scholarly journals Capsaicin and Its Effect on Exercise Performance, Fatigue and Inflammation after Exercise

Nutrients ◽  
2022 ◽  
Vol 14 (2) ◽  
pp. 232
Author(s):  
Gaia Giuriato ◽  
Massimo Venturelli ◽  
Alexs Matias ◽  
Edgard M. K. V. K. Soares ◽  
Jessica Gaetgens ◽  
...  

Capsaicin (CAP) activates the transient receptor potential vanilloid 1 (TRPV1) channel on sensory neurons, improving ATP production, vascular function, fatigue resistance, and thus exercise performance. However, the underlying mechanisms of CAP-induced ergogenic effects and fatigue-resistance, remain elusive. To evaluate the potential anti-fatigue effects of CAP, 10 young healthy males performed constant-load cycling exercise time to exhaustion (TTE) trials (85% maximal work rate) after ingestion of placebo (PL; fiber) or CAP capsules in a blinded, counterbalanced, crossover design, while cardiorespiratory responses were monitored. Fatigue was assessed with the interpolated twitch technique, pre-post exercise, during isometric maximal voluntary contractions (MVC). No significant differences (p > 0.05) were detected in cardiorespiratory responses and self-reported fatigue (RPE scale) during the time trial or in TTE (375 ± 26 and 327 ± 36 s, respectively). CAP attenuated the reduction in potentiated twitch (PL: −52 ± 6 vs. CAP: −42 ± 11%, p = 0.037), and tended to attenuate the decline in maximal relaxation rate (PL: −47 ± 33 vs. CAP: −29 ± 68%, p = 0.057), but not maximal rate of force development, MVC, or voluntary muscle activation. Thus, CAP might attenuate neuromuscular fatigue through alterations in afferent signaling or neuromuscular relaxation kinetics, perhaps mediated via the sarco-endoplasmic reticulum Ca2+ ATPase (SERCA) pumps, thereby increasing the rate of Ca2+ reuptake and relaxation.

2014 ◽  
Vol 306 (4) ◽  
pp. H574-H584 ◽  
Author(s):  
Jack Rubinstein ◽  
Valerie M. Lasko ◽  
Sheryl E. Koch ◽  
Vivek P. Singh ◽  
Vinicius Carreira ◽  
...  

Transient receptor potential cation channels have been implicated in the regulation of cardiovascular function, but only recently has our laboratory described the vanilloid-2 subtype (TRPV2) in the cardiomyocyte, though its exact mechanism of action has not yet been established. This study tests the hypothesis that TRPV2 plays an important role in regulating myocyte contractility under physiological conditions. Therefore, we measured cardiac and vascular function in wild-type and TRPV2−/− mice in vitro and in vivo and found that TRPV2 deletion resulted in a decrease in basal systolic and diastolic function without affecting loading conditions or vascular tone. TRPV2 stimulation with probenecid, a relatively selective TRPV2 agonist, caused an increase in both inotropy and lusitropy in wild-type mice that was blunted in TRPV2−/− mice. We examined the mechanism of TRPV2 inotropy/lusitropy in isolated myocytes and found that it modulates Ca2+ transients and sarcoplasmic reticulum Ca2+ loading. We show that the activity of this channel is necessary for normal cardiac function and that there is increased contractility in response to agonism of TRPV2 with probenecid.


Author(s):  
Noah M. A. d’Unienville ◽  
Henry T. Blake ◽  
Alison M. Coates ◽  
Alison M. Hill ◽  
Maximillian J. Nelson ◽  
...  

Abstract Background Increasing nitric oxide bioavailability may induce physiological effects that enhance endurance exercise performance. This review sought to evaluate the performance effects of consuming foods containing compounds that may promote nitric oxide bioavailability. Methods Scopus, Web of Science, Ovid Medline, EMBASE and SportDiscus were searched, with included studies assessing endurance performance following consumption of foods containing nitrate, L-arginine, L-citrulline or polyphenols. Random effects meta-analysis was conducted, with subgroup analyses performed based on food sources, sex, fitness, performance test type and supplementation protocol (e.g. duration). Results One hundred and eighteen studies were included in the meta-analysis, which encompassed 59 polyphenol studies, 56 nitrate studies and three L-citrulline studies. No effect on exercise performance following consumption of foods rich in L-citrulline was identified (SMD=-0.03, p=0.24). Trivial but significant benefits were demonstrated for consumption of nitrate and polyphenol-rich foods (SMD=0.15 and 0.17, respectively, p<0.001), including performance in time-trial, time-to-exhaustion and intermittent-type tests, and following both acute and multiple-day supplementation, but no effect of nitrate or polyphenol consumption was found in females. Among nitrate-rich foods, beneficial effects were seen for beetroot, but not red spinach or Swiss chard and rhubarb. For polyphenol-rich foods, benefits were found for grape, (nitrate-depleted) beetroot, French maritime pine, Montmorency cherry and pomegranate, while no significant effects were evident for New Zealand blackcurrant, cocoa, ginseng, green tea or raisins. Considerable heterogeneity between polyphenol studies may reflect food-specific effects or differences in study designs and subject characteristics. Well-trained males (V̇O2max ≥65 ml.kg.min-1) exhibited small, significant benefits following polyphenol, but not nitrate consumption. Conclusion Foods rich in polyphenols and nitrate provide trivial benefits for endurance exercise performance, although these effects may be food dependent. Highly trained endurance athletes do not appear to benefit from consuming nitrate-rich foods but may benefit from polyphenol consumption. Further research into food sources, dosage and supplementation duration to optimise the ergogenic response to polyphenol consumption is warranted. Further studies should evaluate whether differential sex-based responses to nitrate and polyphenol consumption are attributable to physiological differences or sample size limitations. Other The review protocol was registered on the Open Science Framework (https://osf.io/u7nsj) and no funding was provided.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
YEN LIN CHEN ◽  
Zdravka Daneva ◽  
Swapnil K. Sonkusare

Introduction: Transient receptor potential vanilloid 4 (TRPV4) channels are a major Ca 2+ entry pathway in vascular endothelial cells. TRPV4 channels are also expressed in vascular smooth muscle cells (SMC). However, the effect of SMC TRPV4 (TRPV4 SMC ) channels on vascular resistance and blood pressure remains controversial. Hypothesis: We hypothesized that TRPV4 SMC channels are essential regulators of vascular function and blood pressure. Methods: Inducible, SMC-specific TRPV4 knockout (TRPV4 SMC -/- ) mice were used. Blood pressure was monitored using radiotelemetry catheters. SMC Ca 2+ signals were recorded with a spinning disk confocal imaging system. Pressure myography studies assessed vascular reactivity in MAs. Results: Resting diastolic blood pressure and mean arterial pressure were lower in TRPV4 SMC -/- mice when compared to control mice. Selective TRPV4 channel agonist, GSK1016790A (GSK101), induced Ca 2+ influx signals in SMCs that were inhibited by TRPV4 channel inhibitor GSK2193874 and were absent in MAs from TRPV4 SMC -/- mice. In pressure myography studies, GSK101 constricted the MAs in control mice, but not in TRPV4 SMC -/- mice. Moreover, MAs from TRPV4 SMC -/- showed lower vasoconstriction in response to phenylephrine, a α1 adrenergic receptor agonist. These results indicated that Ca 2+ influx through TRPV4 SMC channels contributes to vasoconstriction and increased vascular resistance. However, studies of pressure-induced constriction or myogenic tone indicated that MAs from TRPV4 SMC -/- mice exhibit a higher myogenic constriction at pressures ≥ 60 mm Hg. Moreover, membrane depolarization-induced vasoconstriction (KCl, 33 and 60 mM) was also increased in TRPV4 SMC -/- mice when compared to the control mice, indicating that TRPV4 SMC channels oppose pressure- or membrane depolarization-induced vasoconstriction. Conclusions: TRPV4 SMC channels are essential regulators of resting blood pressure. While TRPV4 SMC channels contribute to α1 adrenergic receptor-induced vasoconstriction, they negatively regulate pressure-induced vasoconstriction. The divergent effects of TRPV4 SMC channels on vascular function may be determined by the selective stimulus-TRPV4 SMC channel coupling and downstream signaling mechanisms.


2008 ◽  
Vol 294 (3) ◽  
pp. R874-R883 ◽  
Author(s):  
Samuele M. Marcora ◽  
Andrea Bosio ◽  
Helma M. de Morree

Locomotor muscle fatigue, defined as an exercise-induced reduction in maximal voluntary force, occurs during prolonged exercise, but its effects on cardiorespiratory responses and exercise performance are unknown. In this investigation, a significant reduction in locomotor muscle force (−18%, P < 0.05) was isolated from the metabolic stress usually associated with fatiguing exercise using a 100-drop-jumps protocol consisting of one jump every 20 s from a 40-cm-high platform. The effect of this treatment on time to exhaustion during high-intensity constant-power cycling was measured in study 1 ( n = 10). In study 2 ( n = 14), test duration (871 ± 280 s) was matched between fatigue and control condition (rest). In study 1, locomotor muscle fatigue caused a significant curtailment in time to exhaustion (636 ± 278 s) compared with control (750 ± 281 s) ( P = 0.003) and increased cardiac output. Breathing frequency was significantly higher in the fatigue condition in both studies despite similar oxygen consumption and blood lactate accumulation. In study 2, high-intensity cycling did not induce further fatigue to eccentrically-fatigued locomotor muscles. In both studies, there was a significant increase in heart rate in the fatigue condition, and perceived exertion was significantly increased in study 2 compared with control. These results suggest that locomotor muscle fatigue has a significant influence on cardiorespiratory responses and exercise performance during high-intensity cycling independently from metabolic stress. These effects seem to be mediated by the increased central motor command and perception of effort required to exercise with weaker locomotor muscles.


Author(s):  
Vilton E.L. de Moura e Silva ◽  
Jason M. Cholewa ◽  
François Billaut ◽  
Ralf Jäger ◽  
Marcelo C. de Freitas ◽  
...  

Context: Capsaicinoids and capsinoids (CAP) are natural substances found primarily in chili peppers and other spicy foods that agonize the transient receptor potential vanilloid-1 in the mouth, stomach, and small intestine. Several studies have shown CAP to be a potential antiobesity agent and to exhibit an analgesic effect in both rodents and humans. However, there is no scientific consensus about the effects of CAP on physical exercise performance and its physiological mechanisms of action. Purpose: This systematic review aimed to better elucidate the effects of CAP compounds as ergogenic aids and to discuss underlying mechanisms of action by which this supplement may potentially enhance endurance performance and muscular strength. Conclusions: Among 22 studies included in the review, 14 examined the effects of capsaicinoid or capsinoid compounds on endurance and resistance exercise performance in animals, with 9 studies showing benefits on performance. In humans, 8 studies were included: 3 demonstrated significant acute endurance benefits and 2 showed acute resistance exercise performance benefits compared with a placebo condition. Therefore, while more mechanistic studies are necessary to confirm these outcomes in humans, the available scientific literature appears to suggest that these compounds could be considered an effective nutritional strategy to improve exercise performance.


2019 ◽  
Vol 127 (5) ◽  
pp. 1257-1266 ◽  
Author(s):  
Thomas J. Hureau ◽  
Joshua C. Weavil ◽  
Taylor S. Thurston ◽  
Hsuan-Yu Wan ◽  
Jayson R. Gifford ◽  
...  

We sought to investigate the role of group III/IV muscle afferents in limiting endurance exercise performance, independently of their role in optimizing locomotor muscle O2 delivery. While breathing 100% O2 to ensure a similar arterial O2 content ([Formula: see text]) in both trials, eight male cyclists performed 5-km time trials under control conditions (HCTRL) and with lumbar intrathecal fentanyl (HFENT) impairing neural feedback from the lower limbs. After each time trial, common femoral artery blood flow (FBF) was quantified (Doppler ultrasound) during constant-load cycling performed at the average power of the preceding time trial. The assessment of end-tidal gases, hemoglobin content and saturation, and FBF facilitated the calculation of leg O2 delivery. Locomotor muscle activation during cycling was estimated from vastus lateralis EMG. With electrical femoral nerve stimulation, peripheral and central fatigue were quantified by pre- to postexercise decreases in quadriceps twitch torque (ΔQtw) and voluntary activation (ΔVA), respectively. FBF (~16 mL·min−1·W−1; P = 0.6), [Formula: see text] (~24 mL O2/dL; P = 0.9), and leg O2 delivery (~0.38 mL O2·min−1·W−1; P = 0.9) were not different during HCTRL and HFENT. Mean power output and time to completion were significantly improved by 9% (~310 W vs. ~288 W) and 3% (~479 s vs. ~463 s), respectively, during HFENT compared with HCTRL. Quadriceps muscle activation was 9 ± 7% higher during HFENT compared with HCTRL ( P < 0.05). ΔQtw was significantly greater in HFENT compared with HCTRL (54 ± 8% vs. 39 ± 9%), whereas ΔVA was not different (~5%; P = 0.3) in both trials. These findings reveal that group III/IV muscle afferent feedback limits whole body endurance exercise performance and peripheral fatigue by restricting neural activation of locomotor muscle. NEW & NOTEWORTHY Group III/IV muscle afferent feedback facilitates endurance performance by optimizing locomotor muscle O2 delivery but also limits performance by restricting neural drive to locomotor muscle. To isolate the performance-limiting effect of these sensory neurons, we pharmacologically attenuated their central projection during a cycling time trial while controlling for locomotor muscle O2 delivery. With no difference in leg O2 delivery, afferent blockade attenuated the centrally mediated restriction in motoneuronal output and improved cycling performance.


2013 ◽  
Vol 23 (5) ◽  
pp. 522-532 ◽  
Author(s):  
Matthew W. Hoon ◽  
Nathan A. Johnson ◽  
Phillip G. Chapman ◽  
Louise M. Burke

The purpose of this review was to examine the effect of nitrate supplementation on exercise performance by systematic review and meta-analysis of controlled human studies. A search of four electronic databases and cross-referencing found 17 studies investigating the effect of inorganic nitrate supplementation on exercise performance that met the inclusion criteria. Beetroot juice and sodium nitrate were the most common supplements, with doses ranging from 300 to 600 mg nitrate and prescribed in a manner ranging from a single bolus to 15 days of regular ingestion. Pooled analysis showed a significant moderate benefit (ES = 0.79, 95% CI: 0.23–1.35) of nitrate supplementation on performance for time to exhaustion tests (p = .006). There was a small but insignificant beneficial effect on performance for time trials (ES = 0.11, 95% CI: –0.16–0.37) and graded exercise tests (ES = 0.26, 95% CI: –0.10–0.62). Qualitative analysis suggested that performance benefits are more often observed in inactive to recreationally active individuals and when a chronic loading of nitrate over several days is undertaken. Overall, these results suggest that nitrate supplementation is associated with a moderate improvement in constant load time to exhaustion tasks. Despite not reaching statistical significance, the small positive effect on time trial or graded exercise performance may be meaningful in an elite sport context. More data are required to clarify the effect of nitrate supplementation on exercise performance and to elucidate the optimal way to implement supplementation.


2013 ◽  
Vol 304 (12) ◽  
pp. H1598-H1614 ◽  
Author(s):  
Paulo W. Pires ◽  
Carla M. Dams Ramos ◽  
Nusrat Matin ◽  
Anne M. Dorrance

Maintenance of brain function depends on a constant blood supply. Deficits in cerebral blood flow are linked to cognitive decline, and they have detrimental effects on the outcome of ischemia. Hypertension causes alterations in cerebral artery structure and function that can impair blood flow, particularly during an ischemic insult or during periods of low arterial pressure. This review will focus on the historical discoveries, novel developments, and knowledge gaps in 1) hypertensive cerebral artery remodeling, 2) vascular function with emphasis on myogenic reactivity and endothelium-dependent dilation, and 3) blood-brain barrier function. Hypertensive artery remodeling results in reduction in the lumen diameter and an increase in the wall-to-lumen ratio in most cerebral arteries; this is linked to reduced blood flow postischemia and increased ischemic damage. Many factors that are increased in hypertension stimulate remodeling; these include the renin-angiotensin-aldosterone system and reactive oxygen species levels. Endothelial function, vital for endothelium-mediated dilation and regulation of myogenic reactivity, is impaired in hypertension. This is a consequence of alterations in vasodilator mechanisms involving nitric oxide, epoxyeicosatrienoic acids, and ion channels, including calcium-activated potassium channels and transient receptor potential vanilloid channel 4. Hypertension causes blood-brain barrier breakdown by mechanisms involving inflammation, oxidative stress, and vasoactive circulating molecules. This exposes neurons to cytotoxic molecules, leading to neuronal loss, cognitive decline, and impaired recovery from ischemia. As the population ages and the incidence of hypertension, stroke, and dementia increases, it is imperative that we gain a better understanding of the control of cerebral artery function in health and disease.


2021 ◽  
Vol 8 ◽  
Author(s):  
Liangliang Liu ◽  
Mengting Guo ◽  
Xiaowang Lv ◽  
Zhiwei Wang ◽  
Jigang Yang ◽  
...  

Transient receptor potential vanilloid 4 (TRPV4) channels are widely expressed in systemic tissues and can be activated by many stimuli. TRPV4, a Ca2+-permeable cation channel, plays an important role in the vasculature and is implicated in the regulation of cardiovascular homeostasis processes such as blood pressure, vascular remodeling, and pulmonary hypertension and edema. Within the vasculature, TRPV4 channels are expressed in smooth muscle cells, endothelial cells, and perivascular nerves. The activation of endothelial TRPV4 contributes to vasodilation involving nitric oxide, prostacyclin, and endothelial-derived hyperpolarizing factor pathways. TRPV4 activation also can directly cause vascular smooth muscle cell hyperpolarization and vasodilation. In addition, TRPV4 activation can evoke constriction in some specific vascular beds or under some pathological conditions. TRPV4 participates in the control of vascular permeability and vascular damage, particularly in the lung capillary endothelial barrier and lung injury. It also participates in vascular remodeling regulation mainly by controlling vasculogenesis and arteriogenesis. This review examines the role of TRPV4 in vascular function, particularly in vascular dilation and constriction, vascular permeability, vascular remodeling, and vascular damage, along with possible mechanisms, and discusses the possibility of targeting TRPV4 for therapy.


Sign in / Sign up

Export Citation Format

Share Document