O2 uptake and blood pressure regulation at the onset of exercise: interaction of circadian rhythm and priming exercise

Circadian rhythm has an influence on several physiological functions that contribute to athletic performance. We tested the hypothesis that circadian rhythm would affect blood pressure (BP) responses but not O(2) uptake (Vo(2)) kinetics during the transitions to moderate and heavy cycling exercises. Nine male athletes (peak Vo(2): 60.5 ± 3.2 ml·kg(-1)·min(-1)) performed multiple rides of two different cycling protocols involving sequences of 6-min bouts at moderate or heavy intensities interspersed by a 20-W baseline in the morning (7 AM) and evening (5 PM). Breath-by-breath Vo(2) and beat-by-beat BP estimated by finger cuff plethysmography were measured simultaneously throughout the protocols. Circadian rhythm did not affect Vo(2) onset kinetics determined from the phase II time constant (τ(2)) during either moderate or heavy exercise bouts with no prior priming exercise (τ(2) moderate exercise: morning 22.5 ± 4.6 s vs. evening 22.2 ± 4.6 s and τ(2) heavy exercise: morning 26.0 ± 2.7 s vs. evening 26.2 ± 2.6 s, P > 0.05). Priming exercise induced the same robust acceleration in Vo(2) kinetics during subsequent moderate and heavy exercise in the morning and evening. A novel finding was an overshoot in BP (estimated from finger cuff plethysmography) in the first minutes of each moderate and heavy exercise bout. After the initial overshoot, BP declined in association with increased skin blood flow between the third and sixth minute of the exercise bout. Priming exercise showed a greater effect in modulating the BP responses in the evening. These findings suggest that circadian rhythm interacts with priming exercise to lower BP during exercise after an initial overshoot with a greater influence in the evening associated with increased skin blood flow.     

Effects of prior heavy-intensity exercise during single-leg knee extension on VO2 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.     

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.     

Excessive oxygen uptake during exercise and recovery in heavy exercise

The aim of this study was to determine whether excessive oxygen uptake (Vo2) occurs not only during exercise but also during recovery after heavy exercise. After previous exercise at zero watts for 4 min, the main exercise was performed for 10 min. Then recovery exercise at zero watts was performed for 10 min. The main exercises were moderate and heavy exercises at exercise intensities of 40 % and 70 % of peak Vo2, respectively. Vo2 kinetics above zero watts was obtained by subtracting Vo2 at zero watts of previous exercise (DeltaVo2). Delta Vo2 in moderate exercise was multiplied by the ratio of power output performed in moderate and heavy exercises so as to estimate the Delta Vo2 applicable to heavy exercise. The difference between Delta Vo2 in heavy exercise and Delta Vo2 estimated from the value of moderate exercise was obtained. The obtained Vo2 was defined as excessive Vo2. The time constant of excessive Vo2 during exercise (1.88+/-0.70 min) was significantly shorter than that during recovery (9.61+/-6.92 min). Thus, there was excessive Vo2 during recovery from heavy exercise, suggesting that O2/ATP ratio becomes high after a time delay in heavy exercise and the high ratio continues until recovery.     

Effects of prior heavy exercise on VO(2) kinetics during heavy exercise are related to changes in muscle activity.

We hypothesized that the elevated primary O(2) uptake (VO(2)) amplitude during the second of two bouts of heavy cycle exercise would be accompanied by an increase in the integrated electromyogram (iEMG) measured from three leg muscles (gluteus maximus, vastus lateralis, and vastus medialis). Eight healthy men performed two 6-min bouts of heavy leg cycling (at 70% of the difference between the lactate threshold and peak VO(2)) separated by 12 min of recovery. The iEMG was measured throughout each exercise bout. The amplitude of the primary VO(2) response was increased after prior heavy leg exercise (from mean +/- SE 2.11 +/- 0.12 to 2.44 +/- 0.10 l/min, P < 0.05) with no change in the time constant of the primary response (from 21.7 +/- 2.3 to 25.2 +/- 3.3 s), and the amplitude of the VO(2) slow component was reduced (from 0.79 +/- 0.08 to 0.40 +/- 0.08 l/min, P < 0.05). The elevated primary VO(2) amplitude after leg cycling was accompanied by a 19% increase in the averaged iEMG of the three muscles in the first 2 min of exercise (491 +/- 108 vs. 604 +/- 151% increase above baseline values, P < 0.05), whereas mean power frequency was unchanged (80.1 +/- 0.9 vs. 80.6 +/- 1.0 Hz). The results of the present study indicate that the increased primary VO(2) amplitude observed during the second of two bouts of heavy exercise is related to a greater recruitment of motor units at the onset of exercise.     

Morning-to-evening differences in oxygen uptake kinetics in short-duration cycling exercise

This study analyzed diurnal variations in oxygen (O(2)) uptake kinetics and efficiency during a moderate cycle ergometer exercise. Fourteen physically active diurnally active male subjects (age 23+/-5 yrs) not specifically trained at cycling first completed a test to determine their ventilatory threshold (T(vent)) and maximal oxygen consumption (VO(2max)); one week later, they completed four bouts of testing in the morning and evening in a random order, each separated by at least 24 h. For each period of the day (07:00-08:30 h and 19:00-20:30 h), subjects performed two bouts. Each bout was composed of a 5 min cycling exercise at 45 W, followed after 5 min rest by a 10 min cycling exercise at 80% of the power output associated with T(vent). Gas exchanges were analyzed breath-by-breath and fitted using a mono-exponential function. During moderate exercise, the time constant and amplitude of VO(2) kinetics were significantly higher in the morning compared to the evening. The net efficiency increased from the morning to evening (17.3+/-4 vs. 20.5+/-2%; p<0.05), and the variability of cycling cadence was greater during the morning than evening (+34%; p<0.05). These findings suggest that VO(2) responses are affected by the time of day and could be related to variability in muscle activity pattern.     

Effects of prior heavy exercise on phase II pulmonary oxygen uptake kinetics during heavy exercise.

We tested the hypothesis that heavy-exercise phase II oxygen uptake (VO(2)) kinetics could be speeded by prior heavy exercise. Ten subjects performed four protocols involving 6-min exercise bouts on a cycle ergometer separated by 6 min of recovery: 1) moderate followed by moderate exercise; 2) moderate followed by heavy exercise; 3) heavy followed by moderate exercise; and 4) heavy followed by heavy exercise. The VO(2) responses were modeled using two (moderate exercise) or three (heavy exercise) independent exponential terms. Neither moderate- nor heavy-intensity exercise had an effect on the VO(2) kinetic response to subsequent moderate exercise. Although heavy-intensity exercise significantly reduced the mean response time in the second heavy exercise bout (from 65.2 +/- 4.1 to 47.0 +/- 3.1 s; P < 0.05), it had no significant effect on either the amplitude or the time constant (from 23.9 +/- 1.9 to 25.3 +/- 2.9 s) of the VO(2) response in phase II. Instead, this "speeding" was due to a significant reduction in the amplitude of the VO(2) slow component. These results suggest phase II VO(2) kinetics are not speeded by prior heavy exercise.     

Influence of L-NAME on pulmonary O2 uptake kinetics during heavy-intensity cycle exercise.

We hypothesized that inhibition of nitric oxide synthase (NOS) by N(G)-nitro-L-arginine methyl ester (L-NAME) would alleviate the inhibition of mitochondrial oxygen uptake (Vo(2)) by nitric oxide and result in a speeding of phase II pulmonary Vo(2) kinetics at the onset of heavy-intensity exercise. Seven men performed square-wave transitions from unloaded cycling to a work rate requiring 40% of the difference between the gas exchange threshold and peak Vo(2) with and without prior intravenous infusion of L-NAME (4 mg/kg in 50 ml saline over 60 min). Pulmonary gas exchange was measured breath by breath, and Vo(2) kinetics were determined from the averaged response to two exercise bouts performed in each condition. There were no significant differences between the control (C) and L-NAME conditions (L) for baseline Vo(2), the duration of phase I, or the amplitude of the primary Vo(2) response. However, the time constant of the Vo(2) response in phase II was significantly smaller (mean +/- SE: C: 25.1 +/- 3.0 s; L: 21.8 +/- 3.3 s; P < 0.05), and the amplitude of the Vo(2) slow component was significantly greater (C: 240 +/- 47 ml/min; L: 363 +/- 24 ml/min; P < 0.05) after L-NAME infusion. These data indicate that inhibition of NOS by L-NAME results in a significant (13%) speeding of Vo(2) kinetics and a significant increase in the amplitude of the Vo(2) slow component in the transition to heavy-intensity cycle exercise in men. The speeding of the primary component Vo(2) kinetics after L-NAME infusion indicates that at least part of the intrinsic inertia to oxidative metabolism at the onset of heavy-intensity exercise may result from inhibition of mitochondrial Vo(2) by nitric oxide. The cause of the larger Vo(2) slow-component amplitude with L-NAME requires further investigation but may be related to differences in muscle blood flow early in the rest-to-exercise transition.     

Effects of "priming" exercise on pulmonary O2 uptake and muscle deoxygenation kinetics during heavy-intensity cycle exercise in the supine and upright positions.

We hypothesized that the performance of prior heavy exercise would speed the phase 2 oxygen consumption (VO2) kinetics during subsequent heavy exercise in the supine position (where perfusion pressure might limit muscle O2 supply) but not in the upright position. Eight healthy men (mean +/- SD age 24 +/- 7 yr; body mass 75.0 +/- 5.8 kg) completed a double-step test protocol involving two bouts of 6 min of heavy cycle exercise, separated by a 10-min recovery period, on two occasions in each of the upright and supine positions. Pulmonary O2 uptake was measured breath by breath and muscle oxygenation was assessed using near-infrared spectroscopy (NIRS). The NIRS data indicated that the performance of prior exercise resulted in hyperemia in both body positions. In the upright position, prior exercise had no significant effect on the time constant tau of the VO2 response in phase 2 (bout 1: 29 +/- 10 vs. bout 2: 28 +/- 4 s; P = 0.91) but reduced the amplitude of the VO2 slow component (bout 1: 0.45 +/- 0.16 vs. bout 2: 0.22 +/- 0.14 l/min; P = 0.006) during subsequent heavy exercise. In contrast, in the supine position, prior exercise resulted in a significant reduction in the phase 2 tau (bout 1: 38 +/- 18 vs. bout 2: 24 +/- 9 s; P = 0.03) but did not alter the amplitude of the VO2 slow component (bout 1: 0.40 +/- 0.29 vs. bout 2: 0.41 +/- 0.20 l/min; P = 0.86). These results suggest that the performance of prior heavy exercise enables a speeding of phase 2 VO2 kinetics during heavy exercise in the supine position, presumably by negating an O2 delivery limitation that was extant in the control condition, but not during upright exercise, where muscle O2 supply was probably not limiting.     

Oxidative metabolism and anaerobic glycolysis during repeated exercise

The purpose of the present study was to examine aerobic and muscle anaerobic energy production during supramaximal repeated exercise. Eight subjects performed three 2-min bouts of cycling (EX1-EX3) at an intensity corresponding to about 125 % of VO2 max separated by 15 min of rest. Ventilatory variables were measured breath by breath during the exercise and a muscle biopsy was taken before and after each exercise bout. Blood samples were collected before and after each cycling period and during the recovery periods. Total work in the first 2 min bout of cycling, EX1, [46.3 +/- 2.1 KJ] was greater than in the second, EX2, (p < 0.01) and in the third, EX3, (p < 0.05). The ATP utilization [4.0 +/- 1.4 mmol x (kg dry weight)(-1), EX1] during the three exercise bouts was the same. The decrement in muscle phosphocreatine (PCr) [46.8 +/- 8.5 mmol x (kg dry weight)(-1), EX1] was also similar for the three exercise bouts. Muscle lactate accumulation was greater (p < 0.05) during EX1 compared to EX2 and EX3. The total oxygen consumption was the same for the three exercise bouts, but when it is corrected for the total work performed, oxygen uptake during EX2 (153 +/- 9 ml x KJ(-1)) and EX3 (150 +/- 9 ml x KJ(-1)) was higher (p < 0.01 and p < 0.05, respectively) than during EX1 (139 +/- 8 ml x KJ(-1)). The present data suggest that oxidative metabolism does not compensate for the reduction of anaerobic glycolysis during repeated fatiguing exercise.     

VO(2) kinetics in heavy exercise is not altered by prior exercise with a different muscle group.

We examined whether lactic acidemia-induced hyperemia at the onset of high-intensity leg exercise contributed to the speeding of pulmonary O(2) uptake (VO(2)) after prior heavy exercise of the same muscle group or a different muscle group (i.e., arm). Six healthy male subjects performed two protocols that consisted of two consecutive 6-min exercise bouts separated by a 6-min baseline at 0 W: 1) both bouts of heavy (work rate: 50% of lactate threshold to maximal VO(2)) leg cycling (L1-ex to L2-ex) and 2) heavy arm cranking followed by identical heavy leg cycling bout (A1-ex to A2-ex). Blood lactate concentrations before L1-ex, L2-ex, and A2-ex averaged 1.7 +/- 0.3, 5.6 +/- 0.9, and 6.7 +/- 1.4 meq/l, respectively. An "effective" time constant (tau) of VO(2) with the use of the monoexponential model in L2-ex (tau: 36.8 +/- 4.3 s) was significantly faster than that in L1-ex (tau: 52.3 +/- 8.2 s). Warm-up arm cranking did not facilitate the VO(2) kinetics for the following A2-ex [tau: 51.7 +/- 9.7 s]. The double-exponential model revealed no significant change of primary tau (phase II) VO(2) kinetics. Instead, the speeding seen in the effective tau during L2-ex was mainly due to a reduction of the VO(2) slow component. Near-infrared spectroscopy indicated that the degree of hyperemia in working leg muscles was significantly higher at the onset of L2-ex than A2-ex. In conclusion, facilitation of VO(2) kinetics during heavy exercise preceded by an intense warm-up exercise was caused principally by a reduction in the slow component, and it appears unlikely that this could be ascribed exclusively to systemic lactic acidosis.     

Effect of prior multiple-sprint exercise on pulmonary O2 uptake kinetics following the onset of perimaximal exercise.

We hypothesized that the metabolic acidosis resulting from the performance of multiple-sprint exercise would enhance muscle perfusion and result in a speeding of pulmonary oxygen uptake (VO2)kinetics during subsequent perimaximal-intensity constant work rate exercise, if O2 availability represented a limitation to VO2 kinetics in the control (i.e., no prior exercise) condition. On two occasions, seven healthy subjects completed two bouts of exhaustive cycle exercise at a work rate corresponding to approximately 105% of the predetermined Vo2 peak, separated by 3 x 30-s maximal sprint cycling and 15-min recovery (MAX1 and MAX2). Blood lactate concentration (means +/- SD: MAX1: 1.3 +/- 0.4 mM vs. MAX2: 7.7 +/- 0.9 mM; P < 0.01) was significantly greater immediately before, and heart rate was significantly greater both before and during, perimaximal exercise when it was preceded by multiple-sprint exercise. Near-infrared spectroscopy also indicated that muscle blood volume and oxygenation were enhanced when perimaximal exercise was preceded by multiple-sprint exercise. However, the time constant describing the primary component (i.e., phase II) increase in VO2 was not significantly different between the two conditions (MAX1: 33.8 +/- 5.5 s vs. MAX2: 33.2 +/- 7.7 s). Rather, the asymptotic "gain" of the primary Vo2 response was significantly increased by the performance of prior sprint exercise (MAX1: 8.1 +/- 0.9 ml.min(-1).W(-1) vs. MAX2: 9.0 +/- 0.7 ml.min(-1).W(-1); P < 0.05), such that VO2 was projecting to a higher "steady-state" amplitude with the same time constant. These data suggest that priming exercise, which apparently increases muscle O2 availability, does not influence the time constant of the primary-component VO2 response but does increase the amplitude to which VO2 may rise following the onset of perimaximal-intensity cycle exercise.     

Preexercise metabolic alkalosis induced via bicarbonate ingestion accelerates Vo2 kinetics at the onset of a high-power-output exercise in humans.

The present study investigated the effect of preexercise metabolic alkalosis on the primary component of oxygen uptake (Vo(2)) kinetics, characterized by tau(1). Seven healthy physically active nonsmoking men, aged 22.4 +/- 1.8 (mean +/- SD) yr, maximum Vo(2) (Vo(2 max)) 50.4 +/- 4 ml.min(-1).kg(-1), performed two bouts of cycling, corresponding to 40 and 87% of Vo(2 max), lasting 6 min each, separated by a 20-min pause, once as a control study and a few days later at approximately 90 min after ingestion of 3 mmol/kg body wt of NaHCO(3). Blood samples for measurements of bicarbonate concentration and hydrogen ion concentration were taken from antecubital vein via catheter. Pulmonary Vo(2) was measured continuously breath by breath. The values of tau(1) were calculated by using six various approaches published in the literature. Preexercise level of bicarbonate concentration after ingestion of NaHCO(3) was significantly elevated (P < 0.01) compared with the control study (28.96 +/- 2.11 vs. 24.84 +/- 1.18 mmol/l; P < 0.01), and [H(+)] was significantly (P < 0.01) reduced (42.79 +/- 3.38 nmol/l vs. 46.44 +/- 3.51 nmol/l). This shift (P < 0.01) was also present during both bouts of exercise. During cycling at 40% of Vo(2 max), no significant effect of the preexercise alkalosis on the magnitude of tau(1) was found. However, during cycling at 87% of Vo(2 max), the tau(1) calculated by all six approaches was significantly (P < 0.05) reduced, compared with the control study. The tau(1) calculated as in Borrani et al. (Borrani F, Candau R, Millet GY, Perrey S, Fuchsloscher J, and Rouillon JD. J Appl Physiol 90: 2212-2220, 2001) was reduced on average by 7.9 +/- 2.6 s, which was significantly different from zero with both the Student's t-test (P = 0.011) and the Wilcoxon's signed-ranks test (P = 0.014).     

Prior heavy exercise increases oxygen cost during moderate exercise without associated change in surface EMG.

The aim of this study was to test the hypothesis that prior heavy exercise results in a higher oxygen cost during a subsequent bout of moderate exercise due to changes in muscle activity. Eight male subjects (25+/-2 yr, +/-SE) performed moderate-moderate and moderate-heavy-moderate transitions in work rate (cycling intensity, moderate=90% LT, heavy=80% VO(2) peak). The second bout of moderate exercise was performed after 6 min (C) or 30s (D) of recovery. Pulmonary gas exchange was measured breath-by-breath and surface electromyography was obtained from the vastus lateralis and medialis muscles. Root mean square (RMS) and median power frequency (MDPF) were computed. Prior heavy exercise increased DeltaVO(2)/DeltaWR (C: +2.0+/-0.8 ml min(-1)W(-1), D: +3.4+/-0.8 ml min(-1)W(-1); P<0.05) and decreased exercise efficiency (C: -13.3+/-5.6%, D: -22.2 +/-4.9%; P<0.05) during the second bout of moderate exercise in the absence of changes in RMS. MDPF was slightly elevated ( approximately 2%) during the second bout of moderate exercise, but MDPF was not correlated with V O(2) (r=0.17). These findings suggest that the increased oxygen cost during moderate exercise following heavy exercise is not due to increased muscle activity as assessed by surface electromyography.     

Effects of progressive exercise and hypoxia on human muscle sarcoplasmic reticulum function.

This study examined the effects of progressive exercise to fatigue in normoxia (N) on muscle sarcoplasmic reticulum (SR) Ca(2+) cycling and whether alterations in SR Ca(2+) cycling are related to the blunted peak mechanical power output (PO(peak)) and peak oxygen consumption (Vo(2 peak)) observed during progressive exercise in hypoxia (H). Nine untrained men (20.7 +/- 0.42 yr) performed progressive cycle exercise to fatigue on two occasions, namely during N (inspired oxygen fraction = 0.21) and during H (inspired oxygen fraction = 0.14). Tissue extracted from the vastus lateralis before exercise and at power output corresponding to 50 and 70% of Vo(2 peak) (as determined during N) and at fatigue was used to investigate changes in homogenate SR Ca(2+)-cycling properties. Exercise in H compared with N resulted in a 19 and 21% lower (P < 0.05) PO(peak) and Vo(2 peak), respectively. During progressive exercise in N, Ca(2+)-ATPase kinetics, as determined by maximal activity, the Hill coefficient, and the Ca(2+) concentration at one-half maximal activity were not altered. However, reductions with exercise in N were noted in Ca(2+) uptake (before exercise = 357 +/- 29 micromol x min(-1) x g protein(-1); at fatigue = 306 +/- 26 micromol x min(-1) x g protein(-1); P < 0.05) when measured at free Ca(2+) concentration of 2 microM and in phase 2 Ca(2+) release (before exercise = 716 +/- 33 micromol x min(-1) x g protein(-1); at fatigue = 500 +/- 53 micromol x min(-1) x g protein(-1); P < 0.05) when measured in vitro in whole muscle homogenates. No differences were noted between N and H conditions at comparable power output or at fatigue. It is concluded that, although structural changes in SR Ca(2+)-cycling proteins may explain fatigue during progressive exercise in N, they cannot explain the lower PO(peak) and Vo(2 peak) observed during H.     

Deciphering the metabolic and mechanical contributions to the exercise-induced circulatory response: insights from eccentric cycling

Metabolic demand and muscle mechanical tension are closely coupled during exercise, making their respective drives to the circulatory response difficult to establish. This coupling being altered in eccentric cycling, we implemented an experimental design featuring eccentric vs. concentric constant-load cycling bouts to gain insights into the control of the exercise-induced circulatory response in humans. Heart rate (HR), stroke volume (SV), cardiac output (Q), oxygen uptake (V(.-)(O(2))), and electromyographic (EMG) activity of quadriceps muscles were measured in 11 subjects during heavy concentric (heavy CON: 270 +/- 13 W; V(.-)(O(2)) = 3.59 +/- 0.20 l/min), heavy eccentric (heavy ECC: 270 +/- 13 W, V(.-)(O(2)) = 1.17 +/- 0.15 l/min), and light concentric (light CON: 70 +/- 9 W, V(.-)(O(2)) = 1.14 +/- 0.12 l/min) cycle bouts. Using a reductionist approach, the circulatory responses observed between heavy CON vs. light CON (difference in V(.-)(O(2)) and power output) was ascribed either to metabolic demand, as estimated from heavy CON vs. heavy ECC (similar power output, different V(.-)(O(2))), or to muscle mechanical tension, as estimated from heavy ECC vs. light CON (similar V(.-)(O(2)), different power output). 74% of the Q response was determined by the metabolic demand, also accounting for 65% and 84% of HR and SV responses, respectively. Consequently, muscle mechanical tension determined 26%, 35%, and 16% of the Q, HR, and SV responses, respectively. Q was significantly related to V(.-)(O(2)) (r(2) = 0.83) and EMG activity (r(2) = 0.82; both P < 0.001). These results suggest that the exercise-induced circulatory response is mainly under metabolic control and support the idea that the level of muscle activation plays a role in the cardiovascular regulation during cycle exercise in humans.     

VO2 and heart rate kinetics in cycling: transitions from an elevated baseline.

The purpose of this study was to examine oxygen consumption (VO2) and heart rate kinetics during moderate and repeated bouts of heavy square-wave cycling from an exercising baseline. Eight healthy, male volunteers performed square-wave bouts of leg ergometry above and below the gas exchange threshold separated by recovery cycling at 35% VO2 peak. VO2 and heart rate kinetics were modeled, after removal of phase I data by use of a biphasic on-kinetics and monoexponential off-kinetics model. Fingertip capillary blood was sampled 45 s before each transition for base excess, HCO and lactate concentration, and pH. Base excess and HCO concentration were significantly lower, whereas lactate concentration and pH were not different before the second bout. The results confirm earlier reports of a smaller mean response time in the second heavy bout. This was the result of a significantly greater fast-component amplitude and smaller slow-component amplitude with invariant fast-component time constant. A role for local oxygen delivery limitation in heavy exercise transitions with unloaded but not moderate baselines is presented.     

Comparison of hyperthermic hyperpnea elicited during rest and submaximal, moderate-intensity exercise.

We tested the hypothesis that, in humans, hyperthermic hyperpnea elicited in resting subjects differs from that elicited during submaximal, moderate-intensity exercise. In the rest trial, hot-water legs-only immersion and a water-perfused suit were used to increase esophageal temperature (T(es)) in 19 healthy male subjects; in the exercise trial, T(es) was increased by prolonged submaximal cycling [50% peak O(2) uptake (Vo(2))] in the heat (35 degrees C). Minute ventilation (Ve), ventilatory equivalent for Vo(2) (Ve/Vo(2)) and CO(2) output (Ve/Vco(2)), tidal volume (Vt), and respiratory frequency (f) were plotted as functions of T(es). In the exercise trial, Ve increased linearly with increases (from 37.0 to 38.7 degrees C) in T(es) in all subjects; in the rest trial, 14 of the 19 subjects showed a T(es) threshold for hyperpnea (37.8 +/- 0.5 degrees C). Above the threshold for hyperpnea, the slope of the regression line relating Ve and T(es) was significantly greater for the rest than the exercise trial. Moreover, the slopes of the regression lines relating Ve/Vo(2), Ve/Vco(2), and T(es) were significantly greater for the rest than the exercise trial. The increase in Ve reflected increases in Vt and f in the rest trial, but only f in the exercise trial, after an initial increase in ventilation due to Vt. Finally, the slope of the regression line relating T(es) and Vt or f was significantly greater for the rest than the exercise trial. These findings indicate that hyperthermic hyperpnea does indeed differ, depending on whether one is at rest or exercising at submaximal, moderate intensity.     

The intramuscular contribution to the slow oxygen uptake kinetics during exercise in chronic heart failure is related to the severity of the condition

The mechanism for slow pulmonary O(2) uptake (Vo(2)) kinetics in patients with chronic heart failure (CHF) is unclear but may be due to limitations in the intramuscular control of O(2) utilization or O(2) delivery. Recent evidence of a transient overshoot in microvascular deoxygenation supports the latter. Prior (or warm-up) exercise can increase O(2) delivery in healthy individuals. We therefore aimed to determine whether prior exercise could increase muscle oxygenation and speed Vo(2) kinetics during exercise in CHF. Fifteen men with CHF (New York Heart Association I-III) due to left ventricular systolic dysfunction performed two 6-min moderate-intensity exercise transitions (bouts 1 and 2, separated by 6 min of rest) from rest to 90% of lactate threshold on a cycle ergometer. Vo(2) was measured using a turbine and a mass spectrometer, and muscle tissue oxygenation index (TOI) was determined by near-infrared spectroscopy. Prior exercise increased resting TOI by 5.3 ± 2.4% (P = 0.001), attenuated the deoxygenation overshoot (-3.9 ± 3.6 vs. -2.0 ± 1.4%, P = 0.011), and speeded the Vo(2) time constant (τVo(2); 49 ± 19 vs. 41 ± 16 s, P = 0.003). Resting TOI was correlated to τVo(2) before (R(2) = 0.51, P = 0.014) and after (R(2) = 0.36, P = 0.051) warm-up exercise. However, the mean response time of TOI was speeded between bouts in half of the patients (26 ± 8 vs. 20 ± 8 s) and slowed in the remainder (32 ± 11 vs. 44 ± 16 s), the latter group having worse New York Heart Association scores (P = 0.042) and slower Vo(2) kinetics (P = 0.001). These data indicate that prior moderate-intensity exercise improves muscle oxygenation and speeds Vo(2) kinetics in CHF. The most severely limited patients, however, appear to have an intramuscular pathology that limits Vo(2) kinetics during moderate exercise.     

Effect of pedal rate on primary and slow-component oxygen uptake responses during heavy-cycle exercise.

We hypothesized that a higher pedal rate (assumed to result in a greater proportional contribution of type II motor units) would be associated with an increased amplitude of the O(2) uptake (Vo(2)) slow component during heavy-cycle exercise. Ten subjects (mean +/- SD, age 26 +/- 4 yr, body mass 71.5 +/- 7.9 kg) completed a series of square-wave transitions to heavy exercise at pedal rates of 35, 75, and 115 rpm. The exercise power output was set at 50% of the difference between the pedal rate-specific ventilatory threshold and peak Vo(2), and the baseline power output was adjusted to account for differences in the O(2) cost of unloaded pedaling. The gain of the Vo(2) primary component was significantly higher at 35 rpm compared with 75 and 115 rpm (mean +/- SE, 10.6 +/- 0.3, 9.5 +/- 0.2, and 8.9 +/- 0.4 ml. min(-1). W(-1), respectively; P < 0.05). The amplitude of the Vo(2) slow component was significantly greater at 115 rpm (328 +/- 29 ml/min) compared with 35 rpm (109 +/- 30 ml/min) and 75 rpm (202 +/- 38 ml/min) (P < 0.05). There were no significant differences in the time constants or time delays associated with the primary and slow components across the pedal rates. The change in blood lactate concentration was significantly greater at 115 rpm (3.7 +/- 0.2 mM) and 75 rpm (2.8 +/- 0.3 mM) compared with 35 rpm (1.7 +/- 0.4 mM) (P < 0.05). These data indicate that pedal rate influences Vo(2) kinetics during heavy exercise at the same relative intensity, presumably by altering motor unit recruitment patterns.