Exercise Intensity-Dependent Effects on Cognitive Control Function during and after Acute Treadmill Running in Young Healthy Adults

The aim of the present study was to investigate the effects of acute administration of taurine overload on time to exhaustion (TTE) of high-intensity running performance and alternative maximal accumulated oxygen deficit (MAODALT). The study design was a randomized, placebo-controlled, crossover design. Seventeen healthy male volunteers (age: 25 ± 6 years; maximal oxygen uptake: 50.5 ± 7.6 mL·kg−1·min−1) performed an incremental treadmill-running test until voluntary exhaustion to determine maximal oxygen uptake and exercise intensity at maximal oxygen uptake. Subsequently, participants completed randomly 2 bouts of supramaximal treadmill-running at 110% exercise intensity at maximal oxygen uptake until exhaustion (placebo (6 g dextrose) or taurine (6 g) supplementation), separated by 1 week. MAODALT was determined using a single supramaximal effort by summating the contribution of the phosphagen and glycolytic pathways. When comparing the results of the supramaximal trials (i.e., placebo and taurine conditions) no differences were observed for high-intensity running TTE (237.70 ± 66.00 and 277.30 ± 40.64 s; p = 0.44) and MAODALT (55.77 ± 8.22 and 55.06 ± 7.89 mL·kg−1; p = 0.61), which seem to indicate trivial and unclear differences using the magnitude-based inferences approach, respectively. In conclusion, acute 6 g taurine supplementation before exercise did not substantially improve high-intensity running performance and showed an unclear effect on MAODALT.

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Cognitive Control Deficits in Alcohol Dependence Are a Trait- and State-Dependent Biomarker: An ERP Study

Frontiers in Psychiatry ◽

10.3389/fpsyt.2020.606891 ◽

2020 ◽

Vol 11 ◽

Author(s):

Xiaohong Liu ◽

Hongliang Zhou ◽

Chenguang Jiang ◽

Yanling Xue ◽

Zhenhe Zhou ◽

...

Keyword(s):

Cognitive Control ◽

Alcohol Dependence ◽

Control Function ◽

Event Related Potential ◽

Oddball Paradigm ◽

Group Level ◽

Auditory Oddball ◽

State Dependent ◽

Simple Effect ◽

Time Point

Alcohol dependence (AD) presents cognitive control deficits. Event-related potential (ERP) P300 reflects cognitive control-related processing. The aim of this study was to investigate whether cognitive control deficits are a trait biomarker or a state biomarker in AD. Participants included 30 AD patients and 30 healthy controls (HCs). All participants were measured with P300 evoked by a three-stimulus auditory oddball paradigm at a normal state (time 1, i.e., just after the last alcohol intake) and abstinence (time 2, i.e., just after a 4-week abstinence). The results showed that for P3a and P3b amplitude, the interaction effect for group × time point was significant, the simple effect for group at time 1 level and time 2 level was significant, and the simple effect for time point at AD group level was significant; however, the simple effect for time point at HC group level was not significant. Above results indicated that compared to HCs, AD patients present reductions of P3a/3b amplitude, and after 4-week alcohol abstinence, although P3a/3b amplitudes were improved, they were still lower than those of HCs. For P3a and P3b latencies, no significant differences were observed. These findings conclude that AD patients present cognitive control deficits that are reflected by P3a/3b and that cognitive control deficits in AD are trait- and state-dependent. The implication of these findings is helpful to understand the psychological and neural processes for AD, and these findings suggest that improving the cognitive control function may impact the treatment effect for AD.

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Attenuation of force deficit after lengthening contractions in soleus muscle from trained rats

Journal of Applied Physiology ◽

10.1152/jappl.2000.88.4.1254 ◽

2000 ◽

Vol 88 (4) ◽

pp. 1254-1258 ◽

Cited By ~ 16

Author(s):

Luc E. Gosselin

Keyword(s):

Exercise Training ◽

Exercise Intensity ◽

Muscle Length ◽

Training Group ◽

Treadmill Running ◽

Similar Degree ◽

Lengthening Contractions ◽

Lengthening Contraction ◽

Old Rats

The purposes of this study were 1) to determine the extent to which endurance training reduces the functional deficit induced by lengthening contractions in the soleus (Sol) muscle and 2) to determine whether young and old rats training at a comparable relative exercise intensity would demonstrate a similar protective effect from lengthening-contraction-induced injury. Young (3-mo-old) and old (23-mo-old) male Fischer 344 rats were randomly assigned to either a control or exercise training group [young control (YC), old control (OC), young trained (YT), old trained (OT)]. Exercise training consisted of 10 wk of treadmill running (15% grade, 45 min/day, and 5 days/wk) such that by the end of training the young and old rats were exercising at 27 and 15 m/min, respectively. After training, contractile properties of the Sol muscle were measured in vitro at 26°C. The percent decrease in maximal isometric specific force (Po) was determined after a series of 20 lengthening contractions (20% strain from optimal muscle length, 1 contraction every 5 s). After the lengthening-contraction protocol, Sol muscle Po was decreased by ∼26% (19.6 vs. 14.6 N/cm2) and 28% (14.8 vs. 9.6 N/cm2) in the YC and OC rats, respectively. After exercise training, the reduction in Po was significantly ( P < 0.05) attenuated to a similar degree (∼13%) in both YT rats (18.7 vs. 16.2 N/cm2) and OT rats (15.8 vs. 13.7 N/cm2). It is concluded that exercise training attenuates the force deficit after repeated lengthening contractions to a comparable extent in young and old rats training at a similar exercise intensity.

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Effect of exercise intensity and AICAR on isoform-specific expressions of murine skeletal muscle PGC-1α mRNA: a role of β2-adrenergic receptor activation

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00400.2010 ◽

2011 ◽

Vol 300 (2) ◽

pp. E341-E349 ◽

Cited By ~ 76

Author(s):

Miki Tadaishi ◽

Shinji Miura ◽

Yuko Kai ◽

Emi Kawasaki ◽

Keiichi Koshinaka ◽

...

Keyword(s):

Exercise Intensity ◽

High Intensity ◽

Adrenergic Receptor ◽

Skeletal Muscles ◽

Receptor Activation ◽

High Intensity Exercise ◽

Treadmill Running ◽

Peroxisome Proliferator ◽

Peroxisome Proliferator Activated Receptor ◽

Exercise Induced

There are three isoforms of peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α) mRNA, which promotes mitochondrial biogenesis in skeletal muscles. Compared with PGC-1α-a mRNA, PGC-1α-b or PGC-1α-c mRNA is transcribed by a different exon 1 of the PGC-1α gene. In this study, effects of exercise intensity and 5-aminoimidazole-4-carboxamide-1β-d-ribofuranoside (AICAR) on isoform-specific expressions of PGC-1α were investigated. All isoforms were increased in proportion to exercise intensity of treadmill running (10–30 m/min for 30 min). Preinjection of β2-adrenergic receptor (AR) antagonist (ICI 118551) inhibited the increase in PGC-1α-b and PGC-1α-c mRNAs, but not the increase in PGC-1α-a mRNA, in response to high-intensity exercise. Although high-intensity exercise activated α2-AMP-activated protein kinase (α2-AMPK) in skeletal muscles, inactivation of α2-AMPK activity did not affect high-intensity exercise-induced mRNA expression of all PGC-1α isoforms, suggesting that activation of α2-AMPK is not mandatory for an increase in PGC-1α mRNA by high-intensity exercise. A single injection in mice of AICAR, an AMPK activator, increased mRNAs of all PGC-1α isoforms. AICAR increased blood catecholamine concentrations, and preinjection of β2-AR antagonist inhibited the increase in PGC-1α-b and PGC-1α-c mRNAs but not the increase in PGC-1α-a mRNA. Direct exposure of epitrochlearis muscle to AICAR increased PGC-1α-a but not the -b isoform. These data indicate that exercise-induced PGC-1α expression was dependent on the intensity of exercise. Exercise or AICAR injection increased PGC-1α-b and PGC-1α-c mRNAs via β2-AR activation, whereas high-intensity exercise increased PGC-1α-a expression by a multiple mechanism in which α2-AMPK is one of the signaling pathways.

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Acute effects of cocaine on the neurobiology of cognitive control

Philosophical Transactions of the Royal Society B Biological Sciences ◽

10.1098/rstb.2008.0106 ◽

2008 ◽

Vol 363 (1507) ◽

pp. 3267-3276 ◽

Cited By ~ 91

Author(s):

Hugh Garavan ◽

Jacqueline N Kaufman ◽

Robert Hester

Keyword(s):

Cognitive Control ◽

Cognitive Processes ◽

Impulse Control ◽

Control Function ◽

Brain Regions ◽

Acute Effects ◽

Neurocognitive Dysfunction ◽

Action Monitoring ◽

Motor Response Inhibition ◽

Drug Naïve

Compromised ability to exert control over drug urges and drug-seeking behaviour is a characteristic of addiction. One specific cognitive control function, impulse control, has been shown to be a risk factor for the development of substance problems and has been linked in animal models to increased drug administration and relapse. We present evidence of a direct effect of cocaine on the neurobiology underlying impulse control. In a laboratory test of motor response inhibition, an intravenous cocaine administration improved task performance in 13 cocaine users. This improvement was accompanied by increased activation in right dorsolateral and inferior frontal cortex, regions considered critical for this cognitive function. Similarly, for both inhibitory control and action monitoring processes, cocaine normalized activation levels in lateral and medial prefrontal regions previously reported to be hypoactive in users relative to drug-naive controls. The acute amelioration of neurocognitive dysfunction may reflect a chronic dysregulation of those brain regions and the cognitive processes they subserve. Furthermore, the effects of cocaine on midline function suggest a dopaminergically mediated intersection between cocaine's acute reinforcing effects and its effects on cognitive control.

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