Predicting rate of oxygen consumption from heart rate while little penguins work, rest and play.

The relationship between heart rate (f(H)) and rate of oxygen consumption (V(.)O2) was investigated under changing conditions of ambient temperature, digestive state and exercise state in the little penguin (Eudyptula minor). Both f(H) and V(.)O2 were recorded simultaneously from 12 little penguins while they each (a) rested and exercised within their reported thermo-neutral zone (TNZ), (b) rested and exercised below their reported TNZ and (c) digested a meal of sardines within their reported TNZ. Contrary to our expectations, we found that minimum V(.)O2 did not vary between the two temperatures used. Comparison with values from the literature suggests that both minimum V(.)O2 and the extent of the TNZ in this species may vary along a latitudinal gradient. Furthermore, while minimum V(.)O2 was unchanged at the lower temperature, minimum f(H) was significantly higher, suggesting a hitherto undescribed cardiac response to lowered ambient temperature in an avian species. This response was maintained when the penguins exercised within and below their apparent TNZ as f(H) was significantly greater in cold conditions for a given level of V(.)O2. Furthermore, both f(H) and V(.)O2 were slightly but significantly elevated for a given walking speed during exercise at the lower temperature. This suggests that the penguins may have been close to their TNZ and that the measures employed to counteract heat loss while at rest may have been compromised during exercise. There was no significant difference in the relationship between f(H) and V(.)O2 while the penguins were inactive ina post-digestive state or inactive and digesting a meal within their TNZ, though both of these relationships were significantly different from that during exercise. This suggests that while digestion has no effect on the f(H)/V(.)O2 relationship, for little penguins at least, it is of little value in deriving a predictive relationship for application to active free-ranging animals.     

Predicting rate of oxygen consumption from heart rate while little penguins work, rest and play

The relationship between heart rate (f(H)) and rate of oxygen consumption (V(.)O2) was investigated under changing conditions of ambient temperature, digestive state and exercise state in the little penguin (Eudyptula minor). Both f(H) and V(.)O2 were recorded simultaneously from 12 little penguins while they each (a) rested and exercised within their reported thermo-neutral zone (TNZ), (b) rested and exercised below their reported TNZ and (c) digested a meal of sardines within their reported TNZ. Contrary to our expectations, we found that minimum V(.)O2 did not vary between the two temperatures used. Comparison with values from the literature suggests that both minimum V(.)O2 and the extent of the TNZ in this species may vary along a latitudinal gradient. Furthermore, while minimum V(.)O2 was unchanged at the lower temperature, minimum f(H) was significantly higher, suggesting a hitherto undescribed cardiac response to lowered ambient temperature in an avian species. This response was maintained when the penguins exercised within and below their apparent TNZ as f(H) was significantly greater in cold conditions for a given level of V(.)O2. Furthermore, both f(H) and V(.)O2 were slightly but significantly elevated for a given walking speed during exercise at the lower temperature. This suggests that the penguins may have been close to their TNZ and that the measures employed to counteract heat loss while at rest may have been compromised during exercise. There was no significant difference in the relationship between f(H) and V(.)O2 while the penguins were inactive ina post-digestive state or inactive and digesting a meal within their TNZ, though both of these relationships were significantly different from that during exercise. This suggests that while digestion has no effect on the f(H)/V(.)O2 relationship, for little penguins at least, it is of little value in deriving a predictive relationship for application to active free-ranging animals.     

Long-term fasting decreases mitochondrial avian UCP-mediated oxygen consumption in hypometabolic king penguins

In endotherms, regulation of the degree of mitochondrial coupling affects cell metabolic efficiency. Thus it may be a key contributor to minimizing metabolic rate during long periods of fasting. The aim of the present study was to investigate whether variation in mitochondrial avian uncoupling proteins (avUCP), as putative regulators of mitochondrial oxidative phosphorylation, may contribute to the ability of king penguins (Aptenodytes patagonicus) to withstand fasting for several weeks. After 20 days of fasting, king penguins showed a reduced rate of whole animal oxygen consumption (Vo2; -33%) at rest, together with a reduced abundance of avUCP and peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC1-alpha) mRNA in pectoralis muscle (-54%, -36%, respectively). These parameters were restored after the birds had been refed for 3 days. Furthermore, in recently fed, but not in fasted penguins, isolated muscle mitochondria showed a guanosine diphosphate-inhibited, fatty acid plus superoxide-activated respiration, indicating the presence of a functional UCP. It was calculated that variation in mitochondrial UCP-dependent respiration in vitro may contribute to nearly 20% of the difference in resting Vo2 between fed or refed penguins and fasted penguins measured in vivo. These results suggest that the lowering of avUCP activity during periods of long-term energetic restriction may contribute to the reduction in metabolic rate and hence the ability of king penguins to face prolonged periods of fasting.     

Metabolism and thermoregulation during fasting in king penguins, Aptenodytes patagonicus, in air and water

We measured oxygen consumption rate (Vo(2)) and body temperatures in 10 king penguins in air and water. Vo(2) was measured during rest and at submaximal and maximal exercise before (fed) and after (fasted) an average fasting duration of 14.4 +/- 2.3 days (mean +/- 1 SD, range 10-19 days) in air and water. Concurrently, we measured subcutaneous temperature and temperature of the upper (heart and liver), middle (stomach) and lower (intestine) abdomen. The mean body mass (M(b)) was 13.8 +/- 1.2 kg in fed and 11.0 +/- 0.6 kg in fasted birds. After fasting, resting Vo(2) was 93% higher in water than in air (air: 86.9 +/- 8.8 ml/min; water: 167.3 +/- 36.7 ml/min, P < 0.01), while there was no difference in resting Vo(2) between air and water in fed animals (air: 117.1 +/- 20.0 ml O(2)/min; water: 114.8 +/- 32.7 ml O(2)/min, P > 0.6). In air, Vo(2) decreased with M(b), while it increased with M(b) in water. Body temperature did not change with fasting in air, whereas in water, there were complex changes in the peripheral body temperatures. These latter changes may, therefore, be indicative of a loss in body insulation and of variations in peripheral perfusion. Four animals were given a single meal after fasting and the temperature changes were partly reversed 24 h after refeeding in all body regions except the subcutaneous, indicating a rapid reversal to a prefasting state where body heat loss is minimal. The data emphasize the importance in considering nutritional status when studying king penguins and that the fasting-related physiological changes diverge in air and water.     

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

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

Behavioral and physiological significance of minimum resting metabolic rate in king penguins

Because fasting king penguins (Aptenodytes patagonicus) need to conserve energy, it is possible that they exhibit particularly low metabolic rates during periods of rest. We investigated the behavioral and physiological aspects of periods of minimum metabolic rate in king penguins under different circumstances. Heart rate (f(H)) measurements were recorded to estimate rate of oxygen consumption during periods of rest. Furthermore, apparent respiratory sinus arrhythmia (RSA) was calculated from the f(H) data to determine probable breathing frequency in resting penguins. The most pertinent results were that minimum f(H) achieved (over 5 min) was higher during respirometry experiments in air than during periods ashore in the field; that minimum f(H) during respirometry experiments on water was similar to that while at sea; and that RSA was apparent in many of the f(H) traces during periods of minimum f(H) and provides accurate estimates of breathing rates of king penguins resting in specific situations in the field. Inferences made from the results include that king penguins do not have the capacity to reduce their metabolism to a particularly low level on land; that they can, however, achieve surprisingly low metabolic rates at sea while resting in cold water; and that during respirometry experiments king penguins are stressed to some degree, exhibiting an elevated metabolism even when resting.     

How accurately can we estimate energetic costs in a marine top predator,the king penguin?

King penguins (Aptenodytes patagonicus) are one of the greatest consumers of marine resources. However, while their influence on the marine ecosystem is likely to be significant, only an accurate knowledge of their energy demands will indicate their true food requirements. Energy consumption has been estimated for many marine species using the heart rate-rate of oxygen consumption (f(H) - V(O2)) technique, and the technique has been applied successfully to answer eco-physiological questions. However, previous studies on the energetics of king penguins, based on developing or applying this technique, have raised a number of issues about the degree of validity of the technique for this species. These include the predictive validity of the present f(H) - V(O2) equations across different seasons and individuals and during different modes of locomotion. In many cases, these issues also apply to other species for which the f(H) - V(O2) technique has been applied. In the present study, the accuracy of three prediction equations for king penguins was investigated based on validity studies and on estimates of V(O2) from published, field f(H) data. The major conclusions from the present study are: (1) in contrast to that for walking, the f(H) - V(O2) relationship for swimming king penguins is not affected by body mass; (2) prediction equation (1), log(V(O2) = -0.279 + 1.24log(f(H) + 0.0237t - 0.0157log(f(H)t, derived in a previous study, is the most suitable equation presently available for estimating V(O2) in king penguins for all locomotory and nutritional states. A number of possible problems associated with producing an f(H) - V(O2) relationship are discussed in the present study. Finally, a statistical method to include easy-to-measure morphometric characteristics, which may improve the accuracy of f(H) - V(O2) prediction equations, is explained.     

Improving the precision and accuracy for estimating energy expenditure using the heart rate method

The "heart rate technique" is commonly used to estimate the rate of oxygen consumption (a proxy for energy expenditure) of free-ranging animals. However, a major limitation of this technique is that interindividual variability in the relationship between heart rate (f(H)) and rate of oxygen consumption (Vo2) generates large errors of estimation when the technique is applied to individual free-ranging animals. In this study, we present a new analysis technique that takes advantage of the observation that the f(H) or Vo2 relationships between individuals are frequently parallel and differ only in elevation. This technique offers superior accuracy and precision of Vo2 estimates, reducing the coefficient of variability from 18% to 9% for individual animals in an example application in macaroni penguins. This approach enables application of the heart rate technique to deduce the energetic strategies of individual animals.     

Menstrual cycle phase and oral contraceptive effects on triglyceride mobilization during exercise.

We examined the effects of menstrual cycle phase and oral contraceptive (OC) use on triglyceride mobilization during 90 min of rest and 60 min of leg ergometry exercise at 45 and 65% peak O(2) uptake (Vo(2 peak)) in eight moderately physically active, eumenorrheic women (24.8 +/- 1.2 yr). Subjects were tested during the follicular phase (FP) and the luteal phase (LP) before OC use and during the inactive phase (IP) and high-dose phase (HP) after 4 complete mo of OC use. Glycerol rate of appearance (R(a)), a measure of triglyceride mobilization, was determined in a 3-h postabsorptive state using a primed constant infusion of [1,1,2,3,3-(2)H]glycerol. Before OC use (BOC), there were no significant differences between FP and LP in any of the variables studied. Dietary composition, exercise patterns, plasma glycerol concentrations, growth hormone concentrations, and exercise respiratory exchange ratio did not change with OC use. However, 4 mo of OC use significantly (P < 0.05) increased glycerol R(a) in HP during exercise at 45% Vo(2 peak) (6.2 +/- 0.2, 6.5 +/- 0.4, and 7.7 +/- 1.1 micromol.kg(-1).min(-1) for BOC, IP, and HP, respectively) and in IP and HP at 65% Vo(2 peak) (6.6 +/- 0.1, 8.2 +/- 0.6, and 8.1 +/- 0.7 micromol.kg(-1).min(-1) for BOC, IP, and HP, respectively). Plasma cortisol concentrations were significantly higher with OC use at rest and during exercise at 45 and 65% Vo(2 peak). In summary, although fluctuations of endogenous ovarian steroids have little effect on triglyceride mobilization, the synthetic ovarian steroids found in OCs increase triglyceride mobilization and plasma cortisol concentrations in exercising women. We conclude that the hierarchy of effects of ovarian steroids and their analogs on triglyceride mobilization in exercising women is as follows: energy flux > OC use > recent carbohydrate nutrition, menstrual cycle effects.     

Hypoxia augments muscle sympathetic neural response to leg cycling

It was demonstrated that acute hypoxia increased muscle sympathetic nerve activity (MSNA) by using a microneurographic method at rest, but its effects on dynamic leg exercise are unclear. The purpose of this study was to clarify changes in MSNA during dynamic leg exercise in hypoxia. To estimate peak oxygen uptake (Vo(2 peak)), two maximal exercise tests were conducted using a cycle ergometer in a semirecumbent position in normoxia [inspired oxygen fraction (Fi(O(2)) = 0.209] and hypoxia (Fi(O(2)) = 0.127). The subjects performed four submaximal exercise tests; two were MSNA trials in normoxia and hypoxia, and two were hematological trials under each condition. In the submaximal exercise test, the subjects completed two 15-min exercises at 40% and 60% of their individual Vo(2 peak) in normoxia and hypoxia. During the MSNA trials, MSNA was recorded via microneurography of the right median nerve at the elbow. During the hematological trials, the subjects performed the same exercise protocol as during the MSNA trials, but venous blood samples were obtained from the antecubital vein to assess plasma norepinephrine (NE) concentrations. MSNA increased at 40% Vo(2 peak) exercise in hypoxia, but not in normoxia. Plasma NE concentrations did not increase at 40% Vo(2 peak) exercise in hypoxia. MSNA at 40% and 60% Vo(2 peak) exercise were higher in hypoxia than in normoxia. These results suggest that acute hypoxia augments muscle sympathetic neural activation during dynamic leg exercise at mild and moderate intensities. They also suggest that the MSNA response during dynamic exercise in hypoxia could be different from the change in plasma NE concentrations.     

Substantial working muscle glycerol turnover during two-legged cycle ergometry

We combined tracer and arteriovenous (a-v) balance techniques to evaluate the effects of exercise and endurance training on leg triacylglyceride turnover as assessed by glycerol exchange. Measurements on an exercising leg were taken to be a surrogate for working skeletal muscle. Eight men completed 9 wk of endurance training [5 days/wk, 1 h/day, 75% peak oxygen consumption (Vo(2peak))], with leg glycerol turnover determined during two pretraining trials [45 and 65% Vo(2peak) (45% Pre and 65% Pre, respectively)] and two posttraining trials [65% of pretraining Vo(2peak) (ABT) and 65% of posttraining Vo(2peak) (RLT)] using [(2)H(5)]glycerol infusion, femoral a-v sampling, and measurement of leg blood flow. Endurance training increased Vo(2peak) by 15% (45.2 +/- 1.2 to 52.0 +/- 1.8 mlxkg(-1)xmin(-1), P < 0.05). At rest, there was tracer-measured leg glycerol uptake (41 +/- 8 and 52 +/- 15 micromol/min for pre- and posttraining, respectively) even in the presence of small, but significant, net leg glycerol release (-68 +/- 19 and -50 +/- 13 micromol/min, respectively; P < 0.05 vs. zero). Furthermore, while there was no significant net leg glycerol exchange during any of the exercise bouts, there was substantial tracer-measured leg glycerol turnover during exercise (i.e., simultaneous leg muscle uptake and leg release) (uptake, release: 45% Pre, 194 +/- 41, 214 +/- 33; 65% Pre, 217 +/- 79, 201 +/- 84; ABT, 275 +/- 76, 312 +/- 87; RLT, 282 +/- 83, 424 +/- 75 micromol/min; all P < 0.05 vs. corresponding rest). Leg glycerol turnover was unaffected by exercise intensity or endurance training. In summary, simultaneous leg glycerol uptake and release (indicative of leg triacylglyceride turnover) occurs despite small or negligible net leg glycerol exchange, and furthermore, leg glycerol turnover can be substantially augmented during exercise.     

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

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

Acute effects of hydrogen peroxide on skeletal muscle microvascular oxygenation from rest to contractions

Reactive oxygen species, such as hydrogen peroxide (H(2)O(2)), exert a critical regulatory role on skeletal muscle function. Whether acute increases in H(2)O(2) modulate muscle microvascular O(2) delivery-utilization (Qo(2)/Vo(2)) matching [i.e., microvascular partial pressure of O(2) (Pmv(O(2)))] at rest and following the onset of contractions is unknown. The hypothesis was tested that H(2)O(2) treatment (exogenous H(2)O(2)) would enhance Pmv(O(2)) and slow Pmv(O(2)) kinetics during contractions compared with control. Anesthetized, healthy young Sprague-Dawley rats had their spinotrapezius muscles either exposed for measurement of blood flow (and therefore QO(2)), VO(2), and Pmv(O(2)), or exteriorized for measurement of force production. Electrically stimulated twitch contractions (1 Hz, ~7 V, 2-ms pulse duration, 3 min) were evoked following acute superfusion with Krebs-Henseleit (control) and H(2)O(2) (100 μM). Relative to control, H(2)O(2) treatment elicited disproportionate increases in QO(2) and VO(2) that elevated Pmv(O(2)) at rest and throughout contractions and slowed overall Pmv(O(2)) kinetics (i.e., ~85% slower mean response time; P < 0.05). Accordingly, H(2)O(2) resulted in ~33% greater overall Pmv(O(2)), as assessed by the area under the Pmv(O(2)) curve (P < 0.05). Muscle force production was not altered with H(2)O(2) treatment (P > 0.05), evidencing reduced economy during contractions (~40% decrease in the force/VO(2) relationship; P < 0.05). These findings indicate that, although increasing the driving force for blood-myocyte O(2) flux (i.e., Pmv(O(2))), transient elevations in H(2)O(2) impair skeletal muscle function (i.e., reduced economy during contractions), which mechanistically may underlie, in part, the reduced exercise tolerance in conditions associated with oxidative stress.     

Relationship between resting ventilatory chemosensitivity and maximal oxygen uptake in moderate hypobaric hypoxia.

This study tested the hypothesis that the extent of the decrement in (.)Vo(2max) and the respiratory response seen during maximal exercise in moderate hypobaric hypoxia (H; simulated 2,500 m) is affected by the hypoxia ventilatory and hypercapnia ventilatory responses (HVR and HCVR, respectively). Twenty men (5 untrained subjects, 7 long distance runners, 8 middle distance runners) performed incremental exhaustive running tests in H and normobaric normoxia (N) condition. During the running test, (.)Vo(2), pulmonary ventilation (Ve) and arterial oxyhemoglobin saturation (Sa(O(2))) were measured, and in two ventilatory response tests performed during N, a rebreathing method was used to evaluate HVR and HCVR. Mean HVR and HCVR were 0.36 +/- 0.04 and 2.11 +/- 0.2 l.min(-1).mmHg(-1), respectively. HVR correlated significantly with the percent decrements in (.)Vo(2max) (%d(.)Vo(2max)), Sa(O(2)) [%dSa(O(2)) = (N-H).N(-1).100], and (.)Ve/(.)Vo(2) seen during H condition. By contrast, HCVR did not correlate with any of the variables tested. The increment in maximal Ve between H and N significantly correlated with %d(.)Vo(2max). Our findings suggest that O(2) chemosensitivity plays a significant role in determining the level of exercise hyperventilation during moderate hypoxia; thus, a higher O(2) chemosensitivity was associated with a smaller drop in (.)Vo(2max) and Sa(O(2)) under those conditions.     

Effects of prior very-heavy intensity exercise on indices of aerobic function and high-intensity exercise tolerance.

A recent bout of high-intensity exercise can alter the balance of aerobic and anaerobic energy provision during subsequent exercise above the lactate threshold (theta(L)). However, it remains uncertain whether such "priming" influences the tolerable duration of subsequent exercise through changes in the parameters of aerobic function [e.g., theta(L), maximum oxygen uptake (Vo(2max))] and/or the hyperbolic power-duration (P-t) relationship [critical power (CP) and the curvature constant (W')]. We therefore studied six men performing cycle ergometry to the limit of tolerance; gas exchange was measured breath-by-breath and arterialized capillary blood [lactate] was measured at designated intervals. On different days, each subject completed 1) an incremental test (15 W/min) for estimation of theta(L) and measurement of the functional gain (DeltaVo(2)/DeltaWR) and Vo(2peak) and 2) four constant-load tests at different work rates (WR) for estimation of CP, W', and Vo(2max). All tests were subsequently repeated with a preceding 6-min supra-CP priming bout and an intervening 2-min 20-W recovery. The hyperbolicity of the P-t relationship was retained postpriming, with no significant difference in CP (241 +/- 39 vs. 242 +/- 36 W, post- vs. prepriming), Vo(2max) (3.97 +/- 0.34 vs. 3.93 +/- 0.38 l/min), DeltaVo(2)/DeltaWR (10.7 +/- 0.3 vs. 11.1 +/- 0.4 ml.min(-1).W(-1)), or the fundamental Vo(2) time constant (25.6 +/- 3.5 vs. 28.3 +/- 5.4 s). W' (10.61 +/- 2.07 vs. 16.13 +/- 2.33 kJ) and the tolerable duration of supra-CP exercise (-33 +/- 11%) were each significantly reduced, despite a less-prominent Vo(2) slow component. These results suggest that, following supra-CP priming, there is either a reduced depletable energy resource or a residual fatigue-metabolite level that leads to the tolerable limit before this resource is fully depleted.     

Relationship between maximal oxygen uptake and oxygenation level in inactive muscle at exhaustion in incremental exercise in humans

The aim of the present study was to determine whether the oxygenation level in an inactive muscle during an incremental exercise test, determined by near-infrared spectroscopy, influences the maximal oxygen uptake (Vo2max). The oxygenation level at the onset of incremental exercise was higher than that at rest and started to decrease at a high power output. A minimal level was observed at exhaustion during incremental exercise. Vo2 increased linearly after some delay, and the rate of increase in Vo2 was greater at a higher power output. Heart rate increased linearly after the time delay, and the rate of increase in heart rate did not change. There was a significant correlation between Vo2max and oxygenation level in inactive muscle at exhaustion (r=-0.89). We therefore concluded that the oxygenation level in inactive muscle at exhaustion during incremental exercise is associated with an individual difference in Vo2max.     

The role of exercise intensity in the bone metabolic response to an acute bout of weight-bearing exercise

We compared the effects of exercise intensity (EI) on bone metabolism during and for 4 days after acute, weight-bearing endurance exercise. Ten males [mean ± SD maximum oxygen uptake (Vo(2max)): 56.2 ± 8.1 ml·min(-1)·kg(-1)] completed three counterbalanced 8-day trials. Following three control days, on day 4, subjects completed 60 min of running at 55%, 65%, and 75% Vo(2max). Markers of bone resorption [COOH-terminal telopeptide region of collagen type 1 (β-CTX)] and formation [NH(2)-terminal propeptides of procollagen type 1 (P1NP), osteocalcin (OC), bone-alkaline phosphatase (ALP)], osteoprotegerin (OPG), parathyroid hormone (PTH), albumin-adjusted calcium (ACa), phosphate (PO(4)), and cortisol were measured during and for 3 h after exercise and on four follow-up days (FU1-FU4). At 75% Vo(2max), β-CTX was not significantly increased from baseline by exercise but was higher compared with 55% (17-19%, P < 0.01) and 65% (11-13%, P < 0.05) Vo(2max) in the first hour postexercise. Concentrations were decreased from baseline in all three groups by 39-42% (P < 0.001) at 3 h postexercise but not thereafter. P1NP increased (P < 0.001) during exercise only, while bone-ALP was increased (P < 0.01) at FU3 and FU4, but neither were affected by EI. PTH and cortisol increased (P < 0.001) with exercise at 75% Vo(2max) only and were higher (P < 0.05) than at 55% and 65% Vo(2max) during and immediately after exercise. The increases (P < 0.001) in OPG, ACa, and PO(4) with exercise were not affected by EI. Increasing EI from 55% to 75% Vo(2max) during 60 min of running resulted in higher β-CTX concentrations in the first hour postexercise but had no effect on bone formation markers. Increased bone-ALP concentrations at 3 and 4 days postexercise suggest a beneficial effect of this type of exercise on bone mineralization. The increase in OPG was not influenced by exercise intensity, whereas PTH was increased at 75% Vo(2max) only, which cannot be fully explained by changes in serum calcium or PO(4) concentrations.     

Thigh muscle activation distribution and pulmonary VO2 kinetics during moderate, heavy, and very heavy intensity cycling exercise in humans

The mechanisms underlying the oxygen uptake (Vo(2)) slow component during supra-lactate threshold (supra-LT) exercise are poorly understood. Evidence suggests that the Vo(2) slow component may be caused by progressive muscle recruitment during exercise. We therefore examined whether leg muscle activation patterns [from the transverse relaxation time (T2) of magnetic resonance images] were associated with supra-LT Vo(2) kinetic parameters. Eleven subjects performed 6-min cycle ergometry at moderate (80% LT), heavy (70% between LT and critical power; CP), and very heavy (7% above CP) intensities with breath-by-breath pulmonary Vo(2) measurement. T2 in 10 leg muscles was evaluated at rest and after 3 and 6 min of exercise. During moderate exercise, nine muscles achieved a steady-state T2 by 3 min; only in the vastus medialis did T2 increase further after 6 min. During heavy exercise, T2 in the entire vastus group increased between minutes 3 and 6, and additional increases in T2 were seen in adductor magnus and gracilis during this period of very heavy exercise. The Vo(2) slow component increased with increasing exercise intensity (being functionally zero during moderate exercise). The distribution of T2 was more diverse as supra-LT exercise progressed: T2 variance (ms) increased from 3.6 +/- 0.2 to 6.5 +/- 1.7 between 3 and 6 min of heavy exercise and from 5.5 +/- 0.8 to 12.3 +/- 5.4 in very heavy exercise (rest = 3.1 +/- 0.6). The T2 distribution was significantly correlated with the magnitude of the Vo(2) slow component (P < 0.05). These data are consistent with the notion that the Vo(2) slow component is an expression of progressive muscle recruitment during supra-LT exercise.     

Simultaneous determination of the kinetics of cardiac output, systemic O(2) delivery, and lung O(2) uptake at exercise onset in men

We tested whether the kinetics of systemic O(2) delivery (QaO(2)) at exercise start was faster than that of lung O(2) uptake (Vo(2)), being dictated by that of cardiac output (Q), and whether changes in Q would explain the postulated rapid phase of the Vo(2) increase. Simultaneous determinations of beat-by-beat (BBB) Q and QaO(2), and breath-by-breath Vo(2) at the onset of constant load exercises at 50 and 100 W were obtained on six men (age 24.2 +/- 3.2 years, maximal aerobic power 333 +/- 61 W). Vo(2) was determined using Gr?nlund's algorithm. Q was computed from BBB stroke volume (Q(st), from arterial pulse pressure profiles) and heart rate (f(h), electrocardiograpy) and calibrated against a steady-state method. This, along with the time course of hemoglobin concentration and arterial O(2) saturation (infrared oximetry) allowed computation of BBB QaO(2). The Q, QaO(2) and Vo(2) kinetics were analyzed with single and double exponential models. f(h), Q(st), Q, and Vo(2) increased upon exercise onset to reach a new steady state. The kinetics of QaO(2) had the same time constants as that of Q. The latter was twofold faster than that of Vo(2). The Vo(2) kinetics were faster than previously reported for muscle phosphocreatine decrease. Within a two-phase model, because of the Fick equation, the amplitude of phase I Q changes fully explained the phase I of Vo(2) increase. We suggest that in unsteady states, lung Vo(2) is dissociated from muscle O(2) consumption. The two components of Q and QaO(2) kinetics may reflect vagal withdrawal and sympathetic activation.     

Cardiac output and leg and arm blood flow during incremental exercise to exhaustion on the cycle ergometer.

To determine central and peripheral hemodynamic responses to upright leg cycling exercise, nine physically active men underwent measurements of arterial blood pressure and gases, as well as femoral and subclavian vein blood flows and gases during incremental exercise to exhaustion (Wmax). Cardiac output (CO) and leg blood flow (BF) increased in parallel with exercise intensity. In contrast, arm BF remained at 0.8 l/min during submaximal exercise, increasing to 1.2 +/- 0.2 l/min at maximal exercise (P < 0.05) when arm O(2) extraction reached 73 +/- 3%. The leg received a greater percentage of the CO with exercise intensity, reaching a value close to 70% at 64% of Wmax, which was maintained until exhaustion. The percentage of CO perfusing the trunk decreased with exercise intensity to 21% at Wmax, i.e., to approximately 5.5 l/min. For a given local Vo(2), leg vascular conductance (VC) was five- to sixfold higher than arm VC, despite marked hemoglobin deoxygenation in the subclavian vein. At peak exercise, arm VC was not significantly different than at rest. Leg Vo(2) represented approximately 84% of the whole body Vo(2) at intensities ranging from 38 to 100% of Wmax. Arm Vo(2) contributed between 7 and 10% to the whole body Vo(2). From 20 to 100% of Wmax, the trunk Vo(2) (including the gluteus muscles) represented between 14 and 15% of the whole body Vo(2). In summary, vasoconstrictor signals efficiently oppose the vasodilatory metabolites in the arms, suggesting that during whole body exercise in the upright position blood flow is differentially regulated in the upper and lower extremities.