The VO2 response to exhaustive square wave exercise: influence of exercise intensity and mode

We investigated the oxygen uptake (O₂) response to exhaustive square wave exercise of approximately 2, 5 and 8 min duration in cycling and running. Nine males completed a ramp test and three square wave tests on a motorised treadmill and the same four tests on a cycle ergometer, throughout which gas exchange was assessed (Douglas bag method). The peak O₂ from the ramp test was higher for running than for cycling [mean (SD): 58.4 (2.8) vs. 55.9 (3.7) ml.kg^–1.min^–1; P=0.04]. However O_2max (defined as the highest O₂ achieved in any of the four tests) did not differ between running and cycling [60.0 (2.9) vs. 58.5 (3.3) ml.kg^–1.min^–1; P=0.15]. The peak O₂ was similar (P>0.1) for the 5 and 8 min square wave tests [98.5 (1.8) and 99.2 (2.3) %O_2max for running; 97.0 (4.2) and 97.5 (2.0) %O_2max for cycling] but lower (P<0.001) for the 2-min test [91.8 (2.5) and 89.9 (5.5) %O_2max for running and cycling respectively]. O₂ increased over the final two 30-s collection periods of the 2-min test for cycling [O₂=0.18 (0.15) l.min^–1; P<0.01] but not running [O₂=0.00 (0.09) l.min^–1; P=0.98]. We conclude that in the aerobically fit the peak O₂ for square wave running or cycling at an intensity severe enough to result in exhaustion in approximately 2 min is below O_2max. In running, O₂ plateaus at this sub-maximal rate.     

Muscle oxygenation kinetics at the onset of exercise do not depend on exercise intensity

The purpose of this study was to determine whether the onset kinetics of muscle oxygenation in localized working muscle (mOxy) was affected by differences in exercise intensity. Five healthy male subjects exercised for 6 min at 125 W, 150 W, and 175 W, and 1 min at 300 W on a cycle ergometer. mOxy was estimated by near-infrared spectroscopy (NIRS) with a continuous wave photometer. The NIRS probe was positioned on the vastus lateralis muscle of the right leg. The relative change in mOxy was calculated from the relative change of the oxygenated hemoglobin (OxyHb) and deoxygenated hemoglobin (DeoxyHb) concentration from their resting values ([mOxy]=[OxyHb]–[DeoxyHb]). Assuming an exponential time course with time delay, the time constants of the mOxy were 5.7 (SD 2.2) s at 125 W, 5.6 (SD 1.9) s at 150 W, 6.0 (SD 2.2) s at 175 W, and 5.6 (SD 2.1) s at 300 W. The time delays of the mOxy were 6.7 (SD 4.2) s at 125 W, 8.6 (SD 1.6) s at 150 W, 6.4 (SD 3.0) s at 175 W, and 5.4 (SD 2.9) s at 300 W. The mean response times of the mOxy were 12.5 (SD 2.7) s at 125 W, 14.2 (SD 2.4) s at 150 W, 12.4 (SD 4.4) s at 175 W, and 11.0 (SD 3.1) s at 300 W. These results indicate that the kinetics of mOxy were not affected by differences in exercise intensity.     

The effect of the amount of eccentric exercise on ventilatory response at the onset of exercise

We examined the effect of the amount of eccentric exercise (ECC) on ventilatory response at the onset of exercise. The first 10 s of ventilatory response to exercise while using the leg that had performed a relatively greater number of ECC repetitions was greater than that of the leg that had done relatively fewer repetitions, suggesting that ventilatory response at the onset of exercise varies with the degree of change in muscle condition after ECC.     

(.)VO(2) and EMG activity kinetics during moderate and severe constant work rate exercise in trained cyclists.

The purpose of this study was to compare O(2) uptake ((.)VO(2)) and muscle electromyography activity kinetics during moderate and severe exercise to test the hypothesis of progressive recruitment of fast-twitch fibers in the explanation of the VO(2) slow component. After an incremental test to exhaustion, 7 trained cyclists (mean +/- SD, 61.4 +/- 4.2 ml x min(-1) x kg(- 1)) performed several square-wave transitions for 6 min at moderate and severe intensities on a bicycle ergometer. The (.)VO(2) response and the electrical activity (i.e., median power frequency, MDF) of the quadriceps vastus lateralis and vastus medialis of both lower limbs were measured continuously during exercise. After 2 to 3 min of exercise onset, MDF values increased similarly during moderate and severe exercise for almost all muscles whereas a (.)VO(2) slow component occurred during severe exercise. There was no relationship between the increase of MDF values and the magnitude of the (.)VO(2) slow component during the severe exercise. These results suggest that the origin of the slow component may not be due to the progressive recruitment of fast-twitch fibers.     

The off-transient pulmonary oxygen uptake (VO(2)) kinetics following attainment of a particular VO(2) during heavy-intensity exercise in humans

The oxygen uptake response to moderate-intensity exercise (i.e. < anaerobic threshold (an)) has been characterised with a gain (i.e. response amplitude per increment of work rate) and time constant that do not vary appreciably at different work rates or between the on- and off-transients. Above an, the response becomes more complex with an early component that typically projects to a value that has a gain similar to that of the < an response, but which is supplemented by the addition of a delayed slow kinetic component. We therefore established a constant target VO2 (VO21) for each subject such that with different imposed work rates the contribution to VO21 from the slow phase varied over a wide range. Work rates were chosen so that VO21 was attained at 2-24 min. Five subjects (aged 21-58 years) cycled at four to five different work rates. VO2 was measured breath-by-breath, at VO21 the work rate was abruptly reduced and the subject recovered by cycling unloaded for 15 min. Unlike the on-transient, for which the slow component shows a long delay, the off-transient was best fitted as two simultaneous exponential components. The slower off-transient component had a small amplitude and long time constant, but did not differ significantly among the various tests. The off-transient kinetics for VO2 therefore was independent of the magnitude of the contribution to the slow phase from the on-transient kinetics.     

Caffeine ingestion attenuates the VO(2) slow component during intense exercise

The purpose of this study was to analyze the effects of caffeine ingestion on the slow component of oxygen uptake (DeltaVO(2)) during high-intensity endurance exercise. Nine subjects (8 male and 1 female; age: 21 +/- 1 years; VO(2 max): 57.9 +/- 1.5 ml kg(-1) min(-1)) performed two 9-min tests on a treadmill at a running velocity eliciting 90% of their VO(2 max), 60 min after ingesting either a placebo capsule (PLAC) or a capsule containing a caffeine dose of 5 mg (kg body mass)(-1) [CAFF]. The mean values of DeltaVO(2) were significantly lower in CAFF than in PLAC (83 +/- 31 ml min(-1) vs. 167 +/- 26 ml min(-1), respectively; p < 0.05). These findings suggest that the ergogenic effect of caffeine in a high-intensity endurance exercise shown in previous research may be partly mediated by a possible attenuation of the VO(2) slow component.     

Immediate CO2 storage capacity at the onset of exercise

The purpose of the present study was to obtain the immediate CO2 storage capacity at the onset of exercise. The CO2 stores at the onset of the exercise were calculated from the difference between the respiratory gas exchange ratio (R) and the metabolic gas exchange ratio (RQ: R obtained at 5.5 min of exercise). The CO2 stores per body weight (CO2 stores/w) were linearly related to the CO2 pressure (P'vCO2) determined by the CO2 rebreathing method (r = 0.713, p less than 0.001), the slope being 0.330 ml/(mmHg X kg). The CO2 stores were then corrected for change in O2 stores with exercise, that defined as total CO2 stores. P'vCO2 was also corrected for the effect of lung-bag volume shrinkage and Haldane effect during CO2 rebreathing, that defined as true PvCO2. The total CO2 stores/w were also related linearly to the true PvCO2 (r = 0.725, p less than 0.001), the slope of the regression line defined as the immediate CO2 storage capacity being 0.650 ml/(mmHg X kg).     

Effect of paddling cadence on time to exhaustion and VO2 kinetics at the intensity associated with VO2max in elite white-water kayakers.

The influence of paddling cadence on the time to exhaustion (t.lim) and VO2 kinetics at the intensity associated with VO2max (IVO2max) was examined in seven highly-trained white water kayakers. All subjects were engaged in national or international competitions. Subjects took part in three constant-load tests at IVO2max, each test performed at a different paddling cadence (50, 60 or 70 cycles min(-1). The VO2 kinetics recorded during these constant-load tests at IVO2max were fitted with a mono-exponential equation. A significant increase in t.lim (P <.05) was observed as the paddling cadence increased from 50 to 70 cycles min(-1). No effect was found either on values of VO2peak, post-exercise blood lactate concentration, or on the time at which VO2peak was attained (TAVO2peak). Our results suggest that experienced kayakers may choose a high paddling cadence during physiological assessments at IVO2max. Further experiments are needed in order to identify the physiological significance of t.lim at IVO2max.     

Hyperpnoeic response independent of limb movements at exercise onset in mice

We have shown that constant-load treadmill exercise in mice produces an abrupt ventilatory increase to a maximal level at exercise onset. We examined what caused this abrupt response. We measured ventilation during 30-min constant-load exercise on a treadmill, below the lactate threshold, in conscious mice. Video analysis showed that hyperpnoea started before locomotion began. Incremental changes in speed did not further increase ventilation during the early phase of exercise. Next, we measured ventilatory responses to a sudden movement of the treadmill belt on which the mice were kept in a stationary position by a mesh cover. Hyperpnoea started concurrently with the sudden belt movement. In the absence of locomotion, ventilation increased to the extent reached during exercise hyperpnoea. Finally, the abrupt response showed plasticity but was attenuated by experience. The present study shows the importance of factors independent of limb movements in the hyperpnoeic response during the early phase of treadmill exercise in mice.     

Effects of acute hypoxia on ventilatory response at the onset of cycle exercise in man.

In order to examine whether or not there are initial changes in ventilation at the start of bicycle exercise having work loads of differing intensities are affected with regard to normoxia and to hypoxia accompanying hypocapnia, six healthy male subjects performed submaximal exercise of 30 and 120 W at 60 rpm under normoxic (FIO2 = 0.21) and hypoxic (FIO2 = 0.11) conditions. Resting ventilation was significantly higher in hypoxia than in normoxia. However, no statistically significant differences in the initial change in ventilation at the start of exercise (delta VI assessed breath-by-breath) were found between eucapnic normoxia and hypocapnic hypoxia in both 30 and 120 W exercise. Moreover, blood lactate after exercise did not increase in any conditions as compared with rest. These observations suggest that the neurogenic ventilatory response immediately after submaximal exercise at a work load below the subject's anaerobic threshold is independent from PO2.     

The heart rate increase at the onset of high-work intensity exercise is accelerated by central blood volume loading

Using a water immersion (WI) method, the combined effect of central blood volume (CBV) loading and work intensity on the time course of heart rate (HR) at the onset of upright dynamic exercise was investigated. Seven males cranked a cycle ergometer for 12 min using their un-immersed arms at low-, moderate- and high-work intensities, followed by a 12-min rest. For WI, the pre-exercise resting cardiac output increased by 36%, while HR decreased by 22% [from 76.8 (10.4) to 59.6 (9.8) beats/min]. WI also increased the high-frequency (HF, 0.15–0.40 Hz) component of the HR variability, suggesting an increased vagal activity. During the initial 2 min of the exercise period at low-work intensity, HR increased by 34.9 and 25.8% in the WI and control conditions, respectively. These were 117 and 73% at high-work intensity, indicating more accelerated HR with WI than the control. The plasma norepinephrine concentration increased less during high-work intensity exercise during WI, as compared to exercise during control conditions. In conclusion, the HR increase at the onset of high-work intensity exercise is accelerated by CBV loading but not at low intensity, possibly reflecting vago-sympathetic interaction and reduced baroreflex sensitivity.     

Effects of acute hypoxia on ventilatory response at the onset of submaximal exercise

In order to investigate the effects of acute hypoxia and accompanying hypocapnia on the ventilatory response at the onset of dynamic exercise, four healthy adult men performed 50W rectangular loads on a cycle-ergometer in normoxic (FIO2 = 0.21) and hypoxic (FIO2 = 0.11) conditions. No statistically significant differences in the initial ventilatory responses to exercise (both delta VI and delta VE assessed on a breath-by-breath basis) were found between eucapnic normoxia (PETO2 approximately 95, PETCO2 approximately 42 Torr) and hypocapnic hypoxia (PETO2 approximately 45, PETCO2 approximately 35 Torr). The present findings support the contention that the neurogenic ventilatory drive at the onset of early exercise is independent from PO2 and PCO2.     

Heart rate response at the onset of exercise in an apparently healthy cohort

Background

The exercise test is a powerful non-invasive tool for risk stratifying patients with or suspected of having cardiovascular disease (CVD). Heart rate (HR) response during and following exercise has been extensively studied. However, the clinical utility of HR response at the onset of exercise is less understood. Furthermore, conflicting reports exist regarding whether a faster vs. slower HR acceleration represents a CVD risk marker. The primary study purpose was to describe HR acceleration early in exercise in apparently healthy individuals.

Methods

Retrospective analyses were performed in a sample (N = 947) representing a range of age and fitness (11–78 years; VO_2peak 17–49 mL kg^?1 min^?1). HR response was defined over the initial 7 min of the protocol. Associations between HR acceleration and CVD risk factors were also assessed.

Results

Mean increases in HR were 18 ± 9 and 23 ± 11 beats at minute one, for men and women, respectively (p < 0.05). After adjusting for gender and pre-exercise HR, only modest associations were observed between the change in HR at minute one and body mass index, resting blood pressure, cigarette smoking, physical activity, HR reserve, and cardiorespiratory fitness.

Conclusion

There was wide variability in HR acceleration at the onset of exercise in this apparently healthy cohort. A lower increase in HR during the first minute of exercise was associated with a better CVD risk profile, including higher cardiorespiratory fitness, in apparently healthy individuals. These data suggest a greater parasympathetic influence at the onset of exercise may be protective in an asymptomatic population.     

The effect of exercise intensity on the post-exercise esophageal temperature response

On 2 separate days, nine volunteers aged 23.8 (2.0) years performed 15-min bouts of treadmill running in a temperature-controlled chamber at 29°C at a power output that elicited either 70% (moderate) or 93% (intense) of maximum oxygen consumption. Exercise was followed by a 45-min recovery period. End-exercise esophageal temperature (T _es) was elevated by 0.97°C and 2.17°C above baseline for the moderate and intense exercise trials, respectively. Post-exercise T _es achieved a sustained elevated value of 0.38°C and 0.79°C within 15 min of exercise cessation. Systolic blood pressure (SBP) for both exercise trials became hypotensive for the full recovery period, with the magnitude of the reduction being greater for the intense exercise (P<0.05). Diastolic blood pressure (DBP) was unaffected by exercise intensity and values were lower than baseline between 15 min and 30 min post-exercise (P<0.05). Mean arterial pressure (MAP) was reduced from baseline for both exercise trials, with intense exercise showing a greater decrement (P<0.05). It was shown that the increase in the post-exercise hypotensive response, induced by exercise of increasing intensity, was paralleled by an increase in the magnitude of the post-exercise elevation in T _es (i.e., a difference of 0.41°C between conditions). Electronic Publication     

The VO2 response to submaximal ramp cycle exercise: Influence of ramp slope and training status

The aim of the study was to test whether ramp slope and training status interact in the oxygen uptake (VO2) response during submaximal ramp exercise. Eight cyclists (VO2 peak=67.8+/-3.7 ml min(-1)kg(-1)) and eight physically active students (PA students) (VO2 peak=49.1+/-4.3 ml min(-1)kg(-1)) performed several ramp protocols, respectively, 25 and 40 W min(-1) for the cyclists and 10, 25 and 40 W min(-1) for the PA students. Vo(2) was plotted as a function of time and work rate up to the gas exchange threshold (GET). Faster ramp elicited a significantly shorter mean response time (MRT) in both groups, and MRT was significantly longer for each ramp protocol in the PA students (126+/-32s, 76+/-15s and 50+/-6s for ramp 10, ramp 25 and ramp 40, respectively) compared to the cyclists (61+/-9s and 40+/-11s for ramp 25 and ramp 40, respectively). Ramp 40 showed less steep Delta VO2/Delta W than ramp 25 in both groups (p<0.01) and Delta VO2/Delta W was less steep for each ramp protocol in PA students (p<0.01) (9.82+/-0.30 ml min(-1)W(-1) and 9.33+/-0.45 ml min(-1)W(-1) for ramp 25 and ramp 40, respectively) compared to cyclists (10.31+/-0.40 ml min(-1)W(-1) and 10.05+/-0.48 ml min(-1)W(-1) for ramp 25 and ramp 40, respectively). In the PA students, Delta VO2/Delta W did not differ between ramp 10 and ramp 25. Statistical analysis showed no interaction effects between ramp slope and training status for MRT (p=0.62) and Delta VO2/Delta W (p=0.35).     

Ventilatory response at the onset of voluntary exercise and passive movement in endurance runners

The present study was performed to examine whether or not the ventilatory response at the onset of voluntary exercise and passive movement in endurance runners is the same as in untrained subjects. Twelve long-distance runners belonging to the varsity athletic club and 13 untrained subjects of our university participated as subjects in this study. Maximum oxygen uptake was significantly higher in the endurance runner group [mean (SD) 70.8 (4.7) ml?·?kg^?1?·?min^?1] than in the untrained group [49.8 (6.3) ml?·?kg^?1?·?min^?1]. Cardiorespiratory responses during voluntary exercise and passive movement of alternate flexion-extension of the right and left legs for about 15 s at a frequency of about 60?rpm, were determined by means of breath-by-breath techniques. Minute inspiratory ventilation (V˙ _I), tidal volume (V _T), respiratory frequency (f _b), cardiac output (Q˙ _c), stroke volume (SV) and heart rate (HR) increased significantly immediately at the onset of voluntary exercise and passive movement. The incremental rate for V˙ _I was greater than that for Q˙ _c. Average values and standard deviations of changes in V˙ _I were calculated as the difference between the mean of the first and second breath and the mean of five breaths preceding the exercise or movement. The rates obtained in voluntary exercise and passive movement in the endurance runner group [2.34 (0.82) and 1.72 (0.71 l?·?min^?1), respectively] were significantly (P<0.05) lower than those in the untrained group [4.16 (2.66) and 2.71 (1.56 l?·?min^?1), respectively]. Also changes in V _T and HR were significantly lower in the endurance group than in the untrained group with regard to both voluntary exercise and passive movement. The results suggest that the magnitude of cardiorespiratory responses at the onset of voluntary exercise and passive movement in humans is influenced by chronic endurance training for long periods.     

Skeletal muscle vasodilatation at the onset of exercise

The mechanism for exercise hyperaemia is a century old enigma. Much of the research on the topic has focused on the factors controlling skeletal muscle blood flow during steady-state dynamic exercise. It is likely that the factors which initiate the increase in blood flow are distinct from those which sustain the elevated blood flow. There is now convincing evidence that there is rapid vasodilatation following release of muscle contraction. Metabolic, neural and acetylcholine spillover mechanisms do not appear to explain the initial dilatation. Heretofore there has been only circumstantial evidence regarding the role of potassium released by skeletal muscle fibres. Studies which interrupt potassium-mediated dilatation are just emerging and are not conclusive. In addition, the latency of the vascular smooth muscle response to potassium makes it desirable to identify a mechanism that does not rely on diffusion of a vasoactive agent. Compression of the intramuscular arterioles during contraction could activate a mechanosensitive response by the vascular smooth muscle and/or endothelium. Recent in vitro and in vivo data support the notion that brief periods of mechanical compression elicit rapid vasodilatation. Thus, vascular compression could represent a feedforward mechanism for initiating skeletal muscle vasodilatation at the onset of exercise.     

VO2 responses to different intermittent runs at velocity associated with VO2max.

The purposes of this study were (1) to determine the time sustained above 90% of VO2max in different intermittent running sessions having the same overall time run at the velocity (vVO2max) associated with VO2max, and (2) to test whether the use of a fixed-fraction (50%) of the time to exhaustion at vVO2max (Tlim) leads to longer time spent at a high percentage of VO2max. Subjects were 8 triathletes who, after determination of their track vVO2max and Tlim, performed three intermittent running sessions alternating the velocity between 100% and 50% of vVO2max, termed 30 s-30 s, 60 s-30 s, and 1/2 Tlim, where the overall time at vVO2max was similar (= 3 x Tlim). VO2max achieved in the incremental test was 71.1 +/- 3.9 ml.min-1.kg-1 and Tlim was 236 +/- 49 s. VO2peak and peak heart rate were lower in 30 s-30 s than in the other intermittent runs. The time spent above 90% of VO2max was significantly (p < 0.001) longer either in 60 s-30 s (531 +/- 187 s) or in 1/2 Tlim-1/2 Tlim (487 +/- 176 s) than in 30 s-30 s (149 +/- 33 s). Tlim was negatively correlated with the time (in % of Tlim) spent above 90% of VO2max in 30 s-30 s (r = -0.75, p < 0.05). Tlim was also correlated with the difference of time spent over 90% of VO2max between 60 s-30 s and 30 s-30 s (r = 0.77, p < 0.05), or between 1/2 Tlim-1/2 Tlim and 30 s-30 s (r = 0.97, p < 0.001). The results confirm that vVO2max and Tlim are useful for setting interval-training sessions. However, the use of an individualized fixed-fraction of Tlim did not lead to longer time spent at a high percentage of VO2max compared to when using a fixed work-interval duration.