Acute moderate normobaric hypoxia does not modify circulating thyroid hormone concentrations induced by 1 h of head-out cold-water immersion.

This study tested the hypothesis that acute moderate normobaric hypoxia augments circulating thyroid hormone concentrations during and following 1 h of cold head-out water immersion (HOWI), compared with when cold HOWI is completed during normobaric normoxia. In a randomized crossover single-blind design, 12 healthy adults (27 ± 2 yr, 2 women) completed 1 h of cold (22.0 ± 0.1°C) HOWI breathing either normobaric normoxia ([Formula: see text] = 0.21) or normobaric hypoxia ([Formula: see text] = 0.14). Free and total thyroxine (T3) and triiodothyronine (T4), and thyroid-stimulating hormone (TSH) concentrations were measured in venous blood samples obtained before (baseline), during (15-, 30-, and 60 min), and 15 min following HOWI (post-), and were corrected for changes in plasma volume. Arterial oxyhemoglobin saturation and core (rectal) temperature were measured continuously. Arterial oxyhemoglobin saturation was lower during hypoxia (90 ± 3%) compared with normoxia (98 ± 1%, P < 0.001). Core temperature fell from baseline (normoxia: 37.2 ± 0.4°C, hypoxia: 37.2 ± 0.4°C) to post-cold HOWI (normoxia: 36.4 ± 0.5°C, hypoxia: 36.3 ± 0.5°C, P < 0.001) in both conditions but did not change differently between conditions (condition × time: P = 0.552). Circulating TSH, total T3, free T4, total T3, and free T4 concentrations demonstrated significant main effects of time (all P ≤ 0.024), but these changes did not differ between normoxic and hypoxic conditions (condition × time: all P ≥ 0.163). These data indicate that acute moderate normobaric hypoxia does not modify the circulating thyroid hormone response during 1 h of cold HOWI.NEW & NOTEWORTHY Acute head-out cold (22°C) water immersion (HOWI) decreased core temperature and increased thermogenesis. This thermogenic response was paralleled by the activation of the hypothalamic-pituitary-thyroid axis, as evidenced by changes in thyroid hormones. However, cold HOWI in combination with moderate normobaric hypoxia did not modify the thermogenic nor the circulating thyroid hormone response. This finding suggests that hypoxia-induced alterations in thyroid hormone concentrations are unlikely to acutely contribute to adaptations resulting from repeated cold-water exposures.

Does Physical Inactivity Induce Significant Changes in Human Gut Microbiota? New Answers Using the Dry Immersion Hypoactivity Model.

Gut microbiota, a major contributor to human health, is influenced by physical activity and diet, and displays a functional cross-talk with skeletal muscle. Conversely, few data are available on the impact of hypoactivity, although sedentary lifestyles are widespread and associated with negative health and socio-economic impacts. The study aim was to determine the effect of Dry Immersion (DI), a severe hypoactivity model, on the human gut microbiota composition. Stool samples were collected from 14 healthy men before and after 5 days of DI to determine the gut microbiota taxonomic profiles by 16S metagenomic sequencing in strictly controlled dietary conditions. The α and ß diversities indices were unchanged. However, the operational taxonomic units associated with the Clostridiales order and the Lachnospiraceae family, belonging to the Firmicutes phylum, were significantly increased after DI. Propionate, a short-chain fatty acid metabolized by skeletal muscle, was significantly reduced in post-DI stool samples. The finding that intestine bacteria are sensitive to hypoactivity raises questions about their impact and role in chronic sedentary lifestyles.

TailTimer: A device for automating data collection in the rodent tail immersion assay.

The tail immersion assay is a widely used method for measuring acute thermal pain in a way which is quantifiable and reproducible. It is non-invasive and measures response to a stimulus that may be encountered by an animal in its natural environment. However, quantification of tail withdrawal latency relies on manual timing of tail flick using a stopwatch, and precise temperatures of the water at the time of measurement are most often not recorded. These two factors greatly reduce the reproducibility of tail immersion assay data and likely contribute to some of the discrepancies present among relevant literature. We designed a device, TailTimer, which uses a Raspberry Pi single-board computer, a digital temperature sensor, and two electrical wires, to automatically record tail withdrawal latency and water temperature. We programmed TailTimer to continuously display and record water temperature and to only permit the assay to be conducted when the water is within ± 0.25°C of the target temperature. Our software also records the identification of the animals using a radio frequency identification (RFID) system. We further adapted the RFID system to recognize several specific keys as user interface commands, allowing TailTimer to be operated via RFID fobs for increased usability. Data recorded using the TailTimer device showed a negative linear relationship between tail withdrawal latency and water temperature when tested between 47-50°C. We also observed a previously unreported, yet profound, effect of water mixing speed on latency. In one experiment using TailTimer, we observed significantly longer latencies following administration of oral oxycodone versus a distilled water control when measured after 15 mins or 1 h, but not after 4 h. TailTimer also detected significant strain differences in baseline latency. These findings valorize TailTimer in its sensitivity and reliability for measuring thermal pain thresholds.

Autonomic regulation of the heart and arrhythmogenesis in trained breath-hold divers.

AbstractBreath-hold divers are known to develop cardiac autonomic changes and brady-arrthymias during prolonged breath-holding (BH). The effects of BH-induced hypoxemia were investigated upon both cardiac autonomic status and arrhythmogenesis by comparing breath-hold divers (BHDs) to non-divers (NDs). Eighteen participants (9 BHDs, 9 NDs) performed a maximal voluntary BH with face immersion. BHDs were asked to perform an additional BH at water surface to increase the degree of hypoxemia. Beat-to-beat changes in heart rate (HR), short-term fractal scaling exponent (DFAα1), the number of arrhythmic events [premature ventricular contractions (PVCs), premature atrial contractions (PACs)] and peripheral oxygen saturation (SpO2) were recorded during and immediately following BH. The corrected QT-intervals (QTc) were analyzed pre- and post-acute BH. A regression-based model was used to split BH into a normoxic (NX) and a hypoxemic phase (HX). During the HX phase of BH, BHDs showed a progressive decrease in DFAα1 during BH with face immersion (p < 0.01) and BH with whole-body immersion (p < 0.01) whereas NDs did not (p > 0.05). In addition, BHDs had more arrhythmic events during the HX of BH with whole-body immersion when compared to the corresponding NX phase (5.9 ± 6.7 vs 0.4 ± 1.3; p < 0.05; respectively). The number of PVCs was negatively correlated with SpO2 during BH with whole-body immersion (r = -0.72; p < 0.05). The hypoxemic stage of voluntary BH is concomitant with significant cardiac autonomic changes toward a synergistic sympathetic and parasympathetic stimulation. Co-activation led ultimately to increased bradycardic response and cardiac electrophysiological disturbances.

Carbohydrate saving or biomass maintenance: which is the main determinant of the plant's long-term submergence tolerance?

It is hypothesized that plant submergence tolerance could be assessed from the decline of plant biomass due to submergence, as biomass integrates all eco-physiological processes leading to fitness. An alternative hypothesis stated that the consumption rate of carbohydrate is essential in differing tolerance to submergence. In the present study, the responses of biomass, biomass allocation, and carbohydrate content to simulated long-term winter submergence were assessed in four tolerant and four sensitive perennials. The four tolerant perennials occur in a newly established riparian ecosystem created by The Three Gorges Dam, China. They had 100% survival after 120 days' simulated submergence, and had full photosynthesis recovery after 30 days' re-aeration, and the photosynthetic rate was positively related to the growth during the recovery period. Tolerant perennials were characterized by higher carbohydrate levels, compared with the four sensitive perennials (0% survival) at the end of submergence. Additionally, by using a method which simulates posterior estimates, and bootstraps the confidence interval for the difference between strata means, it was found that the biomass response to post-hypoxia, rather than that to submergence, could be a reliable indicator to assess submergence tolerance. Interestingly, the differences of changes in carbohydrate content between tolerant and sensitive perennials during submergence were significant, which were distinct from the biomass response, supporting the hypothesis that tolerant perennials could sacrifice non-vital components of biomass to prioritize the saving of carbohydrates for later recovery. Our study provides some insight into the underlying mechanism(s) of perennials' tolerance to submergence in ecosystems such as temperate wetland and reservoir riparian.

Hypoxia gradually augments metabolic and thermoperceptual responsiveness to repeated whole-body cold stress in humans.

NEW FINDINGS: What is the central question of this study? In male lowlanders, does hypoxia modulate thermoregulatory effector responses during repeated whole-body cold stress encountered in a single day? What is the main finding and its importance? A ∼10 h sustained exposure to hypoxia appears to mediate a gradual upregulation of endogenous heat production, preventing the progressive hypothermic response prompted by serial cold stimuli. Also, hypoxia progressively degrades mood, and compounds the perceived thermal discomfort, and sensations of fatigue and coldness. ABSTRACT: We examined whether hypoxia would modulate thermoeffector responses during repeated cold stress encountered in a single day. Eleven men completed two ∼10 h sessions, while breathing, in normobaria, either normoxia or hypoxia ( PO2 : 12 kPa). During each session, subjects underwent sequentially three 120 min immersions to the chest in 20°C water (CWI), interspersed by 120 min rewarming. In normoxia, the final drop in rectal temperature (Trec ) was greater in the third (∼1.2°C) than in the first and second (∼0.9°C) CWIs (P < 0.05). The first hypoxic CWI augmented the Trec fall (∼1.2°C; P = 0.002), but the drop in Trec did not vary between the three hypoxic CWIs (P = 0.99). In normoxia, the metabolic heat production ( Ṁ ) was greater during the first half of the third CWI than during the corresponding part of the first CWI (P = 0.02); yet the difference was blunted during the second half of the CWIs (P = 0.89). In hypoxia, by contrast, the increase in Ṁ was augmented by ∼25% throughout the third CWI (P < 0.01). Regardless of the breathing condition, the cold-induced elevation in mean arterial pressure was blunted in the second and third CWI (P < 0.05). Hypoxia aggravated the sensation of coldness (P = 0.05) and thermal discomfort (P = 0.04) during the second half of the third CWI. The present findings therefore demonstrate that prolonged hypoxia mediates, in a gradual manner, metabolic and thermoperceptual sensitization to repeated cold stress.

Muscle temperature kinetics and thermoregulatory responses to 42 °C hot-water immersion in healthy males and females.

PURPOSE: To determine the vastus lateralis muscle temperature kinetics during and after passive heating, to exam the effect of sex on thermoregulatory responses, and the thermal safety and tolerance of the 42 °C hot-water immersion protocol. METHODS: Thirty participants (15 males, 15 females) underwent a 2 h 42 ºC hot-water immersion to the waist level. Vastus lateralis, rectal and skin temperature, thermal sensation, heart rate and blood pressure (BP) were measured during the passive heating and recovery period. Participant recovery was monitored until muscle temperature returned to baseline. RESULTS: Vastus lateralis temperature increased to a maximal value of 39.0 ± 0.11 °C (P < 0.001), reaching a plateau after ~ 83.5 min of hot-water immersion and returning to baseline after ~ 115.8 min of recovery. Despite the anthropometric differences between males and females (e.g., height, body mass, body fat %, and fat thickness; P < 0.05), thermoregulatory responses showed no differences between sexes (P > 0.05). No change was found in systolic BP (~ 117 mmHg; P = 0.061). Peak rectal temperature (38.8 ± 0.14 °C; P < 0.001), heart rate (~ 100 bpm; P < 0.001), and diastolic BP (↓ ~ 13 mmHg; P < 0.001) during the hot-water immersion indicated the safety of the protocol. While skin temperature (~ 35.4 °C; P < 0.001) and thermal sensation (~ 5.95 AU; P < 0.001) confirmed protocol tolerance. CONCLUSION: These data demonstrate lower-body 42 °C hot-water immersion to increase vastus lateralis temperature and plateau ~ 2.8 °C above baseline. This amplitude of muscle temperature change aligns with reported cellular adaptation and muscle growth. Thermal strain incurred from this protocol appears safe and tolerable, positioning it well for health-related prescription.

Water immersion methods do not alter muscle damage and inflammation biomarkers after high-intensity sprinting and jumping exercise.

PURPOSE: The aim of this study was to compare the efficacy of three water immersion interventions performed after active recovery compared to active recovery only on the resolution of inflammation and markers of muscle damage post-exercise. METHODS: Nine physically active men (n = 9; age 20‒35 years) performed an intensive loading protocol, including maximal jumps and sprinting on four occasions. After each trial, one of three recovery interventions (10 min duration) was used in a random order: cold-water immersion (CWI, 10 °C), thermoneutral water immersion (TWI, 24 °C), contrast water therapy (CWT, alternately 10 °C and 38 °C). All of these methods were performed after an active recovery (10 min bicycle ergometer), and were compared to active recovery only (ACT). 5 min, 1, 24, 48, and 96 h after exercise bouts, immune response and recovery were assessed through leukocyte subsets, monocyte chemoattractant protein-1, myoglobin and high-sensitivity C-reactive protein concentrations. RESULTS: Significant changes in all blood markers occurred at post-loading (p < 0.05), but there were no significant differences observed in the recovery between methods. However, retrospective analysis revealed significant trial-order effects for myoglobin and neutrophils (p < 0.01). Only lymphocytes displayed satisfactory reliability in the exercise response, with intraclass correlation coefficient > 0.5. CONCLUSIONS: The recovery methods did not affect the resolution of inflammatory and immune responses after high-intensity sprinting and jumping exercise. It is notable that the biomarker responses were variable within individuals. Thus, the lack of differences between recovery methods may have been influenced by the reliability of exercise-induced biomarker responses.

Prolonged Brackish Water Exposure: A Case Report.

Exposure to and consumption of brackish water are associated with an elevated risk of infection, hypernatremia, and hypothermia. Minimal data exist to support the diagnosis and treatment of patients with long-term brackish water exposure. We present a case of a patient who spent 5 to 10 d semisubmerged in the Elizabeth River in coastal Virginia. A 55-y-old male presented via ambulance after 5 to 10 d of being "stuck in the mud." He was hypernatremic, with a sodium of 176 mEq·L-1, hypothermic to 34.5°C (94.1°F), and hypotensive at 88/50 mm Hg, with a sodium concentration of 176 mEq·L-1 and an osmolality of 412 mosm·kg-1. He developed pneumonia, with respiratory cultures growing Vibrio parahemolyticus, Klebsiella oxytoca, and Shewanella algae. He had pustules, which grew Aeromonas hydrophilia and Aeromonas caviae. A nasogastric tube was placed. Using suction, 500 mL of coarse sand and gravel was removed from his stomach. Antibiotics and intravenous fluids were given. The patient fully recovered after 3 wk and was discharged to rehabilitation. Exposure to brackish water can present a unique set of infectious and metabolic complications. Initial care should include treatment of metabolic derangements, such as hypovolemia, hypernatremia, and hypothermia, and treatment of infections with antibiotics based on knowledge of the most likely causative organisms.

Nervous mechanisms of restraint water-immersion stress-induced gastric mucosal lesion.

Stress-induced gastric mucosal lesion (SGML) is one of the most common visceral complications after trauma. Exploring the nervous mechanisms of SGML has become a research hotspot. Restraint water-immersion stress (RWIS) can induce GML and has been widely used to elucidate the nervous mechanisms of SGML. It is believed that RWIS-induced GML is mainly caused by the enhanced activity of vagal parasympathetic nerves. Many central nuclei, such as the dorsal motor nucleus of the vagus, nucleus of the solitary tract, supraoptic nucleus and paraventricular nucleus of the hypothalamus, mediodorsal nucleus of the thalamus, central nucleus of the amygdala and medial prefrontal cortex, are involved in the formation of SGML in varying degrees. Neurotransmitters/neuromodulators, such as nitric oxide, hydrogen sulfide, vasoactive intestinal peptide, calcitonin gene-related peptide, substance P, enkephalin, 5-hydroxytryptamine, acetylcholine, catecholamine, glutamate, γ-aminobutyric acid, oxytocin and arginine vasopressin, can participate in the regulation of stress. However, inconsistent and even contradictory results have been obtained regarding the actual roles of each nucleus in the nervous mechanism of RWIS-induced GML, such as the involvement of different nuclei with the time of RWIS, the different levels of involvement of the sub-regions of the same nucleus, and the diverse signalling molecules, remain to be further elucidated.

Whole-body active heating does not preserve finger temperature or manual dexterity during cold-water immersion.

Background: Cold-water immersion impairs manual dexterity when finger temperature is below 15°C. This exposes divers to increased risk of error. We hypothesized that whole-body active heating would maintain finger temperatures and dexterity during cold-water immersion. Methods: Twelve subjects (six males) (22 ± 2 years old; BMI 23.9 ± 2.5; body fat 16 ± 6%) completed 60-minute head-out water immersion (HOWI) wearing a 7mm wetsuit and 3mm gloves in thermoneutral water (TN 25°C) and cold water (CW 10°C) while wearing a water-perfused suit (WP) with 37°C water circulated over the torso, arms, and legs. Gross (Minnesota Manual Dexterity Test [MMDT]) and fine (modified Purdue Pegboard [PPT]) dexterity were assessed before, during and after immersion. Core body and skin temperatures were recorded every 10 minutes. Results: MMDT (TN -25 ± 14%; CW -72 ± 23%; WP -67 ± 29%; p<0.05) and PPT (TN -16 ± 9%; CW: -45 ± 10%; WP: -38 ± 13%; p<0.05) performance decreased during immersion. MMDT and PPT did not differ between CW and WP. Immediately following immersion gross dexterity was recovered in all conditions. Post-immersion fine dexterity was still impaired in CW (p<0.01), but not WP or TN. Core and skin temperatures decreased during immersion in CW and WP (p<0.05) but did not differ between CW and WP. Conclusion: Manual dexterity decreased during immersion. Dexterity was further impaired during cold-water immersion and was not maintained by water perfusion active heating. Warm water perfusion did not maintain finger temperature above 15°C but hand temperature remained above these limits, suggesting a need to reassess thermal thresholds for working divers in cold-water conditions.

Attenuated Cardiovascular Responses to the Cold Pressor Test in Concussed Collegiate Athletes.

CONTEXT: Cardiovascular responses to the cold pressor test (CPT) provide information regarding sympathetic function. OBJECTIVE: To determine if recently concussed collegiate athletes had blunted cardiovascular responses during the CPT. DESIGN: Cross-sectional study. SETTING: Laboratory. PATIENTS OR OTHER PARTICIPANTS: A total of 10 symptomatic concussed collegiate athletes (5 men, 5 women; age = 20 ± 2 years) who were within 7 days of diagnosis and 10 healthy control individuals (5 men, 5 women; age = 24 ± 4 years). INTERVENTION(S): The participants' right hands were submerged in agitated ice water for 120 seconds (CPT). MAIN OUTCOME MEASURE(S): Heart rate and blood pressure were continuously measured and averaged at baseline and every 30 seconds during the CPT. RESULTS: Baseline heart rate and mean arterial pressure were not different between groups. Heart rate increased throughout 90 seconds of the CPT (peak increase at 60 seconds = 16 ± 13 beats/min; P < .001) in healthy control participants but remained unchanged in concussed athletes (peak increase at 60 seconds = 7 ± 10 beats/min; P = .08). We observed no differences between groups for the heart rate response (P > .28). Mean arterial pressure was elevated throughout the CPT starting at 30 seconds (5 ± 7 mm Hg; P = .048) in healthy control individuals (peak increase at 120 seconds = 26 ± 9 mm Hg; P < .001). Mean arterial pressure increased in concussed athletes at 90 seconds (8 ± 8 mm Hg; P = .003) and 120 seconds (12 ± 8 mm Hg; P < .001). Healthy control participants had a greater increase in mean arterial pressure starting at 60 seconds (P < .001) and throughout the CPT than concussed athletes (peak difference at 90 seconds = 25 ± 10 mm Hg and 8 ± 8 mm Hg, respectively; P < .001). CONCLUSIONS: Recently concussed athletes had blunted cardiovascular responses to the CPT, which indicated sympathetic dysfunction.

Seawater Immersion Aggravates Early Mitochondrial Dysfunction and Increases Neuronal Apoptosis After Traumatic Brain Injury.

Traumatic brain injury (TBI) is a major cause of death and disability in naval warfare. Due to the unique physiochemical properties of seawater, immersion in it exacerbates TBI and induces severe neural damage and complications. However, the characteristics and underlying mechanisms of seawater-immersed TBI remain unclear. Mitochondrial dysfunction is a major cause of TBI-associated brain damage because it leads to oxidative stress, decrease in energy production, and apoptosis. Thus, the present study aimed to further elucidate the current understanding of the pathology of seawater-immersed TBI, particularly the role of mitochondrial dysfunction, using a well-defined rat model of fluid percussion injury and a stretch injury model comprising cultured neurons. The biochemical and pathological markers of brain-related and neuronal injuries were evaluated. Histological analysis suggested that seawater immersion enhanced brain tissue injury and induced a significant increase in apoptosis in rats with TBI. Additionally, lactate dehydrogenase release occurred earlier and at higher levels in stretched neurons at 24 h after seawater immersion, which was consistent with more severe morphological changes and enhanced apoptosis. Furthermore, seawater immersion induced more rapid decreases in mitochondrial membrane potential, adenosine triphosphate (ATP) content, and H+-ATPase activity in the cortices of TBI rats. In addition, the immunochemical results revealed that seawater immersion further attenuated mitochondrial function in neurons exposed to stretch injury. The increases in neuronal damage and apoptosis triggered by seawater immersion were positively correlated with mitochondrial dysfunction in both in vivo and in vitro models. Thus, the present findings strengthen the current understanding of seawater-immersed TBI. Moreover, because seawater immersion aggravates mitochondrial dysfunction and contributes to post-traumatic neuronal cell death, it is important to consider mitochondria as a therapeutic target for seawater-immersed TBI.

Cold Water Immersion Syndrome and Whitewater Recreation Fatalities.

Sudden death during whitewater recreation often occurs through understandable mechanisms such as underwater entrapment or trauma, but poorly defined events are common, particularly in colder water. These uncharacterized tragedies are frequently called flush drownings by whitewater enthusiasts. We believe the condition referred to as cold water immersion syndrome may be responsible for some of these deaths. Given this assumption, the physiologic alterations contributing to cold water immersion syndrome are reviewed with an emphasis on those factors pertinent to flush drowning.

Ski-Everest (8848 m) Expedition: Digit Skin Temperature Responses to Cold Immersion May Reflect Susceptibility to Cold Injury.

INTRODUCTION: We tested the hypothesis that individual susceptibility to freezing cold injury might be reflected in an attenuated cold-induced vasodilatation (CIVD) response by comparing the CIVD responses of an elite alpinist with a history of freezing cold injury in the feet (case alpinist) with those of an age- and ability- matched noninjured alpinists control group (controls). According to this hypothesis, the vasomotor responses to a CIVD test of the case alpinist would represent a pathophysiological response when compared with the normal physiological response of a noninjured cohort. METHODS: The case alpinist and the controls in the cohort group conducted a cold water immersion test comprising sequential immersion of a hand and foot for 5 min in 35°C water, followed by a 30-min immersion in 8°C water and a 10-min recovery period in room air. During this test we monitored the finger and toe skin temperatures. RESULTS: The case alpinist had a significantly attenuated CIVD response and a lower skin temperature in all injured and noninjured digits during immersion (∼2°C lower than in the control group) and an attenuated recovery of finger skin temperatures (∼6°C lower than in the control group). CONCLUSIONS: The attenuated CIVD response of the case alpinist may reflect a previously unrecognized enhanced susceptibility to frostbite. In addition to the poor vasomotor response observed in the injured toes, he also exhibited a poor vasomotor response in his noninjured fingers. The results of the present study indicate that a test of vasomotor activity during thermal stress may identify individuals predisposed to cold injury.

Modulation of cardiac vascular endothelial growth factor and PGC-1α with regular postexercise cold-water immersion of rats.

Myocardial mitochondrial biogenesis and vascular angiogenesis biomarker responses to postexercise cold-water immersion (CWI) have not been reported. Therefore, to determine those cardiac adaptations, adult male Sprague-Dawley rats were divided into three groups: postexercise CWI (CWI; n = 13), exercise only (Ex; n = 12), and untreated control (CON; n = 10). CWI and Ex were trained for 10 wk, 5 sessions/wk, 30-60 min/session. CWI rats were immersed after each session in cold water (15 min at ~12°C). CON remained sedentary. Left ventricle tissue was obtained 48 h after the last exercise session and analyzed for peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), vascular endothelial growth factor (VEGF), and heat shock protein 70 kDa (Hsp70) protein content and mRNA expression levels. In addition, superoxide dismutase activity and mRNA and malondialdehyde levels were evaluated. Ex and CWI induced higher PGC-1α protein content compared with CON (1.8 ± 0.6-fold, P < 0.001), which was significantly higher in CWI than Ex rats (P = 0.01). VEGF protein (4.3 ± 3.7-fold) and mRNA (10.1 ± 1.1-fold) were markedly increased only in CWI (P < 0.001) relative to CON. CWI and Ex augmented cardiac Hsp70 protein to a similar level relative to CON (P < 0.05); however, Hsp70 mRNA increased only in Ex (P = 0.002). No further differences were observed between groups. These results suggest that postexercise CWI may further enhance cardiac oxidative capacity by increasing the angiogenic and mitochondrial biogenic factors. In addition, CWI does not seem to worsen exercise-induced cardioprotection and oxidative stress. NEW & NOTEWORTHY A regular postexercise cold-water immersion for 10 wk of endurance training augmented the myocardial mitochondrial biogenesis and vascular angiogenesis coactivators peroxisome proliferator-activated receptor γ coactivator-1α and vascular endothelial growth factor, respectively. In addition, postexercise cold-water immersion did not attenuate the exercise-induced increase in the cardioprotective biomarker heat shock protein 70 kDa or increase exercise-induced oxidative stress.

Warm water immersion in patients with chronic heart failure: a pilot study : Shah immerse: HF.

BACKGROUND: Patients with chronic conditions, such as heart failure, swim regularly and most rehabilitation exercises are conducted in warm hydrotherapy pools. However, little is known about the acute effects of warm water immersion (WWI) on cardiac haemodynamics in patients with chronic heart failure (CHF). METHODS: Seventeen patients with CHF (NYHA I and II; mean age 67 years, 88% male, mean left ventricular ejection fraction 33%) and 10 age-matched normal subjects were immersed up to the neck in a hydrotherapy pool (33-35 °C). Cardiac haemodynamics were measured non-invasively, and echocardiography was performed at baseline, during WWI, 3 min after kicking in the supine position and after emerging. RESULTS: In patients with CHF, compared to baseline, WWI immediately increased stroke volume (SV, mean ± standard deviation; from 65 ± 21 to 82 ± 22 mL, p < 0.001), cardiac output (CO, from 4.4 ± 1.4 to 5.7 ± 1.6 L/min, p < 0.001) and cardiac index (CI, from 2.3 ± 0.6 to 2.9 ± 0.70 L/min/m², p < 0.001) with decreased systemic vascular resistance (from 1881 ± 582 to 1258 ± 332 dynes/s/cm5, p < 0.001) and systolic blood pressure (132 ± 21 to 115 ± 23 mmHg, p < 0.001). The haemodynamic changes persisted for 15 min of WWI. In normal subjects, compared to baseline, WWI increased SV (from 68 ± 11 to 80 ± 18 mL, p < 0.001), CO (from 5.1 ± 1.9 to 5.7 ± 1.8 L/min, p < 0.001) and CI (from 2.7 ± 0.9 to 2.9 ± 1.0 L/min/m², p < 0.001).In patients with CHF, compared to baseline, WWI caused an increase in left atrial volume (from 57 ± 44 to 72 ± 46 mL, p = 0.04), without any changes in left ventricular size or function or amino terminal pro B-type natriuretic peptide. CONCLUSIONS: In patients with CHF, WWI causes an acute increase in cardiac output and a fall in systemic vascular resistance. CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov (Identifier: NCT02949544) https://clinicaltrials.gov/ct2/show/NCT02949544?cond=NCT02949544&rank=1 .

Effect of rehydration schedule after four-hour head-out water immersion on running performance and recovery.

Introduction: Head-out water immersion (HOWI) results in diuresis, which could potentially limit performance after egress to land. We examined the effect of rehydration on endurance, cardiovascular stability, and overnight recovery following a four-hour thermoneutral HOWI on 12 subjects. Methods: Twelve males completed a crossover design consisting of no hydration, replacement of fluid loss during immersion (RD), and replacement of fluid after the immersion period (RA). Sixty minutes following immersion, subjects ran to exhaustion at ~80% maximum heart rate. After completing the run, each subject submitted to a head-up tilt test (HUTT). Vital signs and ECG were monitored overnight. Results: HOWI resulted in a transient diuresis in NH and RA, while it was sustained throughout immersion in the RD protocol, resulting in greater urine [l] output (1.27 ± 0.48 (NH), 1.18 ± 0.43 (RA), 2.32 ± 0.77 (RD) (p ⟨ 0.001). Body mass change (%) was greater in NH than RD, but not RA (-1.58 ± 0.56 (NH), -0.66 ± 0.47 (RD), and -0.92 ± 0.76 (RA)). Run times were 17% versus 20% in NH compared to RD and RA, respectively, but were not statistically different. Time to orthostasis during the HUTT did not differ by condition. Overnight heart rate variability and blood pressures were not different. Conclusion: Rehydration during water immersion resulted in a large, sustained diuresis without improving performance or recovery after exiting the water. Loss of body water during thermoneutral HOWI was modest, and both rehydration strategies minimally affected aerobic performance and overnight recovery in young, healthy males.

Cryotherapy: biochemical alterations involved in reduction of damage induced by exhaustive exercise.

When exercises are done in intense or exhaustive modes, several acute biochemical mechanisms are triggered. The use of cryotherapy as cold-water immersion is largely used to accelerate the process of muscular recovery based on its anti-inflammatory and analgesic properties. The present study aimed to study the biochemical effects of cold-water immersion treatment in mice submitted to exercise-induced exhaustion. Swiss albino mice were divided into 4 treatment groups: control, cold-water immersion (CWI), swimming exhaustive protocol (SEP), and SEP+CWI. Treatment groups were subdivided into times of analysis: 0, 1, 3, and 5 days. Exhaustion groups were submitted to one SEP session, and the CWI groups submitted to one immersion session (12 min at 12°C) every 24 h. Reactive species production, inflammatory, cell viability, and antioxidant status were assessed. The SEP+CWI group showed a decrease in inflammatory damage biomarkers, and reactive species production, and presented increased cell viability compared to the SEP group. Furthermore, CWI increased acetylcholinesterase activity in the first two sessions. The present study showed that CWI was an effective treatment after exercise-induced muscle damage. It enhanced anti-inflammatory response, decreased reactive species production, increased cell viability, and promoted redox balance, which could decrease the time for the recovery process.