Heterogeneity of muscle deoxygenation kinetics during two bouts of repeated heavy exercises

This study examines the effect of prior heavy exercise on the spatial distribution of muscle deoxygenation kinetics at the onset of heavy-intensity cycling exercise. Young untrained male adults (n = 16) performed two consecutive bouts of 6 min of high intensity cycle exercise separated by 6 min at 35 W. Muscle deoxygenation (HHb) was monitored continuously by near-infrared spectroscopy at eight sites in the quadriceps. Prior heavy exercise reduced the delay before the increase in HHb (9 ± 2 vs. 5 ± 2 s; P < 0.001). The standard deviation of TD HHb of the eight sites was decreased by the performance of prior exercise (1.1 ± 0.5 vs. 0.8 ± 0.4 s; P < 0.05). The transient decrease in HHb during the first 10 s of exercise was less during the second bout than during the first bout (0.6 ± 0.6 vs. 0.3 ± 0.3 A.U.; P < 0.01). The standard deviation of this decrease was also reduced by prior exercise (0.5 ± 0.3 vs. 0.3 ± 0.2 A.U.; P < 0.01). Lastly, prior exercise decreased significantly the standard deviation of the HHb rise during the time period corresponding to the pulmonary [(V)\dot] \dot{V} O₂ slow component. These results indicate that prior heavy exercise reduced the spatial heterogeneity of muscle deoxygenation kinetics at the early onset of heavy exercise and during the development of the pulmonary [(V)\dot] \dot{V} O₂ slow component. It indicates that the distribution of the [(V)\dot] \dot{V} O₂/O₂ delivery ratio within muscle was improved by the performance of a prior exercise.     

Dynamics of skeletal muscle oxygenation during sequential bouts of moderate exercise

In rat muscle, faster dynamics of microvascular P(O2) (approximately blood flow (Q(m) to O2 uptake (V(O2) ratio) after prior contractions that did not alter blood [lactate] have been considered to be a consequence of faster V(O2) kinetics. However, in humans, prior exercise below the lactate threshold does not affect the pulmonary V(O2) kinetics. To clarify this apparent discrepancy, we examined the effects of prior moderate exercise on the kinetics of muscle oxygenation (deoxyhaemoglobin, [HHb] alpha V(O2m)/Q(m)) and pulmonary V(O2) (V(O2p) in humans. Eight subjects performed two bouts (6 min each) of moderate-intensity cycling separated by 6 min of baseline pedalling. Muscle (vastus lateralis) oxygenation was evaluated by near-infrared spectroscopy and V(O2p) was measured breath-by-breath. The time constant (tau) of the primary component of V(O2p) was not significantly affected by prior exercise (21.5 +/- 9.2 versus 25.6 +/- 9.7 s; Bout 1 versus 2, P= 0.49). The time delay (TD) of [HHb] decreased (11.6 +/- 2.6 versus 7.7 +/- 1.5 s; Bout 1 versus 2, P < 0.05) and tau[HHb] increased (7.0 +/- 3.5 versus 10.2 +/- 4.6 s; Bout 1 versus 2, P < 0.05), while the mean response time (TD + tau) did not change (18.6 +/- 2.7 versus 17.9 +/- 3.9 s) after prior moderate exercise. Thus, prior moderate exercise resulted in shorter onset and slower rate of increase in [HHb] during subsequent exercise. These data suggest that prior exercise altered the dynamic interaction between V(O2m)and Q(m) following the onset of exercise.     

Effects of recovery time on phosphocreatine kinetics during repeated bouts of heavy-intensity exercise

The purpose of this study was to examine the kinetics of phosphocreatine (PCr) breakdown in repeated bouts of heavy-intensity exercise separated by three different durations of resting recovery. Healthy young adult male subjects (n = 7) performed three protocols involving two identical bouts of heavy-intensity dynamic plantar flexion exercise separated by 3, 6, and 15 min of rest. Muscle high-energy phosphates and intracellular acid-base status were measured using phosphorus-31 magnetic resonance spectroscopy. In addition, the change in concentration of total haemoglobin (Delta[Hb(tot)]) and deoxy-haemoglobin (Delta[HHb]) were monitored using near-infrared spectroscopy. Prior exercise resulted in an elevated (P < 0.05) intracellular hydrogen ion ([H(+)](i)) after 3 min (182 +/- 72 (SD) nM; pH 6.73) and 6 min (112 +/- 19 nM; pH 6.95) but not after 15 min (93 +/- 8 nM; pH 7.03) compared to pre-exercise in Con (90 +/- 3 nM; pHi 7.05). The on-transient time constant (tau) of the PCr primary component was not different amongst the exercise bouts. However, in each of the subsequent bouts the amplitude of the PCr slow component, total PCr breakdown, and rise in [H(+)](i) were reduced (P < 0.05). At exercise onset, Delta[Hb(tot)] was increased (P < 0.05) and the Delta[HHb] kinetic response was slowed (P < 0.05) in the exercise after 3 min, consistent with improved muscle perfusion. In summary, neither the level of acidosis or muscle perfusion at the onset of exercise appeared to be directly related to the time course of the on-transient PCr primary component or the magnitude of the PCr slow component during subsequent bouts of exercise.     

Kinetics of estimated human muscle capillary blood flow during recovery from exercise

The kinetic characteristics of muscle capillary blood flow (Qcap) during recovery from exercise are controversial (e.g. one versus two phases). Furthermore, it is not clear how the overall Qcap kinetics are temporally associated with muscle oxygen uptake (VO2m) kinetics. To address these issues, we examined the kinetics of Qcap estimated from the rearrangement of the Fick equation (Qcap=VO2m/C(a-v)O2) using the kinetics of pulmonary VO2 (VO2p, primary component) and deoxy-haemoglobin concentration ([HHb]) as indices of VO2m and C(a - v)O2 (arterio-venous oxygen difference) kinetics, respectively. VO2p (l min-1) was measured breath by breath and [HHb] (microm) was measured by near infrared spectroscopy during moderate (M; below lactate threshold, LT) and heavy exercise (H, above LT) in nine subjects. The kinetics of Qcap were biphasic, with an initial fast phase (tauI; M=9.3+/-4.9 s and H=6.0+/-3.8 s) followed by a slower phase 2 (tauP; M=29.9+/-8.6 s and H=47.7+/-26.0 s). For moderate exercise, the overall kinetics of Qcap (mean response time [MRT], 36.1+/-8.6 s) were significantly slower than the kinetics of VO2p (tauP; 27.8+/-5.3 s) and [HHb] (MRT for [HHb]; 16.2+/-6.3 s). However, for heavy exercise, there was no significant difference between MRT-[HHb] (34.7+/-10.4 s) and tauP for VO2p (32.3+/-6.7 s), while MRT for Qcap (48.7+/-21.8 s) was significantly slower than MRT for [HHb] and tauP for VO2p. In conclusion, during recovery from exercise the estimated Qcap kinetics were biphasic, showing an early rapid decrease in blood flow. In addition, the overall kinetics of Qcap were slower than the estimated VO2m kinetics.     

Determinants of repeated-sprint ability in females matched for single-sprint performance

This study investigated the relationship between VO2max and repeated-sprint ability (RSA), while controlling for the effects of initial sprint performance on sprint decrement. This was achieved via two methods: (1) matching females of low and moderate aerobic fitness (VO2max: 36.4 +/- 4.7 vs 49.6 +/- 5.5 ml kg(-1) min(-1) ; p < 0.05) for initial sprint performance and then comparing RSA, and (2) semi-partial correlations to adjust for the influence of initial sprint performance on RSA. Tests consisted of a RSA cycle test (5 x 6-s max sprints every 30 s) and a VO2max test. Muscle biopsies were taken before and after the RSA test. There was no significant difference between groups for work (W1, 3.44 +/- 0.57 vs 3.58 +/- 0.49 kJ; p = 0.59) or power (P1, 788.1 +/- 99.2 vs 835.2 +/- 127.2 W; p = 0.66) on the first sprint, or for total work (W(tot), 15.2 +/- 2.2 vs 16.6 +/- 2.2 kJ; p = 0.25). However, the moderate VO2max group recorded a smaller work decrement across the five sprints (W(dec), 11.1 +/- 2.5 vs 7.6 +/- 3.4%; p = 0.045). There were no significant differences between the two groups for muscle buffer capacity, muscle lactate or pH at any time point. When a semi-partial correlation was performed, to control for the contribution of W1 to W(dec), the correlation between VO2max and W(dec) increased from r = -0.41 (p > 0.05) to r = -0.50 (p < 0.05). These results indicate that VO2max does contribute to performance during repeated-sprint efforts. However, the small variance in W(dec) explained by VO2max suggests that other factors also play a role.     

Effects of intermittent hypoxia on SaO2, cerebral and muscle oxygenation during maximal exercise in athletes with exercise-induced hypoxemia

In a placebo-controlled study, the effects of intermittent hypoxic exposures (IHE) or a placebo control for 10 days, were examined on the extent of exercise-induced hypoxemia (EIH), cerebral and muscle oxygenation (near-infrared spectroscopy) and [Formula: see text] Eight athletes who had previously displayed EIH (fall in saturation of arterial oxygen (SaO(2)) of >4% from rest) during an incremental maximal exercise test, volunteered for the present research. Prior to (baseline), and 2 days following (post) the IHE or placebo, an incremental maximal exercise test was performed whilst SaO(2), heart rate, cerebral and muscle oxygenation and respiratory gas exchange were measured continuously. After IHE, but not placebo, EIH was less pronounced at [Formula: see text] (IHE group, SaO(2) at [Formula: see text] baseline 91.23 +/- 1.10%, post 94.10 +/- 2.19%; P < 0.01, mean +/- SD). This reduction was reflected in an increased ventilation (NS), a lower end-tidal CO(2) (P < 0.01), and lowered cerebral TOI during heavy exercise [Formula: see text] Conversely, muscle tHb at maximal exercise, was increased (2.4 +/- 1.8 DeltamuM, P = 0.01, mean +/- 95 CL) following IHE, whilst de-oxygenated Hb at 90% of [Formula: see text] was reduced (-0.9 +/- 0.8 DeltamuM, P = 0.02). These data indicate that exposure to IHE can attenuate the degree of EIH. Despite a potential compromise in cerebral oxygenation, exposure to IHE may induce some positive physiological adaptations at the muscle tissue level. We speculate that the unchanged [Formula: see text] following IHE might reflect a balance between these central (cerebral) and peripheral (muscle) adaptations.     

Plasma lactate accumulation is reduced during incremental exercise in untrained women compared with untrained men

The lactate threshold (LT) is commonly reported as not different between sexes, yet lower blood lactate concentrations have been reported in women during submaximal exercise. The purpose of the present study was to measure the changes in plasma lactate concentration [La(-1)] in men and women during incremental cycle ergometer exercise using the same protocol and compare the data using several different methods of analysis. A group of untrained men (n = 21) and women (n = 22) were studied and venous blood drawn at regular intervals during and after exercise for assay of plasma [La(-1)]. Plasma [La(-1)] increased during exercise in both sexes, reaching higher values in men, both at exhaustion (men 8.6 +/- 2.3 mmol l(-1); women 6.2 +/- 2.3 mmol l(-1); P = 0.01) and post-exercise (men 11.8 +/- 2.1 mmol l(-1); women 10.2 +/- 2.4 mmol l(-1); P = 0.03). Logarithmic transformation of the data yielded LT values that were not different between sexes (men 44.2 +/- 12.9; women 50.2 +/- 12.6; %VO2peak; P = 0.45), yet both the 2 and 4 mmol l(-1) fixed concentration LT occurred at lower relative intensities in men (2 mmol l(-1): men 50.9 +/- 12.9; women 66.9 +/- 11.1; %VO2peak; P = 0.01). 4 mmol l(-1): men 75.7 +/- 11.0; women 90.6 +/- 9.2; VO2peak; P = 0.01). However, when the plasma [La(-1)] was examined in both sexes throughout exercise, using a single exponential function, plasma [La(-1)] was significantly lower in women (P < 0.05) at all relative intensities between 30 and 100%VO2peak. While the basis of this sex difference is unknown, reduced plasma [La(-1)] during submaximal exercise in women may offset to some degree the endurance performance disadvantage of their lower VO2peak.     

Dissociation between the time courses of femoral artery blood flow and pulmonary VO2 during repeated bouts of heavy knee extension exercise in humans

It has frequently been demonstrated that prior heavy cycling exercise facilitates pulmonary O(2) kinetics at the onset of subsequent heavy exercise. This might be due to improved muscle perfusion via acidosis-induced vasodilating effects. However, it is difficult to measure the blood flow (BF) to the working muscles (via the femoral artery) during cycling exercise. We therefore selected supine knee extension (KE) exercise as an alternative, and investigated whether the faster O(2) kinetics in the 2nd bout was matched by proportionally faster BF kinetics to the exercising muscle. Nine healthy subjects (aged 21-44 years) volunteered to participate in this study. The protocol consisted of two consecutive 6-min KE exercise bouts in a supine position (work rate: 70-75% of peak power) separated by a 6-min baseline rest (EX1 to EX2). During the protocol, a pulsed Doppler ultrasound technique was utilized to continuously measure the BF in the right femoral artery. The protocol was repeated at least 6 times to characterize the precise kinetics. In agreement with previous studies using cycling exercise, the O(2) kinetics in the 2nd bout were facilitated compared with that in the 1st bout [mean +/-s.d. of the 'effective' time constant (tau): EX1, 68.6 +/- 15.9, versus EX2, 58.0 +/- 14.4 s. Phase II-tau: EX1, 48.7 +/- 9.0, versus EX2, 41.2 +/- 13.3 s. Empirical index of the slow component (Delta O(2(6-3))): EX1, 78 +/- 44, versus EX2, 57 +/- 36 ml min(-1) (P < 0.05)]. However, no substantial difference was observed for the facilitation of the femoral artery BF response to the 1st and 2nd exercise bouts [i.e. the 'effective'tau of the femoral artery BF: EX1, 40.8 +/- 16.9, versus EX2, 39.0 +/- 17.1 s (P > 0.05)]. It was concluded that the faster pulmonary O(2) kinetics during heavy KE exercise following prior heavy exercise was not associated with a similar modulation in the BF to the working muscles.     

Effects of prior heavy exercise,prior sprint exercise and passive warming on oxygen uptake kinetics during heavy exercise in humans

Prior heavy exercise (above the lactate threshold, Th_la) increases the amplitude of the primary oxygen uptake (VO₂) response and reduces the amplitude of the VO₂ slow component during subsequent heavy exercise. The purpose of this study was to determine whether these effects required the prior performance of an identical bout of heavy exercise, or if prior short-duration sprint exercise could cause similar effects. A secondary purpose of this study was to determine the effect of elevating muscle temperature (through passive warming) on VO₂ kinetics during heavy exercise. Nine male subjects performed a 6-min bout of heavy exercise on a cycle ergometer 6 min after: (1) an identical bout of heavy exercise; (2) a 30-s bout of maximal sprint cycling; (3) a 40-min period of leg warming in a hot water bath at 42°C. Prior sprint exercise elevated blood [lactate] prior to the onset of heavy exercise (by ≅5.6 mM) with only a minor increase in muscle temperature (of ≅0.7°C). In contrast, prior warming had no effect on baseline blood lactate concentration, but elevated muscle temperature by ≅2.6°C. Both prior heavy exercise and prior sprint exercise significantly increased the absolute primary VO₂ amplitude (by ≅230 ml·min^–1 and 260 ml·min^–1, respectively) and reduced the amplitude of the VO₂ slow component (by ≅280 ml·min^–1 and 200 ml·min^–1, respectively) during heavy exercise, whereas prior warming had no significant effect on the VO₂ response. We conclude that the VO₂ response to heavy exercise can be markedly altered by both sustained heavy-intensity submaximal exercise and by short-duration sprint exercise that induces a residual acidosis. In contrast, passive warming elevated muscle temperature but had no effect on the VO₂ response. Electronic Publication     

The effect of hypoxia on pulmonary O2 uptake, leg blood flow and muscle deoxygenation during single-leg knee-extension exercise

The effect of hypoxic breathing on pulmonary O(2) uptake (VO(2p)), leg blood flow (LBF) and O(2) delivery and deoxygenation of the vastus lateralis muscle was examined during constant-load single-leg knee-extension exercise. Seven subjects (24 +/- 4 years; mean +/-s.d.) performed two transitions from unloaded to moderate-intensity exercise (21 W) under normoxic and hypoxic (P(ET)O(2)= 60 mmHg) conditions. Breath-by-breath VO(2p) and beat-by-beat femoral artery mean blood velocity (MBV) were measured by mass spectrometer and volume turbine and Doppler ultrasound (VingMed, CFM 750), respectively. Deoxy-(HHb), oxy-, and total haemoglobin/myoglobin were measured continuously by near-infrared spectroscopy (NIRS; Hamamatsu NIRO-300). VO(2p) data were filtered and averaged to 5 s bins at 20, 40, 60, 120, 180 and 300 s. MBV data were filtered and averaged to 2 s bins (1 contraction cycle). LBF was calculated for each contraction cycle and averaged to 5 s bins at 20, 40, 60, 120, 180 and 300 s. VO(2p) was significantly lower in hypoxia throughout the period of 20, 40, 60 and 120 s of the exercise on-transient. LBF (l min(-1)) was approximately 35% higher (P > 0.05) in hypoxia during the on-transient and steady-state of KE exercise, resulting in a similar leg O(2) delivery in hypoxia and normoxia. Local muscle deoxygenation (HHb) was similar in hypoxia and normoxia. These results suggest that factors other than O(2) delivery, possibly the diffusion of O(2,) were responsible for the lower O(2) uptake during the exercise on-transient in hypoxia.     

Effects of a prior high-intensity knee-extension exercise on muscle recruitment and energy cost: a combined local and global investigation in humans

The effects of a priming exercise bout on both muscle energy production and the pattern of muscle fibre recruitment during a subsequent exercise bout are poorly understood. The purpose of the present study was to determine whether a prior exercise bout which is known to increase O₂ supply and to induce a residual acidosis could alter energy cost and muscle fibre recruitment during a subsequent heavy-intensity knee-extension exercise. Fifteen healthy subjects performed two 6 min bouts of heavy exercise separated by a 6 min resting period. Rates of oxidative and anaerobic ATP production, determined with ³¹P-magnetic resonance spectroscopy, and breath-by-breath measurements of pulmonary oxygen uptake were obtained simultaneously. Changes in muscle oxygenation and muscle fibre recruitment occurring within the quadriceps were measured using near-infrared spectroscopy and surface electromyography. The priming heavy-intensity exercise increased motor unit recruitment ( P < 0.05) in the early part of the subsequent exercise bout but did not alter muscle energy cost. We also observed a reduced deoxygenation time delay, whereas the deoxygenation amplitude was increased ( P < 0.01). These changes were associated with an increased oxidative ATP cost after ∼50 s ( P < 0.05) and a slight reduction in the overall anaerobic rate of ATP production (0.11 ± 0.04 m m min⁻¹ W⁻¹ for bout 1 and 0.06 ± 0.11 m m min⁻¹ W⁻¹ for bout 2; P < 0.05). We showed that a priming bout of heavy exercise led to an increased recruitment of motor units in the early part of the second bout of heavy exercise. Considering the increased oxidative cost and the unaltered energy cost, one could suggest that our results illustrate a reduced metabolic strain per fibre.     

Physiological responses at five estimates of critical velocity

The purpose of this study was to compare critical velocity (CV) estimates from five mathematical models, and to examine the oxygen uptake (VO(2)) and heart rate (HR) responses during treadmill runs at the five estimates of CV. Ten subjects (six males and four females) performed one incremental test to determine maximal oxygen consumption (VO(2max)) and four or five randomly ordered constant-velocity trials on a treadmill for the estimation of CV. Five mathematical models were used to estimate CV for each subject including two linear, two nonlinear, and an exponential model. Up to five randomly ordered runs to exhaustion were performed by each subject at treadmill velocities that corresponded to the five CV estimates, and VO(2) and HR responses were monitored throughout each trial. The 3-parameter, nonlinear (Non-3) model produced CV estimates that were significantly (P < 0.05) less than the other four models. During runs at CV estimates, five subjects did not complete 60 min at the their estimate from the Non-3 model, nine did not complete 60 min at their estimate from the Non-2 model, and no subjects completed 60 min at any estimate from the other three models. The mean HR value (179 +/- 18 beats min(-1), HR(peak)) at the end of runs at CV using the Non-3 model was significantly less than the maximal HR (195 +/- 7 beats min(-1), HR(max)) achieved during the incremental trial to exhaustion. However, mean HR(peak) values from runs at all other CV estimates were not significantly different from HR(max). Furthermore, data indicated that mean HR(peak) values increased during runs at CV estimates from the third minute to the end of exercise for all models, and that these increases in VO(2) (range = 367-458 ml min(-1)) were significantly greater than that typically associated with O(2) drift ( approximately 200 ml min(-1)) for all but the exponential model, indicating a VO(2) slow component associated with CV estimates from four of the five models. However, the mean VO(2) values at the end of exercise during the runs at CV estimates for all five mathematical models were significantly less than the mean VO(2max) value. These results suggest that, in most cases, CV estimated from the five models does not represent a fatigueless task. In addition, the mean CV estimates from the five models varied by 18%, and four of the five mean CV estimates were within the heavy exercise domain. Therefore, CV would not represent the demarcation point between heavy and severe exercise domains.     

Electrostimulation improves muscle perfusion but does not affect either muscle deoxygenation or pulmonary oxygen consumption kinetics during a heavy constant-load exercise

Electromyostimulation (EMS) is commonly used as part of training programs. However, the exact effects at the muscle level are largely unknown and it has been recently hypothesized that the beneficial effect of EMS could be mediated by an improved muscle perfusion. In the present study, we investigated rates of changes in pulmonary oxygen consumption and muscle deoxygenation during a standardized exercise performed after an EMS warm-up session. We aimed at determining whether EMS could modify pulmonary O₂ uptake and muscle deoxygenation as a result of improved oxygen delivery. Nine subjects performed a 6-min heavy constant load cycling exercise bout preceded either by an EMS session (EMS) or under control conditions (CONT). and heart rate (HR) were measured while deoxy-(HHb), oxy-(HbO₂) and total haemoglobin/myoglobin (Hb_tot) relative contents were measured using near infrared spectroscopy. EMS significantly increased (P < 0.05) the Hb_tot resting level illustrating a residual hyperaemia. The EMS priming exercise did not affect either the HHb time constant (17.7 ± 14.2 s vs. 13.1 ± 2.3 s under control conditions) or the kinetics (time-constant = 18.2 ± 5.2 s vs. 15.4 ± 4.6 s under control conditions). Likewise, the other parameters were unchanged. Our results further indicated that EMS warm-up improved muscle perfusion through a residual hyperaemia. However, neither nor [HHb] kinetics were modified accordingly. These results suggest that improved O₂ delivery by residual hyperaemia induced by EMS does not accelerate the rate of aerobic metabolism during heavy exercise at least in trained subjects.     

Human femoral artery and estimated muscle capillary blood flow kinetics following the onset of exercise

The purpose of this study was to compare the kinetics of estimated capillary blood flow (Qcap) to those of femoral artery blood flow (QFA) and estimated muscle oxygen uptake (VO2m). Nine healthy subjects performed a series of transitions from rest to moderate (below estimated lactate threshold, 6 min bouts) knee extension exercise. Pulmonary oxygen uptake (VO2) was measured breath by breath, (QFA) was measured continuously using Doppler ultrasound, and deoxyhaemoglobin ([HHb]) was estimated by near-infrared spectroscopy over the rectus femoris throughout the tests. The time course of (Qcap) was estimated by rearranging the Fick equation (i.e. Qcap = VO2m/(a-v)O2), (arterio - venous O2 difference) using the primary component of VO2 to represent VO2m and [HHb] as a surrogate for (a - v)O2. The overall kinetics of QFA (mean response time, MRT, 13.7 +/- 7.0 s), VO2m (tau, 27.8 +/- 9.0 s) and Qcap (MRT, 41.4 +/- 19.0 s) were significantly (P < 0.05) different from each other. We conclude that for moderate intensity knee extension exercise, conduit artery blood flow (QFA) kinetics may not be a reasonable approximation of blood flow kinetics in the microcirculation (Qcap), the site of gas exchange. This temporal dissociation suggests that blood flow may be controlled differently at the conduit artery level than in the microcirculation.     

Influence of prior exercise on muscle [phosphorylcreatine] and deoxygenation kinetics during high-intensity exercise in men

(31)Phosphate-magnetic resonance spectroscopy and near infrared spectroscopy (NIRS) were used for the simultaneous assessment of changes in quadriceps muscle metabolism and oxygenation during consecutive bouts of high-intensity exercise. Six male subjects completed two 6 min bouts of single-legged knee-extension exercise at 80% of the peak work rate separated by 6 min of rest while positioned inside the bore of a 1.5 T superconducting magnet. The total haemoglobin and oxyhaemoglobin concentrations in the area of the quadriceps muscle interrogated with NIRS were significantly higher in the baseline period prior to the second compared with the first exercise bout, consistent with an enhanced muscle oxygenation. Intramuscular phosphorylcreatine concentration ([PCr]) dynamics were not different over the fundamental region of the response (time constant for bout 1, 51 +/- 15 s versus bout 2, 52 +/- 17 s). However, the [PCr] dynamics over the entire response were faster in the second bout (mean response time for bout 1, 72 +/- 16 s versus bout 2, 57 +/- 8 s; P < 0.05), as a consequence of a greater fall in [PCr] in the fundamental phase and a reduction in the magnitude of the 'slow component' in [PCr] beyond 3 min of exercise (bout 1, 10 +/- 6% versus bout 2, 5 +/- 3%; P < 0.05). These data suggest that the increased muscle O(2) availability afforded by the performance of a prior bout of high-intensity exercise does not significantly alter the kinetics of [PCr] hydrolysis at the onset of a subsequent bout of high-intensity exercise. The greater fall in [PCr] over the fundamental phase of the response following prior high-intensity exercise indicates that residual fatigue acutely reduces muscle efficiency.     

The effect of resistive breathing on leg muscle oxygenation using near-infrared spectroscopy during exercise in men

The effect of added respiratory work on leg muscle oxygenation during constant-load cycle ergometry was examined in six healthy adults. Exercise was initiated from a baseline of 20 W and increased to a power output corresponding to 90% of the estimated lactate threshold (moderate exercise) and to a power output yielding a tolerance limit of 11.8 min (+/- 1.4, S.D.) (heavy exercise). Ventilation and pulmonary gas exchange were measured breath-by-breath. Profiles of leg muscle oxygenation were determined throughout the protocol using near-infrared (NIR) spectroscopy (Hamamatsu NIRO 500) with optodes aligned midway along the vastus lateralis of the dominant leg. Four conditions were tested: (i) control (Con) where the subjects breathed spontaneously throughout, (ii) controlled breathing (Con Br) where breathing frequency and tidal volume were matched to the Con profile, (iii) increased work of breathing (Resist Br) in which a resistance of 7 cmH2O l(-1) s(-1) was inserted into the mouthpiece assembly, and (iv) partial leg blood flow occlusion (Leg Occl), where muscle perfusion was reduced by inflating a pressure cuff (approximately 90 mmHg) around the upper right thigh. During Resist Br and Leg Occl, subjects controlled their breathing pattern to reproduce the ventilatory profile of Con. An approximately 3 min period with respiratory resistance or pressure cuff was introduced approximately 4 min after exercise onset. NIR spectroscopy data for reduced haemoglobin-myoglobin (delta[Hb]) were extracted from the continuous display at specific times prior to, during and after removal of the resistance or pressure cuff. While the delta[Hb] increased during moderate- and heavy-intensity exercise, there was no additional increase in delta[Hb] with Resist Br. In contrast, delta[Hb] increased further with Leg Occl, reflecting increased muscle O2 extraction during the period of reduced muscle blood flow. In conclusion, increasing the work of breathing did not increase leg muscle deoxygenation during heavy exercise. Assuming that leg muscle O2 consumption did not decrease, this implies that leg blood flow was not reduced consequent to a redistribution of flow away from the working leg muscle.     

Matching of blood flow to metabolic rate during recovery from moderate exercise in humans

It is unclear whether measurement of limb or conduit artery blood flow during recovery from exercise provides an accurate representation of flow to the muscle capillaries where gas exchange occurs. To investigate this, we: (a) examined the kinetic responses of femoral artery blood flow (QFA), estimated muscle capillary blood flow (Qcap) and estimated muscle oxygen uptake (VO2m) following cessation of exercise; and (b) compared these responses to verify the adequacy of O2 delivery during recovery. Pulmonary VO2 (VO2p) was measured breath by breath, QFA was measured using Doppler ultrasonography, and deoxy-haemoglobin/myoglobin (deoxy-[Hb/Mb]) was estimated by near-infrared spectroscopy over the rectus femoris in nine healthy subjects during a series of transitions from moderate knee-extension exercise to rest. The time course of Qcap was estimated by rearranging the Fick equation [i.e. Qcap(t) alpha VO2m(t)/deoxy-[Hb/Mb](t)], using the primary component of Vo2p to represent VO2m and deoxy-[Hb/Mb] as a surrogate for arteriovenous O2 difference. There were no significant differences among the overall kinetics of VO2m (tau, 31.4+/-8.2 s), QFA [mean response time (MRT), 34.5+/-20.4 s] and Qcap (MRT, 31.7+/-14.7 s). The VO2m kinetics were also significantly correlated (P<0.05) with those of both QFA and Qcap. Both QFA and Qcap appear to be coupled with VO2m during recovery from moderate knee-extension exercise, such that extraction falls (thus cellular energetic state is not further compromised) throughout recovery.     

Prediction of maximal oxygen uptake from the ratings of perceived exertion and heart rate during a perceptually-regulated sub-maximal exercise test in active and sedentary participants

This study assessed whether the accuracy of predicting maximal oxygen uptake (VO2max) from sub-maximal heart rate (HR) and ratings of perceived exertion (RPE) values was moderated by gender and habitual activity. In total, 27 men and 18 women completed two GXTs to determine VO2max and three perceptually-regulated GXTs, incremented by RPE 9, 11, 13, 15 and 17. The RPE and HR were individually regressed against VO2max (approximately 0.96) to enable predictions of VO2max. The VO2max was predicted from three RPE ranges (9-17, 9-15, 9-13). The RPE ranges were extrapolated to RPE(19), RPE(20) and age-predicted maximal HR (HRmax(pred)). ANOVA revealed no differences between measured and predicted VO2max (P > 0.05) when the RPE range 9-17 was extrapolated to RPE(19) and HRmax(pred). Extrapolation of RPE 9-17 to RPE(20) overestimated VO2max (P < 0.05), but no differences were observed when predicted from the RPE ranges 9-15 and 9-13. The prediction of VO2max was not moderated by gender or activity status. Hierarchical regression analysis revealed that HR explained additional variance in VO2max when added to the RPE (2%). Hierarchical multiple regression analysis also indicated that VO2max was significantly correlated with power output at sub-maximal RPE values of 13 and 15 (P < 0.01) in men and women. The addition of HRmax(pred) improved the accuracy of the prediction equation for men (P = 0.05) but not for women. The study confirmed the validity of estimating VO2max from perceptually-regulated, sub-maximal GXT and indicated the potential utility of regression analysis to gauge appropriate sub-maximal exercise intensities.     

Dynamic responses of oxygen uptake at the onset and end of moderate and heavy exercise in trained subjects.

Inconsistencies about dynamic asymmetry between the on- and off-transient responses in VO2 are found in the literature. Therefore the purpose of this study was to examine VO2 on- and off-transients during moderate- and heavy-intensity cycling exercise in trained subjects. Ten men underwent an initial incremental test for the estimation of ventilatory threshold (VT) and, on different days, two bouts of square-wave exercise at moderate (VT) intensities. VO2 kinetics in exercise and recovery were better described by a single exponential model (VT). For moderate exercise, we found a symmetry of VO2 kinetics between the on- and off-transients (i.e., fundamental component), consistent with a system manifesting linear control dynamics. For heavy exercise, a slow component superimposed on the fundamental phase was expressed in both the exercise and recovery, with similar parameter estimates. But the on-transient values of the time constant were appreciably faster than the associated off-transient, and independent of the work rate imposed (VT). Our results do not support a dynamically linear system model of VO2 during cycling exercise in the heavy-intensity domain.     

A comparison of modelling techniques used to characterise oxygen uptake kinetics during the on-transient of exercise

We compared estimates for the phase 2 time constant (tau) of oxygen uptake (VO2) during moderate- and heavy-intensity exercise, and the slow component of VO2 during heavy-intensity exercise using previously published exponential models. Estimates for tau and the slow component were different (P < 0.05) among models. For moderate-intensity exercise, a two-component exponential model, or a mono-exponential model fitted from 20 s to 3 min were best. For heavy-intensity exercise, a three-component model fitted throughout the entire 6 min bout of exercise, or a two-component model fitted from 20 s were best. When the time delays for the two- and three-component models were equal the best statistical fit was obtained; however, this model produced an inappropriately low DeltaVO2/DeltaWR (WR, work rate) for the projected phase 2 steady state, and the estimate of phase 2 tau was shortened compared with other models. The slow component was quantified as the difference between VO2 at end-exercise (6 min) and at 3 min (DeltaVO2 (6-3 min)); 259 ml x min(-1)), and also using the phase 3 amplitude terms (truncated to end-exercise) from exponential fits (409-833 ml x min(-1)). Onset of the slow component was identified by the phase 3 time delay parameter as being of delayed onset approximately 2 min (vs. arbitrary 3 min). Using this delay DeltaVO2 (6-2 min) was approximately 400 ml x min(-1). Use of valid consistent methods to estimate tau and the slow component in exercise are needed to advance physiological understanding.