁻¹ m⁻²; P < 0.001]. Fasting respiratory exchange ratio (RER) decreased significantly in both groups (DE group: pre 0.91 ± 0.06, post 0.88 ± 0.06; D group: pre 0.92 ± 0.07, post 0.86 ± 0.07; P = 0.002). VO_2peak increased significantly in the DE group (pre 27 ± 5, post 32 ± 6 mL kg⁻¹ min⁻¹; P < 0.001), but not in the D group (pre 26 ± 9, post 26 ± 8 mL kg⁻¹ min⁻¹). Lean mass and resistin were preserved only in the DE group (P < 0.05). Fourteen days of CHO-reduced diet improved OGIS and fat oxidation (RER) in obese subjects. The energy-balanced HIIT did not further enhance these parameters, but increased aerobic capacity (VO_2peak) and preserved lean mass and resistin.     

Effect of isokinetic cycling versus weight training on maximal power output and endurance performance in cycling

The aim of this study was to compare the effects of a weight training program for the leg extensors with isokinetic cycling training (80 rpm) on maximal power output and endurance performance. Both strength training interventions were incorporated twice a week in a similar endurance training program of 12 weeks. Eighteen trained male cyclists (VO_2peak 60 ± 1 ml kg⁻¹ min⁻¹) were grouped into the weight training (WT n = 9) or the isokinetic training group (IT n = 9) matched for training background and sprint power (P _max), assessed from five maximal sprints (5 s) on an isokinetic bicycle ergometer at cadences between 40 and 120 rpm. Crank torque was measured (1 kHz) to determine the torque distribution during pedaling. Endurance performance was evaluated by measuring power, heart rate and lactate during a graded exercise test to exhaustion and a 30-min performance test. All tests were performed on subjects’ individual race bicycle. Knee extension torque was evaluated isometrically at 115° knee angle and dynamically at 200° s⁻¹ using an isokinetic dynamometer. P _max at 40 rpm increased in both the groups (~15%; P < 0.05). At 120 rpm, no improvement of P _max was found in the IT training group, which was possibly related to an observed change in crank torque at high cadences (P < 0.05). Both groups improved their power output in the 30-min performance test (P < 0.05). Isometric knee extension torque increased only in WT (P < 0.05). In conclusion, at low cadences, P _max improved in both training groups. However, in the IT training group, a disturbed pedaling technique compromises an improvement of P _max at high cadences.     

<Emphasis Type="Italic">V</Emphasis>O<Subscript>2</Subscript>max during successive maximal efforts

The concept of VO₂max has been a defining paradigm in exercise physiology for >75 years. Within the last decade, this concept has been both challenged and defended. The purpose of this study was to test the concept of VO₂max by comparing VO₂ during a second exercise bout following a preliminary maximal effort exercise bout. The study had two parts. In Study #1, physically active non-athletes performed incremental cycle exercise. After 1-min recovery, a second bout was performed at a higher power output. In Study #2, competitive runners performed incremental treadmill exercise and, after 3-min recovery, a second bout at a higher speed. In Study #1 the highest VO₂ (bout 1 vs. bout 2) was not significantly different (3.95 ± 0.75 vs. 4.06 ± 0.75 l min⁻¹). Maximal heart rate was not different (179 ± 14 vs. 180 ± 13 bpm) although maximal V _E was higher in the second bout (141 ± 36 vs. 151 ± 34 l min⁻¹). In Study #2 the highest VO₂ (bout 1 vs. bout 2) was not significantly different (4.09 ± 0.97 vs. 4.03 ± 1.16 l min⁻¹), nor was maximal heart rate (184 + 6 vs. 181 ± 10 bpm) or maximal V _E (126 ± 29 vs. 126 ± 34 l min⁻¹). The results support the concept that the highest VO₂ during a maximal incremental exercise bout is unlikely to change during a subsequent exercise bout, despite higher muscular power output. As such, the results support the “classical” view of VO₂max.     

The influence of prior cycling on biomechanical and cardiorespiratory response profiles during running in triathletes

The aim of the present study was to determine the effects of 40 km of cycling on the biomechanical and cardiorespiratory responses measured during the running segment of a classic triathlon, with particular emphasis on the time course of these responses. Seven male triathletes underwent four successive laboratory trials: (1) 40 km of cycling followed by a 10-km triathlon run (TR), (2) a 10-km control run (CR) at the same speed as TR, (3) an incremental treadmill test, and (4) an incremental cycle test. The following ventilatory data were collected every minute using an automated breath-by-breath system: pulmonary ventilation (V˙ _E, l · min⁻¹), oxygen uptake (V˙O₂, ml · min⁻¹ · kg⁻¹), carbon dioxide output (ml · min⁻¹), respiratory equivalents for oxygen (V˙ _E/V˙O₂) and carbon dioxide (V˙ _E/V˙CO₂), respiratory exchange ratio (R) respiratory frequency (f, breaths · min⁻¹), and tidal volume (ml). Heart rate (HR, beats · min⁻¹) was monitored using a telemetric system. Biomechanical variables included stride length (SL) and stride frequency (SF) recorded on a video tape. The results showed that the following variables were significantly higher (analysis of variance, P < 0.05) for TR than for CR: V˙O₂ [51.7 (3.4) vs 48.3 (3.9) ml · kg⁻¹ · min⁻¹, respectively], V˙ _E [100.4 (1.4) l · min⁻¹ vs 84.4 (7.0) l · min⁻¹], V˙ _E/V˙O₂ [24.2 (2.6) vs 21.5 (2.7)] V˙ _E/V˙CO₂ [25.2 (2.6) vs 22.4 (2.6)], f [55.8 (11.6) vs 49.0 (12.4) breaths · min⁻¹] and HR [175 (7) vs 168 (9) beats · min⁻¹]. Moreover, the time needed to reach steady-state was shorter for HR and V˙O₂ (1 min and 2 min, respectively) and longer for V˙ _E (7 min). In contrast, the biomechanical parameters, i.e. SL and SF, remained unchanged throughout TR versus CR. We conclude that the first minutes of the run segment after cycling in an experimental triathlon were specific in terms of V˙O₂ and cardiorespiratory variables, and nonspecific in terms of biomechanical variables. Accepted: 7 July 1997     

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.