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H B Rossiter

Publications and source records attributed to H B Rossiter.

18 recordsLinked to original sources
PubMed2005

A test to establish maximum O2 uptake despite no plateau in the O2 uptake response to ramp incremental exercise.

The O2 uptake (Vo2) response to ramp incremental (RI) exercise does not consistently demonstrate plateau-like behavior at the limit of tolerance, and hence the requirements for a maximum Vo2 commonly are not met, despite apparent maximum effort. We sought to determine whether an appended step exercise (SE) test at a work rate greater than that achieved in a preceding ramp test would establish the plateau criterion. Seven healthy male adults performed RI cycle ergometry (20 W/min) to the limit of tolerance, followed by 5-min recovery (20 W) and then an SE test at 105% (RISE-105) of the final work rate (WRpeak) achieved during RI. Five of these subjects also performed an RI test followed by SE at 95% WRpeak (RISE-95). Vo2 was measured breath by breath using a turbine and mass spectrometer. The average of the final 15 s of RI or SE was used to establish respective Vo2 peaks. When Vo2 peak was approached, a constant Vo2 value (e.g., a plateau) was not discernable during any RI or SE component of the tests. Although the WRpeak [mean (SD)] was higher during the SE portion [359 W (SD 31)] than during the RI portion [341 W (SD 29)] of the RISE-105, the peak Vo2 was not different [SE, 4.30 l/min (SD 0.51); RI, 4.33 l/min (SD 0.52); P=0.49; n=7]. Similarly, in the RISE-95 test, WRpeak was 310 W (SD 31) for the SE portion and 326 W (SD 32) for the RI portion, yet the peak Vo2 values were not different [SE, 4.12 l/min (SD 0.53); RI, 4.11 l/min (SD 0.48); P=0.78; n=5]. The lack of notable difference between the Vo2 peaks established at different WRpeak values in our RISE protocols provides the plateau criterion for verification of maximum Vo2 in a single test session, even when the data response profiles do not themselves evidence a plateau.

Adult↗
PubMed2005

Age is no barrier to muscle structural, biochemical and angiogenic adaptations to training up to 24 months in female rats.

Ageing is associated with reduced transport and utilization of O(2), diminishing exercise tolerance. Reductions may occur in cardiac output (delivery), and skeletal muscle oxidative capacity (utilization). To determine the reversibility of the declines in the muscular determinants of these limitations, skeletal muscle morphological, angiogenic and biochemical responses to acute exercise and endurance training were investigated in female Fischer 344 rats (n = 42; seven groups of six rats) aged 6 (Y) and 24 (O) months compared with resting untrained controls (Y(C), O(C)). Treadmill training lasted 8 weeks (10 deg incline, 1 h per day, 5 days per week). Two groups ran at maximum tolerated speeds (Y(TR), O(TR)), while an additional Y group (Y(TM)) trained at O(TR) speed. There was no effect of age on vascular endothelial growth factor gene expression in gastrocnemius muscles after acute exercise. Similarly, age did not impair the effects of training, with increases (P < 0.05; +/-s.e.m.) occurring in all of the following: 1 h exercise running speed (Y(TR) 92 +/- 4% versus O(TR) 140 +/- 25%); citrate synthase (Y(TR) 37 +/- 8% versus O(TR) 97 +/- 33%) and beta-hydroxyacyl-CoA-dehydrogenase (Y(TR) 31 +/- 7%, versus O(TR) 72 +/- 24%) activities; and capillary-to-fibre ratio (Y(TR) 5.2 +/- 0.2% versus O(TR) 8.1 +/- 0.2%). However, Y(TM) muscle was unchanged in each measure compared with Y(C). In conclusion, these muscular responses to training were (1) not reduced by ageing, but (2) dependent on relative and not absolute work rate, since, at the same speed, O(TR) rats showed greater changes than Y(TM). Therefore, increases in exercise tolerance and muscle adaptations are not impaired in female rats up to 24 months of age, and require a smaller absolute exercise stimulus (than young) to be manifest.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed2005

Prior heavy exercise eliminates VO2 slow component and reduces efficiency during submaximal exercise in humans.

We investigated the hypothesis that the pulmonary oxygen uptake (VO2) slow component is related to a progressive increase in muscle lactate concentration and that prior heavy exercise (PHE) with pronounced acidosis alters VO2 kinetics and reduces work efficiency. Subjects (n= 9) cycled at 75% of the peak VO2 (VO2peak) for 10 min before (CON) and after (AC) PHE. VO2 was measured continuously (breath-by-breath) and muscle biopsies were obtained prior to and after 3 and 10 min of exercise. Muscle lactate concentration was stable between 3 and 10 min of exercise but was 2- to 3-fold higher during AC (P < 0.05 versus CON). Acetylcarnitine (ACn) concentration was 6-fold higher prior to AC and remained higher during exercise. Phosphocreatine (PCr) concentration was similar prior to exercise but the decrease was 2-fold greater during AC than during CON. The time constant for the initial VO2 kinetics (phase II) was similar but the asymptote was 14% higher during AC. The slow increase in VO2 between 3 and 10 min of exercise during CON (+7.9 +/- 0.2%) was not correlated with muscle or blood lactate levels. PHE eliminated the slow increase in VO2 and reduced gross exercise efficiency during AC. It is concluded that the VO2 slow component cannot be explained by a progressive acidosis because both muscle and blood lactate levels remained stable during CON. We suggest that both the VO2 slow component during CON and the reduced gross efficiency during AC are related to impaired contractility of the working fibres and the necessity to recruit additional motor units. Despite a pronounced stockpiling of ACn during AC, initial VO2 kinetics were not affected by PHE and PCr concentration decreased to a lower plateau. The discrepancy with previous studies, where initial oxidative ATP generation appears to be limited by acetyl group availability, might relate to remaining fatiguing effects of PHE.

Adaptation, Physiological↗
PubMed2003

The maximally attainable VO2 during exercise in humans: the peak vs. maximum issue.

The quantification of maximum oxygen uptake (V(O2 max)), a parameter characterizing the effective integration of the neural, cardiopulmonary, and metabolic systems, requires oxygen uptake (VO2) to attain a plateau. We were interested in whether a VO2 plateau was consistently manifest during maximal incremental ramp cycle ergometry and also in ascertaining the relationship between this peak VO2 (V(O2 peak)) and that determined from one, or several, maximal constant-load tests. Ventilatory and pulmonary gas-exchange variables were measured breath by breath with a turbine and mass spectrometer. On average, V(O2 peak) [3.51 +/- 0.8 (SD) l/min] for the ramp test did not differ from that extrapolated from the linear phase of the response in 71 subjects. In 12 of these subjects, the V(O2 peak) was less than the extrapolated value by 0.1-0.4 l/min (i.e., a "plateau"), and in 19 subjects, V(O2 peak) was higher by 0.05-0.4 l/min. In the remaining 40 subjects, we could not discriminate a difference. The V(O2 peak) from the incremental test also did not differ from that of a single maximum constant-load test in 38 subjects or from the V(O2 max) in 6 subjects who undertook a range of progressively greater discontinuous constant-load tests. A plateau in the actual VO2 response is therefore not an obligatory consequence of incremental exercise. Because the peak value attained was not different from the plateau in the plot of VO2 vs. work rate (for the constant-load tests), the V(O2 peak) attained on a maximum-effort incremental test is likely to be a valid index of V(O2 max), despite no evidence of a plateau in the data themselves. However, without additional tests, one cannot be certain.

Adult↗
PubMed2003

Negative accumulated oxygen deficit during heavy and very heavy intensity cycle ergometry in humans.

The concept of the accumulated O(2) deficit (AOD) assumes that the O(2) deficit increases monotonically with increasing work rate (WR), to plateau at the maximum AOD, and is based on linear extrapolation of the relationship between measured steady-state oxygen uptake ( VO(2)) and WR for moderate exercise. However, for high WRs, the measured VO(2) increases above that expected from such linear extrapolation, reflecting the superimposition of a "slow component" on the fundamental VO(2) mono-exponential kinetics. We were therefore interested in determining the effect of the VO(2) slow component on the computed AOD. Ten subjects [31 (12) years] performed square-wave cycle ergometry of moderate (40%, 60%, 80% and 90% ), heavy (40%Delta), very heavy (80%Delta) and severe (110% VO(2)(peak)) intensities for 10-15 min, theta(L)where is the estimated lactate threshold and Delta is the WR difference between and VO(2)(peak). VO(2) was determined breath-by-breath. Projected "steady-state" VO(2) values were determined from sub- tests. The measured VO(2) exceeded the projected value after approximately 3 min for both heavy and very heavy intensity exercise. This led to the AOD actually becoming negative. Thus, for heavy exercise, while the AOD was positive [0.63 (0.41) l] at 5 min, it was negative by 10 min [-0.61 (1.05) l], and more so by 15 min [-1.70 (1.64) l]. For the very heavy WRs, the AOD was [0.42 (0.67) l] by 5 min and reached -2.68 (2.09) l at exhaustion. For severe exercise, however, the AOD at exhaustion was positive in each case: +1.69 (0.39) l. We therefore conclude that the assumptions underlying the computation of the AOD are invalid for heavy and very heavy cycle ergometry (at least). Physiological inferences, such as the "anaerobic work capacity", are therefore prone to misinterpretation.

Adult↗
PubMed2003

Effects of dichloroacetate on VO2 and intramuscular 31P metabolite kinetics during high-intensity exercise in humans.

Traditional control theories of muscle O2 consumption are based on an "inertial" feedback system operating through features of the ATP splitting (e.g., [ADP] feedback, where brackets denote concentration). More recently, however, it has been suggested that feedforward mechanisms (with respect to ATP utilization) may play an important role by controlling the rate of substrate provision to the electron transport chain. This has been achieved by activation of the pyruvate dehydrogenase complex via dichloroacetate (DCA) infusion before exercise. To investigate these suggestions, six men performed repeated, high-intensity, constant-load quadriceps exercise in the bore of an magnetic resonance spectrometer with each of prior DCA or saline control intravenous infusions. O2 uptake (Vo2) was measured breath by breath (by use of a turbine and mass spectrometer) simultaneously with intramuscular phosphocreatine (PCr) concentration ([PCr]), [Pi], [ATP], and pH (by 31P-MRS) and arterialized-venous blood sampling. DCA had no effect on the time constant (tau) of either Vo2 increase or PCr breakdown [tauVo2 45.5 +/- 7.9 vs. 44.3 +/- 8.2 s (means +/- SD; control vs. DCA); tauPCr 44.8 +/- 6.6 vs. 46.4 +/- 7.5 s; with 95% confidence intervals averaging < +/-2 s]. DCA, however, resulted in significant (P < 0.05) reductions in 1). end-exercise [lactate] (-1.0 +/- 0.9 mM), intramuscular acidification (pH, +0.08 +/- 0.06 units), and [Pi] (-1.7 +/- 2.1 mM); 2). the amplitude of the fundamental components for [PCr] (-1.9 +/- 1.6 mM) and Vo2 (-0.1 +/- 0.07 l/min, or 8%); and 3). the amplitude of the Vo2 slow component. Thus, although the DCA infusion lessened the buildup of potential fatigue metabolites and reduced both the aerobic and anaerobic components of the energy transfer during exercise, it did not enhance either tauVo2 or tau[PCr], suggesting that feedback, rather than feedforward, control mechanisms dominate during high-intensity exercise.

Adenosine Triphosphate↗
PubMed2002

Dynamics of intramuscular 31P-MRS P(i) peak splitting and the slow components of PCr and O2 uptake during exercise.

The dynamics of pulmonary O(2) uptake (Vo(2)) during the on-transient of high-intensity exercise depart from monoexponentiality as a result of a "slow component" whose mechanisms remain conjectural. Progressive recruitment of glycolytic muscle fibers, with slow O(2) utilization kinetics and low efficiency, has, however, been suggested as a mechanism. The demonstration of high- and low-pH components of the exercising skeletal muscle (31)P magnetic resonance (MR) spectrum [inorganic phosphate (P(i)) peak] at high work rates (thought to be reflective of differences between oxidative and glycolytic muscle fibers) is also consistent with this conjecture. We therefore investigated the dynamics of Vo(2) (using a turbine and mass spectrometry) and intramuscular ATP, phosphocreatine (PCr), and P(i) concentrations and pH, estimated from the (31)P MR spectrum. Eleven healthy men performed prone square-wave high-intensity knee extensor exercise in the bore of a whole body MR spectrometer. A Vo(2) slow component of magnitude 15.9 +/- 6.9% of the phase II amplitude was accompanied by a similar response (11.9 +/- 7.1%) in PCr concentration. Only five subjects demonstrated a discernable splitting of the P(i) peak, however, which began from between 35 and 235 s after exercise onset and continued until cessation. As such, the dynamics of the pH distribution in intramuscular compartments did not consistently reflect the temporal features of the Vo(2) slow component, suggesting that P(i) splitting does not uniquely reflect the activity of oxidative or glycolytic muscle fibers per se.

Adenosine Triphosphate↗
PubMed2002

Dynamic asymmetry of phosphocreatine concentration and O(2) uptake between the on- and off-transients of moderate- and high-intensity exercise in humans.

The on- and off-transient (i.e. phase II) responses of pulmonary oxygen uptake (V(O(2))) to moderate-intensity exercise (i.e. below the lactate threshold, theta;(L)) in humans has been shown to conform to both mono-exponentiality and 'on-off' symmetry, consistent with a system manifesting linear control dynamics. However above theta;(L) the V(O(2)) kinetics have been shown to be more complex: during high-intensity exercise neither mono-exponentiality nor 'on-off' symmetry have been shown to appropriately characterise the V(O(2)) response. Muscle [phosphocreatine] ([PCr]) responses to exercise, however, have been proposed to be dynamically linear with respect to work rate, and to demonstrate 'on-off' symmetry at all work intenisties. We were therefore interested in examining the kinetic characteristics of the V(O(2)) and [PCr] responses to moderate- and high-intensity knee-extensor exercise in order to improve our understanding of the factors involved in the putative phosphate-linked control of muscle oxygen consumption. We estimated the dynamics of intramuscular [PCr] simultaneously with those of V(O(2)) in nine healthy males who performed repeated bouts of both moderate- and high-intensity square-wave, knee-extension exercise for 6 min, inside a whole-body magnetic resonance spectroscopy (MRS) system. A transmit-receive surface coil placed under the right quadriceps muscle allowed estimation of intramuscular [PCr]; V(O(2)) was measured breath-by-breath using a custom-designed turbine and a mass spectrometer system. For moderate exercise, the kinetics were well described by a simple mono-exponential function (following a short cardiodynamic phase for V(O(2))), with time constants (tau) averaging: tauV(O(2))(,on) 35 +/- 14 s (+/- S.D.), tau[PCr](on) 33 +/- 12 s, tauV(O(2))(,off) 50 +/- 13 s and tau[PCr](off) 51 +/- 13 s. The kinetics for both V(O(2)) and [PCr] were more complex for high-intensity exercise. The fundamental phase expressing average tau values of tauV(O(2))(,on) 39 +/- 4 s, tau[PCr](on) 38 +/- 11 s, tauV(O(2))(,off) 51 +/- 6 s and tau[PCr](off) 47 +/- 11 s. An associated slow component was expressed in the on-transient only for both V(O(2)) and [PCr], and averaged 15.3 +/- 5.4 and 13.9 +/- 9.1 % of the fundamental amplitudes for V(O(2)) and [PCr], respectively. In conclusion, the tau values of the fundamental component of [PCr] and V(O(2)) dynamics cohere to within 10 %, during both the on- and off-transients to a constant-load work rate of both moderate- and high-intensity exercise. On average, approximately 90 % of the magnitude of the V(O(2)) slow component during high-intensity exercise is reflected within the exercising muscle by its [PCr] response.

Adult↗
PubMed2002

Complexities in ETS-domain transcription factor function and regulation: lessons from the TCF (ternary complex factor) subfamily. The Colworth Medal Lecture.

The ETS-domain transcription factor family can be divided into a series of subfamilies. Elk-1 represents the founding member of the ternary complex factor (TCF) subfamily. By focusing on the TCF subfamily, we can demonstrate the complexities that exist in the function and regulation of ETS-domain transcription factors. This article focuses on Elk-1 in detail and summarizes the functions of other TCFs. The key themes covered include the domain structure of the TCFs, the mechanisms of complex formation with serum response factor, regulation of TCFs by mitogen-activated protein kinase cascades, and transcriptional regulatory properties of the TCFs. Finally, the emerging role of the TCFs in vivo is discussed. A picture is developing indicating that, while these proteins exhibit significant sequence and functional conservation, key differences in their structure and regulation are being identified which may relate to unique functions of these proteins in vivo.

Amino Acid Sequence↗
PubMed2001

Effects of prior exercise on oxygen uptake and phosphocreatine kinetics during high-intensity knee-extension exercise in humans.

1. A prior bout of high-intensity square-wave exercise can increase the temporal adaptation of pulmonary oxygen uptake (.V(O2)) to a subsequent bout of high-intensity exercise. The mechanisms controlling this adaptation, however, are poorly understood. 2. We therefore determined the dynamics of intramuscular [phosphocreatine] ([PCr]) simultaneously with those of .V(O2) in seven males who performed two consecutive bouts of high-intensity square-wave, knee-extensor exercise in the prone position for 6 min with a 6 min rest interval. A magnetic resonance spectroscopy (MRS) transmit-receive surface coil under the quadriceps muscle allowed estimation of [PCr]; .V(O2) was measured breath-by-breath using a custom-designed turbine and a mass spectrometer system. 3. The .V(O2) kinetics of the second exercise bout were altered compared with the first such that (a) not only was the instantaneous rate of .V(O2) change (at a given level of .V(O2)) greater but the phase II tau was also reduced - averaging 46.6 +/- 6.0 s (bout 1) and 40.7 +/- 8.4 s (bout 2) (mean +/- S.D.) and (b) the magnitude of the later slow component was reduced. 4. This was associated with a reduction of, on average, 16.1% in the total exercise-induced [PCr] decrement over the 6 min of the exercise, of which 4.0% was due to a reduction in the slow component of [PCr]. There was no discernable alteration in the initial rate of [PCr] change. The prior exercise, therefore, changed the multi-compartment behaviour towards that of functionally first-order dynamics. 5. These observations demonstrate that the .V(O2) responses relative to the work rate input for high-intensity exercise are non-linear, as are, it appears, the putative phosphate-linked controllers for which [PCr] serves as a surrogate.

Adult↗
PubMed2001

Influence of exercise intensity on the on- and off-transient kinetics of pulmonary oxygen uptake in humans.

1. The maximal oxygen uptake (V(O(2),peak)) during dynamic muscular exercise is commonly taken as a crucial determinant of the ability to sustain high-intensity exercise. Considerably less attention, however, has been given to the rate at which V(O(2)) increases to attain this maximum (or to its submaximal requirement), and even less to the kinetic features of the response following exercise. 2. Six, healthy, male volunteers (aged 22 to 58 years), each performed 13 exercise tests: initial ramp-incremental cycle ergometry to the limit of tolerance and subsequently, on different days, three bouts of square-wave exercise each at moderate, heavy, very heavy and severe intensities. Pulmonary gas exchange variables were determined breath by breath throughout exercise and recovery from the continuous monitoring of respired volumes (turbine) and gas concentrations (mass spectrometer). 3. For moderate exercise, the V(O(2)) kinetics were well described by a simple mono-exponential function, following a short cardiodynamic phase, with the on- and off-transients having similar time constants (tau(1)); i.e. tau(1,on) averaged 33 +/- 16 s (+/- S.D.) and tau(1,off) 29 +/- 6 s. 4. The on-transient V(O(2)) kinetics were more complex for heavy exercise. The inclusion of a second slow and delayed exponential component provided an adequate description of the response; i.e. tau(1,on) = 32 +/- 17 s and tau(2,on) = 170 +/- 49 s. The off-transient V(O(2)) kinetics, however, remained mono-exponential (tau(1,off) = 42 +/- 11 s). 5. For very heavy exercise, the on-transient V(O(2)) kinetics were also well described by a double exponential function (tau(1,on) = 34 +/- 11 s and tau(2,on) = 163 +/- 46 s). However, a double exponential, with no delay, was required to characterise the off-transient kinetics (i.e. tau(1,off) = 33 +/- 5 s and tau(2,off) = 460 +/- 123 s). 6. At the highest intensity (severe), the on-transient V(O(2)) kinetics reverted to a mono-exponential profile (tau(1,on) = 34 +/- 7 s), while the off-transient kinetics retained a two-component form (tau(1,off) = 35 +/- 11 s and tau(2,off) = 539 +/- 379 s). 7. We therefore conclude that the kinetics of V(O(2)) during dynamic muscular exercise are strikingly influenced by the exercise intensity, both with respect to model order and to dynamic asymmetries between the on- and off-transient responses.

Adult↗
PubMed2001

Effect of prior metabolic rate on the kinetics of oxygen uptake during moderate-intensity exercise.

Pulmonary oxygen uptake (VO2) dynamics during moderate-intensity exercise are often assumed to be dynamically linear (i.e. neither the gain nor the time constant (tau) of the response varies as a function of work rate). However, faster, slower and unchanged VO2 kinetics have been reported during work-to-work transitions compared to rest-to-work transitions, all within the moderate-intensity domain. In an attempt to resolve these discrepancies and to improve the confidence of the parameter estimation, we determined the VO2 response dynamics using the averaged response to repeated exercise bouts in seven healthy male volunteers. Each subject initially performed a ramp-incremental exercise test for the estimation of the lactate threshold (thetaL). They then performed an average of four repetitions of each of three constant-work-rate (WR) tests: (1) between 20 W and a work rate of 50% (WR50) between 20 W and 90% thetaL (step 1-->2), (2) between WR50 and 90% thetaL (step 2-->3), and (3) between 20 W and 90% thetaL (step 1-->3); 6 min was spent at each work rate increment and decrement. Parameters of the kinetic response of phase II VO2 were established by non-linear least-squares fitting techniques. The kinetics of VO2 were significantly slower at the upper reaches of the moderate-intensity domain (step 2-->3) compared to steps 1-->2 and 1-->3 [group mean (SD) phase II tau: step 1-->2 25.3 (4.9) s, step 2-->3 40.0 (7.4) s and step 1-->3 32.2 (6.9) s]. The off-transient values of tau were not significantly different from each other: 36.8 (16.3) s, 38.9 (11.6) s and 30.8 (5.7) s for steps 1-->2, 2-->3 and 1-->3, respectively. Surprisingly, the on-transient gain (G, deltaVO2/deltaWR) was also found to vary among the three steps [G = 10.56 (0.42) ml x min(-1) W(-1) 11.85 (0.64) ml x min(-1) W(-1) and 11.23 (0.52) ml x min(-1) W(-1) for steps 1-->2, 2-->3 and 1-->3, respectively]; the off-transient G did not vary significantly and was close to that for the on-transient step 1-->3 in all cases. Our results do not support a dynamically linear system model of VO2 during cycle ergometer exercise even in the moderate-intensity domain. The greater oxygen deficit per unit power increment in the higher reaches of the moderate-intensity domain necessitates a greater transient lactate contribution to the energy transfer, or a greater phosphocreatine breakdown, or possibly both.

Adult↗
PubMed2000

Intersample fluctuations in phosphocreatine concentration determined by 31P-magnetic resonance spectroscopy and parameter estimation of metabolic responses to exercise in humans.

The ATP turnover rate during constant-load exercise is often estimated from the initial rate of change of phosphocreatine concentration ([PCr]) using 31P-magnetic resonance spectroscopy (MRS). However, the phase and amplitude characteristics of the sample-to-sample fluctuations can markedly influence this estimation (as well as that for the time constant (tau) of the [PCr] change) and confound its physiological interpretation especially for small amplitude responses. This influence was investigated in six healthy males who performed repeated constant-load quadriceps exercise of a moderate intensity in a whole-body MRS system. A transmit- receive surface coil was placed under the right quadriceps, allowing determination of intramuscular [PCr]; pulmonary oxygen uptake (VO2) was simultaneously determined, breath-by-breath, using a mass spectrometer and a turbine volume measuring module. The probability density functions (PDF) of [PCr] and VO2 fluctuations were determined for each test during the steady states of rest and exercise and the PDF was then fitted to a Gaussian function. The standard deviation of the [PCr] and VO2 fluctuations at rest and during exercise (sr and sw, respectively) and the peak centres of the distributions (xc(r) and xc(w)) were determined, as were the skewness (gamma1) and kurtosis (gamma2) coefficients. There was no difference between sr and sw for [PCr] relative to the resting control baseline (s(r) = 1.554 %delta (s.d. = 0.44), s(w) = 1.514 %delta (s.d. = 0.35)) or the PDF peak centres (xc(r) = -0.013 %delta (s.d. = 0.09), xc(w) -0.197 %delta (s.d. = 0.18)). The standard deviation and peak centre of the 'noise' in VO2 also did not vary between rest and exercise (sr = 0.0427 l min(-1) (s.d. = 0.0104), s(w) = 0.0640 l min(-1) (s.d. = 0.0292); xc(r) = -0.0051 l min(-1) (s.d. = 0.0069), xc(w) 0.0022 l min(-1) (s.d. = 0.0034)). Our results demonstrate that the intersample 'noise' associated with [PCr] determination by 31P-MRS may be characterised as a stochastic Gaussian process that is uncorrelated with work rate, as previously described for VO2. This 'noise' can significantly affect the estimation of tau[PCr] and especially the initial rate of change of [PCr], i.e. the fluctuations can lead to variations in estimation of the initial rate of change of [PCr] of more than twofold, if the inherent 'noise' is not accounted for. This 'error' may be significantly reduced in such cases if the initial rate of change is estimated from the time constant and amplitude of the response.

Adenosine Triphosphate↗
PubMed1999

Inferences from pulmonary O2 uptake with respect to intramuscular [phosphocreatine] kinetics during moderate exercise in humans.

1. In the non-steady state of moderate intensity exercise, pulmonary O2 uptake (Vp,O2) is temporally dissociated from muscle O2 consumption (Vm,O2) due to the influence of the intervening venous blood volume and the contribution of body O2 stores to ATP synthesis. A monoexponential model of Vp,O2 without a delay term, therefore, implies an obligatory slowing of Vp,O2 kinetics in comparison to Vm, O2. 2. During moderate exercise, an association of Vm,O2 and [phosphocreatine] ([PCr]) kinetics is a necessary consequence of the control of muscular oxidative phosphorylation mediated by some function of [PCr]. It has also been suggested that the kinetics of Vp,O2 will be expressed with a time constant within 10 % of that of Vm,O2. 3. Vp,O2 and intramuscular [PCr] kinetics were investigated simultaneously during moderate exercise of a large muscle mass in a whole-body NMR spectrometer. Six healthy males performed prone constant-load quadriceps exercise. A transmit-receive coil under the right quadriceps allowed determination of intramuscular [PCr]; Vp,O2 was measured breath-by-breath, in concert with [PCr], using a turbine and a mass spectrometer system. 4. Intramuscular [PCr] decreased monoexponentially with no delay in response to exercise. The mean of the time constants (tauPCr) was 35 s (range, 20-64 s) for the six subjects. 5. Two temporal phases were evident in the Vp, O2 response. When the entire Vp,O2 response was modelled to be exponential with no delay, its time constant (tau'Vp,O2) was longer in all subjects (group mean = 62 s; range, 52-92 s) than that of [PCr], reflecting the energy contribution of the O2 stores. 6. Restricting the Vp,O2 model fit to phase II resulted in matching kinetics for Vp,O2 (group mean tauVp,O2 = 36 s; range, 20-68 s) and [PCr], for all subjects. 7. We conclude that during moderate intensity exercise the phase II tauVp,O2 provides a good estimate of tauPCr and by implication that of Vm,O2 (tauVm,O2).

Adenosine Triphosphate↗
PubMed1999

Simultaneous determination of muscle 31P and O2 uptake kinetics during whole body NMR spectroscopy.

Our understanding of O2 uptake (VO2) control mechanisms during exercise may be improved by the simultaneous determination of the kinetics of intramuscular high-energy phosphate turnover and pulmonary VO2. We therefore developed a technique for remote gas-exchange analysis while subjects exercised in a whole body 1.5-T NMR system. Knee-extension exercise was performed against restraining rubber bands in the prone position. Free induction decays were acquired every 1,875 ms by using a transmit-receive coil, which was placed under the quadriceps. This allowed 31P spectra of intramuscular ATP, Pi, and creatine phosphate dynamics to be determined every 15 s. Airflow was measured with a custom-designed turbine and a 45-ft.-long cable to reach the volume-measuring module. This was located in an adjacent radio-frequency-shielded room, as was the respiratory mass spectrometer, which also used a 45-ft.-long sampling line. The respired gas profiles were not discernibly different from those that used the standard inlet; the increase in the delay was readily incorporated into the breathby-breath algorithm, allowing the VO2 kinetics to be determined in concert with those of intramuscular phosphate metabolism.

Adenosine Triphosphate↗
PubMed1997

Mechanical deformation promotes secretion of IL-1 alpha and IL-1 receptor antagonist.

Both IL-1 alpha and IL-1 beta lack an N terminus secretory sequence, and the mechanism of secretion of these pleiotropic cytokines is incompletely understood. The epidermis contains large quantities of IL-1 alpha in keratinocytes, which may play a role in inducing endothelial adhesion molecules and promoting extravasation of leukocytes. Here we report that mechanical deformation of human keratinocytes leads to rapid release of IL-1 alpha, possibly through transient disruptions in the plasma membrane. Using a device that precisely controls the amplitude of strain on the culture substrate, we found by pulse-chase analysis, Western analysis, and ELISA that the release of IL-1 alpha is dependent on the amplitude of the strain. A cyclic strain of 14% released a small but significant quantity of IL-1 alpha, while strains of 33% released 66 +/- 9% of cytoplasmic IL-1 alpha over 1 h (p < 0.001). Release of IL-1 alpha was accompanied by rapid release of large stores of IL-1R antagonist, approximately 25 to 30 times greater by mass than the quantity of IL-1 alpha released, but only a small fraction of cytoplasmic lactate dehydrogenase. Media conditioned by mechanically stimulated keratinocytes induced expression of E-selectin by human vascular endothelial cells; induction of E-selectin was completely inhibited by an Ab to IL-1 alpha. Therefore, mechanical strain promotes the secretion of IL-1 alpha, and deformation of keratinocytes in the epidermis may activate vascular endothelium through mechanically released IL-1 alpha. This pathophysiologic mechanism may play a role in the anatomic localization of some inflammatory skin diseases, such as psoriasis, which occurs more commonly in locations where the dermis is subjected to repetitive stretch or trauma.

Cell Membrane↗
PubMed1996

The effect of oral creatine supplementation on the 1000-m performance of competitive rowers.

This study investigated the change in 1000-m simulated rowing performance in two matched groups of 19 competitive rowers following a 5-day period of supplementation with placebo (CON group) or creatine at a dose equivalent to 0.25 g creatine monohydrate per kilogram of body mass (BM) (EXP group). Creatine uptake was calculated from the difference between the amount fed and the amount recovered in urine during each 24-h period of supplementation. Total creatine uptake for the EXP group over the 5-day period of supplementation averaged 34.9 +/- 10.9 g (range 20.1-54.9 g), which equated to 3.54 +/- 0.93 mmol kg BM-1. The estimated creatine uptake into muscle was 38.1 +/- 10.0 (range 22.6-56.6) mmol kg dry weight-1 for these subjects. After supplementation with placebo, the CON group showed no change in 1000-m rowing performance (214.0 +/- 30.9 vs 214.1 +/- 31.5 s; P = 0.88). Of these subjects, 7 decreased and 10 increased their performance times (range - 3.1 to 2.7%). By contrast, 16 of the 19 subjects in the EXP group improved their performance times. The mean improvement in rowing performance for the EXP group was 2.3 s (211.0 +/- 21.5 vs 208.7 +/- 21.8 s; P < 0.001), an overall improvement of just over 1% (range - 0.4 to 3.4%). We conclude that in competitive rowers, a 5-day period of creatine supplementation was effective in raising whole-body creatine stores, the magnitude of which provided a positive, though statistically non-significant (r = 0.426, P = 0.088), relationship with 1000-m rowing performance.

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