Fig 1 - uploaded by Ollie Jay
Content may be subject to copyright.
Effect of upright seated recovery posture ( ᮀ ) and recovery in a 15° head-down tilt recovery position ( ‚ ) after 15 min of cycle ergometry at 75%
Source publication
The following study examined the effect of 15 degrees head-down tilt (HDT) on postexercise heat loss and hemodynamic responses. We tested the hypothesis that recovery from dynamic exercise in the HDT position would attenuate the reduction in the heat loss responses of cutaneous vascular conductance (CVC) and sweating relative to upright seated (URS...
Contexts in source publication
Context 1
... condition. The change in T es at the end of exercise relative to preexercise rest was not significantly different be- tween the URS and HDT trials (P 0. (Fig. 1A). T es remained significantly (P 0.006) elevated by 0.22°C (SD 0.12) above preexercise rest after 60 min of URS recovery, but it was 0.15°C (SD 0.08) below preexercise rest after 60 min of HDT ...
Context 2
... after exercise before both HDT and URS recovery trials became lower with postexercise recovery time [F(2.6,13.2) 17.6, P 0.001]. Furthermore %CVC peak was influenced by recovery mode [F(1,5) 49.4, P 0.001] with significantly greater values observed throughout the 60-min postexercise recovery period in the HDT position compared with URS (P 0.05; Fig. ...
Similar publications
The purpose of this study was to evaluate the effect of obesity and mild hypohydration on local sweating (LSR) and cutaneous vascular conductance (CVC) responses during passive heat stress in females. Thirteen obese (age, 24 ± 4 years; 45.4% ± 5.2% body fat) and 12 nonobese (age, 22 ± 2 years; 25.1% ± 3.9% body fat) females were passively heated (1...
Nitric oxide synthase (NOS) contributes to sweating and cutaneous vasodilation during exercise in younger adults. We hypothesized that endothelial NOS (eNOS) and neuronal NOS (nNOS) mediate NOS-dependent sweating, whereas eNOS induces NOS-dependent cutaneous vasodilation in younger adults exercising in the heat. Further, aging may upregulate induci...
We investigated the effect of head-down bed rest (HDBR) for 14 days on thermoregulatory sweating and cutaneous vasodilation in humans. Fluid intake was ad libitum during HDBR. We induced whole body heating by increasing skin temperature for 1 h with a water-perfused blanket through which hot water (42 degrees C) was circulated. The experimental roo...
The cutaneous vascular conductance-esophageal temperature (CVC-Tes) relationship was examined at five work loads (75-200 W) in each of four men to find whether there is a role for exercise intensity in the control of skin blood flow (SkBF). Several factors contributed to our evaluation of the CVC-Tes relationship during work. Laser-Doppler velocime...
Citations
... Therefore, IBP activity could increase peripheral circulation in the lower extremities and enhance the process of physiological recovery. Previously, a position of head-down tilt at 15 • was shown to increase stroke volume, mean arterial pressure, and cutaneous vascular conductance [21,22]. Another study [23] used the same position for 5 min and reported a 36% increase in tibial microvascular flow. ...
... Since the effects of increasing blood flow were achieved on the 15 • head-down tilt [21-23], our IBP protocol had a maximal inclination (up to 90 • ) in expectation of the greatest effects of circulation of blood and body fluids [18]. Considering results from previous head-down tilt studies [21][22][23], the effects of elevation [18], and the Frank−Starling mechanism theory [19], we hypothesized that the lactate removal rate at the end of IBP would be greater than that of passive recovery at the same time point. Due to more voluntary muscle contractions and movements, we further expected higher values of heart rate and energy expenditure in the active recovery condition than in the IBP and passive recovery conditions. ...
... Therefore, we acknowledge the level of accuracy in estimating energy expenditure as a limitation. While accepted, our hypothesis was based on increased blood flow for a body position with 15 • head-down tilt [21][22][23] and the lack of direct measures on blood flow parameters limit us to explain and interpret the observed benefits. As an elevated blood pressure during and after exercise is typical, performing IBP immediately after exercise may be harmful by applying additional pressure to blood vessels. ...
We compared the immediate effects of a cool-down strategy including an inverted body position (IBP: continuous 30-s alternations of supine and IBP) after a short period of an intense treadmill run with active (walking) and passive (seated) methods. Fifteen healthy subjects (22 years, 172 cm, 67 kg) completed three cool-down conditions (in a counterbalanced order) followed by a 5-min static stretch on three separate days. Heart rate, energy expenditure, blood lactate concentration, fatigue perception, and circumference of thighs and calves were recorded at pre- and post-run at 0, 5, 10, 20, and 30 min. At 5 min post-run, subjects performing the IBP condition showed (1) a 22% slower heart rate (p < 0.0001, ES = 2.52) and 14% lower energy expenditure (p = 0.01, ES = 0.48) than in the active condition, and (2) a 23% lower blood lactate than in the passive condition (p = 0.001, ES = 0.82). Fatigue perception and circumferences of thighs and calves did not differ between the conditions at any time point (F10,238 < 0.96, p < 0.99 for all tests). IBP appears to produce an effect similar to that of an active cool-down in blood lactate removal with less energy expenditure. This cool-down strategy is recommended for tournament sporting events with short breaks between matches, such as Taekwondo, Judo, and wrestling.
... Regardless of the method employed, it appears that a baroreceptor modulation of sweating is dependent upon the thermal challenge. Specifically, baroreceptors modulate sweating during and following dynamic exercise (Fortney et al., 1981;Mack et al., 1995Mack et al., , 2001Journeay et al., 2004aJourneay et al., , b, 2007McInnis et al., 2006;Kenny et al., 2008;Paull et al., 2016), but not during passive heat exposure (Solack et al., 1985;Vissing et al., 1994;Wilson et al., 2001Wilson et al., , 2005Cui et al., 2004;Binder et al., 2012;Lynn et al., 2012;Schlader et al., 2015a). ...
In humans, sweating is the most powerful autonomic thermoeffector. The evaporation of sweat provides by far the greatest potential for heat loss and it represents the only means of heat loss when air temperature exceeds skin temperature. Sweat production results from the integration of afferent neural information from peripheral and central thermoreceptors which leads to an increase in skin sympathetic nerve activity. At the neuroglandular junction, acetylcholine is released and binds to muscarinic receptors which stimulate the secretion of a primary fluid by the secretory coil of eccrine glands. The primary fluid subsequently travels through a duct where ions are reabsorbed. The end result is the expulsion of hypotonic sweat on to the skin surface. Sweating increases in proportion with the intensity of the thermal challenge in an attempt of the body to attain heat balance and maintain a stable internal body temperature. The control of sweating can be modified by biophysical factors, heat acclimation, dehydration, and nonthermal factors. The purpose of this article is to review the role of sweating as a heat loss thermoeffector in humans.
... In an experimental setting, the negative impact of this postexercise suppression of heat loss can be observed by the rapid reversal of the individual's hyperthermic state when postural (i.e., head-down tilt) (67) or mechanical (application of positive pressure to the lower limbs, passive leg compressions) (43) interventions are employed to reverse the postexercise hypotension (Table 3). When performed, these manipulations have been shown to reverse the attenuation of SkBF and sweating and enhance the compartmental transfer of heat through the translocation of the blood pooled in the previously hot active muscles to the body core region (43,67). ...
... In an experimental setting, the negative impact of this postexercise suppression of heat loss can be observed by the rapid reversal of the individual's hyperthermic state when postural (i.e., head-down tilt) (67) or mechanical (application of positive pressure to the lower limbs, passive leg compressions) (43) interventions are employed to reverse the postexercise hypotension (Table 3). When performed, these manipulations have been shown to reverse the attenuation of SkBF and sweating and enhance the compartmental transfer of heat through the translocation of the blood pooled in the previously hot active muscles to the body core region (43,67). Baroreceptor loading can lead to lower core temperatures by~0.5°C ...
Performing exercise, especially in the hot conditions, can heat the body causing significant increases in internal body temperature. To offset this increase, powerful and highly developed autonomic thermoregulatory responses (i.e., skin blood flow and sweating) are activated to enhance whole-body heat loss; a response mediated by temperature sensitive receptors in both the skin and the internal core regions of the body. Independent of thermal control of heat loss, nonthermal factors can have profound consequences on the body's ability to dissipate heat during exercise. These include the activation of the body's sensory receptors (i.e., baroreceptors, metaboreceptors, mechanoreceptors, etc.) as well as phenotypic factors such as age, sex, acclimation, fitness, and chronic diseases such as diabetes. The influence of these factors extend into recovery such that marked impairments in thermoregulatory function occur leading to prolonged and sustained elevations in body core temperature. Irrespective of the level of hyperthermia, there is a time-dependent suppression of the body's physiological ability to dissipate heat. This delay in the restoration of postexercise thermoregulation has been associated with disturbances in cardiovascular function which manifests most commonly as postexercise hypotension. This review examines the current knowledge regarding the restoration of thermoregulation postexercise. In addition, the factors that are thought to accelerate or delay the return of body core temperature to resting levels are highlighted with a particular emphasis on strategies to manage heat stress in athletic and/or occupational settings.
... 8 When rowing or cycling, it is relatively easy to receive feedback and maintain HR within the required range. 9,10,11 Steady HR during swimming is not observed since immersion leads to a drop in HR 12 , postural changes after exercise affect HR, 13 while the turn and subsequent under water kicking cause a drop in HR. 14 Moreover, feedback about HR is almost impossible to give. Therefore, swimmers are instructed to swim at a specified velocity rather than at a certain HR level. ...
For training to be optimal, daily training load has to be adapted to the momentary status of the individual athlete, which is often difficult to establish. Therefore, the present study was performed to investigate the predictive value of heart rate recovery (HRR) during a standardized warm-up for training load. Training load was quantified by the variation in heart rate during standardized training in competitive swimmers. Eight female and five male swimmers of Dutch national level participated in the study. They all performed three sessions consisting of a 300-meter warm-up test and a 10 × 100 meter training protocol. Both protocols were swum in front-crawl at individually standardized velocities derived from an incremental step-test. Velocity was related to 75% and 85% Heart Rate Reserve (% HRres) for the warm-up and training, respectively. Relative HRR during the first 60 seconds after the warm-up (HRRw-up) and differences between the actual and intended heart rate for the warm-up and the training (ΔHRw-up and ΔHRtr) were determined. No significant relationship between HRRw-up and ΔHRtr was found (F(1,37) = 2.96, p = 0.09, R(2) = 0.07, SEE = 4.65). There was considerable daily variation in ΔHRtr at a given swimming velocity (73-93% HRres). ΔHRw-up and ΔHRtr were clearly related (F(1,37) = 74.31, p < 0.001, R(2) = 0.67, SEE = 2.78). HRR after a standardized warm-up does not predict heart rate during a directly subsequent and standardized training session. Instead, heart rate during the warm-up protocol seems a promising alternative for coaches to make daily individual-specific adjustments to training programs.
... Notably, similar results have been observed during exercise, yet cardiopulmonary and/or baroreflex unloading consistently reduces sweating rate during post-exercise recovery (Journeay et al., 2004). Baroreflex reloading via lower body positive pressure (Journeay et al., 2004) or head down tilt (Journeay et al., 2007;McInnis et al., 2006) augments sweating and reduces return time to baseline Tcore versus control conditions, subsequently improving thermoregulatory recovery to exercise in warm conditions. It is important to consider the level of hyperthermia with extreme heat stress, and therefore a high thermal drive, superseding non-thermal modulation of sweating (Kondo et al., 2002). ...
Under normothermic, resting conditions, humans dissipate heat from the body at a rate approximately equal to heat production. Small discrepancies between heat production and heat elimination would, over time, lead to significant changes in heat storage and body temperature. When heat production or environmental temperature is high the challenge of maintaining heat balance is much greater. This matching of heat elimination with heat production is a function of the skin circulation facilitating heat transport to the body surface and sweating, enabling evaporative heat loss.
... The body's compromised ability to dissipate heat postexercise has been attributed to the actions of nonthermal factors (21). In fact, numerous studies in the past decade have demonstrated that nonthermal factors (e.g., baroreceptors, muscle mechanoreceptor and metabore-ceptors) have a pivotal role in the modulation of postexercise heat loss and, therefore, core temperature regulation (8,15,17,18,22,28,29). A number of these studies have alluded to the hypothesis that baroreceptor activity associated with postexercise hypotension, characterized by a marked reduction in blood pressure from preexercise levels lasting ϳ2 h (13), is primarily responsible for mediating the attenuation of postexercise heat loss. ...
... However, the metaboreceptor influence was only assessed at 20 min following high-intensity treadmill running to coincide with the approximate point of nadir of postexercise hypotension (19,22,23) and the point at which sweating and cutaneous blood flow have returned to near baseline levels (21). Postexercise hypotension and, therefore, baroreceptor unloading, has a well-documented role in modulating postexercise heat loss (8,17,29). In particular, this is supported by the observation that reversing postexercise hypotension with lower body positive pressure (LBPP) application leads to a greater rate of core temperature decay due to an enhanced rate of heat dissipation associated with elevated sweating and cutaneous blood flow responses (17). ...
... It is well established that changes in baroreflex activity alone can modulate CVC during postexercise recovery (8,17,27,29). Accordingly, in the present study, baroreceptor unloading associated with LBNP application resulted in greater reductions in both forearm and upper back CVC toward baseline resting levels compared with Control and LBPP conditions. On the other hand, the application of LBPP did not affect CVC, which contrasts previous work that mechanically altered baroreceptor loading status via the application of lower body pressure (17,27). ...
We examined whether sustained changes in baroreceptor loading status during prolonged postexercise recovery can alter the metaboreceptors' influence on heat loss. Thirteen young males performed a 1-min isometric handgrip exercise (IHG) at 60% maximal voluntary contraction followed by 2-min of forearm ischemia (to activate metaboreceptors) before and 15, 30, 45 and 60-min after a 15-min intense treadmill running exercise (>90% maximal heart rate) in the heat (35°C). This was repeated on three separate days with continuous lower-body positive (LBPP, +40 mmHg), negative (LBNP, -20 mmHg), or no pressure (Control) from 13- to 65-min postexercise. Sweat rate (ventilated capsule; forearm, chest, upper back) and cutaneous vascular conductance (CVC; forearm, upper back) were measured. Relative to pre-IHG levels, sweating at all sites increased during IHG and remained elevated during ischemia at baseline and similarly at 30, 45, and 60-min postexercise (site average sweat rate increase during ischemia: Control, 0.13±0.02; LBPP, 0.12±0.02; LBNP, 0.15±0.02 mg·min(-1)·cm(-2); all P<0.01), but not at 15-min (all P>0.10). LBPP and LBNP did not modulate the pattern of sweating to IHG and ischemia (all P>0.05). At 15-min postexercise, forearm CVC was reduced from pre-IHG levels during both IHG and ischemia under LBNP only (ischemia: 3.9±0.8 %CVCmax; P<0.02). Therefore, we show metaboreceptors increase postexercise sweating in the mid-to-late stages of recovery (30-60 min), independent of baroreceptor loading status and similarly between skin sites. In contrast, metaboreflex modulation of forearm but not upper back CVC occurs only in the early stages of recovery (15-min) and is dependent upon baroreceptor unloading.
... A relationship between persistent post-exercise hyperthermia and post-exercise hypotension has been postulated such that the post-exercise attenuation in heat loss responses of skin blood flow and sweating was the result of a non-thermal baroreflex-mediated suppression (Kenny & Jay, 2013). This hypothesis was supported by reports demonstrating that reversal of baroreceptor Post-exercise responses in type 1 diabetes unloading (i.e., increases in blood pressure) during the post-exercise period resulted in a reversal in the attenuation of heat loss responses paralleled by a more rapid decay in esophageal temperature (Jackson & Kenny, 2003;McInnis et al., 2006). In the present study, absolute MAP did not differ between groups; however, we did observe a greater reduction in the magnitude of post-exercise hypotension in participants with T1DM (Fig. 5) when compared to controls. ...
Recent data demonstrated that individuals with type 1 diabetes mellitus (T1DM) exhibit impaired sweating and increased rectal temperature (i.e., heat storage) during exercise compared with healthy controls. Our purpose in this study was to investigate the consequences of T1DM on post-exercise thermal homeostasis. Sixteen participants (eight controls matched with eight T1DM) performed 90 min of cycling followed by 60 min of seated recovery. Esophageal and rectal temperatures, sweating (forearm, chest, and upper back), skin blood flow [forearm and upper back, presented as cutaneous vascular conductance (CVC)], and blood pressure [mean arterial pressure (MAP)] were measured at baseline and throughout recovery. Esophageal temperature was similar during baseline and recovery between groups (P = 0.88). However, rectal temperature was elevated in our T1DM group throughout recovery (P = 0.05). Sweating and CVC were similar between groups at all sites from 10-min post-exercise until the end of recovery (P ≥ 0.16). While absolute MAP was similar between groups (P = 0.43), the overall decrease in MAP post-exercise was greater in controls from 20 min (T1DM: − 8 ± 5 vs control: − 13 ± 6 mmHg, P = 0.03) until the end of recovery. We conclude that despite increased heat storage during exercise, individuals with T1DM exhibit a suppression in heat loss similar to their healthy counterparts during recovery.
... • a relative increase in the onset thresholds for sweating and cutaneous vasodilation; and • a concomitant increase in the postexercise core and muscle tissue temperature recovery time (Kenny et al ., 2003a(Kenny et al ., , 2003b. This is further supported by fi ndings that changes in hemodynamic response, such as an increase in stroke volume and mean arterial pressure, induced by the application of positive pressure to the lower limbs ( + 45 mm Hg) (Jackson and Kenny, 2003 ), or head-down tilt (McInnis et al ., 2006 ), attenuates the fall of mean arterial pressure, local skin blood fl ow and sweat rate, and elicits a shorter core temperature recovery time. Similarly, the postexercise attenuation of whole-body heat loss was reversed when a leg compression garment was employed to re-establish normal resting blood pressure levels during a 15-min recovery period interspersed between three successive 15-min exercise bouts performed in the heat (Kenny and Gagnon, 2010 ). ...
An overview of the physiology of human thermoregulation is presented, including a discussion of the principle of heat balance and the various heat exchange pathways together with physiological adaptations during thermal challenges. Thermoeffector responses (i.e., eccrine sweating, cutaneous vasodilation) during heat stress are examined, as well as the thermoregulatory mechanisms activated during passive heat/cold stress, exercise, and postexercise, such as shivering and nonshivering thermogenesis. Aspects related to nonthermal modulators of thermoeffector responses are explored and the effects of body composition, aerobic fitness, heat acclimation, sex, age, chronic disease (i.e., diabetes), hydration, and cardiovascular function on the body's capacity to dissipate heat are discussed.
... The vasoconstrictor system, however, can be affected by the recovery from exercise, as the threshold for vasoconstriction in response to controlled body cooling was also elevated (238). The elevated threshold for vasodilation can be reduced or even prevented by maneuvers to improve cardiac filling and reduce baroreceptor unloading such as head-down tilt or lower body positive pressure (183,280). These observations point to a baroreceptor involvement in the postexercise period. ...
In this review, we focus on significant developments in our understanding of the mechanisms that control the cutaneous vasculature in humans, with emphasis on the literature of the last half-century. To provide a background for subsequent sections, we review methods of measurement and techniques of importance in elucidating control mechanisms for studying skin blood flow. In addition, the anatomy of the skin relevant to its thermoregulatory function is outlined. The mechanisms by which sympathetic nerves mediate cutaneous active vasodilation during whole body heating and cutaneous vasoconstriction during whole body cooling are reviewed, including discussions of mechanisms involving cotransmission, NO, and other effectors. Current concepts for the mechanisms that effect local cutaneous vascular responses to local skin warming and cooling are examined, including the roles of temperature sensitive afferent neurons as well as NO and other mediators. Factors that can modulate control mechanisms of the cutaneous vasculature, such as gender, aging, and clinical conditions, are discussed, as are nonthermoregulatory reflex modifiers of thermoregulatory cutaneous vascular responses. © 2014 American Physiological Society. Compr Physiol 4:33-89, 2014.
... Studies show that, independent of thermal control, the actions of nonthermal factors have important consequences on heat loss responses, and, therefore, core temperature (14,18,19,30,33). Although nonthermal factors, such as mechanoreceptors/muscle pump and central command, have been shown to influence cutaneous blood flow and sweating during recovery, the perturbation in thermoregulatory control following dynamic exercise has primarily been ascribed to a nonthermal baroreflex-mediated response associated with postexercise hypotension (18,23,33,40). ...
... Studies show that, independent of thermal control, the actions of nonthermal factors have important consequences on heat loss responses, and, therefore, core temperature (14,18,19,30,33). Although nonthermal factors, such as mechanoreceptors/muscle pump and central command, have been shown to influence cutaneous blood flow and sweating during recovery, the perturbation in thermoregulatory control following dynamic exercise has primarily been ascribed to a nonthermal baroreflex-mediated response associated with postexercise hypotension (18,23,33,40). However, a recent review on the topic combined evidence from several studies examining metaboreceptor stimulation during passive heat stress (8,26,36) and surmised that other nonthermal factors, such as those associated with metaboreceptor activation, may be involved (24). ...
... Consistent with previous reports (14,18,23,33), we observed a gradual decline in sweat rate during the 20-min recovery period from dynamic exercise. This was reversed by performing IHG exercise and maintained during post-IHG ischemia such that sweat rate was elevated relative to control. ...
Metaboreceptor activation during passive heating is known to influence cutaneous vascular conductance (CVC) and sweat rate (SR). However, whether metaboreceptors modulate the suppression of heat loss following dynamic exercise remains unclear. On separate days, before and after 15-min of high intensity treadmill running in the heat (35°C), eight males performed either: i) no isometric handgrip exercise (IHG) or ischemia (CON); ii) 1-min IHG (60% of maximum, IHG); iii) 1-min IHG followed by 2-min of ischemia (IHG+OCC); iv) 2-min of ischemia (OCC); or v) 1-min IHG followed by 2-min of ischemia with application of lower body negative pressure (IHG+LBNP). SR (ventilated capsule), cutaneous blood flow (Laser-Doppler) and mean arterial pressure (Finometer) were measured continuously before and after dynamic exercise. Following dynamic exercise, CVC was reduced with IHG exercise (P<0.05) and remained attenuated with post-IHG ischemia during IHG+OCC relative to CON (39±2 vs 47±6%, P<0.05). Furthermore, the reduction in CVC was exacerbated by application of LBNP during post-IHG ischemia (35±3%, P<0.05) relative to IHG+OCC. SR increased during IHG exercise (P<0.05) and remained elevated during post-IHG ischemia relative to CON following dynamic exercise (0.94±0.15 vs. 0.53±0.09 mg•min(-1)•cm(-2), P<0.05). In contrast, application of LBNP during post-IHG ischemia had no effect on SR (0.93±0.09 mg•min(-1)•cm(-2), P>0.05) relative to post-IHG ischemia during IHG+OCC. We show that CVC is reduced and that sweat rate is increased by metaboreceptor activation following dynamic exercise. In addition, we show that the metaboreflex-induced loading of the baroreceptors can influence the CVC response, but not the sweating response.
