Blood lactate disappearance at various intensities of recovery exercise

Numerous studies have reported that following intense exercise the rate of blood lactate (La) disappearance is greater during continuous aerobic work than during passive recovery. Recent work indicates that a combination of high- and low-intensity work may be optimal in reducing blood La. We tested this hypothesis by measuring the changes in blood La levels following maximal exercise during four different recovery patterns. Immediately following 50 S of maximal work, subjects (n = 7) performed one of the following recovery treatments for 40 min: 1) passive recovery (PR); 2) cycling at 35% maximal O2 uptake (VO2 max) (35% R); 3) cycling at 65% VO2 max (65% R); 4) cycling at 65% for 7 min followed by cycling at 35% for 33 min (CR). The treatment order was counterbalanced with each subject performing all treatments. Serial blood samples were obtained throughout recovery treatments and analyzed for La. The rate of blood La disappearance was significantly greater (P less than 0.05) in both the 35% R and CR when compared with either the 65% R or PR. No significant difference (P greater than 0.05) existed in the rate of blood La disappearance between the 35% R and CR. These data do not support the hypothesis that exercise recovery at a combination of intensities is superior to a recovery involving continuous submaximal exercise in lowering blood La following maximal work.     

The influence of dietary manipulation on plasma ammonia accumulation during incremental exercise in man

The influence of a pattern of exercise and dietary manipulation, intended to alter carbohydrate (CHO) availability, on pre-exercise acid-base status and plasma ammonia and blood lactate accumulation during incremental exercise was investigated. On three separate occasions, five healthy male subjects underwent a pre-determined incremental exercise test (IET) on an electrically braked cycle ergometer. Each IET involved subjects exercising for 5 min at 30%, 50%, 70% and 95% of their maximal oxygen uptake (VO2max) and workloads were separated by 5 min rest. The first IET took place after 3 days of normal dietary CHO intake. The second and third tests followed 3 days of low or high CHO intake, which was preceded by prolonged exercise to exhaustion in an attempt to deplete muscle and liver glycogen stores. Acid-base status and plasma ammonia and blood lactate levels were measured on arterialised venous blood samples immediately prior to and during the final 15 s of exercise at each workload and for 40 min following the completion of each IET. Three days of low CHO intake resulted in the development of a mild metabolic acidosis in all subjects. Plasma ammonia (NH3) accumulation on the low-CHO diet tended to be greater than normal at each exercise workload. Values returned towards resting levels during each recovery period. After the normal and high-CHO diets plasma NH3 levels did not markedly increase above resting values until after exercise at 95% VO2max. Plasma NH3 levels after the high-CHO diet were similar to those after the normal CHO diet.(ABSTRACT TRUNCATED AT 250 WORDS)     

Similar carbohydrate but enhanced lactate utilization during exercise after 9 wk of acclimatization to 5,620 m

We hypothesized that reliance on lactate as a means of energy distribution is higher after a prolonged period of acclimatization (9 wk) than it is at sea level due to a higher lactate Ra and disposal from active skeletal muscle. To evaluate this hypothesis, six Danish lowlanders (25 +/- 2 yr) were studied at rest and during 20 min of bicycle exercise at 146 W at sea level (SL) and after 9 wk of acclimatization to 5,260 m (Alt). Whole body glucose Ra was similar at SL and Alt at rest and during exercise. Lactate Ra was also similar for the two conditions at rest; however, during exercise, lactate Ra was substantially lower at SL (65 micro mol. min(-1). kg body wt(-1)) than it was at Alt (150 micro mol. min(-1). kg body wt(-1)) at the same exercise intensity. During exercise, net lactate release was approximately 6-fold at Alt compared with SL, and related to this, tracer-calculated leg lactate uptake and release were both 3- or 4-fold higher at Alt compared with SL. The contribution of the two legs to glucose disposal was similar at SL and Alt; however, the contribution of the two legs to lactate Ra was significantly lower at rest and during exercise at SL (27 and 81%) than it was at Alt (45 and 123%). In conclusion, at rest and during exercise at the same absolute workload, CHO and blood glucose utilization were similar at SL and at Alt. Leg net lactate release was severalfold higher, and the contribution of leg lactate release to whole body lactate Ra was higher at Alt compared with SL. During exercise, the relative contribution of lactate oxidation to whole body CHO oxidation was substantially higher at Alt compared with SL as a result of increased uptake and subsequent oxidation of lactate by the active skeletal muscles.     

Cardiorespiratory and metabolic alterations during exercise and passive recovery after three modes of exercise

The objective of this study was to investigate the potential variations in cardiorespiratory and metabolic parameters and running performance among 3 modes of exercise of the same duration, namely, intermittent running with active recovery (AR) or passive recovery (PR) and continuous running (CR) and whether these variations could affect passive recovery time (PRT). Fifteen male physical education students with a subspecialty in soccer were studied (mean age 22.3 ± 2.5 years, training experience 12.3 ± 2.5 years) in the middle of the playing season. The results showed that during exercise, the highest heart rate (HR) and VO2 values were observed in CR, whereas the lowest values in PR followed by AR. Blood lactate (BLa) concentration was higher in PR by 38% compared to that in AR (p < 0.05). The exercise duration was similar between PR and AR tests and longer than in CR. With regard to PRT, the highest HR (186 ± 9 b · min(-1)), VO2 (55.5 ± 5.2 ml · kg(-1) · min(-1)), and BLa (5.1 ± 1.7 mmol · L(-1)) values were found in CR. No differences in HR and VO2 between PR and AR were detected. However, despite the differences in BLa concentration between AR and PR during exercise, the PRT BLa values between these 2 exercise modes were not different. Among the 3 running protocols, only CR appeared to have fully challenged the cardiorespiratory system inducing maximal HR and VO2 responses during exercise and high BLa values in PRT, yet these responses were not associated with better exercise performance compared to intermittent running. Therefore, intermittent exercise, regardless of implementing passive or active interval, might be the preferable exercise mode particularly in activities extended over 30 minutes.     

Muscle interstitial glucose and lactate levels during dynamic exercise in humans determined by microdialysis.

The purpose of the present study was to use the microdialysis technique to determine skeletal muscle interstitial glucose and lactate concentrations during dynamic incremental exercise in humans. Microdialysis probes were inserted into the vastus lateralis muscle, and subjects performed knee extensor exercise at workloads of 10, 20, 30, 40, and 50 W. The in vivo probe recoveries determined at rest by the internal reference method for glucose and lactate were 28.7 +/- 2.5 and 32.0 +/- 2.7%, respectively. As exercise intensity increased, probe recovery also increased, and at the highest workload probe recovery for glucose (61.0 +/- 3.9%) and lactate (66. 3 +/- 3.6%) had more than doubled. At rest the interstitial glucose concentration (3.5 +/- 0.2 mM) was lower than both the arterial (5.6 +/- 0.2 mM) and venous (5.3 +/- 0.3 mM) plasma water glucose levels. The interstitial glucose levels remained lower (P < 0.05) than the arterial and venous plasma water glucose concentrations during exercise at all intensities and at 10, 20, 30, and 50 W, respectively. At rest the interstitial lactate concentration (2.5 +/- 0.2 mM) was higher (P < 0.05) than both the arterial (0.9 +/- 0. 2 mM) and venous (1.1 +/- 0.2 mM) plasma water lactate levels. This relationship was maintained (P < 0.05) during exercise at workloads of 10, 20, and 30 W. These data suggest that interstitial glucose delivery at rest is flow limited and that during exercise changes in the interstitial concentrations of glucose and lactate mirror the changes observed in the venous plasma water compartments. Furthermore, skeletal muscle contraction results in an increase in the diffusion coefficient of glucose and lactate within the interstitial space as reflected by an elevation in probe recovery during exercise.     

Decreased exercise blood lactate concentrations after respiratory endurance training in humans

For many years, it was believed that ventilation does not limit performance in healthy humans. Recently, however, it has been shown that inspiratory muscles can become fatigued during intense endurance exercise and decrease their exercise performance. Therefore, it is not surprising that respiratory endurance training can prolong intense constant-intensity cycling exercise. To investigate the effects of respiratory endurance training on blood lactate concentration and oxygen consumption (VO2) during exercise and their relationship to performance, 20 healthy, active subjects underwent 30 min of voluntary, isocapnic hyperpnoea 5 days a week, for 4 weeks. Respiratory endurance tests, as well as incremental and constant-intensity exercise tests on a cycle ergometer, were performed before and after the 4-week period. Respiratory endurance increased from 4.6 (SD 2.5) to 29.1 (SD 4.0) min (P < 0.001) and cycling endurance time was prolonged from 20.9 (SD 5.5) to 26.6 (SD 11.8) min (P < 0.01) after respiratory training. The VO2 did not change at any exercise intensity whereas blood lactate concentration was lower at the end of the incremental [10.4 (SD 2.1) vs 8.8 (SD 1.9) mmol x l(-1), P < 0.001] as well as at the end of the endurance exercise [10.4 (SD 3.6) vs 9.6 (SD 2.7) mmol x l(-1), P < 0.01] test after respiratory training. We speculate that the reduction in blood lactate concentration was most likely caused by an improved lactate uptake by the trained respiratory muscles. However, reduced exercise blood lactate concentrations per se are unlikely to explain the improved cycling performance after respiratory endurance training.     

Effect of motivational music on lactate levels during recovery from intense exercise

The effects of music played during an exercise task on athletic performance have been previously studied. Yet, these results are not applicable for competitive athletes, who can use music only during warm-up or recovery from exercise. Therefore, the aim of this study was to determine the effect of motivational music (music that stimulates or inspires physical activity) during recovery from intense exercise, on activity pattern, rate of perceived exertion (RPE), and blood lactate concentration. Twenty young, active men (mean age 26.2 ± 2.1 years) performed a 6-minute run at peak oxygen consumption speed (predetermined from the VO(2) max test). The mean heart rate (HR), RPE, number of steps (determined by step counter), and blood lactate concentrations were determined at 3, 6, 9, 12, and 15 minutes during the recovery from the exercise, with and without motivational music (2 separate sessions, at random order). There was no difference in the mean HR during the recovery with and without music. Listening to motivational music during the recovery was associated with increased voluntary activity of the participants, determined by increased number of steps (499.4 ± 220.1 vs. 413.2 ± 150.6 steps, with and without music, respectively; p ≤ 0.05). The increased number of steps during the recovery was accompanied by a significantly greater decrease in blood lactate concentration percentage (28.1 ± 12.2 vs. 22.8 ± 10.9%, with and without music, respectively, p ≤ 0.05). This was associated with a greater decrease in RPE (77.7 ± 14.4 vs. 73.1 ± 14.7% with and without music, respectively; p ≤ 0.05). Our results suggest that listening to motivational music during nonstructured recovery from intense exercise leads to increased activity, faster lactate clearance, and reduced RPE and therefore may be used by athletes in their effort to enhance recovery.     

Rate of decline in blood lactate after cycling exercise in endurance-trained and -untrained subjects

The purpose of this study was to compare the rate of decline in blood lactate (La) levels in nine trained men [maximal O2 consumption (VO2max) 65.5 +/- 3.3 ml.kg-1.min-1] and eight untrained men (VO2max 42.2 +/- 2.8 ml.kg-1.min-1) during passive recovery from a 3-min exercise bout. Trained and untrained subjects cycled at 85 and 80% VO2max, respectively, to produce similar peak blood La concentrations. Twenty samples of arterialized venous blood were drawn from a heated hand vein during 60 min of recovery and analyzed in an automated La analyzer. The data were then fitted to a biexponential function, which closely described the observed data (r = 0.97-0.98). There was no difference in the coefficient expressing the rate of decline in blood La for trained and untrained groups (0.0587 +/- 0.0111 vs. 0.0579 +/- 0.0100, respectively). However, trained subjects demonstrated a faster time-to-peak La (P = 0.01), indicative of a faster efflux of La from muscle to blood. Thus the rate of decline in blood La after exercise does not appear to be affected by training. The faster decline previously reported for trained subjects may be due to the use of a linear rather than a biexponential curve fit.     

Influence of light physical activity on cardiac responses during recovery from exercise in humans

To examine the influence of light exercise on cardiac responses during recovery from exercise, we measured heart rate (HR), stroke volume (SV), and cardiac output (Q˙ _c) in five healthy untrained male subjects in an upright position before, during, and after 10-min steady-state cycle exercise at an exercise intensity of 170 W, corresponding to a mean of 68 (SD 4)% of maximal oxygen uptake. The recovery phase was evaluated separately for three different conditions: 10 min of complete rest (passive recovery), 7 min of pedalling at 20-W exercise intensity followed by 3 min of rest (partially active recovery), and 7 min of pedalling at 40-W exercise intensity followed by 3 min of rest (partially active recovery), on an upright cycle ergometer. The time courses of decreases in HR in the two active recovery phases at different exercise intensities were almost identical to those in the passive recovery phase. However, the subsequent HR reductions during the rest after active recovery at 20 W and at 40 W were mean 7.5 (SD 4.4) and mean 10.0 (SD 3.1) beats · min⁻¹, respectively, both of which were significantly larger (P<0.05 and P<0.005) than the corresponding reduction [1.4 (SD 2.5) beats · min⁻¹] for passive recovery. The SV values at the two exercise intensities during the active recovery periods were maintained at levels similar to that during 170-W steady-state exercise. In contrast, the SV during passive recovery decreased gradually to a level significantly below the initial baseline level at rest before exercise (P<0.05). The resultant time courses of CO values during active recovery were significantly higher (each P<0.05) than that during passive recovery. It was concluded from these findings that light post-exercise physical activity plays an important role in facilitating the venous return from the muscles and in restoring the elevated HR to the pre-exercise resting level. Accepted: 17 September 1997     

Time course of muscular blood metabolites during forearm rhythmic exercise in hypoxia

O2 concentration, PO2, PCO2, pH, osmolarity, lactate (LA), and hemoglobin (Hb) concentrations in deep forearm venous blood were repeatedly measured during submaximal exercise of forearm muscles. Concentrations of arterial blood gases were determined at rest and during exercise. Experiments were conducted under normoxia and hypobaric hypoxia (PB = 465 Torr). In arterial blood, data obtained during exercise were the same as those obtained during rest under either normoxia or hypoxia. In venous muscular blood, PO2 and O2 concentration were lower at rest and during exercise in hypoxia. The muscular arteriovenous O2 difference during exercise in hypoxia was increased by no more than 10% compared with normoxia, which implied that muscular blood flow during exercise also increased by the same percentage, if we assume that exercise O2 consumption was not affected by hypoxia. Despite increased [LA], the magnitude of changes in PCO2 and pH in hypoxia were smaller than in normoxia during exercise and recovery; this finding is probably due to the increased blood buffer value induced by the greater amount of reduced Hb in hypoxia. Hence all the changes occurring in hypoxia showed that local metabolism was less affected than we expected from the decrease in arterial PO2. The rise in [Hb] that occurred during exercise was lower in hypoxia. Possible underlying mechanisms of the [Hb] rise during exercise are discussed.     

Decreased exercise muscle lactate release after high altitude acclimatization

Blood lactate concentration during exercise decreases after acclimatization to high altitude, but it is not clear whether there is decreased lactate release from the exercising muscle or if other mechanisms are involved. We measured iliac venous and femoral arterial lactate concentrations and iliac venous blood flow during cycle exercise before and after acclimatization to 4,300 m. During hypoxia, at a given O2 consumption the venous and arterial lactate concentrations, the venous and arterial concentration differences, and the net lactate release were lower after acclimatization than during acute altitude exposure. While breathing O2-enriched air after acclimatization at a given O2 consumption the venous and arterial lactate concentrations and the venous and arterial concentration differences were significantly lower, and the net lactate release tended to be lower than while breathing ambient air at sea level before acclimatization. We conclude that the lower lactate concentration in venous and arterial blood during exercise after altitude acclimatization reflected less net release of lactate by the exercising muscles, and that this likely resulted from the acclimatization process itself rather than the hypoxia per se.     

Attenuated hepatosplanchnic uptake of lactate during intense exercise in humans.

We evaluated whether the increase in blood lactate with intense exercise is influenced by a low hepatosplanchnic blood flow as assessed by indocyanine green dye elimination and blood sampling from an artery and the hepatic vein in eight men. The hepatosplanchnic blood flow decreased from a resting value of 1.6 +/- 0.1 to 0.7 +/- 0.1 (SE) l/min during exercise. Yet the hepatosplanchnic O2 uptake increased from 67 +/- 3 to 93 +/- 13 ml/min, and the output of glucose increased from 1.1 +/- 0.1 to 2.1 +/- 0.3 mmol/min (P < 0.05). Even at the lowest hepatosplanchnic venous hemoglobin O2 saturation during exercise of 6%, the average concentration of glucose in arterial blood was maintained close to the resting level (5.2 +/- 0.2 vs. 5.5 +/- 0.2 mmol/l), whereas the difference between arterial and hepatic venous blood glucose increased to a maximum of 22 mmol/l. In arterial blood, the concentration of lactate increased from 1.1 +/- 0.2 to 6.0 +/- 1.0 mmol/l, and the hepatosplanchnic uptake of lactate was elevated from 0.4 +/- 0.06 to 1.0 +/- 0.05 mmol/min during exercise (P < 0.05). However, when the hepatosplanchnic venous hemoglobin O2 saturation became low, the arterial and hepatosplanchnic venous blood lactate difference approached zero. Even with a marked reduction in its blood flow, exercise did not challenge the ability of the liver to maintain blood glucose homeostasis. However, it appeared that the contribution of the Cori cycle decreased, and the accumulation of lactate in blood became influenced by the reduced hepatosplanchnic blood flow.     

Muscle pump and central command during recovery from exercise in humans.

We sought to determine the relative contributions of cessation of skeletal muscle pumping and withdrawal of central command to the rapid decrease in arterial pressure during recovery from exercise. Twelve healthy volunteers underwent three exercise sessions, each consisting of a warm-up, 3 min of cycling at 60% of maximal heart rate, and 5 min of one of the following recovery modes: seated (inactive), loadless pedaling (active), and passive cycling. Mean arterial pressure (MAP), cardiac output, thoracic impedance, and heart rate were measured. When measured 15 s after exercise, MAP decreased less (P < 0.05) during the active (-3 +/- 1 mmHg) and passive (-6 +/- 1 mmHg) recovery modes than during inactive (-18 +/- 2 mmHg) recovery. These differences in MAP persisted for the first 4 min of recovery from exercise. Significant maintenance of central blood volume (thoracic impedance), stroke volume, and cardiac output paralleled the maintenance of MAP during active and passive conditions during 5 min of recovery. These data indicate that engaging the skeletal muscle pump by loadless or passive pedaling helps maintain MAP during recovery from submaximal exercise. The lack of differences between loadless and passive pedaling suggests that cessation of central command is not as important.     

Blood lactate production and recovery from anaerobic exercise in trained and untrained boys

Blood lactate production and recovery from anaerobic exercise were investigated in 19 trained (AG) and 6 untrained (CG) prepubescent boys. The exercises comprised 3 maximal test performances; 2 bicycle ergometer tests of different durations (15 s and 60 s), and running on a treadmill for 23.20 +/- 2.61 min to measure maximal oxygen uptake. Blood samples were taken from the fingertip to determine lactate concentrations and from the antecubital vein to determine serum testosterone. Muscle biopsies were obtained from vastus lateralis. Recovery was passive (seated) following the 60 s test but that following the treadmill run was initially active (10 min), and then passive. Peak blood lactate was highest following the 60 s test (AG, 13.1 +/- 2.6 mmol.1-1 and CG, 12.8 +/- 2.3 mmol.1-1). Following the 15 s test and the treadmill run, peak lactate values were 68.7 and 60.6% of the 60 s value respectively. Blood lactate production was greater (p less than 0.001) during the 15 s test (0.470 +/- 0.128 mmol.1-1.s-1) than during the 60 s test (0.184 +/- 0.042 mmol.1-1.s-1). Although blood lactate production was only nonsignificantly greater in AG, the amount of anaerobic work in the short tests was markedly greater (p less than 0.05-0.01) in AG than CG. Muscle fibre area (type II%) and serum testosterone were positively correlated (p less than 0.05) with blood lactate production in both short tests. Blood lactate elimination was greater (p less than 0.001) at the end of the active recovery phase than in the next (passive) phase.(ABSTRACT TRUNCATED AT 250 WORDS)     

Exercise hyperventilation in patients with McArdle's disease

This study was undertaken to determine if patients who lack muscle phosphorylase (i.e., McArdle's disease), and therefore the ability to produce lactic acid during exercise, demonstrate a normal hyperventilatory response during progressive incremental exercise. As expected these patients did not increase their blood lactate above resting levels, whereas the blood lactate levels of normal subjects increased 8- to 10-fold during maximal exercise. The venous pH of the normal subjects decreased markedly during exercise that resulted in hyperventilation. The patients demonstrated a distinct increase in ventilation with respect to O2 consumption similar to that seen in normal individuals during submaximal exercise. However their hyperventilation resulted in an increase in pH because there was no underlying metabolic acidosis. End-tidal partial pressures of O2 and CO2 also reflected a distinct hyperventilation in both groups at approximately 70-85% maximal O2 consumption. These data show that hyperventilation occurs during intense exercise, even when there is no increase in plasma [H+]. Since arterial CO2 levels were decreasing and O2 levels were increasing during the hyperventilation, it is possible that nonhumoral stimuli originating in the active muscles or in the brain elicit the hyperventilation observed during intense exercise.     

Effect of exercise duration during incremental exercise on the determination of anaerobic threshold and the onset of blood lactate accumulation

To determine the effect of the duration of incremental exercise on the point at which arterial blood lactate concentration (HLa) increases above the resting value (anaerobic threshold: AT) and on the point at which HLa reaches a constant value of 4 mM (onset of blood lactate accumulation: OBLA), eight male students performed two different kinds of incremental exercise. A comparison of arterial HLa and venous HLa was made under both conditions of incremental exercise. The incremental bicycle exercise tests consisted of 25 W increase every minute (1-min test) and every 4 min (4-min test). At maximal exercise, there were no significant differences in either gas exchange parameters or HLa values for the two kinds of incremental exercise. However, the peak workloads attained during the two exercises were significantly different (P less than 0.01). At OBLA and AT, there were no significant differences in gas exchange parameters during the 1-min and 4-min tests except for the workload (at OBLA P less than 0.01; at AT P less than 0.05). When venous blood HLa was used instead of arterial HLa for a 4-min test, AT was not significantly different from that obtained by arterial HLa, but OBLA was significantly different from that obtained by arterial HLa (P less than 0.05). On the other hand, for the 1-min test, venous HLa values yielded significantly higher AT and OBLA compared with those obtained using arterial HLa (P less than 0.01). It was concluded that when arterial blood was used, there was no effect of duration of workload increase in an incremental exercise test on the determination of the AT and OBLA expressed in VO2.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiovascular limitations of active recovery from strenuous exercise.

Recovery from muscle fatigue after exercise is known to have two beneficial effects: improved blood lactate elimination and a central nervous recuperation of the capacity for exercise. This study indicates circulatory mechanisms that might limit active recovery. Ten subjects were seated on a cycle ergometer and performed arm cranking exercise at an anaerobic intensity which was for each individual in three periods of 6 min, alternating with recovery intervals of 14 min. In two randomly assigned tests, recovery consisted either of passive sitting (control) or cycling at 80 W for 12 min. Both tests terminated with an identical final passive rest period of 25 min. In the cycling test arm cranking led to a heart rate increase which was further elevated with each repetition, while in the control test no differences were shown among the cranking periods. No corresponding difference was found for oxygen consumption. During the 25 min of final rest, the cycling test showed arterial hypotension and elevated heart rate both of which were absent in the control tests. Venous-occlusion-plethysmography revealed a postcranking forearm hyperaemia. In the cycling test hyperaemia was markedly reduced with the onset of cycling due to vasoconstriction; this effect was absent in the control test. A reduction in blood lactate occurred faster in the cycling test, mainly at the onset of cycling. Total plasma fluid loss combined with forearm fluid uptake was accentuated and prolonged by cycling recovery. Recovery exercise performed by muscles other than those that were fatigued could have led to arterial hypotension (shock-index about 1) through both plasma fluid loss and additional vasodilatation depending on the muscle mass involved.(ABSTRACT TRUNCATED AT 250 WORDS)     

Control of cutaneous vascular conductance and sweating during recovery from dynamic exercise in humans.

The purpose of the study was to examine the effect of 1) passive (assisted pedaling), 2) active (loadless pedaling), and 3) inactive (motionless) recovery modes on mean arterial pressure (MAP), skin blood flow (SkBF), and sweating during recovery after 15 min of dynamic exercise. It was hypothesized that an active recovery mode would be most effective in attenuating the fall in MAP, SkBF, and sweating during exercise recovery. Six male subjects performed 15 min of cycle ergometer exercise at 70% of their predetermined peak oxygen consumption followed by 15 min of 1) active, 2) passive, or 3) inactive recovery. Mean skin temperature (T(sk)), esophageal temperature (T(es)), SkBF, sweating, cardiac output (CO), stroke volume (SV), heart rate (HR), total peripheral resistance (TPR), and MAP were recorded at baseline, end exercise, and 2, 5, 8, 12, and 15 min postexercise. Cutaneous vascular conductance (CVC) was calculated as the ratio of laser-Doppler blood flow to MAP. In the active and passive recovery modes, CVC, sweat rate, MAP, CO, and SV remained elevated over inactive values (P < 0.05). The passive mode was equally as effective as the active mode in maintaining CO, SV, MAP, CVC, and sweat rate above inactive recovery. Sweat rate was different among all modes after 8 min of recovery (P < 0.05). TPR during active recovery remained significantly lower than during recovery in the passive and inactive modes (P < 0.05). No differences in either T(es) or T(sk) were observed among conditions. Given that MAP was higher during passive and active recovery modes than during inactive recovery suggests differences in CVC may be due to differences in baroreceptor unloading and not factors attributed to central command. However, differences in sweat rate may be influenced by factors such as central command and mechanoreceptor stimulation.     

Effect of respiratory acidosis on metabolism in exercise

Five healthy males took part in two separate studies. In one study subjects breathed air (control, C) and in the other 5% CO2 in 21% O2 (respiratory acidosis, RA). Measurements were made at rest, during exercise at 30 and 60% maximal O2 uptake (VO2 max), (20 min each) and in recovery. RA was associated with higher arterial CO2 partial pressure (PCO2) and bicarbonate and lower pH than C. The increase with exercise in plasma lactate (mmol . l-1) was less in RA than C from 1.0 +/- 0.15 (SE) (C = 1.1 +/- 0.17) at rest to 5.3 +/- 1.25 (C = 6.8 +/- 0.98) at 60% VO2 max (P less than 0.10). Plasma pyruvate, alanine, and glycerol concentrations increased with exercise; free fatty acids did not change. There were no significant differences between RA and C in any of these metabolites. Norepinephrine concentrations were similar at rest but increased to a greater extent during exercise in RA than C (P less than 0.02). Epinephrine levels were also higher in RA than C at 60% VO2 max (NS); the two subjects in whom lactate was not lower with RA showed the greatest increase in epinephrine. Exercise in RA was associated with higher heart rates (P less than 0.05), blood pressures (NS), and ventilation (P less than 0.01). In hypercapnia the metabolic effects of acidosis are modified by increased levels of circulating catecholamines.     

Plasma ATP concentration and venous oxygen content in the forearm during dynamic handgrip exercise

Background  

It has been proposed that adenosine triphosphate (ATP) released from red blood cells (RBCs) may contribute to the tight coupling between blood flow and oxygen demand in contracting skeletal muscle. To determine whether ATP may contribute to the vasodilatory response to exercise in the forearm, we measured arterialised and venous plasma ATP concentration and venous oxygen content in 10 healthy young males at rest, and at 30 and 180 seconds during dynamic handgrip exercise at 45% of maximum voluntary contraction (MVC).