Effect of hyperthermia on simulated muscle activation in female when crossing obstacle.

It is well known that hyperthermia greatly impairs neuromuscular function and dynamic balance. However, whether a greater level of hyperthermia could potentially alter the lower limb simulated muscle activation when crossing an obstacle in female participants remains unknown. Therefore we examined the effect of a systematic increase in oral temperature on lower limb simulated muscle activation when crossing an obstacle in female participants. Eighteen female participants were recruited where they underwent a control trial (Con) and two progressive passive heating trials with Δ 1°C and Δ 2°C increase of oral temperature (Toral) using a 45°C water bath. In each trial, we assessed lower limb simulated muscle activation when crossing an obstacle height of 10%, 20%, and 30% of the participant's leg length and toe-off, toe-above-obstacle and heel-strike events were identified and analyzed. In all events, the lower limb simulated muscle activation were greater in Δ2°C than Δ1°C and Con when both leading and trailing limbs crossed the obstacle height of 20% and 30% leg length (all p < 0.001). However, the lower limb simulated muscle activation were not different between Δ1°C and Con across all obstacle heights (p > 0.05). This study concluded that a greater level of hyperthermia resulted in a greater lower limb simulated muscle activation to ensure safety and stability when females cross an obstacle height of 20% leg length or higher.

Interactive effects of exercise intensity and recovery posture on post-exercise hypotension.

Post-exercise reduction in blood pressure, termed post-exercise hypotension (PEH), is relevant for both acute and chronic health reasons and potentially for peripheral cardiovascular adaptations. We investigated the interactive effects of exercise intensity and recovery postures (seated, supine, and standing) on PEH. Thirteen normotensive men underwent a VO2max test on a cycle ergometer and 5 exhaustive constant load trials to determine critical power (CP) and the gas exchange threshold (GET). Subsequently, work-matched exercise trials were performed at two discrete exercise intensities (10% > CP and 10% < GET), with one hour of recovery in each of three postures. For both exercise intensities, standing posture resulted in a more substantial PEH (all P < 0.01). For both standing and seated recovery postures, the higher exercise intensity led to larger reductions in systolic, diastolic and mean arterial pressures (all P < 0.01), whereas in the supine recovery posture, the reduction in diastolic and mean arterial pressures was unaffected by prior exercise intensity (both P > 0.05). PEH is more pronounced during recovery from exercise performed above critical power versus below GET. However, the effect of exercise intensity on PEH is largely abolished when recovery is performed in the supine posture.

Comparing thermoregulatory responses between short and long moderate intensity intermittent exercise protocols with the same duty cycle.

To date, the thermoregulatory response between continuous and intermittent exercises has been investigated whilst limited studies are available to examine the thermoregulatory responses between different modes of intermittent exercises. We sought to determine the effect of two patterns of short duration intermittent exercises (180:180 (3-min) and 30:30 s (30-s) work: rest) on thermoregulatory responses in a temperate environment (25 °C, 50% RH, vapor pressure: 1.6 kPa) with low airflow (0.2 m/s). Twelve male participants (Age:24.0(5.0) year; VO2max: 53(8) mL.kg-1.min-1; BSA:1.7(0.1) m2) cycled at 50% VO2max for 60 min in 3-min and 30-s intervals to result in the same 30-min net exercise duration. Core and skin temperatures, the percent increase of skin blood flow (forearm and chest) from baseline and local sweat rate (forearm and chest) were not different between 3-min and 30-s (all P > 0.35) from the onset of exercise to the end of the exercise. Similarly, the mean body temperature onsets of skin blood flow (forearm and chest) and local sweat rates (forearm and chest) were not different between different mode of intermittent exercises (all P > 0.1). Furthermore, thermal sensitivities of skin blood flow (forearm and chest) and local sweat rate (forearm and chest) with increasing mean body temperature were not different between different mode of intermittent exercises (all P > 0.1). We conclude that intermittent exercises with different work periods at moderate exercise intensity did not alter core temperature and thermoeffector responses in a temperate environment. (241/250).

Caffeine intake enhances peak oxygen uptake and performance during high-intensity cycling exercise in moderate hypoxia.

PURPOSE: We investigated whether caffeine consumption can enhance peak oxygen uptake ([Formula: see text]) by increasing peak ventilation during an incremental cycling test, and subsequently enhance time to exhaustion (TTE) during high-intensity cycling exercise in moderate normobaric hypoxia. METHODS: We conducted a double-blind, placebo cross-over design study. Sixteen recreational male endurance athletes (age: 20 ± 2 years, [Formula: see text]: 55.6 ± 3.6 ml/kg/min, peak power output: 318 ± 40 W) underwent an incremental cycling test and a TTE test at 80% [Formula: see text] (derived from the placebo trial) in moderate normobaric hypoxia (fraction of inspired O2: 15.3 ± 0.2% corresponding to a simulated altitude of ~ 2500 m) after consuming either a moderate dose of caffeine (6 mg/kg) or a placebo. RESULTS: Caffeine consumption resulted in a higher peak ventilation [159 ± 21 vs. 150 ± 26 L/min; P < 0.05; effect size (ES) = 0.31]. [Formula: see text] (3.58 ± 0.44 vs. 3.47 ± 0.47 L/min; P < 0.01; ES = 0.44) and peak power output (308 ± 44 vs. 302 ± 44 W; P = 0.02, ES = 0.14) were higher following caffeine consumption than during the placebo trial. During the TTE test, caffeine consumption enhanced minute ventilation (P = 0.02; ES = 0.28) and extended the TTE (426 ± 74 vs. 358 ± 75 s; P < 0.01, ES = 0.91) compared to the placebo trial. There was a positive correlation between the percent increase of [Formula: see text] following caffeine consumption and the percent increase in TTE (r = 0.49, P < 0.05). CONCLUSION: Moderate caffeine consumption stimulates breathing and aerobic metabolism, resulting in improved performance during incremental and high-intensity endurance exercises in moderate normobaric hypoxia.

Whole-body passive heating at moderate hyperthermic state impairs static and dynamic balance in healthy females.

BACKGROUND: Whether static and dynamic balances can be impaired with increasing core temperature in female participants remains unknown. PURPOSE: We tested the hypothesis that static and dynamic balances can be further impaired with systematic increases of core temperature by Δ1 °C and Δ 2 °C using whole-body passive heating. METHOD: Eighteen female participants underwent a control trial (Con) and two progressive passive heating trials with Δ 1 °C and Δ 2 °C increase of oral temperature (TOral) using 45 °C water bath. In each trial, we assessed static balance with both eye open and closed and assessed dynamic balance using obstacle crossing at 10 %, 20 % and 30 % of the participant's leg length. RESULTS: Static balance was not different between Con and Δ1 °C but was different between Δ1 °C and Δ 2 °C in an eye closed condition. Furthermore, Δ 2 °C greatly impaired both static and dynamic balances when compared to Con. The joint angles and toe clearance increased while leading heel-obstacle distance decreased during crossing obstacles at the height of 20 % and 30 % leg length with leading limbs in the Δ2 °C compared to Δ 1 °C and Con (All P < 0.05). However, no differences in joint kinematics and toe clearance with trailing limbs were observed (All P > 0.05). CONCLUSION: In female participants, static and dynamic balances only became impaired when TOral increased 2 °C from baseline.

The effects of high-intensity exercise training and detraining with and without active recovery on postexercise hypotension in young men.

Whether high-intensity exercise training and detraining combined with skeletal muscle pump (MP) could alter the magnitude of postexercise hypotension has not been investigated. We therefore sought to determine whether the combination of MP (unloaded back-pedaling) with 4 weeks of high-intensity exercise training and detraining could alter the magnitude of postexercise hypotension. Fourteen healthy men underwent 4 weeks of high-intensity exercise training (5 consecutive days per week for 15 min per session at 40% of the difference between the gas exchange threshold and maximal oxygen uptake [i.e., Δ40%]) followed by detraining for 4 weeks. Assessments were conducted at Pre-training (Pre), Post-training (Post) and after Detraining with (MP) and without MP (Con). The exercise test in the Pre, Post and the Detraining consisted of 15 min exercise at Δ40% followed by 1 h of recovery. At all time-points, the postexercise reduction in mean arterial pressure (MAP) was reduced in MP compared to Con (all p < 0.01). Four weeks of high-intensity exercise training resulted in a reduction in the magnitude of postexercise hypotension (i.e., the change in MAP from baseline was mitigated) across both trials (All p < 0.01) when compared to Pre and Detraining. Following Detraining, the reduction of MAP from baseline was reduced compared to Pre, but was not different from Post. We conclude that high-intensity exercise training combined with skeletal MP reduces the magnitude of postexercise hypotension, and this effect is partially retained for 4 weeks following the complete cessation of high-intensity exercise training.

The effect of transcranial direct current stimulation on bilateral asymmetry and joint angles of the lower limb for females when crossing obstacles.

BACKGROUND: Gait asymmetry is often accompanied by the bilateral asymmetry of the lower limbs. The transcranial direct current stimulation (tDCS) technique is widely used in different populations and scenarios as a potential tool to improve lower limb postural control. However, whether cerebral cortex bilateral tDCS has an interventional effect on postural control as well as bilateral symmetry when crossing obstacles in healthy female remains unknown. METHODS: Twenty healthy females were recruited in this prospective study. Each participant walked and crossed a height-adjustable obstacle. Two-way repeated ANOVA was used to evaluate the effect of group (tDCS and sham-tDCS) and height (30%, 20%, and 10% leg length) on the spatiotemporal and maximum joint angle parameters for lower limb crossing obstacles. The Bonferroni post-hoc test and paired t-test were used to determine the significance of the interaction effect or main effect. The statistically significant differences were set at p < 0.05. RESULTS: The Swing time (SW) gait asymmetry (GA), Stance time (ST) GA, leading limb hip-knee-ankle maximum joint angles and trailing limb hip-knee maximum joint angles decreased in the tDCS condition compared to the sham-tDCS condition at 30%, 20% leg's length crossing height except for 10% leg's length, whereas there was a significant decrease in SW/ST GA between the tDCS condition and the sham-tDCS condition at 30%, 20%, 10% leg's length crossing height (P < 0.05). CONCLUSION: We conclude that tDCS intervention is effective to reduce bilateral asymmetry in spatio-temporal parameters and enhance dynamic balance in female participants during obstacle crossing when the heights of the obstacles were above 10% of the leg's length. TRIAL REGISTRATION NO: ChiCTR2100053942 (date of registration on December 04, 2021). Prospectively registered in the Chinese Clinical Trial Registry.

Critical power is a key threshold determining the magnitude of post-exercise hypotension in non-hypertensive young males.

The effect of different exercise intensities on the magnitude of post-exercise hypotension has not been rigorously clarified with respect to the metabolic thresholds that partition discrete exercise intensity domains (i.e., critical power and the gas exchange threshold (GET)). We hypothesized that the magnitude of post-exercise hypotension would be greater following isocaloric exercise performed above versus below critical power. Twelve non-hypertensive men completed a ramp incremental exercise test to determine maximal oxygen uptake and the GET, followed by five exhaustive constant load trials to determine critical power and W' (work available above critical power). Subsequently, criterion trials were performed at four discrete intensities matched for total work performed (i.e., isocaloric) to determine the impact of exercise intensity on post-exercise hypotension: 10% above critical power (10% > CP), 10% below critical power (10% < CP), 10% above GET (10% > GET) and 10% below GET (10% < GET). The post-exercise decrease (i.e., the minimum post-exercise values) in mean arterial (10% > CP: -12.7 ± 8.3 vs. 10% < CP: v3.5 ± 2.9 mmHg), diastolic (10% > CP: -9.6 ± 9.8 vs. 10% < CP: -1.4 ± 5.0 mmHg) and systolic (10% > CP: -23.8 ± 7.0 vs. 10% < CP: -9.9 ± 4.3 mmHg) blood pressures were greater following exercise performed 10% > CP compared to all other trials (all P < 0.01). No effects of exercise intensity on the magnitude of post-exercise hypotension were observed during exercise performed below critical power (all P > 0.05). Critical power represents a threshold above which the magnitude of post-exercise hypotension is greatly augmented. NEW FINDINGS: What is the central questions of this study? What is the influence of exercise intensity on the magnitude of post-exercise hypotension with respect to metabolic thresholds? What is the main finding and its importance? The magnitude of post-exercise hypotension is greatly increased following exercise performed above critical power. However, below critical power, there was no clear effect of exercise intensity on the magnitude of post-exercise hypotension.

Galanin receptors modulate cutaneous vasodilation elicited by whole-body and local heating but not thermal sweating in young adults.

Galanin receptor subtypes GAL1, GAL2, and GAL3 are involved in several biological functions. We hypothesized that 1) GAL3 receptor activation contributes to sweating but limits cutaneous vasodilation induced by whole-body and local heating without a contribution of GAL2; and 2) GAL1 receptor activation attenuates both sweating and cutaneous vasodilation during whole-body heating. Young adults underwent whole-body (n = 12, 6 females) and local (n = 10, 4 females) heating. Forearm sweat rate (ventilated capsule) and cutaneous vascular conductance (CVC; ratio of laser-Doppler blood flow to mean arterial pressure) were assessed during whole-body heating (water-perfusion suit circulated with warm (35 °C) water), while CVC was also assessed by local forearm heating (from 33 °C to 39 °C and elevated to 42 °C thereafter; each level of heating maintained for ∼30 min). Sweat rate and CVC were evaluated at four intradermal microdialysis forearm sites treated with either 1) 5% dimethyl sulfoxide (control), 2) M40, a non-selective GAL1 and GAL2 receptor antagonist, 3) M871 to selectively antagonize GAL2 receptor, or 4) SNAP398299 to selectively antagonize GAL3 receptor. Sweating was not modulated by any GAL receptor antagonist (P > 0.169), whereas only M40 reduced CVC (P ≤ 0.003) relative to control during whole-body heating. Relative to control, SNAP398299 augmented the initial and sustained increase in CVC during local heating to 39 °C, and the transient increase at 42 °C (P ≤ 0.028). We confirmed that while none of the galanin receptors modulate sweating during whole-body heating, GAL1 receptors mediate cutaneous vasodilation. Further, GAL3 receptors blunt cutaneous vasodilation during local heating.

Indoor thermal comfort research using human participants: Guidelines and a checklist for experimental design.

Thermal comfort dictates our alliesthesia and behavioural responses in indoor environments with the primary aim of maintaining the thermal homeostasis of our human body. The recent advances in neurophysiology research have suggested that thermal comfort is a physiological response that is regulated by the deviations of both skin and core temperatures. Therefore, when conducting thermal comfort using indoor occupants in an indoor environment, proper experimental design and standardisation should be followed. However, there is no published source that provides an educational guideline on how to properly implement the thermal comfort experiment in an indoor environment using indoor occupants (normal occupational activities and during sleep in a home-based setting). Therefore, the primary purpose of this work is to illustrate how to conduct indoor thermal comfort related experiments using human trials in both normal occupational activities and during sleep in a home-based setting. Furthermore, we hope that the information presented in this article will result in better experimental design when conducting the experiment on thermal comfort using indoor occupants (occupational and home-based environments). Due to this reason, special emphasis will be focused on the experimental design, selection of participants and experimental standardisation. The key summary of this article is that thermal comfort related to indoor occupants in an indoor environment should perform priori sample analysis and follow the proper experimental design and standardisation as outlined in this article.

Induction and decay of seasonal acclimatization on whole body heat loss responses during exercise in a hot humid environment with different air velocities.

Whether whole body heat loss and thermoregulatory function (local sweat rate and skin blood flow) are different between summer and autumn and between autumn and winter seasons during exercise with different air flow in humid heat remain unknown. We therefore tested the hypotheses that whole body sweat rate (WBSR), evaporated sweat rate, and thermoregulatory function during cycling exercise in autumn would be higher than in winter but would be lower than in summer under hot-humid environment (32 C, 75% RH). We also tested the hypothesis that the increase of air velocity would enhance evaporated sweat rate and sweating efficiency across winter, summer, and autumn seasons. Eight males cycled for 1 h at 40% V̇o2max in winter, summer, and autumn seasons. Using an electric fan, air velocity increased from 0.2 m/s to 1.1 m/s during the final 20 min of cycling. The autumn season resulted in a lower WBSR, unevaporated sweat rate, and a higher sweating efficiency compared with summer (all P ≤ 0.05) but WBSR and unevaporated sweat rate in autumn were higher than in winter and thus sweating efficiency was lower when compared with winter only at the air velocity of 0.2 m/s (All P ≤ 0.05). Furthermore, evaporated sweat rate and core temperature (Tcore) were not different among winter, summer, and autumn seasons (All P > 0.19). In conclusion, changes in WBSR across different seasons do not alter Tcore during exercise in a hot humid environment. Furthermore, increasing air velocity enhances evaporated sweat rate and sweating efficiency across all seasons.

Astragalosides Supplementation Enhances Intrinsic Muscle Repair Capacity Following Eccentric Exercise-Induced Injury.

Astragalosides have been shown to enhance endurance exercise capacity in vivo and promote muscular hypertrophy in vitro. However, it remains unknown whether astragalosides supplementation can alter inflammatory response and enhance muscle recovery after damage in humans. We therefore aimed to evaluate the effect of astragalosides supplementation on muscle's intrinsic capacity to regenerate and repair itself after exercise-induced damage. Using a randomized double-blind placebo-controlled cross-over design, eleven male participants underwent 7 days of astragalosides supplementation (in total containing 4 mg of astragalosides per day) or a placebo control, following an eccentric exercise protocol. Serum blood samples and variables related to muscle function were collected prior to and immediately following the muscle damage protocol and also at 2 h, and 1, 2, 3, 5, and 7 days of the recovery period, to assess the pro-inflammatory cytokine response, the secretion of muscle regenerative factors, and muscular strength. Astragalosides supplementation reduced biomarkers of skeletal muscle damage (serum CK, LDH, and Mb), when compared to the placebo, at 1, 2, and 3 days following the muscle damage protocol. Astragalosides supplementation suppressed the secretion of IL-6 and TNF-α, whilst increasing the release of IGF-1 during the initial stages of muscle recovery. Furthermore, following astragaloside supplementation, muscular strength returned to baseline 2 days earlier than the placebo. Astragalosides supplementation shortens the duration of inflammation, enhances the regeneration process and restores muscle strength following eccentric exercise-induced injury.

Increased Asymmetry of Lower Limbs and Leading Joint Angles during Crossing Obstacles in Healthy Male with Cold Exposure.

Lower ambient temperatures impair neuromuscular function and balance. However, whether lower ambient temperatures could alter joint angles and symmetry of lower limbs during crossing obstacles in males still remains unknown. Therefore, we investigated whether there is reduction of ambient temperature (20°C; 15°C; 10°C) on lower limbs joint angles and symmetry when crossing obstacles in males. On three different occasions, eighteen male participants underwent 30 min exposure to three different environmental temperatures (10°C, 15°C, and 20°C), which was followed by the obstacle crossing test at 10%, 20%, and 30% of the participant leg length. In each trial, we assessed joint angles and symmetry of lower limbs when crossing obstacles at 10%, 20%, and 30% of the participants' leg length. The results showed that leading limb maximum joint angles were greater in 10°C than in 15°C and 20°C when leading limb crossed obstacle heights of 20% and 30% leg length (p < 0.05). Trailing limb maximum joint angles were not different (p > 0.05). Lower limb asymmetry increased when participants crossed obstacle heights of 20% and 30% leg length at 10°C (p < 0.05). This study concluded that in male participants, cold exposure can increase lower limb asymmetry to increase falling risk when crossing obstacles. Also, the increased leading limb joint angles and constant trailing limb joint angles increase safety during crossing obstacles.

Do E2 and P4 contribute to the explained variance in core temperature response for trained women during exertional heat stress when metabolic rates are very high?

PURPOSE: Women remain underrepresented in the exercise thermoregulation literature despite their participation in leisure-time and occupational physical activity in heat-stressful environments continuing to increase. Here, we determined the relative contribution of the primary ovarian hormones (estrogen [E2] and progesterone [P4]) alongside other morphological (e.g., body mass), physiological (e.g., sweat rates), functional (e.g., aerobic fitness) and environmental (e.g., vapor pressure) factors in explaining the individual variation in core temperature responses for trained women working at very high metabolic rates, specifically peak core temperature (Tpeak) and work output (mean power output). METHODS: Thirty-six trained women (32 ± 9 year, 53 ± 9 ml·kg-1·min-1), distinguished by intra-participant (early follicular and mid-luteal phases) or inter-participant (ovulatory vs. anovulatory vs. oral contraceptive pill user) differences in their endogenous E2 and P4 concentrations, completed a self-paced 30-min cycling work trial in warm-dry (2.2 ± 0.2 kPa, 34.1 ± 0.2 °C, 41.4 ± 3.4% RH) and/or warm-humid (3.4 ± 0.1 kPa, 30.2 ± 1.2 °C, 79.8 ± 3.7% RH) conditions that yielded 115 separate trials. Stepwise linear regression was used to explain the variance of the dependent variables. RESULTS: Models were able to account for 60% of the variance in Tpeak ([Formula: see text]2: 41% core temperature at the start of work trial, [Formula: see text]2: 15% power output, [Formula: see text]2: 4% [E2]) and 44% of the variance in mean power output ([Formula: see text]2: 35% peak aerobic power, [Formula: see text]2: 9% perceived exertion). CONCLUSION: E2 contributes a small amount toward the core temperature response in trained women, whereby starting core temperature and peak aerobic power explain the greatest variance in Tpeak and work output, respectively.

TMEM16A blockers T16Ainh-A01 and benzbromarone do not modulate the regulation of sweating and cutaneous vasodilatation in humans in vivo.

NEW FINDINGS: What is the central question of this study? Do transmembrane member 16A (TMEM16A) blockers modulate the activation of heat loss responses of sweating and cutaneous vasodilatation? What are the main finding and its importance? Relative to the vehicle control site, TMEM16A blockers T16Ainh-A01 and benzbromarone had no effect on sweat rate or cutaneous vascular conductance during whole-body heating inducing a 1.1 ± 0.1°C increase in core temperature above baseline resting levels. These results suggest that TMEM16A blockers T16Ainh-A01 and benzbromarone do not modulate the regulation of sweating and cutaneous vasodilatation during whole-body heat stress. ABSTRACT: Animal and in vitro studies suggest that transmembrane member 16A (TMEM16A), a Ca2+ -activated Cl- channel, contributes to regulating eccrine sweating. However, direct evidence supporting this possibility in humans is lacking. We assessed the hypothesis that TMEM16A blockers attenuate sweating during whole-body heating in humans. Additionally, we assessed the associated changes in the heat loss response of cutaneous vasodilatation to determine if a functional role of TMEM16A may exist. Twelve young (24 ± 2 years) adults (six females) underwent whole-body heating using a water-perfused suit to raise core temperature 1.1 ± 0.1°C above baseline. Sweat rate and cutaneous vascular conductance (normalized to maximal conductance via administration of sodium nitroprusside) were evaluated continuously at four forearm skin sites treated continuously by intradermal microdialysis with (1) lactated Ringer's solution (control), (2) 5% dimethyl sulfoxide (DMSO) serving as a vehicle control, or (3) TMEM16A blockers 1 mM T16Ainh-A01 or 2 mM benzbromarone dissolved in 5% DMSO solution. All drugs were administered continuously via intradermal microdialysis. Whole-body heating increased core temperature progressively and this was paralleled by an increase in sweat rate and cutaneous vascular conductance at all skin sites. However, sweat rate (all P > 0.318) and cutaneous vascular conductance (all P ≥ 0.073) did not differ between the vehicle control site relative to the TMEM16A blocker-treated sites. Collectively, our findings indicate that TMEM16A blockers T16Ainh-A01 and benzbromarone do not modulate the regulation of sweating and cutaneous vasodilatation during whole-body heating in young adults in vivo.

Astragalus membranaceus Enhances Myotube Hypertrophy through PI3K-Mediated Akt/mTOR Signaling Phosphorylation.

Astragalus membranaceus (AM) is classified as a high-class traditional herbal medicine, which has strengthened vitality and multifunctional pharmacological activities, but limited empirical evidence is available to support its effects in muscular hypertrophy. It evokes skeletal muscle hypertrophy by increasing anabolic pathway, which is essential to prevent sarcopenia in elderly population. In this study, we examined the effects of AM on skeletal muscle hypertrophy by focusing on the molecular mechanism. We employed an in vitro model to investigate whether AM-treated skeletal muscle, as represented by myotube C2C12 cells, was hypertrophic, and to further investigate the efficacy of AM-activated phosphorylation of PI3K/Akt/mTOR signaling that must occur prior to myotube hypertrophy. The results showed that the myotubes formed larger multinucleated myotubes with increased diameter and thickness (1.16-fold relative to control group, p < 0.05). Administration of PI3K and mTOR inhibitors abolished AM-induced muscular hypertrophy. Moreover, AM-induced PI3K-mediated myotube hypertrophy was accompanied by the activation of Akt and mTOR signaling. We concluded that the AM is a nutritional activator to enhance muscular hypertrophy by increasing PI3K/Akt/mTOR signaling phosphorylation. As the AM is effective in myotube hypertrophy, AM and its derivatives may be promising candidates for ergogenic aid to prevent sarcopenia.

Head, Face and Neck Cooling as Per-cooling (Cooling During Exercise) Modalities to Improve Exercise Performance in the Heat: A Narrative Review and Practical Applications.

It is well known that uncompensable heat stress greatly impairs endurance and team sport-related performance because an increase in the core temperature directly induces a greater magnitude of the central fatigue in the heat than in thermal neutral environments. Numerous studies have been conducted in an attempt to discover reliable cooling strategies for improving endurance performance and repeated sprint ability while exercising in the heat. Whole-body pre-cooling has been shown to improve endurance performance in both dry and humid heat. Despite this, the reduction in thermal perceptions associated with pre-cooling gradually narrows during intense exercise. Hence, effective per-cooling strategies to improve athletic performance in the heat are required. Unfortunately, due to practical issues, adopting pre-cooling approaches as a per-cooling (cooling during exercise) modality to improve athletic performance is impractical. Thus, we sought to examine the impact of head, neck and face cooling on athletic performance in heat. According to current evidence, cooling the head, neck and face reduced local skin temperature in the areas where cooling was applied, resulting in improved local perceptual sensations. In the heat, neck cooling during exercise improves athletic performance in both endurance and team sports athletes. Furthermore, from a practical standpoint, neck cooling is preferred over head, face and combined head/face and neck cooling for both endurance and team sport athletes in the heat. Nonetheless, for all athletes who have access to water, face cooling is a recommended cooling strategy. There is a lack of research on the systematic selection of per-cooling modalities to improve athletic performance based on environmental conditions and the nature of sports. In addition, powerful but portable head, neck and face cooling systems are urgently needed to assist athletes in improving their performance in hot conditions.

TRPA1 Channel Activation With Cinnamaldehyde Induces Cutaneous Vasodilation Through NOS, but Not COX and KCa Channel, Mechanisms in Humans.

ABSTRACT: Transient receptor potential ankyrin 1 (TRPA1) channel activation induces cutaneous vasodilation in humans in vivo. However, the mechanisms underlying this response remains equivocal. We hypothesized that nitric oxide synthase (NOS) and Ca2+ activated K+ (KCa) channels contribute to the TRPA1 channel-induced cutaneous vasodilation with no involvement of cyclooxygenase (COX). Cutaneous vascular conductance (CVC) in 9 healthy young adults was assessed at 4 dorsal forearm skin sites treated by intradermal microdialysis with (1) 1.985% dimethyl sulfoxide + 0.015% lactated Ringer solution with propylene glycol (vehicle control), (2) 10 mM l-NAME, a nonselective NOS inhibitor, (3) 10 mM ketorolac, a nonselective COX inhibitor, or (4) 50 mM tetraethylammonium, a nonselective KCa channel blocker. Cinnamaldehyde, a TRPA1 channel activator, was administered to each skin site in a dose-dependent manner (2.9%, 8.8%, 26%, and 80%, each lasting ≥30 minutes). Administration of ≥8.8% cinnamaldehyde increased CVC from baseline at the vehicle control site by as much as 27.4% (95% confidence interval of 5.3; P < 0.001). NOS inhibitor attenuated the cinnamaldehyde-induced increases in CVC at the 8.8%, 26%, and 80% concentrations relative to the vehicle control site (all P ≤ 0.05). In contrast, both the COX inhibitor and KCa channel blockers did not attenuate the cinnamaldehyde induced-increases in CVC relative to the vehicle control site for all concentrations (all P ≥ 0.130). We conclude that in human skin in vivo, NOS plays a role in modulating the regulation of cutaneous vasodilation in response to TRPA1 channel activation with no detectable contributions of COX and KCa channels.

Measurement error of self-paced exercise performance in athletic women is not affected by ovulatory status or ambient environment.

Measurement error(s) of exercise tests for women are severely lacking in the literature. The purpose of this investigation was to 1) determine whether ovulatory status or ambient environment were moderating variables when completing a 30-min self-paced work trial and 2) provide test-retest norms specific to athletic women. A retrospective analysis of three heat stress studies was completed using 33 female participants (31 ± 9 yr, 54 ± 10 mL·min-1·kg-1) that yielded 130 separate trials. Participants were classified as ovulatory (n = 19), anovulatory (n = 4), and oral contraceptive pill users (n = 10). Participants completed trials ∼2 wk apart in their (quasi-) early follicular and midluteal phases in two of moderate (1.3 ± 0.1 kPa, 20.5 ± 0.5°C, 18 trials), warm-dry (2.2 ± 0.2 kPa, 34.1 ± 0.2°C, 46 trials), or warm-humid (3.4 ± 0.1 kPa, 30.2 ± 1.1°C, 66 trials) environments. We quantified reliability using limits of agreement, intraclass correlation coefficient (ICC), standard error of measurement (SEM), and coefficient of variation (CV). Test-retest reliability was high, clinically valid (ICC = 0.90, P < 0.01), and acceptable with a mean CV of 4.7%, SEM of 3.8 kJ (2.1 W), and reliable bias of -2.1 kJ (-1.2 W). The various ovulatory status and contrasting ambient conditions had no appreciable effect on reliability. These results indicate that athletic women can perform 30-min self-paced work trials ∼2 wk apart with an acceptable and low variability irrespective of their hormonal status or heat-stressful environments.NEW & NOTEWORTHY This study highlights that aerobically trained women perform 30-min self-paced work trials ∼2 wk apart with acceptably low variability and their hormonal/ovulatory status and the introduction of greater ambient heat and humidity do not moderate this measurement error.