Simon Marwood

Beetroot juice supplementation speeds O2 uptake kinetics and improves exercise tolerance during severe-intensity exercise initiated from an elevated metabolic rate

Recent research has suggested that dietary nitrate (NO3(-)) supplementation might alter the physiological responses to exercise via specific effects on type II muscle. Severe-intensity exercise initiated from an elevated metabolic rate would be expected to enhance the proportional activation of higher-order (type II) muscle fibers. The purpose of this study was, therefore, to test the hypothesis that, compared with placebo (PL), NO3(-)-rich beetroot juice (BR) supplementation would speed the phase II VO2 kinetics (τ(p)) and enhance exercise tolerance during severe-intensity exercise initiated from a baseline of moderate-intensity exercise. Nine healthy, physically active subjects were assigned in a randomized, double-blind, crossover design to receive BR (140 ml/day, containing ~8 mmol of NO3(-)) and PL (140 ml/day, containing ~0.003 mmol of NO3(-)) for 6 days. On days 4, 5, and 6 of the supplementation periods, subjects completed a double-step exercise protocol that included transitions from unloaded to moderate-intensity exercise (U→M) followed immediately by moderate to severe-intensity exercise (M→S). Compared with PL, BR elevated resting plasma nitrite concentration (PL: 65 ± 32 vs. BR: 348 ± 170 nM, P < 0.01) and reduced the VO2 τ(p) in M→S (PL: 46 ± 13 vs. BR: 36 ± 10 s, P < 0.05) but not U→M (PL: 25 ± 4 vs. BR: 27 ± 6 s, P > 0.05). During M→S exercise, the faster VO2 kinetics coincided with faster near-infrared spectroscopy-derived muscle [deoxyhemoglobin] kinetics (τ; PL: 20 ± 9 vs. BR: 10 ± 3 s, P < 0.05) and a 22% greater time-to-task failure (PL: 521 ± 158 vs. BR: 635 ± 258 s, P < 0.05). Dietary supplementation with NO3(-)-rich BR juice speeds VO2 kinetics and enhances exercise tolerance during severe-intensity exercise when initiated from an elevated metabolic rate.

Tricarboxylic acid cycle intermediate pool size: functional importance for oxidative metabolism in exercising human skeletal muscle.

The tricarboxylic acid (TCA) cycle is the major final common pathway for oxidation of carbohydrates, lipids and some amino acids, which produces reducing equivalents in the form of nicotinamide adenine dinucleotide and flavin adenine dinucleotide that result in production of large amounts of adenosine triphosphate (ATP) via oxidative phosphorylation. Although regulated primarily by the products of ATP hydrolysis, in particular adenosine diphosphate, the rate of delivery of reducing equivalents to the electron transport chain is also a potential regulatory step of oxidative phosphorylation. The TCA cycle is responsible for the generation of ≈67% of all reducing equivalents per molecule of glucose, hence factors that influence TCA cycle flux will be of critical importance for oxidative phosphorylation. TCA cycle flux is dependent upon the supply of acetyl units, activation of the three non-equilibrium reactions within the TCA cycle, and it has been suggested that an increase in the total concentration of the TCA cycle intermediates (TCAi) is also necessary to augment and maintain TCA cycle flux during exercise.This article reviews the evidence of the functional importance of the TCAi pool size for oxidative metabolism in exercising human skeletal muscle. In parallel with increased oxidative metabolism and TCA cycle flux during exercise, there is an exercise intensity-dependent 4- to 5-fold increase in the concentration of the TCAi. TCAi concentration reaches a peak after 10–15 minutes of exercise, and thereafter tends to decline. This seems to support the suggestion that the concentration of TCAi may be of functional importance for oxidative phosphorylation. However, researchers have been able to induce dissociations between TCAi pool size and oxidative energy provision using a variety of nutritional, pharmacological and exercise interventions.Brief periods of endurance training (5 days or 7 weeks) have been found to result in reduced TCAi pool expansion at the start of exercise (same absolute work intensity) in parallel with either equivalent or increased oxidative energy provision. Cycloserine inhibits alanine aminotransferase, which catalyses the predominant anaplerotic reaction in exercising human muscle. When infused into contracting rat hindlimb muscle, TCAi pool expansion was reduced by 25% with no significant change in oxidative energy provision or power output. Glutamine supplementation has been shown to enhance TCAi pool expansion at the start of exercise with no increase in oxidative energy provision. In summary, there is a consistent dissociation between the extent of TCAi pool expansion at the onset of exercise and oxidative energy provision.At the other end of the spectrum, the parallel loss of TCAi, glycogen and adenine nucleotides and accumulation of inosine monophosphate during prolonged exercise has led to the suggestion that there is a link between muscle glycogen depletion, reduced TCA cycle flux and the development of fatigue. However, analysis of serial biopsies during prolonged exercise demonstrated dissociation between muscle TCAi content and both muscle glycogen content and muscle oxygen uptake. In addition, the delay in fatigue development achieved through increased carbohydrate availability does not attenuate TCAi reduction during prolonged exercise. Therefore, TCAi concentration in whole muscle homogenate does not seem to be of functional importance. However, TCAi content can currently only be measured in whole muscle homogenate rather than the mitochondrial subfraction where TCA cycle reactions occur. In addition, anaplerotic flux rather than TCAi content per se is likely to be of greater importance in determining TCA cycle flux, since TCAi content is probably merely reflective of anaplerotic substrate concentration. Methodological advances are required to allow researchers to address the questions of whether oxidative phosphorylation is limited by mitochondrial TCAi content and/or anaplerotic flux.

Faster pulmonary oxygen uptake kinetics in trained versus untrained male adolescents.

UNLABELLED Exercise training results in a speeding of pulmonary oxygen uptake (VO2) kinetics at the onset of exercise in adults; however, only limited research has been conducted with children and adolescents. PURPOSE The aim of the present study was to examine VO2 and muscle deoxygenation kinetics in trained and untrained male adolescents. METHODS Sixteen trained (15 +/- 0.8 yr, VO2peak = 54.7 +/- 6.2 mL x kg-1 x min-1, self-assessed Tanner stage range 2-4) and nine untrained (15 +/- 0.6 yr, VO2peak = 43.1 +/- 5.2 mL x kg-1 x min-1, Tanner stage range 2-4) male adolescents performed two 6-min exercise transitions from a 3-min baseline of 10 W to a workload equivalent to 80% lactate threshold separated by a minimum of 1 h of passive rest. Oxygen uptake (breath-by-breath) and muscle deoxygenation (deoxyhemoglobin signal from near-infrared spectroscopy) were measured continuously throughout baseline and exercise transition. RESULTS The time constant of the fundamental phase of VO2 kinetics was significantly faster in trained versus untrained subjects (trained: 22.3 +/- 7.2 s vs untrained: 29.8 +/- 8.4 s, P = 0.03). In contrast, neither the time constant (trained: 9.7 +/- 2.9 s vs untrained: 10.1 +/- 3.4 s, P = 0.78) nor the mean response time (trained: 17.4 +/- 2.5 s vs untrained: 18.3 +/- 2.3 s, P = 0.39) of muscle deoxygenation kinetics differed with training status. CONCLUSIONS The present data suggest that exercise training results in faster VO2 kinetics in male adolescents, although inherent capabilities cannot be ruled out. Because muscle deoxygenation kinetics were unchanged, it is likely that faster VO2 kinetics were due to adaptations to both the cardiovascular system and the peripheral musculature.

Skeletal muscle ATP turnover by 31P magnetic resonance spectroscopy during moderate and heavy bilateral knee extension

Heavy‐intensity exercise causes a progressive increase in energy demand that contributes to exercise limitation. This inefficiency arises within the locomotor muscles and is thought to be due to an increase in the ATP cost of power production; however, the responsible mechanism is unresolved. We measured whole‐body O2 uptake and skeletal muscle ATP turnover by combined pulmonary gas exchange and magnetic resonance spectroscopy during moderate and heavy exercise in humans. Muscle ATP synthesis rate increased throughout constant‐power heavy exercise, but this increase was unrelated to the progression of whole‐body inefficiency. Our data indicate that the increased ATP requirement is not the sole cause of inefficiency during heavy exercise, and other mechanisms, such as increased O2 cost of ATP resynthesis, may contribute.

No effect of glutamine ingestion on indices of oxidative metabolism in stable COPD

COPD patients have reduced muscle glutamate which may contribute to an impaired response of oxidative metabolism to exercise. We hypothesised that prior glutamine supplementation would enhance V(O2) peak, V(O2) at lactate threshold and speed pulmonary oxygen uptake kinetics in COPD. 13 patients (9 males, age 66±5 years, mean±SD) with severe COPD (mean FEV(1) 0.88±0.23l, 33±7% predicted) performed on separate days ramp cycle-ergometry (5-10 W min(-1)) to volitional exhaustion and subsequently square-wave transitions to 80% estimated lactate threshold (LT) following consumption of either placebo (CON) or 0.125 g kg bm(-1) of glutamine (GLN) in 5 ml kg bm(-1) placebo. Oral glutamine had no effect on peak or V(O2) at LT, {V(O2) peak: CON=0.70±0.1 l min(-1) vs. GLN=0.73±0.2 l min(-1); LT: CON=0.57±0.1 l min(-1) vs. GLN=0.54±0.1 lmin(-1)} or V(O2) kinetics {tau: CON=68±22 s vs. GLN=68±16 s}. Ingestion of glutamine before exercise did not improve indices of oxidative metabolism in this patient group.

No effect of glutamine supplementation and hyperoxia on oxidative metabolism and performance during high-intensity exercise

Abstract Glutamine enhances the exercise-induced expansion of the tricarboxylic acid intermediate pool. The aim of the present study was to determine whether oral glutamine, alone or in combination with hyperoxia, influenced oxidative metabolism and cycle time-trial performance. Eight participants consumed either placebo or 0.125 g · kg body mass−1 of glutamine in 5 ml · kg body mass−1 placebo 1 h before exercise in normoxic (control and glutamine respectively) or hyperoxic (FiO2 = 50%; hyperoxia and hyperoxia + glutamine respectively) conditions. Participants then cycled for 6 min at 70% maximal oxygen uptake ([Vdot]O2max) immediately before completing a brief high-intensity time-trial (∼4 min) during which a pre-determined volume of work was completed as fast as possible. The increment in pulmonary oxygen uptake during the performance test (Δ[Vdot]O2max, P = 0.02) and exercise performance (control: 243 s, s x = 7; glutamine: 242 s, s x = 3; hyperoxia: 231 s, s x = 3; hyperoxia + glutamine: 228 s, s x = 5; P < 0.01) were significantly improved in hyperoxic conditions. There was some evidence that glutamine ingestion increased Δ[Vdot]O2max in normoxia, but not hyperoxia (interaction drink/FiO2, P = 0.04), but there was no main effect or impact on performance. Overall, the data show no effect of glutamine ingestion either alone or in combination with hyperoxia, and thus no limiting effect of the tricarboxylic acid intermediate pool size, on oxidative metabolism and performance during maximal exercise.

Sex influence on myocardial function with exercise in adolescents

Ventricular systolic functional response to exercise has been reported to be superior in adult men compared to women. This study explored myocardial responses to maximal upright progressive exercise in late pubertal males and females.

Effects of magnitude and frequency of variations in external power output on simulated cycling time-trial performance

Abstract Mechanical models of cycling time-trial performance have indicated adverse effects of variations in external power output on overall performance times. Nevertheless, the precise influences of the magnitude and number of these variations over different distances of time trial are unclear. A hypothetical cyclist (body mass 70 kg, bicycle mass 10 kg) was studied using a mathematical model of cycling, which included the effects of acceleration. Performance times were modelled over distances of 4–40 km, mean power outputs of 200–600 W, power variation amplitudes of 5–15% and variation frequencies of 2–32 per time-trial. Effects of a “fast-start” strategy were compared with those of a constant-power strategy. Varying power improved 4-km performance at all power outputs, with the greatest improvement being 0.90 s for ± 15% power variation. For distances of 16.1, 20 and 40 km, varying power by ± 15% increased times by 3.29, 4.46 and 10.43 s respectively, suggesting that in long-duration cycling in constant environmental conditions, cyclists should strive to reduce power variation to maximise performance. The novel finding of the present study is that these effects are augmented with increasing event distance, amplitude and period of variation. These two latter factors reflect a poor adherence to a constant speed.

Prior exercise speeds pulmonary oxygen uptake kinetics and increases critical power during supine but not upright cycling

What is the central question of this study? Critical power (CP) represents the highest work rate for which a metabolic steady state is attainable. The physiological determinants of CP are unclear, but research suggests that CP might be related to the time constant of phase II oxygen uptake kinetics ( τV̇O2 ). What is the main finding and its importance? We provide the first evidence that τV̇O2 is mechanistically related to CP. A reduction of τV̇O2 in the supine position was observed alongside a concomitant increase in CP. This effect may be contingent on measures of oxygen availability derived from near‐infrared spectroscopy.

Effects of power variation on cycle performance during simulated hilly time-trials

Abstract It has previously been shown that cyclists are unable to maintain a constant power output during cycle time-trials on hilly courses. The purpose of the present study is therefore to quantify these effects of power variation using a mathematical model of cycling performance. A hypothetical cyclist (body mass: 70 kg, bicycle mass: 10 kg) was studied using a mathematical model of cycling, which included the effects of acceleration. Performance was modelled over three hypothetical 40-km courses, comprising repeated 2.5-km sections of uphill and downhill with gradients of 1%, 3%, and 6%, respectively. Amplitude (5–15%) and distance (0.31–20.00 km) of variation were modelled over a range of mean power outputs (200–600 W) and compared to sustaining a constant power. Power variation was typically detrimental to performance; these effects were augmented as the amplitude of variation and severity of gradient increased. Varying power every 1.25 km was most detrimental to performance; at a mean power of 200 W, performance was impaired by 43.90 s (±15% variation, 6% gradient). However at the steepest gradients, the effect of power variation was relatively independent of the distance of variation. In contrast, varying power in parallel with changes in gradient improved performance by 188.89 s (±15% variation, 6% gradient) at 200 W. The present data demonstrate that during hilly time-trials, power variation that does not occur in parallel with changes in gradient is detrimental to performance, especially at steeper gradients. These adverse effects are substantially larger than those previously observed during flat, windless time-trials.