Plant-based diets benefit aerobic performance and do not compromise strength/power performance: a systematic review and meta-analysis.

Plant-based diets have emerged as athletic performance enhancers for various types of exercise. Therefore, the present study evaluated the effectiveness of plant-based diets on aerobic and strength/power performances, as well as on BMI of physically active individuals. This systematic review and meta-analysis was conducted and reported according to the guidelines outlined in the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement. A systematic search of electronic databases, including PubMed, Web of Science and SPORTDiscus, was performed. On the basis of the search and inclusion criteria, four and six studies evaluating the effects of plant-based diets on aerobic and strength/power performances in humans were, respectively, included in the systematic review and meta-analysis. Plant-based diets had a moderate but positive effect on aerobic performance (0·55; 95 % CI 0·29, 0·81) and no effect on strength/power performance (-0·30; 95 % CI -0·67, 0·07). The altogether analyses of both aerobic and strength/power exercises revealed that athletic performance was unchanged (0·01; 95 % CI -0·21, 0·22) in athletes who adopted plant-based diets. However, a small negative effect on BMI (-0·27; 95 % CI -0·40, -0·15) was induced by these diets. The results indicate that plant-based diets have the potential to exclusively assist aerobic performance. On the other hand, these diets do not jeopardise strength/power performance. Overall, the predicted effects of plant-based diets on physical performance are impactless, even though the BMI of their adherents is reduced.

TRPV1 inactivation alters core body temperature and serum corticosterone levels: Impacts on clock genes expression in the liver and adrenal glands.

PURPOSE: TRPV1 desensitization or blockade promotes hyperthermia in rodents. Daily changes in core body temperature (Tc), spontaneous locomotor activity (SLA), and glucocorticoids are temporal cues for peripheral clocks. Thus, this study aimed to evaluate the effects of both desensitization and blockade of TRPV1 on Tc, SLA, blood corticosterone, and the clock genes Per1 and Bmal1 in the liver and adrenal. METHODS AND RESULTS: Resiniferatoxin (RTX, 20 µg kg-1) known to desensitize the intra-abdominal TRPV1 channels was i. p. administered in adult male rats. One day after, RTX rats displayed higher Tc than vehicle rats (control) in the light and dark phases. RTX rats showed higher corticosterone at zeitgeber time (ZT) 6 and ZT12 compared to ZT0. Control rats showed a rise in corticosterone at ZT12. RTX abolished the Per1 peak in both the liver and adrenal glands, whereas it enhanced the peak of Bmal1 expression in the liver and decreased it in adrenal glands. Circadian variation in Tc and SLA was unaffected despite higher Tc being found along the light phase up to 5 days after RTX injection. Acute blockade of TRPV1 with the antagonist AMG-517 injected at ZT0 increased Tc and reduced corticosterone without affecting SLA. In the liver, while AMG-517 did not affect Per1, it increased Bmal1 mRNA. In adrenal glands, AMG-517 increased Per1 and did not affect Bmal1 expression. Although rats exposed to a 60-min 34 °C environment showed similar hyperthermia to that observed in AMG-517 rats, neither corticosterone nor liver nor adrenal clock genes changed. CONCLUSIONS: Inactivation of TRPV1 by abdominal desensitization or by antagonism alters the time-of-day changes of clock genes expression in the liver and adrenal, as well as corticosterone. TRPV1 may be necessary for signaling cyclical temporal cues for clock genes in the periphery but less critical for the circadian profile of Tc and SLA.

Determinants of body core temperatures at fatigue in rats subjected to incremental-speed exercise: The prominent roles of ambient temperature, distance traveled, initial core temperature, and measurement site.

Understanding the factors that underlie the physical exercise-induced increase in body core temperature (TCORE) is essential to developing strategies to counteract hyperthermic fatigue and reduce the risk of exertional heatstroke. This study analyzed the contribution of six factors to TCORE attained at fatigue in Wistar rats (n = 218) subjected to incremental-speed treadmill running: ambient temperature (TAMB), distance traveled, initial TCORE, body mass, measurement site, and heat loss index (HLI). First, we ran hierarchical multiple linear regression analyses with data from different studies conducted in our laboratory (n = 353 recordings). We observed that TAMB, distance traveled, initial TCORE, and measurement site were the variables with predictive power. Next, regression analyses were conducted with data for each of the following TCORE indices: abdominal (TABD), brain cortex (TBRAIN), or colonic (TCOL) temperature. Our findings indicated that TAMB, distance traveled (i.e., an exercise performance-related variable), initial TCORE, and HLI predicted the three TCORE indices at fatigue. Most intriguingly, HLI was inversely related to TABD and TBRAIN but positively associated with TCOL. Lastly, we compared the temperature values at fatigue among these TCORE indices, and the following descendent order was noticed - TCOL, TABD, and TBRAIN - irrespective of TAMB where experiments were conducted. In conclusion, TCORE in rats exercised to fatigue depends primarily on environmental conditions, performance, pre-exercise TCORE, and measurement site. Moreover, the influence of cutaneous heat loss on TCOL is qualitatively different from the influence on TABD and TBRAIN, and the temperature values at fatigue are not homogenous within the body core.

Norepinephrine modulation of heat dissipation in female rats lacking estrogen.

Postmenopausal hot flushes are caused by lack of estradiol (E2) but their neuroendocrine basis is still poorly understood. Here, we investigated the interrelationship between norepinephrine and hypothalamic neurons, with emphasis on kisspeptin neurons in the arcuate nucleus (ARC), as a regulatory pathway in the vasomotor effects of E2. Ovariectomized (OVX) rats displayed increased tail skin temperature (TST), and this increase was prevented in OVX rats treated with E2 (OVX + E2). Expression of Fos in the hypothalamus and the number of ARC kisspeptin neurons coexpressing Fos were increased in OVX rats. Likewise, brainstem norepinephrine neurons of OVX rats displayed higher Fos immunoreactivity associated with the increase in TST. In the ARC, the density of dopamine-ß-hydroxylase (DBH)-immunoreactive (ir) fibers was not altered by E2 but, importantly, DBH-ir terminals were found in close apposition to kisspeptin cells, revealing norepinephrine inputs to ARC kisspeptin neurons. Intracerebroventricular injection of the α2-adrenergic agonist clonidine (CLO) was used to reduce central norepinephrine release, confirmed by the decreased 3-methoxy-4-hydroxyphenylglycol/norepinephrine ratio in the preoptic area and ARC. Accordingly, CLO treatment in OVX rats reduced ARC Kiss1 mRNA levels and TST to the values of OVX + E2 rats. Conversely, CLO stimulated Kiss1 expression in the anteroventral periventricular nucleus (AVPV) and increased luteinizing hormone secretion. These findings provide evidence that augmented heat dissipation in OVX rats involves the increase in central norepinephrine that modulates hypothalamic areas related to thermoregulation, including ARC kisspeptin neurons. This neuronal network is suppressed by E2 and its imbalance may be implicated in the vasomotor symptoms of postmenopausal hot flushes.

Exercise capacity in different stages of hypertension in spontaneously hypertensive rats.

BACKGROUND: The aim of the present study was to investigate the exercise capacity of hypertensive rats at different stages of development of hypertension and to determine the most suitable index to evaluate the exercise capacity in different strains. METHODS: Male spontaneously hypertensive rat (SHR) and normotensive Wistar rats (NWR) of 5, 8, 12 and 16 weeks were submitted to the exercise capacity test. The exercise running time was measured and the workload was calculated. RESULTS: Normotensive and hypertensive rats when assess the exercise capacity by exercise running time exhibited a reduction in exercise performance over time. Moreover, hypertensive rats showed lower exercise capacity compared to normotensive control when analyzed by workload. CONCLUSIONS: The present results indicate that hypertensive rats exhibit reduced exercise capacity compared to normotensive rats regardless of age assessed. Beside that, in experiments with strains with different body mass the most reliable index to assess exercise capacity is workload.

Spontaneously hypertensive rats have greater impairments in regulating abdominal temperature than brain cortex temperature following physical exercise.

This study aimed to evaluate the changes in brain (Tbrain) and abdominal (Tabd) temperatures in spontaneously hypertensive rats (SHRs) following fatiguing exercise. Male normotensive Wistar rats (NWRs) and SHRs were used at 16 weeks of age. Their arterial pressure was measured by tail plethysmography prior to the experiments to confirm the hypertensive status of the SHRs. Then, the rats underwent implantation of an abdominal temperature sensor to measure Tabd and a guide cannula in the frontal cortex to enable the insertion of a thermistor to measure Tbrain. After a familiarization period, each animal was subjected to incremental speed exercises until fatigue in either a temperate (25 °C) or warm (32 °C) environment, followed by a 60-min post-exercise period at the same temperature at which they exercised. Tbrain, Tabd and tail-skin temperature (Tskin) were measured every min throughout the experiments. SHRs exhibited higher Tabd values than NWRs, and these higher values were transiently and persistently observed at 25 °C and 32 °C, respectively. For example, at 32 °C, Tabd was 0.84 °C higher in SHRs at the 25th min (large effect size). In contrast, regardless of the ambient temperature, SHRs exhibited similar Tbrain values as NWRs, indicating preserved Tbrain regulation following exercise in hypertensive rats. SHRs presented higher Tskin during the last half of the post-exercise period at 25 °C, whereas no inter-group differences were observed at 32 °C. In conclusion, the present results highlight that SHRs, an animal model that mimics uncontrolled essential hypertension in humans, exhibited greater impairments in regulating Tabd than Tbrain during the post-exercise period.

Nitrate supplementation improves physical performance specifically in non-athletes during prolonged open-ended tests: a systematic review and meta-analysis.

Nitrate (NO3 -) is an ergogenic nutritional supplement that is widely used to improve physical performance. However, the effectiveness of NO3 - supplementation has not been systematically investigated in individuals with different physical fitness levels. The present study analysed whether different fitness levels (non-athletes v. athletes or classification of performance levels), duration of the test used to measure performance (short v. long duration) and the test protocol (time trials v. open-ended tests v. graded-exercise tests) influence the effects of NO3 - supplementation on performance. This systematic review and meta-analysis was conducted and reported according to the guidelines outlined in the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement. A systematic search of electronic databases, including PubMed, Web of Science, SPORTDiscus and ProQuest, was performed in August 2017. On the basis of the search and inclusion criteria, fifty-four and fifty-three placebo-controlled studies evaluating the effects of NO3 - supplementation on performance in humans were included in the systematic review and meta-analysis, respectively. NO3 - supplementation was ergogenic in non-athletes (mean effect size (ES) 0·25; 95 % CI 0·11, 0·38), particularly in evaluations of performance using long-duration open-ended tests (ES 0·47; 95 % CI 0·23, 0·71). In contrast, NO3 - supplementation did not enhance the performance of athletes (ES 0·04; 95 % CI -0·05, 0·15). After objectively classifying the participants into different performance levels, the frequency of trials showing ergogenic effects in individuals classified at lower levels was higher than that in individuals classified at higher levels. Thus, the present study indicates that dietary NO3 - supplementation improves physical performance in non-athletes, particularly during long-duration open-ended tests.

Attenuation of Ca2+ homeostasis, oxidative stress, and mitochondrial dysfunctions in diabetic rat heart: insulin therapy or aerobic exercise?

We tested the effects of swimming training and insulin therapy, either alone or in combination, on the intracellular calcium ([Ca(2+)]i) homeostasis, oxidative stress, and mitochondrial functions in diabetic rat hearts. Male Wistar rats were separated into control, diabetic, or diabetic plus insulin groups. Type 1 diabetes mellitus was induced by streptozotocin (STZ). Insulin-treated groups received 1 to 4 UI of insulin daily for 8 wk. Each group was divided into sedentary or exercised rats. Trained groups were submitted to swimming (90 min/day, 5 days/wk, 8 wk). [Ca(2+)]i transient in left ventricular myocytes (LVM), oxidative stress in LV tissue, and mitochondrial functions in the heart were assessed. Diabetes reduced the amplitude and prolonged the times to peak and to half decay of the [Ca(2+)]i transient in LVM, increased NADPH oxidase-4 (Nox-4) expression, decreased superoxide dismutase (SOD), and increased carbonyl protein contents in LV tissue. In isolated mitochondria, diabetes increased Ca(2+) uptake, susceptibility to permeability transition pore (MPTP) opening, uncoupling protein-2 (UCP-2) expression, and oxygen consumption but reduced H2O2 release. Swimming training corrected the time course of the [Ca(2+)]i transient, UCP-2 expression, and mitochondrial Ca(2+) uptake. Insulin replacement further normalized [Ca(2+)]i transient amplitude, Nox-4 expression, and carbonyl content. Alongside these benefits, the combination of both therapies restored the LV tissue SOD and mitochondrial O2 consumption, H2O2 release, and MPTP opening. In conclusion, the combination of swimming training with insulin replacement was more effective in attenuating intracellular Ca(2+) disruptions, oxidative stress, and mitochondrial dysfunctions in STZ-induced diabetic rat hearts.

Temperature Control of Hypertensive Rats during Moderate Exercise in Warm Environment.

The control of body temperature in Spontaneously Hypertensive Rat (SHR) subjected to exercise in warm environment was investigated. Male SHR and Wistar rats were submitted to moderate exercise in temperate (25°C) and warm (32°C) environments while body and tail skin temperatures, as well as oxygen consumption, were registered. Total time of exercise, workload performed, mechanical efficiency and heat storage were determined. SHR had increased heat production and body temperature at the end of exercise, reduced mechanical efficiency and increased heat storage (p < 0.05). Furthermore, these rats also showed a more intense and faster increase in body temperature during moderate exercise in the warm environment (p < 0.05). The lower mechanical efficiency seen in SHR was closely correlated with their higher body temperature at the point of fatigue in warm environment (p < 0.05). Our results indicate that SHR exhibit significant differences in body temperature control during moderate exercise in warm environment characterized by increased heat production and heat storage during moderate exercise in warm environment. The combination of these responses result in aggravated hyperthermia linked with lower mechanical efficiency. Key PointsThe practice of physical exercise in warm environment has gained importance in recent decades mainly because of the progressive increases in environmental temperature;To the best of our knowledge, these is the first study to analyze body temperature control of SHR during moderate exercise in warm environment;SHR showed increased heat production and heat storage that resulted in higher body temperature at the end of exercise;SHR showed reduced mechanical efficiency;These results demonstrate that when exercising in a warm environment the hypertensive rat exhibit differences in temperature control.

Cardiovascular and electrocardiographic parameters after tonin administration in Wistar rats.

In order to understand the mechanisms of interaction between tonin-angiotensin and renin-angiotensin systems (RAS) we evaluated, "in vivo" and "in vitro", in Wistar rats, cardiovascular and electrocardiographic parameters after tonin administration. Arterial pressure (AP) and electrocardiogram (ECG) were recorded in awake animals before and after tonin administration. Langendorff technique was used to analyze cardiac function in isolated heart in the presence of tonin and video motion edge detection system was used to evaluate the effect of tonin upon contractile function of isolated rat ventricular cardiomyocytes. After tonin infusion rats presented significantly higher diastolic and mean arterial pressure (MAP) and heart rate (HR) as compared with control. The ECG analysis revealed shorter RR interval, increase in the low-frequency (LF) range of the heart rate variability (HRV) power (%) and decrease in the high-frequency (HF) of HRV power (%). Isolated hearts perfused with tonin presented an increase in the arterial coronary pressure (ACP) and decline in the ventricular systolic tension (ST), maximal (dT/dt+) and minimal (dT/dt) contractility. The rates of contraction and relaxation of isolated ventricular cardiomyocytes were significantly increased due to the presence of tonin. The angiotensin II (Ang II) levels in the coronary sinus effluent increased in the presence of tonin in a dose-dependent manner and the effect of tonin upon ACP was completely blocked by candesartan. Tonin is able to generate the vasoconstrictor peptide Ang II in the isolated heart of the rat and the cardiovascular response induced by tonin was completely blocked by candesartan, an indication that the action of Ang II on Ang II type 1 (AT1) receptors is the major mechanism of the heart effects. Tonin affects cardiomyocyte contractile function which may be due to interference with Ca(2+) handling.