Dot VO Research Articles

The Aetiology of Reduced Cardiorespiratory Fitness Among Adults with Severe Traumatic Brain Injury and the Relationship with Physical Activity: A Narrative Review

Reduced cardiorespiratory fitness or cardiorespiratory deconditioning is a secondary physical impairment commonly reported to affect people after traumatic brain injury (TBI), both in the short- and long-term. Eleven studies have measured peak oxygen uptake${\rm ({\dot V}O}_{{\rm 2peak}} )$to evaluate fitness in this population. The mean (SD)${\rm \dot VO}_{{\rm 2peak}}$from these studies was 27.2 (6.7) mL.kg−1·min−1, which is markedly below the average fitness level of age-matched healthy individuals. The aetiology of cardiorespiratory deconditioning has not been well evaluated among people with TBI; however, studies on prolonged bed rest and studies on the acute consequences of TBI inform our current understanding. The primary aim of this paper is to present a model to describe the physiological factors contributing to the development of cardiorespiratory deconditioning among people with severe TBI. We propose that both central and peripheral factors contribute to reduced fitness, and that these changes occur because of both the initial brain damage and trauma sustained and the prolonged and initially extreme physical inactivity that is commonly experienced after this type of injury. Reduced fitness can significantly affect the ability to return to pre-injury activities. Given that reintegration into the community is a key goal of rehabilitation among people with TBI, interventions that can prevent or reverse reduced fitness need to be implemented.

Cardiovascular and metabolic responses at rest and to exercise during 48 hours of head-out immersion: a case report

Head-out immersion in water (HIW) leads to several cardiovascular adjustments. Cardiac output increases by increasing stroke volume with no substantial changes in heart rate (HR) at rest. Therefore, total peripheral resistance to blood flow declines, leading to elevated O2 delivery. During exercise, cardiac output increases for a given workload while the HR response differs in relation to exercise intensity: it does not change during moderate exercise, but decreases during intense exercise. Oxygen uptake does not change either at rest or during exercise. In this case report, we report data on the cardiovascular and metabolic responses in a 29-year-old man at rest and during constant-load exercise during 48 h of HIW. The subject performed constant-load exercise on cycloergometer at 50% VO2max in the laboratory and during 48 h of HIW. Pulmonary gas exchange, VO2 kinetics, HR and rate of perceived exertion were determined. At rest, HR was similar but \(\dot VO_2 \) increased during HIW relative to the laboratory. During exercise, the metabolic cost of exercise was similar and HR was the same during HIW and in the laboratory. \(\dot VO_2 \) kinetics were faster during HIW. The cardiovascular and metabolic responses at rest and during moderate exercise to a few hours of HIW are not different from those during 48 h of HIW.

Maximal oxygen consumption and energy cost of running after a long-lasting running race: the 100 km of Sahara

The purpose of this study was to investigate the effects of a 120 km desert running race (5 stages over 4 days) on the main physiologic parameters related to the individual aerobic work capacity. Incremental treadmill tests were carried out on 7 recreational long-distance runners (age: 50.4±11.8 years; body mass: 76.0±8.5 kg; mean±SD) before and 3–5 days after the competition. Maximal oxygen consumption (\( \dot VO_{2max} \)), ventilatory threshold and heart rate were obtained by standard methods; the mean energy cost of running (Cr) above resting was calculated during the same protocol from the slope of the oxygen consumption versus running speed. After the race, the subjects exhibited significant (p<0.05) reductions only in \( \dot VO_{2max} \) (averaging 7%; from 46.7±5.1 to 43.2±4.4 ml · kg−1 · mm−1) and in maximal heart rate (averaging 3%; from 172.4±14.1 to 166.7±14.5 beats · min−1). Knowledge of Cr (3.78±0.31 J · kg−1 · m−1 and 3.74±0.48 J · kg−1 · m−1, before and after the race respectively) allowed us to estimate the overall daily energy requirement, about 20 850 kJ. \( \dot VO_{2max} \) and the maximal heart rate seem to be the main variables affected by prolonged strenuous runs followed by insufficient rest periods.

The VCO2/VO2 relationship during heavy, constant work rate exercise reflects the rate of lactic acid accumulation.

Oxygen uptake (VO2) kinetics have been reported to be modified when lactic acid accumulates; however little attention has been given to the simultaneous carbon dioxide production (VCO2) kinetics. To demonstrate how VCO2 changes as a function of VO2 when lactic acid is buffered by bicarbonate, eight healthy subjects performed 6-min constant work rate cycle ergometer exercise tests at moderate, heavy and very heavy exercise intensities. VCO2 and VO2 were measured breath-by-breath, and arterial blood samples were obtained every 7.5 s during the first 3 min of exercise, and were analyzed for pH, partial pressure of carbon dioxide, standard bicarbonate, and lactate. VCO2 abruptly increased relative to VO2 between 40 and 50 s after the start of exercise for the high exercise intensities. These gas exchange events were observed to correlate well with the time and VO2 at which lactic acid increased and plasma bicarbonate decreased (r = 0.90, r = 0.95, respectively). We conclude that bicarbonate buffering of lactic acid can be determined from the acceleration of VCO2 relative to VO2 kinetics in response to constant work rate exercise and the increase is quantitatively related to the magnitude of the lactic acid increase. This is easily visualized from a plot of VCO2 as a function of VO2.

Comparison of a modified Fick method with thermodilution for determining cardiac output in critically ill patients on mechanical ventilation

We compared a modified Fick method for measuring cardiac output against the thermodilution method in 11 critically-ill patients on mechanical ventilation. Oxygen consumption (VO2) was calculated indirectly, by measuring the carbon dioxide elimination (VCO2) during steady state and by assuming an average respiratory quotient of 0.9. For a total of 129 measurements, the mean difference in cardiac output between both methods was 0.03 +/- 1.3 l/min (95% confidence interval, -0.19 to 0.25 l/min, p = 0.7) standard deviation, with the largest differences being measured in the low cardiac output range (less than 5 l/min). No statistically significant difference was found between the cardiac output values obtained with either method. These data showed a good correlation between the two methods and suggest that the modified Fick method may be useful in determining cardiac output in seriously ill patients on mechanical ventilation not requiring pulmonary arterial catheterisation, or where facilities for undertaking metabolic measurements are not available.

Effect of ?-adrenergic blockade on $$\left( {\dot VO_2 } \right)$$ kinetics during pseudorandom binary sequence exercise

The effect of β-adrenergic blockade on the dynamic response characteristics of oxygen uptake\(\left( {\dot VO_2 } \right)\) was examined in seven healthy men. Cycle ergometer exercise consisted of a pseudorandom binary sequence (PRBS) with 15 units per sequence, each unit lasting 15 s, for a total period of 225 s. Work rate was either 25 W or 125 W. Six identical sequences were performed continuously in a single exercise test. Each subject was studied on three occasions after 48 h treatment of placebo (CON); a nonselective β-blocker, propranolol (PROP); and a β1-selective blocker, metoprolol (MET).\(\dot V_{O_2 } \) was measured breath-by-breath. The data were analyzed in the frequency domain by Fourier analysis to yield amplitude and phase shift coefficients for the relationship between the input work rate and output\(\dot V_{O_2 } \). Time domain analysis was performed on the cross-correlational analysis of\(\dot V_{O_2 } \) (output) · work rate (input) to determine the total lag time. The amplitude of the\(\dot V_{O_2 } \) · W−1 relationship was lower (P<0.0022) and the phase shift was greater (P<0.0039) with β-blockade compared to CON; no differences were found between PROP and MET. The total lag time was longer (P<0.0053) in PROP (34.3±2.2s) and MET (34.4±1.6s) compared to CON (29.8±1.3s). These data indicate that β-adrenergic blockade causes a significant slowing of kinetics of the O2 transport system as determined by both frequency and time domain analysis. In addition, the PRBS exercise test is a sensitive indicator of change in function of the O2 transport system.

Acclimation effects on routine oxygen consumption of the Antarctic fish Pogonophryne scotti (Artedidraconidae)

Routine oyxgen consumption ( $$\dot VO_2$$ ) of the artedidraconid fish Pogonophryne scotti at-1°C is determined using a flow-through respirometer. The metabolic rate during an 8 to 12 h acclimation period is found to exceed the actual routine metabolic level by a factor of 2 to 4. $$\dot VO_2$$ of 7 P. scotti varies between 2.5 mg/h and 4.4 mg/h for fish weighing 58 g to 210 g. The exponent of the oxygen consumption/weight equation is 0.46. From this relation, routine $$\dot VO_2$$ of a 100 g fish is calculated as 2.9 mg/h. The significance of acclimation times and the use of standardized methods for future respiration measurements of Antarctic fish are discussed.

Breath-by-breath measurement of alveolar gas exchange with a slow-response gas analyser.

The O2-paramagnetic or polarographic and CO2-infra-red expired gas analyser have a response delay which results in an underestimation in breath-by-breath $$\dot vO_2 $$ and $$\dot vCO_2 $$ calculations. In this study, correction for this delay has been made. After measuring the step response of the O2-polarographic and CO2-infra-red analyser, the damping factor and the natural angular frequency were determined as well as the time constant, assuming the response was a first-order one. $$\dot vO_2 $$ and $$\dot vCO_2 $$ were calculated when the response of the analyser was corrected for the first- and second-order responses using the inverse Laplace transform. For the uncorrected $$\dot vO_2 $$ and $$\dot vCO_2 $$ , values from the breath-by-breath method were 27·5 and 18·1 per cent systematically underestimated (p<0·001) compared with those of the Douglas bag method. When correction for the first-order response was made, values of the breath-by-breath method became equivalent to those of the Douglas bag method for $$\dot vCO_2 $$ whereas there was still a 17·5 per cent systematic underestimation (p<0·001) for $$\dot vO_2 $$ . The correction for the second-order response gave equivalence and significant correlation (p<0·001) between the values of both methods for $$\dot vO_2 $$ and $$\dot vCO_2 $$ . These results might indicate that breath-by-breath measurement of alveolar gas exchange with a slow-response gas analyser is valid when a second-order response delay correction is used.

Mass spectrometer system for long-term continuous measurements of v.O2 and v.CO2 during artificial ventilation.

A system for online measurement of respiratory gas exchange in patients undergoing artificial ventilation is described. Expired flow is measured either by a continuous tracer gas injection or by a pneumotachometer. Both systems have a similar degree of accuracy when compared with a reference method (the Douglas bag method). Validation of the whole system by the burning of methanol with a known respiratory quotient is performed. The accuracy of the measurements is within 1·6 per cent. The major problem is that physiological signals recorded from a ventilated patient contain artefacts which may lead to erroneous computations. An algorithm is developed to identify and disregard artefacted signals or an unsteady state of the patient. The technique used for data processing allows reliable continuous measurement of respiratory gas exchange for periods up to 24 h without interfering with the nursing or the ventilatory management.

Gut and whole body O2 deficit during and excess uptake after hypoxia.

Adams and Cain (1983) found that non-muscle regions of the body decreased their share of excess post-hypoxic oxygen uptake (\(\dot VO\)O2) with longer periods of hypoxia. They suggested that part of non-muscle \(\dot VO\)O2 was not obligated for energy production. Mortillaro and Granger (1977) showed that intestine followed a similar pattern of excess \(\dot VO\)O2 when arterial occlusion created an O2 deficit. Shepherd (1978) showed that an arterial PO2 of 46 Torr decreased intestinal \(\dot VO\)O2 26% but, in contrast, hindlimb \(\dot VO\)O2 was unaffected by an arterial PO2 of 36 Torr (Cain & Chapler, 1979) while, at the same time, whole body \(\dot VO\)O2 was decreased approximately 12%. These data, and the fact that gut \(\dot VO\)O2 is 20–25% that of whole body, even though intestine accounts for <5% of body weight, implicated gut as a bigger contributor of O2 excess used in recovery. Since Shepherd (1978) did not measure \(\dot VO\)O2 during recovery and Mortillaro and Granger (1977) did not use hypoxia, there was no information on the intestinal O2 deficit/excess relationship during and after hypoxia. In addition, its contribution to whole body O2 deficit/excess remained in question. Thus, the purposes of these experiments were to 1) measure the gut O2 deficit/excess relationship during acute hypoxic hypoxia, 2) determine the contribution of gut in whole body O2 deficit and excess and 3) ascertain the means by which intestine copes with acute bouts of hypoxic hypoxia.

Cognitive performance during successive sustained physical work episodes

The effects of physical work (30% of $$\dot VO_2 $$ max), sleep loss (3-h nap during a 48-h operation), continuous work (CW), and time of day on cognitive performance were assessed (by ANOVA) in this repeated-measures study comparing two groups (exercise/nonexercise) of healthy young men (N=22). Treadmill walking did not accentuate or attenuate sleep loss effects on performance; however, sleep loss alone did degrade visual vigilance and memory for words. Time-of-day fluctuations were found in choice reaction time, logical reasoning, and word memory. Visual vigilance for nonexercising subjects degraded sooner on the 2nd CW day than it did for exercising subjects. A 3-h nap at 0400 h after 1 17-h CW day was not immediately recuperative. These findings indicate that exercise at 30% of $$\dot VO_2 $$ max does not compound sleep-loss effects in cognitive performance. Indeed, physical activity during video terminal monitoring may delay any sleep-loss decrement. Variability of many cognitive abilities throughout the day appeared to show a greater effect than the sleep-loss and exercise effects over 2 days.

Effects of pressure on oxygen consumption in cottid fish from Lake Baikal

Rates of oxygen consumption in shallow dwelling cottid fish from Lake Baikal were unaffected by a change in pressure from 11 to 51 ata. The metabolic rate of deep cottids decreased by 72% when the pressure was decreased by 50% from that corresponding to habitat depth. Recovery from decreased pressures was incomplete in deep fish, suggesting that measurements of $$\dot VO_2 $$ in deep dwelling fish in the literature may underestimate actual rates.

Oxygen consumption inNeomysis americana (Crustacea: Mysidacea), and the effects of naphthalene exposure

Oxygen uptake (\(\dot VO{_2}\)) of individual mysids was measured in a novel continuous flow respirometer for 24-h periods, and in a sealed chamber respirometer for several hours. Mysids were acclimated 30–100d under conditions which allowed complete life-cycle cultivation.\(\dot VO{_2}\) was normalized for mysid size using an unconventional linear regression: log (\(\dot VO{_2}\)) vs log (body water). Compared to the conventional regression, log (\(\dot VO{_2}\)) vs log (body mass), the new approach showed two advantages: significantly greater coefficient of determination,r2, and removal of differences in\(\dot VO{_2}\) between sexes. Minimum rates of oxygen uptake measured in the continuous flow respirometer were lower than sealed chamber measurements, and may more accurately reflect standard metabolic rate. Hourly data also showed a daily cycle when adjusted to represent a standard size mysid. Exposure to ca 1.1 mg l-1 naphthalene increased\(\dot VO{_2}\) and the range of spontaneous\(\dot VO{_2}\) shown by the mysids; exposure to ca 0.1 mgl-1 naphthalene depressed the range of\(\dot VO{_2}\). Both exposures caused aberrations in the daily cycle.

Adipocyte diameter and lipolytic activity in marathon runners: Relationship with body fatness

Fifteen highly trained marathon runners gave their consent to participate in a study designed to investigate the effects of exercise-training on adipose tissue morphology and metabolism. They were submitted to an adipose tissue biopsy in the suprailiac region and their results were compared with an age and weight matched control group. As expected, runners were characterized by a lower percent body fat. They also had a significantly smaller mean fat cell diameter. Moreover, runners had significantly higher basal, epineprine sub-maximal, and epinephrine maximal stimulated lipolysis than controls. \(\dot VO_2\) max and body fatness were significantly correlated to adipocytes lipolysis. However, when seven runners were paired for mean fat cell diameter and percent body fat with seven sedentary control subjects, no differences in lipolytic activities were observed. These results indicate that high adipose tissue lipolytic activity is associated with low percent body fat in highly trained endurance runners.

Hemodynamic responses of runners and water polo players during exertion in water

Six trained water polo swimmers and five trained runners exercised on a modified bicycle ergometer for 30 min at 60% \(\dot VO_2\) max while immersed to the neck in 20, 25, 30, and 35‡ C water. Metabolic rates in both groups were found to be independent of water temperature, averaging 33.9±2.7 ml·kg−1·min−1. Cardiac output averaged 16.4±1.2 l·min−1 for the runners and 17.6±1.6 l·min−1 for the swimmers and was found to be independent of water temperature or time. Runners were able to maintain stroke volume throughout the duration of the exercise at 30 and 35‡ C, while swimmers' stroke volumes declined significantly by 9.2 and 11.5% respectively, in these environments. Swimmers exercising in 20‡ C water maintained their stroke volume while the stroke volume of the runners declined significantly by 10.5% after the initial 10 min of exercise. The heart rates of the swimmers were consistently higher than the runners in all water temperatures. Percent changes in plasma volume were greater in the runners, with both groups following a parabolic response curve, the greatest efflux occurring in cold water. These results indicate that although cardiac output was similar for trained swimmers and runners during immersion exercise, differences in heart rate and stroke volume existed and were related to the duration of exercise and the temperature of the water. The mediums in which these athletes train may explain these differences in response.

The time course of ammonia and lactate accumulation in blood during bicycle exercise

The time course of venous blood ammonia and lactate formation has been investigated on 5 separate occasions in each of two subjects. Blood was sampled from a free flowing catheter for every 30 s during a ramp bicycle test to exhaustion. In each subject blood ammonia was rapidly elevated even at work rates as low as 40–50% of \(\dot VO_2\) max. On cessation of exercise blood concentrations fell rapidly. Lactate concentration in blood on the other hand was more slowly elevated during the test and continued to rise in the usual fashion after the completion of the work. It is suggested that ammonia may be a primary toxin during exhaustive exercise inducing changes, which ultimately become incapacitating, in essential metabolic functions.

Effects of DL-propranolol on exercise heart rate and maximal rates of oxygen consumption inScaphiopus intermontanus

Lymphatic injection of propranolol (0.2–10 μg) into toads decreased exercise heart rate in a dose-dependent manner. There was a significant linear corrleation between exercise heart rate and maximal oxygen consumption rates $$(\dot VO_2 \max )$$ . These data are consistent with the hypothesis that blood oxygen transport is the limiting process for $$\dot VO_2 $$ max in anuran amphibians.

VO2 peak during free swimming using the backward extrapolation of the O2 recovery curve.

The purpose of this study was to evaluate the accuracy and feasibility of estimating oxygen consumption (VO2) during maximal swimming by using the backward extrapolation (BE) of the VO2 recovery curve to time zero. Two series of experiments were conducted. In the first, the validity of the BE method was ascertained by comparing the VO2 peak values obtained during free swimming (Douglas bag technique) with those estimated by the BE method during recovery after the same tests. These results were also compared with VO2 peak measured during uphill treadmill running. VO2 peak measured during maximal free swimming and estimated by the BE method during the recovery period of that test, were not significantly different. No significant difference was found between VO2 peak uphill treadmill running and free swimming. In the second series of experiments, VO2 peak was measured in each of 28 swimmers during uphill running (conventional method) and during unimpeded swimming using the BE method. The mean value was significantly higher during swimming (mean = 3.37) than during running (mean = 3.23). Seventy-five percent of the subjects had higher VO2 peak during swimming. The swimming speed during maximal swimming effort was 10% higher when the BE method was used then when the same subjects were tested by the conventional Douglas bag technique. The BE method is reliable and valid way to measure VO2 peak in maximal swimming and allows the swimmer to use his specifically trained musculature fully.

A critical look at currently used indirect indices of myocardial oxygen consumption.

Myocardial oxygen consumption indices that are frequently applied to man such as tension-time index (TTI), pressure-rate product (P·HR) and triple product (TP) have not been fully validated so far. These easily obtainable indices and a modified TTI\((\overline P \cdot \sqrt {HR} )\), therefore, were examined in 10 closed-chest dogs with very broad variations of hemodynamics and oxygen consumption (3–36 ml/min·100 g) analyzing 162 steady states. Myocardial blood flow was directly measured by a differential pressure coronary sinus catheter.\(M\dot VO_2 \) was varied by administration of catecholamines and other inotropic drugs, atropine, beta-blocking agents and hypo- and hypervolemia. Over a wide range of hemodynamic states, correlations with directly measured\(M\dot VO_2 \) of TTI (r=0.63), P·HR (r=0.87), TP (r=0.65) and\(\overline P \cdot \sqrt {HR} \) (r=0.80) are not satisfactory due to neglect of contractility and cardiac volumes by these terms. Better correlations are obtained when relating these indices to\(M\dot VO_2 \) under different inotropic states. At normal and moderately increased contractility, correlations with\(M\dot VO_2 \) rose as follows: TTI (r=0.96), P·HR (r=0.91), TP (r=0.96) and\(\overline P \cdot \sqrt {HR} \) (r=0.94). Significant rises in correlation are due to the close relationship between peak pressure and dP/dtmax at only moderately increased contraction velocity. Correlation differences within this inotropic range must be related to incorporation or neglect of ejection time as a partial determinant of\(M\dot VO_2 \). At markedly increased contractility, results for these indices, however, are in part very poor: TTI (r=0.40), P·HR (r=0.81), TP (r=0.38) and\(\overline P \cdot \sqrt {HR} \) (r=0.76). Within this inotropic state neglect of dP/dtmax as a major determinant of\(M\dot VO_2 \) and the inverse relationship between ejection time and dP/dtmax mainly account for these correlation shifts. It is concluded that non-invasively obtainable indices, currently in use, are no reliable predictors of actual overall\(M\dot VO_2 \) of the left ventricle if the contractile state of the myocardium is not checked invasively before. The broad variability of the relation of the energy demand of velocity of tension development to maintenance of systolic wall tension is not sufficiently considered by these terms. Appropriate caution, therefore, is necessary when applying those indirect indices of\(M\dot VO_2 \) to humans.

Body temperature and heart rate relationships during submaximal bicycle ergometer exercises.

Twenty-three male subjects performed submaximal exercise at approximately 80%\(\dot VO_2\) max on a bicycle ergometer. Rectal temperature, skin temperatures, and heart rate measurements were taken during the exercise and during the corresponding recovery periods.