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Biomedical subjects

Andrew M Jones

Publications and source records attributed to Andrew M Jones.

At least 19 recordsLinked to original sources
PubMed2026

The effects of nitrate and nitrite supplementation on mitochondrial respiration in permeabilized muscle fibres in young healthy adults.

Nitric oxide (NO) is a direct regulator of mitochondrial respiration. Nitrate (NO3-) and nitrite (NO2-) are good sources of NO, but whether their effects on mitochondrial respiration differ between in vivo and in vitro administration remains unclear. In Study 1, 8 participants consumed NO3- -rich beetroot juice (BR) (∼12.8 mmol NO3-) and NO3- -depleted placebo beetroot juice (PL) (∼0.08 mmol NO3-) acutely and chronically for 2 weeks in a randomised, double-blind, crossover design. A substrate-uncoupler-inhibitor titration (SUIT) protocol was used to assess mitochondrial respiration using high-resolution respirometry (oxygen tension: ∼200-450 μM) in permeabilized muscle fibres. In Study 2, skeletal muscle samples were collected from 11 participants. In a randomised, crossover design, different doses (0, 1.5, and 3.0 μM) of sodium nitrite (NaNO2) were administered to permeabilized muscle fibres. Mitochondrial respiration was measured using the same SUIT protocol under lower oxygen tension (∼50-200 μM). Although muscle NO3- concentration significantly increased after both acute and chronic BR supplementation, mitochondrial respiration and exercise performance did not differ between PL and BR in either condition. Similarly, absolute oxygen flux across different respiratory states were not different between different doses of NaNO2. However, the leak control ratio, reflecting the degree of uncoupling of mitochondrial respiration, was significantly higher with 3.0 μM NaNO2 administration (0.12 ± 0.05) compared to 0 μM NaNO2 administration (0.09 ± 0.04, P = 0.03). These findings, involving both in vivo and in vitro administration approaches, albeit in the presence of relatively high oxygen concentrations, suggest that neither NO3- nor NO2- improves mitochondrial respiration, at least in young healthy adults.

Humans↗
PubMed2006

Coagulopathy in two patients with cystic fibrosis treated with ciprofloxacin.

We report two cases of prolonged blood clotting times as demonstrated by a raised international normalised ratio and elevated activated partial thromboplastin time in patients with cystic fibrosis taking ciprofloxacin. The potential mechanisms of a coagulopathy of this picture as an adverse drug reaction with ciprofloxacin are discussed along with the possible clinical consequences for patients with cystic fibrosis.

Adolescent↗
PubMed2006

Effects of baseline metabolic rate on pulmonary O2 uptake on-kinetics during heavy-intensity exercise in humans.

We hypothesised that initiating heavy-intensity exercise from an elevated baseline metabolic rate would result in slower Phase II O2 uptake V(O2) kinetics and a greater overall 'gain' in V(O2) per unit increase in work rate. Seven healthy males performed a series of like-transitions on a cycle ergometer: (1) from light exercise to 'moderate' exercise (80% of the gas exchange threshold, GET; L-->M); (2) from light exercise to 'heavy' exercise (40% of the difference between GET and V(O2) peak; L-->H); (3) from moderate exercise to heavy exercise (M-->H). The Phase II time constant (tau) was significantly (P<0.01) greater in the M-->H condition (48+/-11 s) compared to the L-->M and L-->H conditions (26+/-6 s versus 27+/-4 s, respectively). Moreover, the end-exercise 'gain' values were significantly different between the three conditions (L-->M, 8.1+/-0.7 mL min-1 W-1; L-->H, 9.7+/-0.4 mL min-1 W-1; M-->H, 10.7+/-0.7 mL min-1 W-1; P<0.05). This 'non-linearity' in the pulmonary V(O2) response to exercise might be attributed, at least in part, to differences in the metabolic properties of the muscle fibres recruited in the abrupt transition from a lower to a higher work rate.

Adult↗
PubMed2006

Effects of "priming" exercise on pulmonary O2 uptake and muscle deoxygenation kinetics during heavy-intensity cycle exercise in the supine and upright positions.

We hypothesized that the performance of prior heavy exercise would speed the phase 2 oxygen consumption (VO2) kinetics during subsequent heavy exercise in the supine position (where perfusion pressure might limit muscle O2 supply) but not in the upright position. Eight healthy men (mean +/- SD age 24 +/- 7 yr; body mass 75.0 +/- 5.8 kg) completed a double-step test protocol involving two bouts of 6 min of heavy cycle exercise, separated by a 10-min recovery period, on two occasions in each of the upright and supine positions. Pulmonary O2 uptake was measured breath by breath and muscle oxygenation was assessed using near-infrared spectroscopy (NIRS). The NIRS data indicated that the performance of prior exercise resulted in hyperemia in both body positions. In the upright position, prior exercise had no significant effect on the time constant tau of the VO2 response in phase 2 (bout 1: 29 +/- 10 vs. bout 2: 28 +/- 4 s; P = 0.91) but reduced the amplitude of the VO2 slow component (bout 1: 0.45 +/- 0.16 vs. bout 2: 0.22 +/- 0.14 l/min; P = 0.006) during subsequent heavy exercise. In contrast, in the supine position, prior exercise resulted in a significant reduction in the phase 2 tau (bout 1: 38 +/- 18 vs. bout 2: 24 +/- 9 s; P = 0.03) but did not alter the amplitude of the VO2 slow component (bout 1: 0.40 +/- 0.29 vs. bout 2: 0.41 +/- 0.20 l/min; P = 0.86). These results suggest that the performance of prior heavy exercise enables a speeding of phase 2 VO2 kinetics during heavy exercise in the supine position, presumably by negating an O2 delivery limitation that was extant in the control condition, but not during upright exercise, where muscle O2 supply was probably not limiting.

Adaptation, Physiological↗
PubMed2006

Time required for the restoration of normal heavy exercise VO2 kinetics following prior heavy exercise.

Prior heavy exercise markedly alters the O2 uptake (VO2) response to subsequent heavy exercise. However, the time required for VO2 to return to its normal profile following prior heavy exercise is not known. Therefore, we examined the VO2 responses to repeated bouts of heavy exercise separated by five different recovery durations. On separate occasions, nine male subjects completed two 6-min bouts of heavy cycle exercise separated by 10, 20, 30, 45, or 60 min of passive recovery. The second-by-second VO2 responses were modeled using nonlinear regression. Prior heavy exercise had no effect on the primary VO2 time constant (from 25.9 +/- 4.7 s to 23.9 +/- 8.8 s after 10 min of recovery; P = 0.338), but it increased the primary VO2 amplitude (from 2.42 +/- 0.39 to 2.53 +/- 0.41 l/min after 10 min of recovery; P = 0.001) and reduced the VO2 slow component (from 0.44 +/- 0.13 to 0.21 +/- 0.12 l/min after 10 min of recovery; P < 0.001). The increased primary amplitude was also evident after 20-45 min, but not after 60 min, of recovery. The increase in the primary VO2 amplitude was accompanied by an increased baseline blood lactate concentration (to 5.1 +/- 1.0 mM after 10 min of recovery; P < 0.001). Baseline blood lactate concentration was still elevated after 20-60 min of recovery. The priming effect of prior heavy exercise on the VO2 response persists for at least 45 min, although the mechanism underpinning the effect remains obscure.

Adult↗
PubMed2006

Influence of acute plasma volume expansion on VO2 kinetics, VO2 peak, and performance during high-intensity cycle exercise.

The purpose of this study was to examine the influence of acute plasma volume expansion (APVE) on oxygen uptake (V(O2)) kinetics, V(O2peak), and time to exhaustion during severe-intensity exercise. Eight recreationally active men performed "step" cycle ergometer exercise tests at a work rate requiring 70% of the difference between the gas-exchange threshold and V(O2max) on three occasions: twice as a "control" (Con) and once after intravenous infusion of a plasma volume expander (Gelofusine; 7 ml/kg body mass). Pulmonary gas exchange was measured breath by breath. APVE resulted in a significant reduction in hemoglobin concentration (preinfusion: 16.0 +/- 1.0 vs. postinfusion: 14.7 +/- 0.8 g/dl; P < 0.001) and hematocrit (preinfusion: 44 +/- 2 vs. postinfusion: 41 +/- 3%; P < 0.01). Despite this reduction in arterial O(2) content, APVE had no effect on V(O2) kinetics (phase II time constant, Con: 33 +/- 15 vs. APVE: 34 +/- 12 s; P = 0.74), and actually resulted in an increased V(O2peak) (Con: 3.90 +/- 0.56 vs. APVE: 4.12 +/- 0.55 l/min; P = 0.006) and time to exhaustion (Con: 365 +/- 58 vs. APVE: 424 +/- 64 s; P = 0.04). The maximum O(2) pulse was also enhanced by the treatment (Con: 21.3 +/- 3.4 vs. APVE: 22.7 +/- 3.4 ml/beat; P = 0.04). In conclusion, APVE does not alter V(O2) kinetics but enhances V(O2peak) and exercise tolerance during high-intensity cycle exercise in young recreationally active subjects.

Adult↗
PubMed2006

Socioeconomic inequalities in health: a comparative longitudinal analysis using the European Community Household Panel.

This study measures socioeconomic inequalities in health across European Union Member States between 1994 and 2001. The analysis is based on the European Community Household Panel Users' Database (ECHP-UDB) and uses two binary indicators of health limitations for the full 8 waves of available data. Short- and long-run concentration indices together with mobility and health achievement indices are derived for indicators of severe health limitation and any health limitation. Results demonstrate the existence of socioeconomic inequality in health across Member States in both the short-term (1 year) and the long-term (up to 8 years), with health limitations concentrated among those with lower incomes. For all countries, the long-run indices show that income-related inequalities in health widen over time, in the sense that the longer the period over which an individual's health and income are measured the greater the measure of income-related health inequality. The ranking of countries according to their prevalence of illness differs from ranking by overall health achievement, which takes account of inequalities. This means that an equity-efficiency trade-off has to be faced in evaluating the performance of different countries and in comparing countries with diverse health and social welfare systems.

Cross-Sectional Studies↗
PubMed2006

Influence of blood donation on O2 uptake on-kinetics, peak O2 uptake and time to exhaustion during severe-intensity cycle exercise in humans.

We hypothesized that the reduction of O2-carrying capacity caused by the withdrawal of approximately 450 ml blood would result in slower phase II O2 uptake (VO2) kinetics, a lower VO2peak and a reduced time to exhaustion during severe-intensity cycle exercise. Eleven healthy subjects (mean +/- S.D. age 23 +/- 6 years, body mass 77.2 +/- 11.0 kg) completed 'step' exercise tests from unloaded cycling to a severe-intensity work rate (80% of the difference between the predetermined gas exchange threshold and the VO2peak) on two occasions before, and 24 h following, the voluntary donation of approximately 450 ml blood. Oxygen uptake was measured breath-by-breath, and VO2 kinetics estimated using non-linear regression techniques. The blood withdrawal resulted in a significant reduction in haemoglobin concentration (pre: 15.4 +/- 0.9 versus post: 14.7 +/- 1.3 g dl(-1); 95% confidence limits (CL): -0.04, -1.38) and haematocrit (pre: 44 +/- 2 versus post: 41 +/- 3%; 95% CL: -1.3, -5.1). Compared to the control condition, blood withdrawal resulted in significant reductions in VO2peak (pre: 3.79 +/- 0.64 versus post: 3.64 +/- 0.61 l min(-1); 95% CL: -0.04, - 0.27) and time to exhaustion (pre: 375 +/- 129 versus post: 321 +/- 99 s; 95% CL: -24, -85). However, the kinetic parameters of the fundamental VO2 response, including the phase II time constant (pre: 29 +/- 8 versus post: 30 +/- 6 s; 95% CL: 5, -3), were not altered by blood withdrawal. The magnitude of the VO2 slow component was significantly reduced following blood donation owing to the lower VO2peak attained. We conclude that a reduction in blood O2-carrying capacity, achieved through the withdrawal of approximately 450 ml blood, results in a significant reduction in VO2peak and exercise tolerance but has no effect on the fundamental phase of the VO2 on-kinetics during severe-intensity exercise.

Adult↗
PubMed2006

Influence of crank rate on the slow component of pulmonary O(2) uptake during heavy arm-crank exercise.

The principal aim of this study was to examine the influence of variations in crank rate on the slow component of the pulmonary oxygen uptake ((.)VO(2)) response to heavy-intensity arm-crank ergometry (ACE). We hypothesized that, for the same external work rate, a higher crank rate would elicit a greater amplitude of the (.)VO(2) "slow component". Eleven healthy males (mean (+/- SD) age, 25 ((+/-6) y; body mass, 89.1 ((+/-10.7) kg; ACE (.)VO(2)(peak), 3.36 ((+/-0.47) L x min(-1)) volunteered to participate. The subjects initially completed an incremental exercise test for the determination of (.)VO(2)(peak) and peak power on an electrically braked arm ergometer. Subsequently, they completed "step" transitions from an unloaded baseline to a work rate requiring 70% of peak power: 2 at a crank rate of 50 r x min(-1) (LO) and 2 at a crank rate of 90 r x min(-1) (HI). Pulmonary gas exchange was measured on a breath-by-breath basis and (.)VO(2) kinetics were evaluated from the mean response to each condition using non-linear regression techniques. In contradiction to our hypothesis, the (.)VO(2) slow component was significantly greater at 50 r x min(-1) than at 90 r x min(-1) (LO: 0.60 +/- 0.30 vs. HI: 0.47 +/- 0.21 L x min(-1); p < 0.05). The mean value for the localized rating of perceived exertion was also higher at 50 r x min(-1) than at 90 r x min(-1) (LO: 16.7 +/- 1.4 vs. HI: 15.2 +/- 1.3; p < 0.05), but there was no significant difference in end-exercise blood lactate concentration. It is possible that differences in muscle tension development and blood flow resulted in a greater contribution of "low-efficiency" type II muscle fibres to force production at the lower crank rate in ACE, and that this was linked to the greater (.)VO(2) slow component. However, other factors such as greater isometric contraction of the muscles of the trunk and legs at the lower crank rate might also be implicated.

Adult↗
PubMed2006

Influence of continuous and interval training on oxygen uptake on-kinetics.

PURPOSE: To examine the relative effectiveness of moderate-intensity continuous training and high-intensity interval training on pulmonary O2 uptake (VO2) kinetics at the onset of moderate- and severe-intensity cycle exercise in previously sedentary subjects. METHODS: Twenty-three healthy subjects (11 males; mean +/- SD age 24 +/- 5 yr; VO2peak 34.3 +/- 5.5 mL x kg(-1) x min(-1)) were assigned to one of three groups: a continuous training group that completed three to four sessions per week of 30-min duration at 60% VO2peak (LO); an interval training group that completed three to four sessions per week involving 20 x 1-min exercise bouts at 90% VO2peak separated by 1-min rest periods (HI); or a control group (CON). Before and after the 6-wk intervention period, all subjects completed a series of step exercise tests to moderate and severe work rates during which pulmonary VO2 was measured breath-by-breath. RESULTS: ANOVA revealed that continuous and interval training were similarly effective in reducing the phase II VO2 time constant during moderate (LO: from 31 +/- 8 to 23 +/- 5 s; HI: from 32 +/- 9 to 21 +/- 4 s; both P < 0.05; CON: from 30 +/- 6 to 29 +/- 7 s; NSD) and severe exercise (LO: from 35 +/- 6 to 24 +/- 7 s; HI: from 32 +/- 11 to 24 +/- 7 s; both P < 0.05; CON: from 27 +/- 7 to 25 +/- 5 s; NSD) and in reducing the amplitude of the VO2 slow component (LO: from 0.38 +/- 0.10 to 0.29 +/- 0.09 L x min(-1); HI: from 0.41 +/- 0.28 to 0.30 +/- 0.28 L x min(-1); both P < 0.05; CON: from 0.54 +/- 0.22 to 0.66 +/- 0.38 L.min; NSD). CONCLUSIONS: Six weeks of low-intensity continuous training and high-intensity interval training were similarly effective in enhancing VO2 on-kinetics following step transitions to moderate and severe exercise in previously untrained subjects.

Adult↗
PubMed2006

Sodium bicarbonate ingestion alters the slow but not the fast phase of VO2 kinetics.

PURPOSE: The influence of metabolic alkalosis (ALK) on pulmonary O2 uptake (pVO2) kinetics during high-intensity cycle exercise is controversial. The purpose of this study was to examine the influence of ALK induced by sodium bicarbonate (NaHCO3) ingestion on pVO2 kinetics, using a sufficient number of repeat-step transitions to provide high confidence in the results obtained. METHODS: Seven healthy males completed step tests to a work rate requiring 80% pVO2max on six separate occasions: three times after ingestion of 0.3 g x kg(-1) body mass NaHCO3 in 1 L of fluid, and three times after ingestion of a placebo (CON). Blood samples were taken to assess changes in acid-base balance, and pVO2 was measured breath-by-breath. RESULTS: NaHCO3 ingestion significantly increased blood pH and [bicarbonate] both before and during exercise relative to the control condition (P < 0.001). The time constant of the phase II pVO2 response was not different between conditions (CON: 29 +/- 6 vs ALK: 32 +/- 7 s; P = 0.21). However, the onset of the pVO2 slow component was delayed by NaHCO3 ingestion (CON: 120 +/- 19 vs ALK: 147 +/- 34 s; P < 0.01), resulting in a significantly reduced end-exercise pVO2 (CON: 2.88 +/- 0.19 vs ALK: 2.79 +/- 0.23 L x min(-1); P < 0.05). CONCLUSIONS: Metabolic alkalosis has no effect on phase II pVO2 kinetics but alters the pVO2 slow-component response, possibly as a result of the effects of NaHCO3 ingestion on muscle pH.

Acid-Base Imbalance↗
PubMed2005

Influence of initial metabolic rate on pulmonary O2 uptake on-kinetics during severe intensity exercise.

We hypothesised that the fundamental (Phase II) component of pulmonary oxygen uptake (VO(2)) kinetics would be significantly slower when step transitions to severe intensity cycle exercise were initiated from elevated baseline metabolic rates, and that this would be associated with evidence for a greater activation of higher-order (i.e. type II) muscle fibres. Seven male subjects (age 22-34 years) completed repeat step transitions to a severe (S) work rate, estimated to require 100% VO(2) peak, from a baseline of: (1) 3 min of unloaded cycling (L-->S); (2) 6 min of moderate exercise (M-->S); (3) 6 min of heavy exercise (H-->S). Pulmonary gas exchange and the electromyogram (EMG) of the m. vastus lateralis were measured throughout all exercise tests. The Phase II VO(2) kinetics became progressively slower at higher baseline metabolic rates (tau was 37 +/- 6, 59 +/- 23, and 93 +/- 50 s for L-->S, M-->S, and H-->S, respectively; P < 0.05 between L-->S and H-->S). Both the integrated EMG and the mean power frequency were significantly higher immediately before the step transition to severe exercise when it was initiated from higher metabolic rates. Although indirect, these data suggest that the slower Phase II VO(2) kinetics observed at higher baseline metabolic rates was related to alterations in muscle activation and fibre recruitment patterns.

Adult↗
PubMed2005

Influence of hyperoxia on pulmonary O2 uptake kinetics following the onset of exercise in humans.

The purpose of this study was to examine the influence of hyperoxic gas (50% O2 in N2) inspiration on pulmonary oxygen uptake (V(O2)) kinetics during step transitions to moderate, severe and supra-maximal intensity cycle exercise. Seven healthy male subjects completed repeat transitions to moderate (90% of the gas exchange threshold, GET), severe (70% of the difference between the GET and V(O2) peak) and supra-maximal (105% V(O2) peak) intensity work rates while breathing either normoxic (N) or hyperoxic (H) gas before and during exercise. Hyperoxia had no significant effect on the Phase II V(O2) time constant during moderate (N: 28+/-3s versus H: 31+/-7s), severe (N: 32+/-9s versus H: 33+/-6s) or supra-maximal (N: 37+/-9s versus H: 37+/-9s) exercise. Hyperoxia resulted in a 45% reduction in the amplitude of the V(O2) slow component during severe exercise (N: 0.60+/-0.21 L min(-1) versus H: 0.33+/-0.17 L min(-1); P < 0.05) and a 15% extension of time to exhaustion during supra-maximal exercise (N: 173+/-28 s versus H: 198+/-41 s; P < 0.05). These results indicate that the Phase II V(O2) kinetics are not normally constrained by (diffusional) O2 transport limitations during moderate, severe or supra-maximal intensity exercise in young healthy subjects performing upright cycle exercise.

Adult↗
PubMed2005

Influence of recombinant human erythropoietin treatment on pulmonary O2 uptake kinetics during exercise in humans.

We hypothesized that 4 weeks of recombinant human erythropoietin (RhEPO) treatment would result in a significant increase in haemoglobin concentration ([Hb]) and arterial blood O(2)-carrying capacity and that this would (1) increase peak pulmonary oxygen uptake during ramp incremental exercise, and (2) speed kinetics during 'severe'-, but not 'moderate'- or 'heavy'-intensity, step exercise. Fifteen subjects (mean +/- s.d. age 25 +/- 4 years) were randomly assigned to either an experimental group which received a weekly subcutaneous injection of RhEPO (150 IU kg(-1); n = 8), or a control group (CON) which received a weekly subcutaneous injection of sterile saline (10 ml; n = 7) as a placebo, for four weeks. The subjects and the principal researchers were both blind with respect to the group assignment. Before and after the intervention period, all subjects completed a ramp test for determination of the gas exchange threshold (GET) and , and a number of identical 'step' transitions from 'unloaded' cycling to work rates requiring 80% GET (moderate), 70% of the difference between the GET and (heavy), and 105% (severe) as determined from the initial ramp test. Pulmonary gas exchange was measured breath-by-breath. There were no significant differences between the RhEPO and CON groups for any of the measurements of interest ([Hb], kinetics) before the intervention. Four weeks of RhEPO treatment resulted in a 7% increase both in [Hb] (from 15.8 +/- 1.0 to 16.9 +/- 0.7 g dl(-1); P < 0.01) and (from 47.5 +/- 4.2 to 50.8 +/- 10.7 ml kg(-1).min(-1); P < 0.05), with no significant change in CON. RhEPO had no significant effect on kinetics for moderate (Phase II time constant, from 28 +/- 8 to 28 +/- 7 s), heavy (from 37 +/- 12 to 35 +/- 11 s), or severe (from 33 +/- 15 to 35 +/- 15 s) step exercise. Our results indicate that enhancing blood O(2)-carrying capacity and thus the potential for muscle O(2) delivery with RhEPO treatment enhanced the peak but did not influence kinetics, suggesting that the latter is principally regulated by intracellular (metabolic) factors, even during exercise where the requirement is greater than the , at least in young subjects performing upright cycle exercise.

Double-Blind Method↗
PubMed2005

Pulmonary O2 uptake on-kinetics in rowing and cycle ergometer exercise.

The purpose of this study was to characterise, for the first time, the pulmonary O2 uptake (V(O2)) on-kinetic responses to step transitions to moderate and heavy intensity rowing ergometer exercise, and to compare the responses to those observed during upright cycle ergometer exercise. We hypothesised that the recruitment of a greater muscle mass in rowing ergometer exercise (Row) might limit muscle perfusion and result in slower Phase II V(O2) kinetics compared to cycle exercise (Cyc). Eight healthy males (aged 28+/-5 years) performed a series of step transitions to moderate (90% of the mode-specific gas exchange threshold, GET) and heavy (50% of the difference between the mode-specific GET and V(O2) max) work rates, for both Row and Cyc exercise. Pulmonary V(O2) was measured breath-by-breath and the V(O2) on-kinetics were described using standard non-linear regression techniques. With the exception of delta V(O2)delta WR which was approximately 12% greater for Row, the V(O2) kinetic responses were similar between the exercise modes. There was no significant difference in the time constant describing the Phase II V(O2) kinetics between the exercise modes for either moderate (rowing: 25.9+/-6.8 s versus cycling: 25.7+/-8.6 s) or heavy (rowing: 26.5+/-3.0 s versus cycling: 27.8+/-5.1s) exercise. Furthermore, there was no significant difference in the amplitude of the V(O2) slow component between the exercise modes (rowing: 0.34+/-0.13 L min(-1) versus cycling: 0.35+/-0.12 L min(-1)). These data suggest that muscle V(O2) increases towards the anticipated steady-state requirement at essentially the same rate following a step increase in ATP turnover in the myocytes, irrespective of the mode of exercise, at least in subjects with no particular sport specialism. The recruitment of a greater muscle mass in rowing compared to cycling apparently did not compromise muscle perfusion sufficiently to result either in slower Phase II V(O2) kinetics or a greater V(O2) slow component amplitude during heavy exercise.

Adult↗