Respiratory muscle reserve in rats during heavy exercise

Gosselin, Luc E., David Megirian, Joshua Rodman, DonnaMueller, and Gaspar A. Farkas. Respiratory muscle reserve in ratsduring heavy exercise. J. Appl.Physiol. 83(4): 1405-1409, 1997.The extent towhich the respiratory pump muscles limit maximal aerobic capacity inquadrupeds is not entirely clear. To examine the effect of reducedrespiratory muscle reserve on aerobic capacity, whole bodypeak oxygen consumption(O_{2 peak}) wasmeasured in healthy Sprague-Dawley rats before and after Sham,unilateral, or bilateral hemidiaphragm denervation (Dnv) surgery.O_{2 peak} wasdetermined by using a graded treadmill running test.Hemidiaphragm paralysis was verified after testing byrecording the absence of electromyographic activity duringinspiration. Before surgery, O_{2 peak} averaged 86, 87, and 92 ml · kg¹ · min¹for the Sham, unilateral, and bilateral Dnv groups, respectively. Twoweeks after surgery, there was no significant change inO_{2 peak} foreither the Sham or unilateral Dnv group. However,O_{2 peak} decreased~19% in the bilateral Dnv group 2 wk after surgery. These findingsstrongly suggest that the pulmonary system in rats is designed suchthat during heavy exercise, the remaining respiratory pump muscles areable to compensate for the loss of one hemidiaphragm, but not of both.

     

Adaptation of rat skeletal muscle to creatine depletion: AMP deaminase and AMP deamination.

AMP deaminase catalyzes deamination of the AMP formed in contracting muscles to inosine 5'-monophosphate (IMP). Slow-twitch muscle has only approximately 30% as high a level of AMP deaminase activity as fast-twitch muscle in the rat, and rates of IMP formation during intense contractile activity are much lower in slow-twitch muscle. We found that feeding the creatine analogue beta-guanidinopropionic acid (beta-GPA) to rats, which results in creatine depletion, causes a large decrease in muscle AMP deaminase. This adaptation was used to evaluate the role of AMP deaminase activity level in accounting for differences in IMP production in slow-twitch and fast-twitch muscles. beta-GPA feeding for 3 wk lowered AMP deaminase activity in fast-twitch epitrochlearis muscle to a level similar to that found in the normal slow-twitch soleus muscle but had no effect on the magnitude of the increase in IMP in response to intense contractile activity. Despite a similar decrease in ATP in the normal soleus and the epitrochlearis from beta-GPA-fed rats, the increase in IMP was only approximately 30% as great in the soleus in response to intense contractile activity. These results demonstrate that the accumulation of less IMP in slow- compared with fast-twitch skeletal muscle during contractile activity is not due to the lower level of AMP deaminase in slow-twitch muscle.     

Regulation of glycogen phosphorylase and PDH during exercise in human skeletal muscle during hypoxia

The present study examined the acute effects of hypoxia on the regulation of skeletal muscle metabolism at rest and during 15 min of submaximal exercise. Subjects exercised on two occasions for 15 min at 55% of their normoxic maximal oxygen uptake while breathing 11% O(2) (hypoxia) or room air (normoxia). Muscle biopsies were taken at rest and after 1 and 15 min of exercise. At rest, no effects on muscle metabolism were observed in response to hypoxia. In the 1st min of exercise, glycogenolysis was significantly greater in hypoxia compared with normoxia. This small difference in glycogenolysis was associated with a tendency toward a greater concentration of substrate, free P(i), in hypoxia compared with normoxia. Pyruvate dehydrogenase activity (PDH(a)) was lower in hypoxia at 1 min compared with normoxia, resulting in a reduced rate of pyruvate oxidation and a greater lactate accumulation. During the last 14 min of exercise, glycogenolysis was greater in hypoxia despite a lower mole fraction of phosphorylase a. The greater glycogenolytic rate was maintained posttransformationally through significantly higher free [AMP] and [P(i)]. At the end of exercise, PDH(a) was greater in hypoxia compared with normoxia, contributing to a greater rate of pyruvate oxidation. Because of the higher glycogenolytic rate in hypoxia, the rate of pyruvate production continued to exceed the rate of pyruvate oxidation, resulting in significant lactate accumulation in hypoxia compared with no further lactate accumulation in normoxia. Hence, the elevated lactate production associated with hypoxia at the same absolute workload could in part be explained by the effects of hypoxia on the activities of the rate-limiting enzymes, phosphorylase and PDH, which regulate the rates of pyruvate production and pyruvate oxidation, respectively.     

Effects of acute hypoxia on cerebral and muscle oxygenation during incremental exercise.

To determine if fatigue at maximal aerobic power output was associated with a critical decrease in cerebral oxygenation, 13 male cyclists performed incremental maximal exercise tests (25 W/min ramp) under normoxic (Norm: 21% Fi(O2)) and acute hypoxic (Hypox: 12% Fi(O2)) conditions. Near-infrared spectroscopy (NIRS) was used to monitor concentration (microM) changes of oxy- and deoxyhemoglobin (Delta[O2Hb], Delta[HHb]) in the left vastus lateralis muscle and frontal cerebral cortex. Changes in total Hb were calculated (Delta[THb] = Delta[O2Hb] + Delta[HHb]) and used as an index of change in regional blood volume. Repeated-measures ANOVA were performed across treatments and work rates (alpha = 0.05). During Norm, cerebral oxygenation rose between 25 and 75% peak power output {Power(peak); increased (inc) Delta[O2Hb], inc. Delta[HHb], inc. Delta[THb]}, but fell from 75 to 100% Power(peak) {decreased (dec) Delta[O2Hb], inc. Delta[HHb], no change Delta[THb]}. In contrast, during Hypox, cerebral oxygenation dropped progressively across all work rates (dec. Delta[O2Hb], inc. Delta[HHb]), whereas Delta[THb] again rose up to 75% Power(peak) and remained constant thereafter. Changes in cerebral oxygenation during Hypox were larger than Norm. In muscle, oxygenation decreased progressively throughout exercise in both Norm and Hypox (dec. Delta[O2Hb], inc. Delta [HHb], inc. Delta[THb]), although Delta[O2Hb] was unchanged between 75 and 100% Power peak. Changes in muscle oxygenation were also greater in Hypox compared with Norm. On the basis of these findings, it is unlikely that changes in cerebral oxygenation limit incremental exercise performance in normoxia, yet it is possible that such changes play a more pivotal role in hypoxia.     

Human muscle sarcoplasmic reticulum function during submaximal exercise in normoxia and hypoxia.

In this study, the response of the sarcoplasmic reticulum (SR) to prolonged exercise, performed in normoxia (inspired O(2) fraction = 0.21) and hypoxia (inspired O(2) fraction = 0.14) was studied in homogenates prepared from the vastus lateralis muscle in 10 untrained men (peak O(2) consumption = 3.09 +/- 0.25 l/min). In normoxia, performed at 48 +/- 2.2% peak O(2) consumption, maximal Ca(2+)-dependent ATPase activity was reduced by approximately 25% at 30 min of exercise compared with rest (168 +/- 10 vs. 126 +/- 8 micromol.g protein(-1) x min(-1)), with no further reductions observed at 90 min (129 +/- 6 micromol x g protein(-1) x min(-1)). No changes were observed in the Hill coefficient or in the Ca(2+) concentration at half-maximal activity. The reduction in maximal Ca(2+)-dependent ATPase activity at 30 min of exercise was accompanied by oxalate-dependent reductions (P < 0.05) in Ca(2+) uptake by approximately 20% (370 +/- 22 vs. 298 +/- 25 micromol x g protein(-1) x min(-1)). Ca(2+) release, induced by 4-chloro-m-cresol and assessed into fast and slow phases, was decreased (P < 0.05) by approximately 16 and approximately 32%, respectively, by 90 min of exercise. No differences were found between normoxia and hypoxia for any of the SR properties examined. It is concluded that the disturbances induced in SR Ca(2+) cycling with prolonged moderate-intensity exercise in human muscle during normoxia are not modified when the exercise is performed in hypoxia.     

Effects of hypoxic hypoxia on O2 uptake and heart rate kinetics during heavy exercise

Engelen, Marielle, Janos Porszasz, Marshall Riley, KarlmanWasserman, Kazuhira Maehara, and Thomas J. Barstow. Effects ofhypoxic hypoxia on O₂ uptake andheart rate kinetics during heavy exercise. J. Appl.Physiol. 81(6): 2500-2508, 1996.It is unclearwhether hypoxia alters the kinetics ofO₂ uptake(O₂) during heavy exercise[above the lactic acidosis threshold (LAT)] and how thesealterations might be linked to the rise in blood lactate. Eight healthyvolunteers performed transitions from unloaded cycling to the sameabsolute heavy work rate for 8 min while breathing one of threeinspired O₂ concentrations: 21%(room air), 15% (mild hypoxia), and 12% (moderate hypoxia). Breathing12% O₂ slowed the time constantbut did not affect the amplitude of the primary rise inO₂ (period of first2-3 min of exercise) and had no significant effect on either thetime constant or the amplitude of the slowO₂ component (beginning2-3 min into exercise). Baseline heart rate was elevated inproportion to the severity of the hypoxia, but the amplitude andkinetics of increase during exercise and in recovery were unaffected bylevel of inspired O₂.We conclude that the predominant effect of hypoxia during heavyexercise is on the early energetics as a slowed time constant forO₂ and an additionalanaerobic contribution. However, the sum total of the processesrepresenting the slow component of O₂ is unaffected.

     

Efflux of Ca2+ from fragmented sarcoplasmic reticulum during AMP deamination

Deamination of AMP in skeletal muscle sarcoplasmic reticulum followed by an increase in pH from 6,5 up to 8,0 leads in a liberation of part of Ca2+ from the SR vesicles. This effect is enhanced by K+, which activate the deamination, and is suppressed by Mg2+, which inhibit the reaction. The activating effect of AMP on Ca2+ efflux from the vesicles markedly decreases after AMP deaminase dissociation from the vesicles and is restored after reconstitution of their deaminase activity. Substitution of IMP for AMP causes a decrease of Ca2+ efflux from the vesicles. The data obtained are in good agreement with the assumption that the ammonium formation from AMP can favour the release of Ca2+ from some vesicles of SR.     

Dietary nitrate improves muscle but not cerebral oxygenation status during exercise in hypoxia

Exercise tolerance is impaired in hypoxia, and it has recently been shown that dietary nitrate supplementation can reduce the oxygen (O(2)) cost of muscle contractions. Therefore, we investigated the effect of dietary nitrate supplementation on arterial, muscle, and cerebral oxygenation status, symptoms of acute mountain sickness (AMS), and exercise tolerance at simulated 5,000 m altitude. Fifteen young, healthy volunteers participated in three experimental sessions according to a crossover study design. From 6 days prior to each session, subjects received either beetroot (BR) juice delivering 0.07 mmol nitrate/kg body wt/day or a control drink (CON). One session was in normoxia with CON (NOR(CON)); the two other sessions were in hypoxia (11% O(2)), with either CON (HYP(CON)) or BR (HYP(BR)). Subjects first cycled for 20 min at 45% of peak O(2) consumption (VO(2)peak; EX(45%)) and thereafter, performed a maximal incremental exercise test (EX(max)). Whole-body VO(2), arterial O(2) saturation (%SpO(2)) via pulsoximetry, and tissue oxygenation index of both muscle (TOI(M)) and cerebral (TOI(C)) tissue by near-infrared spectroscopy were measured. Hypoxia per se substantially reduced VO(2)peak, %SpO(2), TOI(M), and TOI(C) (NOR(CON) vs. HYP(CON), P < 0.05). Compared with HYP(CON), VO(2) at rest and during EX(45%) was lower in HYP(BR) (P < 0.05), whereas %SpO(2) was higher (P < 0.05). TOI(M) was ～4-5% higher in HYP(BR) than in HYP(CON) both at rest and during EX(45%) and EX(max) (P < 0.05). TOI(C) as well as the incidence of AMS symptoms were similar between HYP(CON) and HYP(BR) at any time. Hypoxia reduced time to exhaustion in EX(max) by 36% (P < 0.05), but this ergolytic effect was partly negated by BR (+5%, P < 0.05). Short-term dietary nitrate supplementation improves arterial and muscle oxygenation status but not cerebral oxygenation status during exercise in severe hypoxia. This is associated with improved exercise tolerance against the background of a similar incidence of AMS.     

Ear oximetry during combined hypoxia and exercise

Ear oximetry is widely used to detect arterial O2 desaturation during exercise in patients with cardiopulmonary disease. Although oximeters have been evaluated for accuracy, response time, and the influence of skin pigmentation, tests of their reliability have not been reported during strenuous exercise. Accordingly, we compared arterial O2 saturation (Sao2) measurements obtained by Hewlett-Packard (HP, model 47201A) and Biox II oximeters with those determined directly from arterial blood in six healthy volunteers during progressive exercise while rebreathing hypoxic gas mixtures. The relationship between the HP oximeter value and blood Sao2 was described by the equation: HP = 0.93 (Sao2) + 5.37 and for the Biox II: Biox = 0.55 (Sao2) + 38.97. With these equations, at a blood Sao2 value of 90%, the underestimation by both oximeters was less than 2%. At a blood value of 70%, the HP oximeter overestimated blood Sao2 by 0.7%, whereas the Biox II showed an overestimation of 10.7%. Below blood Sao2 of 83%, the Biox II tended to overestimate blood Sao2 by an amount greater than the error of the instrument, whereas the HP estimations were within the error of the instrument over all levels of blood Sao2 studied. We conclude that the HP oximeter provides valid estimates of Sao2 during exercise but that the Biox II oximeter, although reflecting qualitative changes in oxygenation that occur during exercise, does not provide accurate records of the degree of desaturation.     

Cerebral perturbations during exercise in hypoxia

Reduction of aerobic exercise performance observed under hypoxic conditions is mainly attributed to altered muscle metabolism due to impaired O(2) delivery. It has been recently proposed that hypoxia-induced cerebral perturbations may also contribute to exercise performance limitation. A significant reduction in cerebral oxygenation during whole body exercise has been reported in hypoxia compared with normoxia, while changes in cerebral perfusion may depend on the brain region, the level of arterial oxygenation and hyperventilation induced alterations in arterial CO(2). With the use of transcranial magnetic stimulation, inconsistent changes in cortical excitability have been reported in hypoxia, whereas a greater impairment in maximal voluntary activation following a fatiguing exercise has been suggested when arterial O(2) content is reduced. Electromyographic recordings during exercise showed an accelerated rise in central motor drive in hypoxia, probably to compensate for greater muscle contractile fatigue. This accelerated development of muscle fatigue in moderate hypoxia may be responsible for increased inhibitory afferent signals to the central nervous system leading to impaired central drive. In severe hypoxia (arterial O(2) saturation <70-75%), cerebral hypoxia per se may become an important contributor to impaired performance and reduced motor drive during prolonged exercise. This review examines the effects of acute and chronic reduction in arterial O(2) (and CO(2)) on cerebral blood flow and cerebral oxygenation, neuronal function, and central drive to the muscles. Direct and indirect influences of arterial deoxygenation on central command are separated. Methodological concerns as well as future research avenues are also considered.     

Acute responses in muscle mitochondrial and cytosolic enzyme activities during heavy intermittent exercise.

To examine the effects of repetitive bouts of heavy exercise on the maximal activities of enzymes representative of the major metabolic pathways and segments, 13 untrained volunteers [peak aerobic power (Vo(2 peak)) = 44.3 +/- 2.3 ml.kg(-1).min(-1)] cycled at approximately 91% Vo(2 peak) for 6 min once per hour for 16 h. Maximal enzyme activities (V(max), mol.kg(-1).protein.h(-1)) were measured in homogenates from tissue extracted from the vastus lateralis before and after exercise at repetitions 1 (R1), 2 (R2), 9 (R9), and 16 (R16). For the mitochondrial enzymes, exercise resulted in reductions (P < 0.05) in cytochrome-c oxidase (COX, 14.6%), near significant reductions in malate dehydrogenase (4.06%; P = 0.06) and succinic dehydrogenase (4.82%; P = 0.09), near significant increases in beta-hydroxyacyl-CoA dehydrogenase (4.94%; P = 0.08), and no change in citrate synthase (CS, 2.88%; P = 0.37). For the cytosolic enzymes, exercise reduced (P < 0.05) V(max) in hexokinase (Hex, 4.4%), creatine phosphokinase (9.0%), total phosphorylase (13.5%), phosphofructokinase (16.6%), pyruvate kinase (PK, 14.1%) and lactate dehydrogenase (10.7%). Repetition-dependent reductions (P < 0.05) in V(max) were observed for CS (R1, R2 > R16), COX (R1, R2 > R16), Hex (1R, 2R > R16), and PK (R9 > R16). It is concluded that heavy exercise results in transient reductions in a wide range of enzymes involved in different metabolic functions and that in the case of selected enzymes, multiple repetitions of the exercise reduce average V(max).     

Effects of PDH activation by dichloroacetate in human skeletal muscle during exercise in hypoxia

During the onset of exercise in hypoxia, the increased lactate accumulation is associated with a delayed activation of pyruvate dehydrogenase (PDH; Parolin ML, Spreit LL, Hultman E, Hollidge-Horvat MG, Jones NL, and Heigenhauser GJF. Am J Physiol Endocrinol Metab 278: E522-E534, 2000). The present study investigated whether activation of PDH with dichloroacetate (DCA) before exercise would reduce lactate accumulation during exercise in acute hypoxia by increasing oxidative phosphorylation. Six subjects cycled on two occasions for 15 min at 55% of their normoxic maximal oxygen uptake after a saline (control) or DCA infusion while breathing 11% O(2). Muscle biopsies of the vastus lateralis were taken at rest and after 1 and 15 min of exercise. DCA increased PDH activity at rest and at 1 min of exercise, resulting in increased acetyl-CoA concentration and acetylcarnitine concentration at rest and at 1 min. In the first minute of exercise, there was a trend toward a lower phosphocreatine (PCr) breakdown with DCA compared with control. Glycogenolysis was lower with DCA, resulting in reduced lactate concentration ([lactate]), despite similar phosphorylase a mole fractions and posttransformational regulators. During the subsequent 14 min of exercise, PDH activity was similar, whereas PCr breakdown and muscle [lactate] were reduced with DCA. Glycogenolysis was lower with DCA, despite similar mole fractions of phosphorylase a, and was due to reduced posttransformational regulators. The results from the present study support the hypothesis that lactate production is due in part to metabolic inertia and cannot solely be explained by an oxygen limitation, even under conditions of acute hypoxia.     

Myoelectric evidence of peripheral muscle fatigue during exercise in severe hypoxia: some references to m. vastus lateralis myosin heavy chain composition

Integrated electromyography (iEMG) of the m. vastus lateralis was analysed during cycle ergometry in male subjects (n = 8). Two work trials were conducted, one under normoxia (N), the other under environmental normobaric hypoxia (EH in which the oxygen fraction in inspired gas = 0.116), each trial lasting 10 min. The absolute power output (180 W) was the same for both trials and was equivalent to 77 (4)% of maximum heart rate in trial N. Maximal voluntary isometric contractions were performed after each trial to assess changes in force, muscle fibre conduction velocity (MFCV), electromechanical delay (EMD), median frequency of EMG (MF) and maximal iEMG (iEMG_max). Biopy samples of muscle were obtained from the m. vastus medialis before testing. Myosin heavy chain (MHC) differences were determined through sodium dodecyl-polyacrylamide gel electrophoresis followed by densitometric analysis. No differences in submaximal iEMG were observed between EH and N trials during the first minute of work. At the end of both work trials iEMG was significantly elevated compared with starting values, however the iEMG recorded in EH exceeded N values by 15%. At the end of the EH trials the following were observed: a decrease in isometric force, MFCV and MF with an increase in EMD and the iEMG_max/force ratio. The iEMG_max was unchanged. No differences in any of these variables were observed after the N trial. Mean (SD) lactate concentrations following EH and N trials were 9.2 (4.4) mmol · 1⁻¹ and 3.5 (1.1) mmol · 1⁻¹, respectively. Results indicate that an increased motor unit recruitment and rate coding was needed in EH to maintain the required power output. The increased motor unit recruitment and rate coding were associated with myoelectric evidence of “peripheral” muscle fatigue. Subjects with higher compositions of type II MHC accumulated more lactate and displayed greater reductions in MF and MFCV during fatigue. Accepted: 16 June 1996     

Reversal of muscle fatigue during 16 h of heavy intermittent cycle exercise.

This study examined the effects of extended sessions of heavy intermittent exercise on quadriceps muscle fatigue and weakness. Twelve untrained volunteers (10 men and 2 women), with a peak oxygen consumption of 44.3 +/- 2.3 ml.kg(-1).min(-1), exercised at approximately 91% peak oxygen consumption for 6 min once per hour for 16 h. Muscle isometric properties assessed before and after selected repetitions (R1, R2, R4, R7, R12, and R15) were used to quantitate fatigue (before vs. after repetitions) and weakness (before vs. before repetitions). Muscle fatigue at R1 was indicated by reductions (P < 0.05) in peak twitch force (135 +/- 13 vs. 106 +/- 11 N) and by a reduction (P < 0.05) in the force-frequency response, which ranged between approximately 53% at 10 Hz (113 +/- 12 vs. 52.6 +/- 7.4 N) and approximately 17% at 50 Hz (324 +/- 27 vs. 270 +/- 30 N). No recovery of force, regardless of stimulation frequency, was observed during the 54 min between R1 and R2. At R2 and for all subsequent repetitions, no reduction in force, regardless of stimulation frequency, was generally found after the exercise. The only exception was for R2, where, at 20 Hz, force was reduced (P < 0.05) by 18%. At R15, force before repetitions for high frequencies (i.e., 100 Hz) returned to R1 (333 +/- 29 vs. 324 +/- 27 N), whereas force at low frequency (i.e., 10 Hz) was only partially (P < 0.05) recovered (113 +/- 12 vs. 70 +/- 6.6 N). It is concluded that multiple sessions of heavy exercise can reverse the fatigue noted early and reduce or eliminate weakness depending on the frequency of stimulation.     

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.     

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.     

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.