Modelling human power and endurance

A generalised three component hydraulic model has been proposed to represent the human bioenergetic processes relating internal energy stores to performance during exercise, and into recovery. Further development of the model allows testable predictions to be made. In particular in this paper I examine certain hypotheses of chemical fuel shortage as a subgroup of the potential causes of fatigue, and their implications for maximal power and for endurance. The assumption that the limitation to sustainable power is direct proportionality to the glycogen store remaining, appears the most feasible. Based on this assumption, equations for the decline in maximum attainable power over time, the endurance at fixed workrates and the endurance at incremental tests (as a function of the increment slope) are obtained. Using published data for fit males, the maximum exertable power declines after about 6 s at 972 W to very low levels after about 2 min. For constant powers selected between 208 and 927 W, endurance declines from ad infinitum to only 6 s. Endurance at VO2max is predicted to be about 9 min. For incremental exercise tests of slope ranging from 30 W/min to 60 W/min, endurance lessens from 14 to 9 min. In these tests the anaerobic threshold is reached in times between 6 and 3 min. Although the power at termination of a test increases with incremental slope, terminal oxygen consumption is effectively constant. Almost all these model predictions are observed to correspond well with published experimental findings. These results suggest that the model can be used to represent an adequate overview of the operation of the human bioenergetic system.     

Oxygen uptake, acid-base status, and performance with varied inspired oxygen fractions

Six subjects rode a bicycle ergometer on three occasions breathing 17, 21, or 60% oxygen. In addition to rest and recovery periods, each subject worked for 10 min at 55% of maximal oxygen uptake (VO2 max) and then to exhaustion at approximately 90% VO2 max. Performance time, inspired and expired gas fractions, ventilation, and arterialized venous oxygen tension (PO2), carbon dioxide tension (PCO2), lactate, and pH were measured. VO2, carbon dioxide output, [H+]a, and [HCO3-]a were calculated. Performance times were longer in hyperoxia than in normoxia or hypoxia. However, VO2 was not different at exhaustion in normoxia compared with hypoxia or hyperoxia. During exercise, hypoxia was associated with increased lactate levels and decreased [H+]a, PCO2, and [HCO3-]a. The opposite trends were generally associated with hyperoxia. At exhaustion, [H+]a was not different under any inspired oxygen fraction. These results support the contention that oxygen is not limiting for exercise of this intensity and duration. The results also suggest that [H+] is a possible limiting factor and that the effect of oxygen on performance is perhaps related to control of [H+].     

The influence of exercise intensity on the power spectrum of heart rate variability

The power spectral analysis of R-R interval variability (RRV) has been estimated by means of an autoregressive method in seven sedentary males at rest, during steady-state cycle exercise at 21 percent maximal oxygen uptake (%VO2max), SEM 2%, 49% VO2max, SEM 2% and 70% VO2max, SEM 2% and during recovery. The RRV, i.e. the absolute power of the spectrum, decreased 10, 100 and 500 times in the three exercise intensities, returning to resting value during recovery. In the RRV power spectrum three components have been identified: (1) high frequency peak (HF), central frequency about 0.24 Hz at rest and recovery, and 0.28 Hz, SEM 0.02, 0.37 Hz, SEM 0.03 and 0.48 Hz, SEM 0.06 during the three exercise intensities, respectively; (2) low frequency peak (LF), central frequency about 0.1 Hz independent of the metabolic state; (3) very low frequency component (VLF), less than 0.05 Hz, no peak observed. The HF peak power, as a percentage of the total power (HF%), averaged 16%, SEM 5% at rest and did not change during exercise, whereas during recovery it decreased to 5%-10%. The LF% and VLF% were about 50% and 35% at rest and during low exercise intensity, respectively. At higher intensities, LF% decreased to 16% and VLF% increased to 70%. During recovery a return to resting values occurred. The HF component may reflect the increased respiratory rate and the LF peak changes the resetting of the baroreceptor reflex with exercise. The hypothesis is made that VLF fluctuations in heart rate might be partially mediated by the sympathetic system.     

Enhancement of fat metabolism by repeated bouts of moderate endurance exercise.

This study compared the fat metabolism between "a single bout of prolonged exercise" and "repeated bouts of exercise" of equivalent exercise intensity and total exercise duration. Seven men performed three trials: 1) a single bout of 60-min exercise (Single); 2) two bouts of 30-min exercise, separated by a 20-min rest between exercise bouts (Repeated); and 3) rest. Each exercise was performed with a cycle ergometer at 60% of maximal oxygen uptake. In the Single and Repeated trials, serum glycerol, growth hormone, plasma epinephrine, and norepinephrine concentrations increased significantly (P<0.05) during the first 30-min exercise bout. In the Repeated trial, serum free fatty acids (FFA), acetoacetate, and 3-hydroxybutyrate concentrations showed rapid increases (P<0.05) during a subsequent 20-min rest period. During the second 30-min exercise bout, FFA and epinephrine responses were significantly greater in the Repeated trial than in the Single trial (P<0.05). Moreover, the Repeated trial showed significantly lower values of insulin and glucose than the Single trial. During the 60-min recovery period after the exercise, FFA, glycerol, and 3-hydroxybutyrate concentrations were significantly higher in the Repeated trial than in the Single trial (P<0.05). The relative contribution of fat oxidation to the energy expenditure showed significantly higher values (P<0.05) in the Repeated trial than in the Single trial during the recovery period. These results indicate that repeated bouts of exercise cause enhanced fat metabolism compared with a single bout of prolonged exercise of equivalent total exercise duration.     

Energy expenditure of heavy to severe exercise and recovery

A method of indirect calorimetry is proposed that attempts to better quantify the energy expenditure associated with heavy/severe exercise and the recovery from that exertion. To accomplish this objective, the energy expenditure associated with rapid anaerobic glycolysis is separated from that of mitochondrial respiration both during and after heavy/severe exercise. This model contrasts with those hypotheses that employ oxygen uptake as the sole measure of energy expenditure (e.g. the oxygen debt) or that utilizing a measure of anaerobic energy expenditure while ignoring the recovery energy expenditure. Anaerobic metabolism and its energy promoting effect on oxidative recovery must be independently acknowledged regardless of the eventual fate of lactate.     

Metaboreceptor-mediated muscle oxygen saturation during recovery following isometric handgrip exercise

The aim of the present study was to determine whether oxygen supply to non-exercised muscle during recovery following fatiguing exercise is influenced by accumulated metabolites within exercised muscle. Twelve healthy male subjects performed 2-min isometric handgrip exercise at 40% maximal voluntary contraction with their right hand and the exercise was followed by a 3-min recovery period. Muscle oxygen saturation (SmO(2)) determined by near-infrared spatially resolved spectroscopy was used as an index of oxygen supply to non-exercised muscle and was measured in biceps brachii and tibialis anterior muscles on the left side. Compared to the pre-exercise baseline level, SmO(2) in the biceps brachii muscle (SmO(2BB)) increased significantly from 30 sec to 1 min after the start of exercise, while SmO(2) in the tibialis anterior muscle (SmO(2TA)) remained stable during the initial 1 min of exercise. Both SmO(2BB) and SmO(2TA) began to decrease at about 1 min and continued to decrease thereafter. Due to the initial increase in SmO(2BB), only SmO(2TA) showed a significant decrease during exercise. During recovery, SmO(2BB) did not differ significantly from the pre-exercise baseline level, whereas SmO(2TA) remained significantly lower until about 1.5 min of recovery and then it did not differ significantly from the baseline level. In another bout, subjects performed handgrip exercise of the same intensity, but post-exercise arterial occlusion (PEAO) of the exercised muscle was imposed for 2 min immediately after the end of exercise. During PEAO, SmO(2BB) decreased significantly compared to the baseline level, whereas SmO(2TA) remained significantly lower until the end of PEAO. The significant decrease in SmO(2BB) and the prolongation of decrease in SmO(2TA) by PEAO suggests that the recovery of SmO(2) in the non-exercised arm and leg is mediated by muscle metaboreceptors.     

On a model of human bioenergetics

A three component hydraulic model has been proposed to represent the energy flows during human exercise and recovery. This model was accompanied by a sketch indicative of the graphical solution but had not been solved mathematically. This paper describes the model and demonstrates the method of mathematical solution, illustrated with a numerical example. Plotted graphically, this particular solution differs from both the "sketch solution" and from what actually happens under experimental conditions. These points of discrepancy are discussed with a view to their rectification and the development of a refined model.     

The physiological response of diploid and triploid brook trout to exhaustive exercise

Using triploidy as an experimental model, we examined whether cell size limits the post-exercise recovery process in fish. Because triploids generally possess larger cells, which could affect many physiological and biochemical processes, we hypothesized that triploids would take longer to recover from exhaustive exercise compared to diploids. To test this, we measured plasma lactate, glucose and osmolality, and white muscle energy stores (glycogen, phosphocreatine and ATP) and lactate before and immediately following exhaustive exercise and during recovery at 2 and 4 h post-exercise. In addition, oxygen consumption and ammonia excretion rates were determined before and after exhaustive exercise. Overall, diploid and triploid brook trout showed similar metabolic responses exercise, but plasma osmolality, white muscle lactate, white muscle ATP and post-exercise oxygen consumption rates recovered earlier in triploids compared to diploids. The results of this study suggest that the characteristic larger cell size of triploidy does not limit the physiological response to, or recovery from, exhaustive exercise.     

The effects of two levels of caffeine ingestion on excess postexercise oxygen consumption in untrained women

The effects of two levels of caffeine ingestion (5 mg.kg-1, CAF1, and 10 mg.kg-1, CAF2) on postexercise oxygen consumption was investigated in six untrained women aged 20.5 (SEM 0.5) years. After a test to determine maximal oxygen consumption (VO2max) each subject underwent three test sessions at 55% VO2max either in a control condition (CON) or with the CAF1 or CAF2 dose of caffeine. During exercise, oxygen consumption was found to be significantly higher in the CAF1 and CAF2 trials, compared to CON (P < 0.05). During the hour postexercise, oxygen consumption in CAF1 and CAF2 remained significantly higher than in CON (P < 0.05). At all times throughout the exercise, free fatty acid (FFA) concentrations were significantly higher in the caffeine trials than in CON. The FFA concentrations 1 h postexercise (+60 min) were further elevated above resting values for all three trials. Caffeine ingestion caused the greatest elevation above resting levels being 1.89 (SEM 0.19) mmol.l-1 and 1.96 (SEM 0.22) mmol.l-1 for the CAF1 and CAF2 trials, respectively. This was significantly higher (P < 0.0001) than the CON level which was 0.97 (SEM 0.19) mmol.l-1. Respiratory exchange ratio (R) values became significantly lower (P < 0.05) in CAF1 and CAF2 compared to CON at the onset of exercise and continued to decrease during the activity. Throughout the recovery period, R values were significantly lower for both caffeine trials compared to CON. The results of this study would suggest that caffeine is useful in significantly increasing metabolic rate above normal levels in untrained women during, as well as after, exercising at 55% VO2max.     

Changes in plasma and erythrocyte K+ during hypercapnia and different grades of exercise in trout.

Trout were exposed to hypercapnia, two levels of aerobic exercise, or three successive periods of supramaximal exercise to evaluate the effects on erythrocyte and plasma K+. During aerobic exercise, plasma K+ increased slightly with the intensity of work, while no change was found in the erythrocyte K+ content. In contrast, both hypercapnia and supramaximal exercise induced a net erythrocyte K+ uptake. This uptake changed to a net loss of K+ as arterial pH and hemoglobin-bound oxygen saturation returned to control values during recovery. The maximal rates of net K+ uptake found during hypercapnia and supramaximal exercise corresponded to 195 and 350 mumol.kg fish-1.h-1, respectively, and the maximal rates of net K+ loss found during recovery corresponded in both cases to approximately 130 mumol.kg fish-1.h-1. Hypercapnia had only a minor effect on plasma K+, but return to normocapnic conditions induced a 0.8 mM rise in plasma K+. Of this increase, approximately 70% could be accounted for by the simultaneous net release of erythrocyte K+. Each period of supramaximal exercise induced an elevated plasma K+ level, resulting in accumulation of plasma K+ despite slight decreases in plasma K+ in between the exercise periods. At the same time the net erythrocyte K+ uptake caused an estimated reduction in plasma K+ of 1.5 mM. It is concluded that both hypercapnia and supramaximal exercise cause profound net changes in the erythrocyte K+ content with significant effects on plasma K+.     

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)     

Ventilatory Responses of Teleost Fish to Exercise and Thermal Stress

Exercise and thermal stress both markedly raise the oxygen demandof fish. The control of ventilation under these two conditionsis apparently quite different and contrasts between speciesare noteworthy. Under both exercise and thermal stress, changes in respiratorypumping amplitude tend to be greater than changes in ventilatoryfrequency in most species. Respiratory pump uncoupling duringthermal stress is frequently seen in trout but much less soin bullhead catfish or bluegills. In fish that actively ventilate the gills while swimming, thecontrol for this probably depends on swimming muscle reflexesrather than blood humoral factors. This control mechanism mayoperate in a reverse fashion in fish that use ram-jet ventilation.During recovery from severe exercise and during thermal stressthe control of gill ventilation is apparently humoral. Of thepossible factors, blood oxygen and possibly also pH are consideredto be the most important. Evidence is summarized that suggeststhe error detector is on the arterial side of the gas exchanger.     

Acute effects of dry immersion upon blood supply of calf muscles during upright exercise

Healthy males performed upright exercise before and after three days of dry immersion. During exercise, calf blood flow, heart rate, and oxygen consumption were measured. Immersion resulted in increased heart rate and oxygen ventilatory equivalent, and decreased calf blood flow. Implications for the alterations in blood flow dynamics are discussed.     

Postexercise muscle and liver glycogen metabolism in male and female rats

Male and female Wistar rats were run for 5 min at 1.7 mph at a 17% grade to determine whether a sex difference exists in the rate of glycogen resynthesis during recovery in fast-twitch red muscle, fast-twitch white muscle, and liver. Rats were killed at one of three time points: immediately after the exercise bout, and at 1 or 4 h later. Males had significantly higher resting muscle glycogen levels (P less than 0.05). Exercise resulted in significant glycogen depletion in both sexes (P less than 0.01). Males utilized approximately 50% more glycogen during the exercise bout than females (P less than 0.05). During the food-restricted 4-h recovery period, muscle glycogen was repleted significantly during the 1st h (P less than 0.05). Liver glycogen was not depleted as a result of the exercise bout, but fell during the first h of recovery (P less than 0.05) and remained low during the subsequent 3 h. The greater glycogen utilization in red and white fast-twitch muscle during exercise by males could represent a true sex difference but could also be attributable in part to the males having performed more work as a result of 20% greater body mass. We conclude that no sex difference was observed in the rates of muscle glycogen repletion after exercise or in liver glycogen metabolism during and after exercise, and rapid postexercise muscle glycogen repletion occurred at a time of accelerated liver glycogen depletion.     

On the kinetics of anaerobic power

ABSTRACT: BACKGROUND: This study investigated two different mathematical models for the kinetics of anaerobic power. Model 1 assumes that the work power is linear with the work rate, while model 2 assumes a linear relationship between the alactic anaerobic power and the rate of change of the aerobic power. In order to test these models, a cross country skier ran with poles on a treadmill at different exercise intensities. The aerobic power, based on the measured oxygen uptake, was used as input to the models, whereas the simulated blood lactate concentration was compared with experimental results. Thereafter, the metabolic rate from phosphocreatine break down was calculated theoretically. Finally, the models were used to compare phosphocreatine break down during continuous and interval exercises. RESULTS: Good similarity was found between experimental and simulated blood lactate concentration during steady state exercise intensities. The measured blood lactate concentrations were lower than simulated for intensities above the lactate threshold, but higher than simulated during recovery after high intensity exercise when the simulated lactate concentration was averaged over the whole lactate space. This fit was improved when the simulated lactate concentration was separated into two compartments; muscles + internal organs and blood. Model 2 gave a better behavior of alactic energy than Model 1 when compared against invasive measurements presented in the literature. During continuous exercise, model 2 showed that the alactic energy storage decreased with time, whereas model 1 showed a minimum value when steady state aerobic conditions were achieved. During interval exercise the two models showed similar patterns of alactic energy. CONCLUSIONS: The current study provides useful insight on the kinetics of anaerobic power. Overall, our data indicates that blood lactate levels can be accurately modeled during steady state, and suggests a linear relationship between the alactic anaerobic power and the rate of change of the aerobic power.     

Cerebral blood flow and metabolism during exercise: implications for fatigue.

During exercise: the Kety-Schmidt-determined cerebral blood flow (CBF) does not change because the jugular vein is collapsed in the upright position. In contrast, when CBF is evaluated by (133)Xe clearance, by flow in the internal carotid artery, or by flow velocity in basal cerebral arteries, a approximately 25% increase is detected with a parallel increase in metabolism. During activation, an increase in cerebral O(2) supply is required because there is no capillary recruitment within the brain and increased metabolism becomes dependent on an enhanced gradient for oxygen diffusion. During maximal whole body exercise, however, cerebral oxygenation decreases because of eventual arterial desaturation and marked hyperventilation-related hypocapnia of consequence for CBF. Reduced cerebral oxygenation affects recruitment of motor units, and supplemental O(2) enhances cerebral oxygenation and work capacity without effects on muscle oxygenation. Also, the work of breathing and the increasing temperature of the brain during exercise are of importance for the development of so-called central fatigue. During prolonged exercise, the perceived exertion is related to accumulation of ammonia in the brain, and data support the theory that glycogen depletion in astrocytes limits the ability of the brain to accelerate its metabolism during activation. The release of interleukin-6 from the brain when exercise is prolonged may represent a signaling pathway in matching the metabolic response of the brain. Preliminary data suggest a coupling between the circulatory and metabolic perturbations in the brain during strenuous exercise and the ability of the brain to access slow-twitch muscle fiber populations.     

Allantoin formation and urate and glutathione exchange in human muscle during submaximal exercise.

Seven males performed two exhaustive cycling bouts (EX1 and EX2) at a work-rate of 90% of maximal oxygen uptake, separated by 60 min. During EX1 there was a significant accumulation of urate (from 0.16 +/- 0.02 to 0.27 +/- 0.03 micromol/kg d.w.) and allantoin (from 0.39 +/- 0.05 to 0.69 +/- 0.14 micromol/kg d.w.) in the muscle. An uptake of urate was observed in early recovery from EX1 (0-9 min: 486 +/- 136 micromol; p <.05). There was no exchange of total glutathione or cysteine over the muscle either during or after exercise, and muscle and plasma total glutathione remained unaltered (p <.05). The glycogen levels were lowered by 40% at the onset of EX2, yet the level of oxidative stress in EX1 and EX2 was similar as evidenced by a similar increase in muscle allantoin in both exercise bouts. The data suggest that urate is utilized as antioxidant in human skeletal muscle and that reactive oxygen species are formed in muscle during intense submaximal exercise. No net exchange of glutathione appears to occur over the muscle either at rest, during exercise or in recovery. Moreover, when an exhaustive exercise bout is repeated with lowered glycogen levels, the level of oxidative stress is not different than that of the first bout.     

Skeletal muscle phosphocreatine recovery in exercise-trained humans is dependent on O2 availability.

In skeletal muscle, phosphocreatine (PCr) recovery from submaximal exercise has become a reliable and accepted measure of muscle oxidative capacity. During exercise, O2 availability plays a role in determining maximal oxidative metabolism, but the relationship between O2 availability and oxidative metabolism measured by 31P-magnetic resonance spectroscopy (MRS) during recovery from exercise has never been studied. We used 31P-MRS to study exercising human gastrocnemius muscle under conditions of varied fractions of inspired O2 (FIO2) to test the hypothesis that varied O2 availability modulates PCr recovery from submaximal exercise. Six male subjects performed three bouts of 5-min steady-state submaximal plantar flexion exercise followed by 5 min of recovery in a 1.5-T magnet while breathing three different FIO2 concentrations (0.10, 0. 21, and 1.00). Under each FIO2 treatment, the PCr recovery time constants were significantly different, being longer in hypoxia [33. 5 +/- 4.1 s (SE)] and shorter in hyperoxia (20.0 +/- 1.8 s) than in normoxia (25.0 +/- 2.7 s) (P 相似文献   

Blood flow and muscle oxygen uptake at the onset and end of moderate and heavy dynamic forearm exercise

We hypothesized that forearm blood flow (FBF) during moderate intensity dynamic exercise would meet the demands of the exercise and that postexercise FBF would quickly recover. In contrast, during heavy exercise, FBF would be inadequate causing a marked postexercise hyperemia and sustained increase in muscle oxygen uptake (VO(2musc)). Six subjects did forearm exercise (1-s contraction/relaxation, 1-s pause) for 5 min at 25 and 75% of peak workload. FBF was determined by Doppler ultrasound, and O(2) extraction was estimated from venous blood samples. In moderate exercise, FBF and VO(2musc) increased within 2 min to steady state. Rapid recovery to baseline suggested adequate O(2) supply during moderate exercise. In contrast, FBF was not adequate during heavy dynamic exercise. Immediately postexercise, there was an approximately 50% increase in FBF. Furthermore, we observed for the first time in the recovery period an increase in VO(2musc) above end-exercise values. During moderate exercise, O(2) supply met requirements, but with heavy forearm exercise, inadequate O(2) supply during exercise caused accumulation of a large O(2) deficit that was repaid during recovery.     

Retention of intravenously infused [13C]bicarbonate is transiently increased during recovery from hard exercise.

The effects of exercise on energy substrate metabolism persist into the postexercise recovery period. We sought to derive bicarbonate retention factors (k) to correct for carbon tracer oxidized, but retained from pulmonary excretion before, during, and after exercise. Ten men and nine women received a primed-continuous infusion of [(13)C]bicarbonate (sodium salt) under three different conditions: 1) before, during, and 3 h after 90 min of exercise at 45% peak oxygen consumption (Vo(2peak)); 2) before, during, and 3 h after 60 min of exercise at 65% Vo(2peak); and 3) during a time-matched resting control trial, with breath samples collected for determination of (13)CO(2) excretion rates. Throughout the resting control trial, k was stable and averaged 0.83 in men and women. During exercise, average k in men was 0.93 at 45% Vo(2peak) and 0.94 at 65% Vo(2peak), and in women k was 0.91 at 45% Vo(2peak) and 0.92 at 65% Vo(2peak), with no significant differences between intensities or sexes. After exercise at 45% Vo(2peak), k returned rapidly to control values in men and women, but following exercise at 65% Vo(2peak), k was significantly less than control at 30 and 60 min postexercise in men (0.74 and 0.72, respectively, P < 0.05) and women (0.75 and 0.76, respectively, P < 0.05) with no significant postexercise differences between men and women. We conclude that bicarbonate/CO(2) retention is transiently increased in men and women for the first hour of postexercise recovery following endurance exercise bouts of hard but not moderate intensity.