Prior Heavy-intensity Exercise Research Articles

Prior heavy-intensity exercise's enhancement of oxygen-uptake kinetics and short-term high-intensity exercise performance independent of aerobic-training status.

Prior high-intensity exercise can improve exercise performance during severe-intensity exercise. These positive alterations have been attributed, at least in part, to enhancement of overall oxygen-uptake (VO2) kinetics. To determine the effects of prior heavy-intensity exercise on VO2 kinetics and short-term high-intensity exercise performance in individuals with different aerobic-training statuses. Fifteen active subjects (UT; VO2max = 43.8 ± 6.3 mL · kg-1 · min-1) and 10 well-trained endurance cyclists (T; VO2max = 66.7 ± 6.7 mL · kg-1 · min-1) performed the following protocols: an incremental test to determine lactate threshold and VO2max, 4 maximal constant-load tests to estimate critical power, and two 3-min bouts of cycle exercise, involving 2 min of constant-work-rate exercise at severe intensity followed by a 1-min all-out sprint test. This trial was performed without prior intervention and 10 min after prior heavy-intensity exercise (ie, 6 min at 90% critical power). The mean response time of VO2 was shortened after prior exercise for both UT (30.7 ± 9.2 vs 24.1 ± 7.2 s) and T (31.8 ± 5.2 vs 25.4 ± 4.3 s), but no group-by-condition interaction was detected. The end-sprint performance (ie, mean power output) was improved in both groups (UT ~4.7%, T ~2.0%; P < .05) by prior exercise. The effect of prior heavy-intensity exercise on overall VO2 kinetics and short-term high-intensity exercise performance is independent of aerobic-training status.

The Positive Effects of Priming Exercise on Oxygen Uptake Kinetics and High-Intensity Exercise Performance Are Not Magnified by a Fast-Start Pacing Strategy in Trained Cyclists

The purpose of this study was to determine both the independent and additive effects of prior heavy-intensity exercise and pacing strategies on the VO2 kinetics and performance during high-intensity exercise. Fourteen endurance cyclists (VO2max = 62.8±8.5 mL.kg−1.min−1) volunteered to participate in the present study with the following protocols: 1) incremental test to determine lactate threshold and VO2max; 2) four maximal constant-load tests to estimate critical power; 3) six bouts of exercise, using a fast-start (FS), even-start (ES) or slow-start (SS) pacing strategy, with and without a preceding heavy-intensity exercise session (i.e., 90% critical power). In all conditions, the subjects completed an all-out sprint during the final 60 s of the test as a measure of the performance. For the control condition, the mean response time was significantly shorter (p<0.001) for FS (27±4 s) than for ES (32±5 s) and SS (32±6 s). After the prior exercise, the mean response time was not significantly different among the paced conditions (FS = 24±5 s; ES = 25±5 s; SS = 26±5 s). The end-sprint performance (i.e., mean power output) was only improved (∼3.2%, p<0.01) by prior exercise. Thus, in trained endurance cyclists, an FS pacing strategy does not magnify the positive effects of priming exercise on the overall VO2 kinetics and short-term high-intensity performance.

Effects of prior heavy-intensity exercise on oxygen uptake and muscle deoxygenation kinetics of a subsequent heavy-intensity cycling and knee-extension exercise

This study examined the effects of prior heavy-intensity exercise on the adjustment of pulmonary oxygen uptake (VO(2p)) and muscle deoxygenation Δ[HHb] during the transition to subsequent heavy-intensity cycling (CE) or knee-extension (KE) exercise. Nine young adults (aged 24 ± 5 years) performed 4 repetitions of repeated bouts of heavy-intensity exercise separated by light-intensity CE and KE, which included 6 min of baseline exercise, a 6-min step of heavy-intensity exercise (H1), 6-min recovery, and a 6-min step of heavy-intensity exercise (H2). Exercise was performed at 50 r·min(-1) or contractions per minute per leg. Oxygen uptake (VO(2)) mean response time was ∼20% faster (p < 0.05) during H2 compared with H1 in both modalities. Phase 2 time constants (τ) were not different between heavy bouts of CE (H1, 29.6 ± 6.5 s; H2, 28.0 ± 4.6 s) or KE exercise (H1, 31.6 ± 6.7 s; H2, 29.8 ± 5.6 s). The VO(2) slow component amplitude was lower (p < 0.05) in H2 in both modalities (CE, 0.19 ± 0.06 L·min(-1); KE, 0.12 ± 0.07 L·min(-1)) compared with H1 (CE, 0.29 ± 0.09 L·min(-1); KE, 0.18 ± 0.07 L·min(-1)), with the contribution of the slow component to the total VO(2) response reduced (p < 0.05) in H2 during both exercise modes. The effective τHHb was similar between bouts for CE (H1, 18.2 ± 3.0 s; H2, 18.0 ± 3.6 s) and KE exercise (H1, 26.0 ± 7.0 s; H2, 24.0 ± 5.8 s). The ΔHHb slow component was reduced during H2 in both CE and KE (p < 0.05). In conclusion, phase 2 VO(2p) was unchanged with priming exercise; however, a faster mean response time of VO(2p) during the heavy-intensity exercise preceded by a priming heavy-intensity exercise was attributed to a smaller slow component and reduced muscle deoxygenation indicative of improved muscle O(2) delivery during the second bout of exercise.

Effects of Priming Exercise on V˙O2 Kinetics and the Power-Duration Relationship

This study aimed to investigate the influence of prior heavy- and severe-intensity exercise on the oxygen uptake (V·O₂) kinetics and the power-duration relationship. Ten cyclists performed 13 exercise tests during a 4-wk period, consisting of a ramp test to determine the gas exchange threshold (GET) and the peak V·O₂, followed by a series of square-wave tests to exhaustion under three conditions: no prior exercise (control), prior heavy exercise (6 min at a work rate above GET but below critical power [CP)], and prior severe exercise (6 min at a work rate above the CP). Pulmonary gas exchange was measured throughout the exhaustive exercise bouts and the parameters of the power-duration relationship (CP and the curvature constant, W') were determined from the linear work-time model. Prior heavy exercise increased the amplitude of the primary V·O₂ response (by ∼ 0.19 ± 0.28 L·min(-1), P = 0.001), reduced the V·O₂ slow component trajectory (by 0.04 ± 0.09 L·min(-2), P = 0.002), and increased the time to exhaustion (by ∼ 52 ± 92 s, P = 0.005). The CP was unchanged (control vs prior heavy: 284 ± 47 vs 283 ± 44 W; 95% confidence interval, -7 to 5 W), whereas the W' was increased by heavy-intensity priming (16.0 ± 4.8 vs 18.7 ± 4.8 kJ; 95% confidence interval, 0.3-5.2 kJ). Severe-intensity exercise had a similar effect on the V·O₂ kinetics but had no effect on the time to exhaustion, the CP (275 ± 45 W), or the W' (16.7 ± 4.7 kJ). Prior heavy-intensity exercise primes the V·O₂ kinetics and increases the amount of work that can be performed above the CP.

Effect of hyperventilation and prior heavy exercise on O2 uptake and muscle deoxygenation kinetics during transitions to moderate exercise

The effect of hyperventilation-induced hypocapnic alkalosis (HYPO) and prior heavy-intensity exercise (HVY) on pulmonary O(2) uptake (VO(2p)) kinetics were examined in young adults (n = 7) during moderate-intensity exercise (MOD). Subjects completed leg cycling exercise during (1) normal breathing (CON, P(ET)CO(2) approximately 40 mmHg) and (2) controlled hyperventilation (HYPO, P(ET)CO(2) approximately 20 mmHg) throughout the protocol, with each condition repeated on four occasions. The protocol consisted of two MOD transitions (MOD1, MOD2) to 80% estimated lactate threshold with MOD2 preceded by HVY (Delta50%); each transition lasted 6 min and was preceded by 20 W cycling. VO(2p) was measured breath-by-breath and concentration changes in oxy- and deoxy-hemoglobin/myoglobin (Delta[HHb]) of the vastus lateralis muscle were measured by near-infrared spectroscopy. Adjustment of VO(2p) and Delta[HHb] were modeled using a mono-exponential equation by non-linear regression. During MOD1, the phase 2 time constant (tau) for VO(2p)(tauVO(2p)) was greater (P < 0.05) in HYPO (45 +/- 24 s) than CON (28 +/- 17 s). During MOD2, tauVO(2p) was reduced (P < 0.05) in both conditions (HYPO: 24 +/- 7 s, CON: 20 +/- 8 s). The Delta[Hb(TOT)] and Delta[O(2)Hb] were greater (P < 0.05) prior to and throughout MOD2. The Delta[HHb] mean response time was similar in MOD1 and MOD2, and between conditions, however, the MOD1 Delta[HHb] amplitude was greater (P < 0.05) in HYPO compared to CON, with no differences between conditions in MOD2. These findings suggest that the speeding of VO(2p) kinetics after prior HVY in HYPO was related, in part, to an increase in microvascular perfusion.

Prior heavy exercise elevates pyruvate dehydrogenase activity and muscle oxygenation and speeds O2uptake kinetics during moderate exercise in older adults

The adaptation of pulmonary oxygen uptake (VO(2)(p)) kinetics during the transition to moderate-intensity exercise is slowed in older compared with younger adults; however, this response is faster following a prior bout of heavy-intensity exercise. We have examined VO(2)(p) kinetics, pyruvate dehydrogenase (PDH) activation, muscle metabolite contents, and muscle deoxygenation in older adults [n = 6; 70 +/- 5 (67-74) yr] during moderate-intensity exercise (Mod(1)) and during moderate-intensity exercise preceded by heavy-intensity warm-up exercise (Mod(2)). The phase 2 VO(2)(p) time constant (tauVO(2)(p)) was reduced (P < 0.05) in Mod(2) (29 +/- 5 s) compared with Mod(1) (39 +/- 14 s). PDH activity was elevated (P < 0.05) at baseline prior to Mod(2) (2.1 +/- 0.6 vs. 1.2 +/- 0.3 mmol acetyl-CoA x min(-1) x kg wet wt(-1)), and the delay in attaining end-exercise activity was abolished. Phosphocreatine breakdown during exercise was reduced (P < 0.05) at both 30 s and 6 min in Mod(2) compared with Mod(1). Near-infrared spectroscopy-derived indices of muscle oxygenation were elevated both prior to and throughout Mod(2), while muscle deoxygenation kinetics were not different between exercise bouts consistent with elevated perfusion and O(2) availability. These results suggest that in older adults, faster VO(2)(p) kinetics following prior heavy-intensity exercise are likely a result of prior activation of mitochondrial enzyme activity in combination with elevated muscle perfusion and O(2) availability.

Prior exercise speeds pulmonary O2 uptake kinetics by increases in both local muscle O2 availability and O2 utilization

The effect of prior exercise on pulmonary O(2) uptake (Vo(2)(p)), leg blood flow (LBF), and muscle deoxygenation at the onset of heavy-intensity alternate-leg knee-extension (KE) exercise was examined. Seven subjects [27 (5) yr; mean (SD)] performed step transitions (n = 3; 8 min) from passive KE following no warm-up (HVY 1) and heavy-intensity (Delta50%, 8 min; HVY 2) KE exercise. Vo(2)(p) was measured breath-by-breath; LBF was measured by Doppler ultrasound at the femoral artery; and oxy (O(2)Hb)-, deoxy (HHb)-, and total (Hb(tot)) hemoglobin/myoglobin of the vastus lateralis muscle were measured continuously by near-infrared spectroscopy (NIRS; Hamamatsu NIRO-300). Phase 2 Vo(2)(p), LBF, and HHb data were fit with a monoexponential model. The time delay (TD) from exercise onset to an increase in HHb was also determined and an HHb effective time constant (HHb - MRT = TD + tau) was calculated. Prior heavy-intensity exercise resulted in a speeding (P < 0.05) of phase 2 Vo(2)(p) kinetics [HVY 1: 42 s (6); HVY 2: 37 s (8)], with no change in the phase 2 amplitude [HVY 1: 1.43 l/min (0.21); HVY 2: 1.48 l/min (0.21)] or amplitude of the Vo(2)(p) slow component [HVY 1: 0.18 l/min (0.08); HVY 2: 0.18 l/min (0.09)]. O(2)Hb and Hb(tot) were elevated throughout the on-transient following prior heavy-intensity exercise. The tauLBF [HVY 1: 39 s (7); HVY 2: 47 s (21); P = 0.48] and HHb-MRT [HVY 1: 23 s (4); HVY 2: 21 s (7); P = 0.63] were unaffected by prior exercise. However, the increase in HHb [HVY 1: 21 microM (10); HVY 2: 25 microM (10); P < 0.001] and the HHb-to-Vo(2)(p) ratio [(HHb/Vo(2)(p)) HVY 1: 14 microM x l(-1) x min(-1) (6); HVY 2: 17 microM x l(-1) x min(-1) (5); P < 0.05] were greater following prior heavy-intensity exercise. These results suggest that the speeding of phase 2 tauVo(2)(p) was the result of both elevated local O(2) availability and greater O(2) extraction evidenced by the greater HHb amplitude and HHb/Vo(2)(p) ratio following prior heavy-intensity exercise.

Prior heavy-intensity exercise elevates Pyruvate Dehydrogenase activity and speeds O2 uptake kinetics during moderate-intensity exercise in healthy older adults

Prior heavy-intensity exercise elevates Pyruvate Dehydrogenase activity and speeds O2 uptake kinetics during moderate-intensity exercise in healthy older adults

Prior exercise delays the onset of acidosis during incremental exercise

The effects of prior moderate- and prior heavy-intensity exercise on the subsequent metabolic response to incremental exercise were examined. Healthy, young adult subjects (n = 8) performed three randomized plantar-flexion exercise tests: 1) an incremental exercise test (approximately 0.6 W/min) to volitional fatigue (Ramp); 2) Ramp preceded by 6 min of moderate-intensity, constant-load exercise below the intracellular pH threshold (pHT; Mod-Ramp); and 3) Ramp preceded by 6 min of heavy-intensity, constant-load exercise above pHT (Hvy-Ramp); the constant-load and incremental exercise periods were separated by 6 min of rest. (31)P-magnetic resonance spectroscopy was used to continuously monitor intracellular pH, phosphocreatine concentration ([PCr]), and inorganic phosphate concentration ([P(i)]). No differences in exercise performance or the metabolic response to exercise were observed between Ramp and Mod-Ramp. However, compared with Ramp, a 14% (SD 10) increase (P < 0.01) in peak power output (PPO) was observed in Hvy-Ramp. The improved exercise performance in Hvy-Ramp was accompanied by a delayed (P = 0.01) onset of intracellular acidosis [Hvy-Ramp 60.4% PPO (SD 11.7) vs. Ramp 45.8% PPO (SD 9.4)] and a delayed (P < 0.01) onset of rapid increases in [P(i)]/[PCr] [Hvy-Ramp 61.5% PPO (SD 12.0) vs. Ramp 45.1% PPO (SD 9.1)]. In conclusion, prior heavy-intensity exercise delayed the onset of intracellular acidosis and enhanced exercise performance during a subsequent incremental exercise test.

Prior heavy exercise elevates pyruvate dehydrogenase activity and speeds O2 uptake kinetics during subsequent moderate‐intensity exercise in healthy young adults

The adaptation of pulmonary oxygen uptake (.VO2) during the transition to moderate-intensity exercise (Mod) is faster following a prior bout of heavy-intensity exercise. In the present study we examined the activation of pyruvate dehydrogenase (PDHa) during Mod both with and without prior heavy-intensity exercise. Subjects (n = 9) performed a Mod(1)-heavy-intensity-Mod(2) exercise protocol preceded by 20 W baseline. Breath-by-breath .VO2 kinetics and near-infrared spectroscopy-derived muscle oxygenation were measured continuously, and muscle biopsy samples were taken at specific times during the transition to Mod. In Mod(1), PDHa increased from baseline (1.08 +/- 0.2 mmol min(-1) (kg wet wt)(-1)) to 30 s (2.05 +/- 0.2 mmol min(-1) (kg wet wt)(-1)), with no additional change at 6 min exercise (2.07 +/- 0.3 mmol min(-1) (kg wet wt)(-1)). In Mod(2), PDHa was already elevated at baseline (1.88 +/- 0.3 mmol min(-1) (kg wet wt)(-1)) and was greater than in Mod(1), and did not change at 30 s (1.96 +/- 0.2 mmol min(-1) (kg wet wt)(-1)) but increased at 6 min exercise (2.70 +/- 0.3 mmol min(-1) (kg wet wt)(-1)). The time constant of .VO2 was lower in Mod(2) (19 +/- 2 s) than Mod(1) (24 +/- 3 s). Phosphocreatine (PCr) breakdown from baseline to 30 s was greater (P < 0.05) in Mod(1) (13.6 +/- 6.7 mmol (kg dry wt)(-1)) than Mod(2) (6.5 +/- 6.2 mmol (kg dry wt)(-1)) but total PCr breakdown was similar between conditions (Mod(1), 14.8 +/- 7.4 mmol (kg dry wt)(-1); Mod(2), 20.1 +/- 8.0 mmol (kg dry wt)(-1)). Both oxyhaemoglobin and total haemoglobin were elevated prior to and throughout Mod(2) compared with Mod(1). In conclusion, the greater PDHa at baseline prior to Mod(2) compared with Mod(1) may have contributed in part to the faster .VO2 kinetics in Mod(2). That oxyhaemoglobin and total haemoglobin were elevated prior to Mod(2) suggests that greater muscle perfusion may also have contributed to the observed faster .VO2 kinetics. These findings are consistent with metabolic inertia, via delayed activation of PDH, in part limiting the adaptation of pulmonary .VO2 and muscle O2 consumption during the normal transition to exercise.

The Effect of Prior Moderate- and Heavy-Intensity Running on the VO2 Response to Exhaustive Severe-Intensity Running

We tested the hypothesis that prior heavy-intensity exercise reduces the difference between asymptotic oxygen uptake (VO2) and maximum oxygen uptake (VO2max) during exhaustive severe-intensity running lasting ?2 minutes. Ten trained runners each performed 2 ramp tests to determine peak VO2 (VO2peak) and speed at ventilatory threshold. They performed exhaustive square-wave runs lasting ?2 minutes, preceded by either 6 minutes of moderate-intensity running and 6 minutes rest (SEVMOD) or 6 minutes of heavy-intensity running and 6 minutes rest (SEVHEAVY). Two transitions were completed in each condition. VO2 was determined breath by breath and averaged across the 2 repeats of each test; for the square-wave test, the averaged VO2 response was then modeled using a monoexponential function. The amplitude of the VO2 response to severe-intensity running was not different in the 2 conditions (SEVMOD vs SEVHEAVY; 3925 +/- 442 vs 3997 +/- 430 mL/min, P = .237), nor was the speed of the response (?; 9.2 +/- 2.1 vs 10.0 +/- 2.1 seconds, P = .177). VO2peak from the square-wave tests was below that achieved in the ramp tests (91.0% +/- 3.2% and 92.0% +/- 3.9% VO2peak, P < .001). There was no difference in time to exhaustion between conditions (110.2 +/- 9.7 vs 111.0 +/- 15.2 seconds, P = .813). The results show that the primary VO2 response is unaffected by prior heavy exercise in running performed at intensities at which exhaustion will occur before a slow component emerges.

Phosphocreatine Metabolism and Acidosis during Repeated Bouts of Heavy-Intensity Exercise Separated by 15-min Rest

Prior heavy-intensity exercise (HVY) results in a reduced reliance on substrate-level phosphorylation during a subsequent exercise bout when the bouts are separated by 6-min rest. Proposed mechanisms for this response have been associated with acidosis and lactate accumulation. PURPOSE: To determine if a similar favourable energetic response in the second exercise is evident when the bouts are separated by 15-min of rest. In this condition intracellular acid-base status will have returned to pre-exercise resting levels prior to the second bout. METHODS: Healthy young adult male subjects (n = 7) performed a 6-min bout of HVY isotonic plantar flexion exercise (HVY1) followed by 15-min of rest, then an identical 6-min bout (HVY2). Muscle phosphocreatine (PCr) and intracellular acid-base status were measured using 3-tesla 31P-magnetic resonance spectroscopy. Each subject repeated the protocol three times. PCr was expressed as percent (%) of average pre-HVY1 resting value. RESULTS: Prior to the onset of exercise, resting intracellular hydrogen ion ([H+]i) was not different (P = 0.11) at the onset of exercise in HVY1 [94 nM (SD 4)] and HVY2 [99 nM (SD 8)]. The increase in [H+]i during exercise was reduced ∼ 45% during HVY2, with end-exercise [H+]i lower (P < 0.01) in HVY2 [139 nM (SD 38)] than HVY1 [167 nM (SD 48)]. Resting [PCr] was greater (P = 0.03) in HVY2 [101.8% (SD 2.1)] than HVY1, while at end-exercise, [PCr] was greater (P = 0.02) in HVY2 [55.1% (SD 15.1)] than HVY1 [48.7 % (SD 10.9)]. CONCLUSIONS: The lower accumulation of [H+]i (and presumably lactate accumulation) in HVY2 (delta [H+]i 40 nM) than HVY1 (delta [H+]i 73 nM), along with the decreased PCr breakdown, are consistent with reduced substrate-level phosphorylation. Therefore, these results demonstrate that the benefits of prior heavy-intensity exercise are evident after 15-min of rest, when intracellular acid-base status has returned to pre-exercise resting levels.

Effects of prior heavy-intensity exercise during single-leg knee extension on v̇o2 kinetics and limb blood flow

The effects of prior heavy-intensity exercise on O(2) uptake (Vo(2)) kinetics of a second heavy exercise may be due to vasodilation (associated with metabolic acidosis) and improved muscle blood flow. This study examined the effect of prior heavy-intensity exercise on femoral artery blood flow (Qleg) and its relationship with Vo(2) kinetics. Five young subjects completed five to eight repeats of two 6-min bouts of heavy-intensity one-legged, knee-extension exercise separated by 6 min of loadless exercise. Vo(2) was measured breath by breath. Pulsed-wave Doppler ultrasound was used to measure Qleg. Vo(2) and blood flow velocity data were fit using a monoexponential model to identify phase II and phase III time periods and estimate the response amplitudes and time constants (tau). Phase II Vo(2) kinetics was speeded on the second heavy-intensity exercise [mean tau (SD), 29 (10) s to 24 (10) s, P < 0.05] with no change in the phase II (or phase III) amplitude. Qleg was elevated before the second exercise [1.55 (0.34) l/min to 1.90 (0.25) l/min, P < 0.05], but the amplitude and time course [tau, 25 (13) s to 35 (13) s] were not changed, such that throughout the transient the Qleg (and DeltaQleg/DeltaVo(2)) did not differ from the prior heavy exercise. Thus Vo(2) kinetics were accelerated on the second exercise, but the faster kinetics were not associated with changes in Qleg. Thus limb blood flow appears not to limit Vo(2) kinetics during single-leg heavy-intensity exercise nor to be the mechanism of the altered Vo(2) response after heavy-intensity prior exercise.

Vo2 And Muscle Deoxygenation Kinetics In Moderateintensity Exercise

Hyperventilation-induced respiratory-alkalosis (R-ALK) was shown to slow the adaptation of pulmonary O2 uptake (VO2) during moderate-intensity exercise (MOD; Leigh, MSc thesis (UWO), 2003). Also prior heavy-intensity exercise (HVY) was shown to speed VO2 kinetics in young adults exhibiting “slow” VO2 kinetics without warm-up (Gurd, MSc thesis (UWO), 2003). PURPOSE To examine the combined effects of R-ALK and HVY on VO2 kinetics at the onset of MOD. METHODS Young male adults (n = 7; age, 23±3 yrs; mean ± SD) completed 4 repetitions of leg cycling exercise during normal breathing (CON; PETCO2 ∼40 mmHg) and controlled hyperventilation (R-ALK; PETCO2 ∼20 mmHg). The protocol consisted of two step transitions in work rate (MOD1 and MOD2) from 20W to 80% estimated lactate threshold, with MOD2 preceded by HVY (Δ50%); each transition was preceded and followed by 20W exercise. VO2 and heart rate (HR) were measured breath-by-breath and beat-by-beat, respectively. Changes in deoxy- (HHb), oxy- (O2Hb) and total hemoglobin (HbTOT) of the vastus lateralis were measured continuously by nearinfrared spectroscopy (NIRS; Hamamatsu, NIRO 300). Adaptation of VO2, HR and HHb were modeled using a mono-exponential equation and non-linear regression techniques. RESULTS The phase 2 VO2 time constant (τVO2) during MOD1 was greater (p < 0.05) in R-ALK (45±24 s) than CON (28±17 s). After HVY, τVO2 was reduced (p < 0.05) in R-ALK only, such that there was no difference between conditions (R-ALK: 24±7 s; CON: 20±8 s). The HHb mean response time (TD + τHHb) was not different amongst conditions (R-ALK: MOD1, 20±3 s, MOD2, 22±10 s; CON: MOD1, 23±2 s, MOD2, 22±7 s). Prior to exercise transitions, baseline HbTOT was elevated (p < 0.05) after (R-ALK: 5±7 μM; CON: 6±6 μM) compared to before HVY (R-ALK: −7±4 μM; CON: −6±3 μM), with no difference between conditions. CONCLUSION In MOD1 the slower VO2 kinetics, but similar HHb kinetics, in R-ALK compared to CON is consistent with a blood flow limitation within the muscle during R-ALK. After HVY, improved muscle perfusion and O2 delivery was seen in both conditions, however the speeding of VO2 kinetics seen in only R-ALK, is consistent with a removal of a blood flow limitation in R-ALK but not CON. Supported by NSERC, Canada.

Vo2 And Muscle Deoxygenation Kinetics In Moderateintensity Exercise

Hyperventilation-induced respiratory-alkalosis (R-ALK) was shown to slow the adaptation of pulmonary O2 uptake (VO2) during moderate-intensity exercise (MOD; Leigh, MSc thesis (UWO), 2003). Also prior heavy-intensity exercise (HVY) was shown to speed VO2 kinetics in young adults exhibiting “slow” VO2 kinetics without warm-up (Gurd, MSc thesis (UWO), 2003). PURPOSE To examine the combined effects of R-ALK and HVY on VO2 kinetics at the onset of MOD. METHODS Young male adults (n = 7; age, 23±3 yrs; mean ± SD) completed 4 repetitions of leg cycling exercise during normal breathing (CON; PETCO2 ∼40 mmHg) and controlled hyperventilation (R-ALK; PETCO2 ∼20 mmHg). The protocol consisted of two step transitions in work rate (MOD1 and MOD2) from 20W to 80% estimated lactate threshold, with MOD2 preceded by HVY (Δ50%); each transition was preceded and followed by 20W exercise. VO2 and heart rate (HR) were measured breath-by-breath and beat-by-beat, respectively. Changes in deoxy- (HHb), oxy- (O2Hb) and total hemoglobin (HbTOT) of the vastus lateralis were measured continuously by nearinfrared spectroscopy (NIRS; Hamamatsu, NIRO 300). Adaptation of VO2, HR and HHb were modeled using a mono-exponential equation and non-linear regression techniques. RESULTS The phase 2 VO2 time constant (τVO2) during MOD1 was greater (p < 0.05) in R-ALK (45±24 s) than CON (28±17 s). After HVY, τVO2 was reduced (p < 0.05) in R-ALK only, such that there was no difference between conditions (R-ALK: 24±7 s; CON: 20±8 s). The HHb mean response time (TD + τHHb) was not different amongst conditions (R-ALK: MOD1, 20±3 s, MOD2, 22±10 s; CON: MOD1, 23±2 s, MOD2, 22±7 s). Prior to exercise transitions, baseline HbTOT was elevated (p < 0.05) after (R-ALK: 5±7 μM; CON: 6±6 μM) compared to before HVY (R-ALK: −7±4 μM; CON: −6±3 μM), with no difference between conditions. CONCLUSION In MOD1 the slower VO2 kinetics, but similar HHb kinetics, in R-ALK compared to CON is consistent with a blood flow limitation within the muscle during R-ALK. After HVY, improved muscle perfusion and O2 delivery was seen in both conditions, however the speeding of VO2 kinetics seen in only R-ALK, is consistent with a removal of a blood flow limitation in R-ALK but not CON. Supported by NSERC, Canada.

Prior heavy-intensity exercise speeds V̇o2 kinetics during moderate-intensity exercise in young adults

The effect of prior heavy-intensity warm-up exercise on subsequent moderate-intensity phase 2 pulmonary O2 uptake kinetics (tauVO2) was examined in young adults exhibiting relatively fast (FK; tauVO2 < 30 s; n = 6) and slow (SK; tauVO2 > 30 s; n = 6) VO2 kinetics in moderate-intensity exercise without prior warm up. Subjects performed four repetitions of a moderate (Mod1)-heavy-moderate (Mod2) protocol on a cycle ergometer with work rates corresponding to 80% estimated lactate threshold (moderate intensity) and 50% difference between lactate threshold and peak VO2 (heavy intensity); each transition lasted 6 min, and each was preceded by 6 min of cycling at 20 W. VO2 and heart rate (HR) were measured breath-by-breath and beat-by-beat, respectively; concentration changes of muscle deoxyhemoglobin (HHb), oxyhemoglobin, and total hemoglobin were measured by near-infrared spectroscopy (Hamamatsu NIRO 300). tauVO2 was lower (P < 0.05) in Mod2 than in Mod1 in both FK (20 +/- 5 s vs. 26 +/- 5 s, respectively) and SK (30 +/- 8 s vs. 45 +/- 11 s, respectively); linear regression analysis showed a greater "speeding" of VO2 kinetics in subjects exhibiting a greater Mod1 tauVO2. HR, oxyhemoglobin, and total hemoglobin were elevated (P < 0.05) in Mod2 compared with Mod1. The delay before the increase in HHb was reduced (P <0.05) in Mod2, whereas the HHb mean response time was reduced (P <0.05) in FK (Mod2, 22 +/- 3 s; Mod1, 32 +/- 11 s) but not different in SK (Mod2, 36 +/- 13 s; Mod1, 34 +/- 15 s). We conclude that improved muscle perfusion in Mod2 may have contributed to the faster adaptation of VO2, especially in SK; however, a possible role for metabolic inertia in some subjects cannot be overlooked.

Effects of prior heavy-intensity exercise on pulmonary O2 uptake and muscle deoxygenation kinetics in young and older adult humans

Pulmonary O2 uptake (VO2p) and muscle deoxygenation kinetics were examined during moderate-intensity cycling (80% lactate threshold) without warm-up and after heavy-intensity warm-up exercise in young (n = 6; 25 +/- 3 yr) and older (n = 5; 68 +/- 3 yr) adults. We hypothesized that heavy warm-up would speed VO2p kinetics in older adults consequent to an improved intramuscular oxygenation. Subjects performed step transitions (n = 4; 6 min) from 20 W to moderate-intensity exercise preceded by either no warm-up or heavy-intensity warm-up (6 min). VO2p was measured breath by breath. Oxy-, deoxy-(HHb), and total hemoglobin and myoglobin (Hb(tot)) of the vastus lateralis muscle were measured continuously by near-infrared spectroscopy (NIRS). VO2p (phase 2; tau) and HHb data were fit with a monoexponential model. After heavy-intensity warm-up, oxyhemoglobin (older subjects: 13 +/- 9 microM; young subjects: 9 +/- 8 microM) and Hb(tot) (older subjects: 12 +/- 8 microM; young subjects: 14 +/- 10 microM) were elevated (P < 0.05) relative to the no warm-up pretransition baseline. In older adults, tauVO2p adapted at a faster rate (P < 0.05) after heavy warm-up (30 +/- 7 s) than no warm-up (38 +/- 5 s), whereas in young subjects, tauVO2p was similar in no warm-up (26 +/- 7 s) and heavy warm-up (25 +/- 5 s). HHb adapted at a similar rate in older and young adults after no warm-up; however, in older adults after heavy warm-up, the adaptation of HHb was slower (P < 0.01) compared with young and no warm-up. These data suggest that, in older adults, VO2p kinetics may be limited by a slow adaptation of muscle blood flow and O2 delivery.

Prior Heavy Exercise Improves VO2 Kinetics and Muscle Oxygenation During Moderate Exercise in Young Adults

0164 PURPOSE: To examine the effect of prior heavy-intensity exercise on the adaptation of pulmonary O2 uptake (ôVO2) during moderate-intensity exercise in young adults with fast and slow VO2 kinetics. METHODS: Healthy young adults were divided into two groups: ôVO2 < 30s (FK; n = 6) and ôVO2 > 30s (SK; n = 6). Each subject performed 4 repetitions of a MOD1-HVY-MOD2 protocol from 20W to work rates corresponding to 80% of the estimated lactate threshold (θL) (MOD1; MOD2), and 50% of the difference between θL and VO2peak (HVY). Each transition lasted 6 min and each was separated by 6 min cycling at 20 W. VO2 was measured breath-by-breath and heart rate (HR) was measured beat-by-beat. The change in total (HbTOT), Oxy-(HbO2), and Deoxy-hemoglobin (HHb) concentrations were monitored continuously by near-infrared spectroscopy (Hamamatsu NIRO 300). Phase II VO2 (ôVO2) kinetics, and HHb (ôHHb) kinetics were modelled using a mono-exponential equation and non-linear regression techniques. RESULTS: τVO2 decreased (P<0.05) in Mod2 in both FK (Mod1, 26±5 s, Mod2, 20±5 s; P<0.05) and SK (Mod1, 45±11 s, Mod2, 30±8 s, P<0.05) with the decrease being greater in subjects having a greater τVO2 in Mod1. Baseline HR, HbTOT and Hb O2 were elevated (P<0.05) in Mod2 compared to Mod1. The delay prior to an increase in HHb(TD HHb) was decreased in Mod2 (FK, 12±4 s; SK, 9±3 s) compared to Mod2 (FK, 19±4 s; SK, 15±3 s) but τHHb was not changed (FK: Mod1, 13±8 s, Mod2, 10±2 (P>0.05); SK: Mod1, 19±12 s; Mod2, 27±12 (P = 0.065)). CONCLUSION: In young adults, a greater “speeding” of VO2 kinetics was seen following HVY in those subjects having a greater τVO2 in Mod1. The faster adaptation may be related to both an improved muscle perfusion (i.e. higher HR, HbTOT and HbO 2 prior to Mod2) and to an accelerated rate of O2 utilization relative to perfusion (i.e. shorter HHb TD). Supported by NSERC, Canada

Facial cooling-induced bradycardia does not slow pulmonary V.O2 kinetics at the onset of high-intensity exercise.

The mechanism(s) underlying the attenuation of the slow component of pulmonary O2 uptake (Vo2) by prior heavy-intensity exercise is (are) poorly understood but may be ascribed to either an intramuscular-metabolic or a circulatory modification resulting from "priming" exercise. We investigated the effects of altering the circulatory dynamics by delayed vagal withdrawal to the circulation induced by the cold face stimulation (CFS) on the Vo2 kinetics during repeated bouts of heavy-intensity cycling exercise. Five healthy subjects (aged 21-43 yr) volunteered to participate in this study and initially performed two consecutive 6-min leg cycling exercise bouts (work rate: 50% of the difference between lactate threshold and maximal Vo2) separated by 6-min baseline rest without CFS as a control (N1 and N2). CFS was then applied separately, by gel-filled cold compresses to the face for 2-min spanning the rest-exercise transition, to each of the first bout (CFS1) or second bout (CFS2) of repeated heavy-intensity exercise. In the control protocol, Vo2 responses in N2 showed a facilitated adaptation compared with those in N1, mainly attributable to the reduction of slow component. CFS application successfully slowed and delayed the heart rate (HR) kinetics (P < 0.05) on transition to exercise [HR time constant; N1: 55.6 +/- 16.0 (SD) vs. CFS1: 69.0 +/- 12.8 s and N2: 55.5 +/- 11.8 vs. CFS2: 64.0 +/- 17.5 s]; however, it did not affect the "primary" Vo2 kinetics [Vo2 time constant; N1: 23.7 +/- 7.9 (SD) vs. CFS1: 20.9 +/- 3.8 s, and N2: 23.3 +/- 10.3 vs. CFS2: 17.4 +/- 6.3 s]. In conclusion, increased vagal withdrawal delayed and slowed the circulatory response but did not alter the Vo2 kinetics at the onset of supra-lactate threshold cycling exercise. As the facilitation of Vo2 subsequent to prior heavy leg cycling exercise is not attenuated by slowing the central circulation, it seems unlikely that this facilitation is exclusively determined by a blood flow-related mechanism.

Oxygen uptake kinetics for moderate exercise are speeded in older humans by prior heavy exercise.

This study examined the effect of heavy-intensity warm-up exercise on O(2) uptake (VO(2)) kinetics at the onset of moderate-intensity (80% ventilation threshold), constant-work rate exercise in eight older (65 +/- 2 yr) and seven younger adults (26 +/- 1 yr). Step increases in work rate from loadless cycling to moderate exercise (Mod(1)), heavy exercise, and moderate exercise (Mod(2)) were performed. Each exercise bout was 6 min in duration and separated by 6 min of loadless cycling. VO(2) kinetics were modeled from the onset of exercise by use of a two-component exponential model. Heart rate (HR) kinetics were modeled from the onset of exercise using a single exponential model. During Mod(1), the time constant (tau) for the predominant rise in VO(2) (tau VO(2)) was slower (P < 0.05) in the older adults (50 +/- 10 s) than in young adults (19 +/- 5 s). The older adults demonstrated a speeding (P < 0.05) of VO(2) kinetics when moderate-intensity exercise (Mod(2)) was preceded by high-intensity warm-up exercise (tau VO(2), 27 +/- 3 s), whereas young adults showed no speeding of VO(2) kinetics (tau VO(2), 17 +/- 3 s). In the older and younger adults, baseline HR preceding Mod(2) was elevated compared with Mod(1), but the tau for HR kinetics was slowed (P < 0.05) in Mod(2) only for the older adults. Prior heavy-intensity exercise in old, but not young, adults speeded VO(2) kinetics during Mod(2). Despite slowed HR kinetics in Mod(2) in the older adults, an elevated baseline HR before the onset of Mod(2) may have led to sufficient muscle perfusion and O(2) delivery. These results suggest that, when muscle blood flow and O(2) delivery are adequate, muscle O(2) consumption in both old and young adults is limited by intracellular processes within the exercising muscle.