Biology subjects

Andrade-Souza, V. A.

Publications and source records attributed to Andrade-Souza, V. A..

3 recordsLinked to original sources

bioRxiv2020

Changes in insulin resistance do not occur in parallel with changes in mitochondrial content and function in male rats

Aims/hypothesisTo investigate if there is a causal relationship between changes in insulin resistance and mitochondrial respiratory function and content in rats fed a high fat diet (HFD) with or without concurrent exercise training. We hypothesised that provision of a high fat diet (HFD) would increase insulin resistance and decrease mitochondrial characteristics (content and function), and that exercise training would improve both mitochondrial characteristics and insulin resistance in rats fed a HFD. MethodsMale Wistar rats were given either a chow diet or a high fat diet (HFD) for 12 weeks. After 4 weeks of the dietary intervention, half of the rats in each group began eight weeks of interval training. In vivo glucose and insulin tolerance was assessed, as was ex vivo glucose uptake in epitrochlearis muscle. Mitochondrial respiratory function was assessed in permeabilised soleus and white gastrocnemius (WG) muscles. Mitochondrial content was determined by measurement of citrate synthase (CS) activity and protein expression of components of the electron transport system (ETS). ResultsHFD rats had impaired glucose and insulin tolerance. HFD did not change CS activity in the soleus; however, it did increase CS activity in WG (Chow 5.9 {+/-} 0.5, HFD 7.2 {+/-} 0.7 mol h-1 kg protein-1). Protein expression of components of the ETS and mitochondrial respiratory function (WG Chow 65.2 {+/-} 8.4, HFD 88.6 {+/-} 8.7 pmol O2 s-1 mg-1) were also increased by HFD. Exercise training improved glucose and insulin tolerance in the HFD rats. Exercise training did not alter CS activity in either muscle. Mitochondrial respiratory function was increased with exercise training in the chow fed animals in soleus muscle, but not in WG. This exercise effect was absent in the HFD animals. Mitochondrial characteristics did not consistently correlate with insulin or glucose tolerance. Conclusions/interpretationHFD induced insulin resistance, but it did not negatively affect any of the measured mitochondrial characteristics. Exercise training improved insulin resistance, but without changes in mitochondrial respiration and content. The lack of an association between mitochondrial characteristics and insulin resistance was reinforced by the absence of strong correlations between these measures. Our results suggest that defects in mitochondrial respiration and content are not responsible for insulin resistance in HFD rats.

physiology↗

bioRxiv2019

Caffeine but not acetaminophen increases 4-km cycling time-trial performance

Acetaminophen has been combined with caffeine for therapeutic purpose, but the effect of co-ingestion of acetaminophen and caffeine on exercise performance has not been investigated. The aim of this study was to determine the effect of isolated and combined ingestion of caffeine and acetaminophen on performance during a 4-km cycling time-trial. In a double-blind, crossover design, eleven men, accustomed to cycling recreationally, completed a 4-km cycling time-trial one hour after the ingestion of cellulose (PLA), acetaminophen (20 mg{middle dot}kg-1 body mass, ACT), caffeine (5 mg{middle dot}kg-1 body mass, CAF) or combined acetaminophen and caffeine (20 and 5 mg{middle dot}kg-1 body mass, respectively, ACTCAF). The perception of pain and rating of perceived exertion were recorded every 1-km, and electromyography and oxygen uptake were continually recorded and averaged each 1-km. Plasma lactate concentration was measured before and immediately after the trial. The time and mean power during the 4-km cycling time-trial was significantly improved (P < 0.05) in CAF (407.9 {+/-} 24.5 s, 241.4 {+/-} 16.1 W) compared to PLA (416.1 {+/-} 34.1 s, 234.1 {+/-} 19.2 W) and ACT (416.2 {+/-} 26.6 s, 235.8 {+/-} 19.7 W). However, there was no difference between ACTCAF (411.6 {+/-} 27.7 s, 238.7 {+/-} 18.7 W) and the other conditions (P > 0.05). The perception of pain, rating of perceived exertion, electromyography, oxygen uptake, and plasma lactate were similar across the conditions (P > 0.05). In conclusion, caffeine but not acetaminophen increases power output ultimately increasing performance during a 4-km cycling time-trial.

physiology↗

bioRxiv2019

Exercise twice-a-day potentiates skeletal muscle signalling responses associated with mitochondrial biogenesis in humans, which are independent of lowered muscle glycogen content

Endurance exercise begun with reduced muscle glycogen stores seems to potentiate skeletal muscle protein abundance and gene expression. However, it is unknown whether this greater signalling responses is due to low muscle glycogen per se or to performing two exercise sessions in close proximity - as a first exercise session is necessary to reduce the muscle glycogen stores. In the present study, we manipulated the recovery duration between a first muscle glycogen-depleting exercise and a second exercise session, such that the second exercise session started with reduced muscle glycogen in both approaches but was performed either two or 15 h after the first exercise session (so-called "twice-a-day" and "once-daily" approaches, respectively). We found that exercise twice-a-day increased the nuclear abundance of transcription factor EB (TFEB) and nuclear factor of activated T cells (NFAT) and potentiated the transcription of peroxisome proliferator-activated receptor-coactivator 1 alpha (PGC-1), peroxisome proliferator-activated receptor alpha (PPAR) and peroxisome proliferator-activated receptor beta/delta (PPAR{beta}/{delta}) genes, in comparison with the once-daily exercise. These results suggest that the elevated molecular signalling reported with previous "train-low" approaches can be attributed to performing two exercise sessions in close proximity rather than the reduced muscle glycogen content per se. The twice-a-day approach might be an effective strategy to induce adaptations related to mitochondrial biogenesis and fat oxidation.

molecular biology↗