[show abstract][hide abstract] ABSTRACT: 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.
[show abstract][hide abstract] ABSTRACT: Background
Short bouts of exercise can reduce cravings, attentional bias (AB) and substance use among abstaining smokers and snackers. Only one study has shown reduced alcohol cravings following exercise but none have investigated the effects on attentional bias. The aim of the present study was to examine whether a single session of exercise reduces AB towards alcohol-related images and alcohol urges among high alcohol consumers.
The study involved 20 abstaining (for ≥3 days) alcohol drinkers, consuming more than weekly recommendations, with a mean age (SD) = 20.8 (0.8) years. Participants were initially randomised in a counterbalanced cross-over design to undertake either (1) 15 min of brisk walking or (2) 15 min of passive seating on different days. Participants completed an adapted dot probe task, with matched neutral and alcohol images randomly presented for either 200 ms or 1000 ms to respectively measure initial (IAB) or maintained attentional bias (MAB) pre- and post-treatment. The Alcohol Urge Questionnaire (AUQ) was administered before, immediately after, and 5 and 10 min post treatment.
A two-way fully repeated measures ANOVA revealed a significant condition × time interaction for MAB F(1, 17) = 6.96, p = 0.017, and AUQ scores F(1.47, 27.96) = 60.19, p < 0.001. MAB was significantly reduced following the exercise compared with the control condition. Differences in AUQ between conditions were significant at all assessments post treatment.
A short bout of exercise, compared with a passive control condition, may acutely reduce MAB to alcohol cues and alcohol urges, and thus may help with self-regulation of alcohol consumption.