Heart rate variability during exertional heat stress: effects of heat production and treatment

Purpose

We assessed the efficacy of different treatments (i.e., treatment with ice water immersion vs. natural recovery) and the effect of exercise intensities (i.e., low vs. high) for restoring heart rate variability (HRV) indices during recovery from exertional heat stress (EHS).

Methods

Nine healthy adults (26 ± 3 years, 174.2 ± 3.8 cm, 74.6 ± 4.3 kg, 17.9 ± 2.8 % body fat, 57 ± 2 mL·kg·^?1 min^?1 peak oxygen uptake) completed four EHS sessions incorporating either walking (4.0–4.5 km·h^?1, 2 % incline) or jogging (~7.0 km·h^?1, 2 % incline) on a treadmill in a hot-dry environment (40 °C, 20–30 % relative humidity) while wearing a non-permeable rain poncho for a slow or fast rate of rectal temperature (T _re) increase, respectively. Upon reaching a T _re of 39.5 °C, participants recovered until T _re returned to 38 °C either passively or with whole-body immersion in 2 °C water. A comprehensive panel of 93 HRV measures were computed from the time, frequency, time–frequency, scale-invariant, entropy and non-linear domains.

Results

Exertional heat stress significantly affected 60/93 HRV measures analysed. Analyses during recovery demonstrated that there were no significant differences between HRV measures that had been influenced by EHS at the end of passive recovery vs. whole-body cooling treatment (p > 0.05). Nevertheless, the cooling treatment required statistically significantly less time to reduce T _re (p < 0.001).

Conclusions

While EHS has a marked effect on autonomic nervous system modulation and whole-body immersion in 2 °C water results in faster cooling, there were no observed differences in restoration of autonomic heart rate modulation as measured by HRV indices with whole-body cold-water immersion compared to passive recovery in thermoneutral conditions.     

HPA and SAS responses to increasing core temperature during uncompensable exertional heat stress in trained and untrained males

Increases in core temperature (T _c) augment stress hormones and neurotransmitters; however, the effect of different T _c tolerated with varying fitness levels during uncompensable exertional heat stress (EHS) is unclear. The purpose was to examine the hypothalamic–pituitary–adrenal (HPA) axis and sympathetic-adrenomedullary system (SAS) responses during uncompensable EHS in trained (TR) versus untrained (UT) males. Twelve TR and 11 UT ( [(V)dot]textO_2textpeak = 70 ±2 dot{V}{text{O}}_{{2{text{peak}}}} = 70 pm 2 and 50 ± 1 mL kg of lean body mass⁻¹ min⁻¹) walked on a treadmill to exhaustion (EXH) in 40°C (dry), dressed in protective clothing. PRE and 0.5°C T _c increments from 38.0–40.0°C/EXH venous blood was obtained. Cortisol responded to absolute thermal strain, increasing throughout EHS and independent of fitness. Adrenocorticotropic Hormone, Norepinephrine, and Dehydroepiandrosterone–Sulphate responded to relative thermal strain with similar EXH values, despite higher T _c tolerated for TR (39.7°C) than UT (39.0°C). Epinephrine, Growth Hormone (GH), and Aldosterone increased initially, with a plateau above 38.5°C T _c. Findings demonstrate the complexity of the HPA axis, SAS, and T _c relationship, with the stress pathways responding largely to relative thermal strain, although some hormones exhibited a clamping response likely as a protective mechanism. For the TR, evidence existed for a reduced pituitary sensitivity to glucocorticoids and the amplified GH may have contributed to their greater T _c tolerated.     

Blunted cutaneous vasoconstriction and increased frequency of presyncope during an orthostatic challenge under moderate heat stress in the morning

Purpose

In normothermia, the tolerance time to presyncope during an orthostatic challenge is shortened during the early morning. Heat stress reduces tolerance to presyncope and the degree of cutaneous vasoconstriction prior to presyncope. However, whether these changes show diurnal variations remains unknown. Therefore, we examined diurnal changes in orthostatic tolerance and cutaneous vascular conductance (CVC) during an orthostatic challenge under moderate heat stress.

Methods

Each lower body negative pressure (LBNP) under normothermia and whole body heat stress was applied for 7 min or until the appearance of presyncopal symptoms in 16 males at both 08:00 (a.m.) and 17:00 hours (p.m.). Measurements included internal and skin temperatures, forearm skin blood flow, arterial pressure, and heart rate. CVC was calculated as skin blood flow/mean arterial pressure, normalized to CVC prior to LBNP and expressed as %CVC.

Results

The average tolerance time in eight subjects exhibiting presyncopal symptoms due to LBNP and moderate heat stress was significantly shorter in the a.m. than in the p.m. (3.7 ± 0.8 versus 6.7 ± 0.3 min, respectively; P = 0.005). Neither %CVC during LBNP in these subjects under moderate heat stress nor normothermia were significantly decreased in the a.m. (P > 0.05, respectively).

Conclusions

These findings indicate an orthostatic challenge even during moderate heat stress that led to an increase in the frequency of presyncope, especially in the morning. The reduction in tolerance was accompanied by blunted cutaneous vasoconstriction prior to presyncope. Hence, diurnal changes in cutaneous vascular responses during combined orthostatic and heat stresses should contribute, at least partly, to heat-induced orthostatic intolerance in the morning.     

The electrocardiogram during emotional and physical stress

The electrocardiographic response pattern during exercise at low and high heart rate was compared with the response pattern during emotional stress. Qualitative differences between exercise and emotional stress were obtained, i.e. during exercise the ST segment was more depressed, T-wave amplitudes were larger and QT and PQ were significantly shorter than during emotional stress. The results do not support the suggestion that emotional stress evokes an exercise-like cardiovascular response pattern, which may lead to a metabolically maladaptive situation. The results are in accordance with the hypothesis that the ECG changes during emotional stress are similar to the ECG changes during right stellate stimulation, while the ECG changes during exercise are similar to the ECG changes obtained during left stellate stimulation.     

Skin cooling aids cerebrovascular function more effectively under severe than moderate heat stress

Skin surface cooling has been shown to improve orthostatic tolerance; however, the influence of severe heat stress on cardiovascular and cerebrovascular responses to skin cooling remains unknown. Nine healthy males, resting supine in a water-perfusion suit, were heated to +1.0 and +2.0°C elevation in body core temperature (T _c). Blood flow velocity in the middle cerebral artery (transcranial Doppler ultrasound), mean arterial pressure (MAP; photoplethysmography), stroke volume (SV; Modelflow), total peripheral resistance (TPR; Modelflow), heart rate (HR; ECG) and the partial pressure of end-tidal carbon dioxide (P_ETCO₂) were measured continuously during 1-min baseline and 3-min lower body negative pressure (LBNP, −15 mm Hg) when heated without and again with skin surface cooling. Nine participants tolerated +1°C and six participants reached +2°C. Skin cooling elevated (P = 0.004) MAP ~4% during baseline and LBNP at +1°C T _c. During LBNP, skin cooling increased SV (9%; P = 0.010) and TPR (0.9 mm Hg L⁻¹ min, P = 0.013) and lowered HR (13 b min⁻¹, P = 0.012) at +1°C T _c and +2°C T _c collectively. At +2°C T _c, skin cooling elevated P_ETCO₂ ~4.3 mm Hg (P = 0.011) and therefore reduced cerebral vascular resistance ~0.1 mm Hg cm⁻¹ s at baseline and LBNP (P = 0.012). In conclusion, skin cooling under severe heating and mild orthostatic stress maintained cerebral blood flow more effectively than it did under moderate heating, in conjunction with elevated carbon dioxide pressure, SV and arterial resistance.     

Increased resistance to heat shock of isolated hearts from rats adapted to moderate physical exercise

Hearts isolated from rats adapted to physical activity through moderate regular exercise (swimming) were more resistant to heat shock than hearts from unadapted controls. Thus, 15-min perfusion of control hearts with a solution heated to 42°C significantly depressed contraction amplitudes and caused a contracture amounting to 36% of the initial contraction amplitude, as well as increased release of creatine kinase into the perfusate. In the hearts from adapted rats, contraction amplitude was, on average, 2.3-fold greater and the contracture 3.2 times less marked than in the control animals; the test and control hearts did not differ significantly in the release of creatine kinase. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 119, N ^o 3, pp. 256–258, March, 1995 Presented by S. S. Debov, Member of the Russian Academy of Medical Sciences     

Cardiovascular responses to facial cooling during low and moderate intensity exercise

Summary To investigate the hypothesis that facial cooling (FC) exerts a greater influence on the cardiovascular system at lower versus higher levels of exercise, this study examined the effect of facial cooling [mean (SE): 0 (2)°C at 0.8 m·s^–1 wind velocity] during 30 min low [35% maximum oxygen consumption ( O_2max)] and moderate (70% O_2max) levels of cycle ergometry in the supine position. Five male subjects were assigned in random order to four exercise conditions: (1) FC at 35% O_2max(FC35), (2) no cooling (NFC35), (3) FC at 70% O_2max(FC70), and (4) no cooling (NFC70). Heart rate (f _c), stroke volume (V _s), and cardiac output ( _c) were measured at rest and every 10 min of exercise using impedance cardiography. During FC35, the change in f _c [mean (SE)] was significantly lower (P < 0.05) than NFC35 at 10 [22 (5) vs 31 (3) beats· min^–1], 20 [29 (6) vs 35 (3) beats·min^–1], and 30 [29 (5) vs 38 (4) beats·min^–1] min. No differences in f _c were observed between FC70 and NFC70. Furthermore, FC had no effect on V _s or _cat either exercise intensity. However, when comparing the FC70 and NFC70 conditions, there was a significant main effect (P<0.05) in mean arterial pressure (P _a) response with cooling despite the fact that neither V _s or _cwere different from the NFC70 control. The increase (P < 0.05) in the estimated change in systemic vascular resistance ( _a· _c ^–1) could partly explain the relative rise in _aat FC70. No pressor effect of cooling was observed at 35% O_2max. The results suggest that the FC condition promotes exercise bradycardia at low levels of exercise and exerts a greater pressor response during moderate exercise.     

Perceived exertion of absolute work during a military physical training program

The purpose of this study was to compare the rating of perceived exertion (RPE) and heart rate (HR) in two groups of 60 military personnel who differed in their level of fitness as determined by maximal oxygen uptake ( O₂ max). At an initial testing period (T ₁), Group I represented a sample of personnel not participating in a training program while Group II had engaged in an endurance program (2–4 mile run/day) for 5 months. Six months later (T ₂), Groups I and II were retested after having participated in the program for 6 and 11 months, respectively. RPE and HR were measured at the end of each min of a 6-min run at an absolute workload of 6 mph, 0% grade on the treadmill. At T ₁, Group II had a significantly lower HR at each min of work but no difference existed in RPE between groups at any time during the run. At T ₂, both groups showed a significant decrease in HR and RPE during each min when compared longitudinally. The data suggest that the perception of the intensity of absolute work does not differ in groups differing in their level of fitness when studied cross-sectionally. However, significant reductions in perceived exertion occur following physical training.     

Influence of nonthermal baroreceptor modulation of heat loss responses during uncompensable heat stress

We evaluated the hypothesis that with increasing levels of hyperthermia, thermal influences would predominate over nonthermal baroreceptor control of cutaneous vascular conductance (CVC) and local sweat rate (LSR). On separate days, eight male participants were positioned in either an upright seated posture (URS) or a 15° head-down tilt (HDT) posture in a thermoneutral condition and during passive heating, until mean body temperature (T _body) increased by 1.5°C. Hemodynamic [heart rate (HR), cardiac output, mean arterial pressure (MAP)] and thermal responses [T _re, CVC, LSR] were measured continuously. MAP showed a gradual decrease in the early- to mid-stages of heating for both HDT and URS. At a T _body > 0.6°C, MAP achieved a stable, albeit reduced level from baseline resting for the duration of the heating, whereas MAP decreased significantly throughout the heating period in the URS position (p < 0.001). CVC increased rapidly in the early stages of heating and achieved a stable elevated level in both HDT and URS at the mid-stage of heating (T _body increase ≤ 0.45°C) for the duration of the heating period (i.e., to a T _body increase of 1.5°C). A similar pattern of response was observed in LSR. A rapid increase in LSR was observed in the early- to mid-stages of heating (T _body increase ≤ 0.75°C), followed by a slower increase until the end of heating. Responses were similar between conditions. We conclude that despite a significant nonthermal drive, as evidenced by a significant difference in MAP between conditions in the late stages of heating, the thermoeffector activity governing CVC and LSR responses are primarily modulated by thermal input.     

Systemic hypoxia promotes lymphocyte apoptosis induced by oxidative stress during moderate exercise

Blood undergoes oxidative stress during severe hypoxia or intense exercise. Excessive exposure to oxidative stress induces replicative senescence and apoptosis of lymphocytes. This study determines how various exercises with/without hypoxia affect lymphocyte subset mobilization and oxidative stress-induced lymphocyte apoptosis. Eighteen sedentary males randomly engaged in two normoxic exercise bouts [severe exercise (SE) (up to VO_2max) and moderate-intensity exercise (ME) (50%VO_2max) while exposed to 21%O₂], two hypoxic exercise bouts (ME while exposed to 12%O₂ and 15%O₂) and two hypoxic resting conditions (resting while exposed to 12%O₂ and 15%O₂) in a normobaric hypoxia chamber. Under normoxic conditions, SE but not ME (1) increased the percentages of senescent (CD28⁻ and CD57⁺)/activated (CD62L⁻ and CD11a⁺)-form lymphocytes mobilized into the peripheral blood compartment; (2) decreased the levels of surface thiol and intracellular total (t-GSH) and reduced-form glutathione (r-GSH) of lymphocytes in blood; and (3) further enhanced the extents of H₂O₂-induced mitochondria trans-membrane potential diminishing, caspases 3/8/9 activation, poly(ADP-ribose) polymerase cleavage and phosphotidyl serine exposure in blood lymphocytes. However, no significant change occurred in the subset mobilization, antioxidant levels or apoptosis of lymphocytes following exposure to either 12%O₂ or 15%O₂. Although both 12%O₂ and 15%O₂ ME increased the mobilization of senescent/activated-form lymphocytes, only 12%O₂ ME enhanced H₂O₂-induced lymphocyte thiol, t-GSH and r-GSH consumption and apoptotic responses. Therefore, we conclude that the 12%O₂ exposure increases the mobilization of senescent/activated-form lymphocytes into the peripheral blood compartment and simultaneously enhances oxidative stress-induced lymphocyte apoptosis by diminishing cellular antioxidant levels during exercise.     

Plasma volume during heat stress and exercise in women

Summary Five women were studied during exercise and passive heating to determine whether PV dynamics were affected by the menstrual cycle. The exercise bout (80% peak) on a modified cycle ergometer and the passive heat stress were done in a hot environment (T_a=50°C, P_w=1.61kPa) during the follicular and luteal phase. Esophageal temperature (T_es) was measured continuously. Blood samples were drawn after each 0.2° C increase in T_es and was measured at that time. Initial PV was estimated at rest during the follicular phase. PV changes from rest were calculated at each T_es from Hb and Hct. During passive heating, PV decreased by a mean volume of 156 (±80) ml to 2.83 (±0.09)l in the follicular phase. During the luteal phase, there was a larger volume reduction (300±100 ml) during passive heating, and the final PV was lower than in the follicular phase and averaged 2.47±0.181. During exercise, PV decreased 463 (±90) ml to 2.50 (±0.11) l in the follicular and 381 (±70) ml to 2.50 (±0.23) l in the luteal phase. These data indicate that there is a menstrual cycle effect on PV dynamics during passive heating such that more fluid is shifted out of the vasculature during the luteal phase. During severe exercise there is a greater fluid loss during the follicular phase, yet the final PV is not different between phases.     

Antidiuretic hormone and evaporative weight loss during heat stress

Summary In order to investigate the effects of vasopressin (ADH) on evaporative weight loss during heat exposure, four modifications of a single experiment were used. In all experiments the subjects (co-authors) initially ingested an amount of tap water equal to 2% of their body weight. During 3 out of 4 experiments urinary and evaporative weight loss was replenished at 15 min intervals while no further water was ingested in the 4th experiment. Following a 2 hr period at room temperature (25–27.8°C), the subjects entered the heat chamber maintained at 43–44°C D. B., 28–29°C W. B. Heat exposure for 3 experiments lasted 2 hrs, while for a 4th exposure the time lapse was 4 hrs. Vasopressin (5 units) was injected intramuscularly at the beginning of the last hour of heat exposure in two experiments wherein water replacement took place. Vasopressin injection had no apparent effect on rates of evaporative weight loss. For these experiments the effects of exercise, hypohydration and probably subject anxiety could be ruled out as influencing these results.This work was supported by N. I. H. grants 5 RO1 HE-07075 and 1K3 HE 25,110     

Severe ethanol stress inhibits yeast proteasome activity at moderate temperatures but not at low temperatures

Since yeast research under laboratory conditions is usually conducted at 25–30°C (moderate temperature range), most of the findings on yeast physiology are based on analyses in this temperature range. Due to inefficiencies in cultivation and analysis, insufficient information is available on yeast physiology in the low-temperature range, although alcoholic beverage production is often conducted at relatively low temperatures (around 15°C). Recently, we reported that severe ethanol stress (10% v/v) inhibits proteasomal proteolysis in yeast cells under laboratory conditions at 28°C. In this study, proteasomal proteolysis at a low temperature (15°C) was evaluated using cycloheximide chase analysis of a short-lived protein (Gic2-3HA), an auxin-inducible degron system (Paf1-AID*-6FLAG), and Spe1-3HA, which is degraded ubiquitin-independently by the proteasome. At 15°C, proteasomal proteolysis was not inhibited under severe ethanol stress, and sufficient proteasomal activity was maintained. These results provide novel insights into the effects of low temperature and ethanol on yeast physiology.     

A low carbohydrate diet affects autonomic modulation during heavy but not moderate exercise

The aim of this study was to examine the effects of low carbohydrate (CHO) availability on heart rate variability (HRV) responses during moderate and severe exercise intensities until exhaustion. Six healthy males (age, 26.5 ± 6.7 years; body mass, 78.4 ± 7.7 kg; body fat %, 11.3 ± 4.5%; [(V)\dot] \textO_{2 max} , \dot{V} {\text{O}}_{{2{ \max }}} , 39.5 ± 6.6 mL kg⁻¹ min⁻¹) volunteered for this study. All tests were performed in the morning, after 8–12 h overnight fasting, at a moderate intensity corresponding to 50% of the difference between the first (LT₁) and second (LT₂) lactate breakpoints and at a severe intensity corresponding to 25% of the difference between the maximal power output and LT₂. Forty-eight hours before each experimental session, the subjects performed a 90-min cycling exercise followed by 5-min rest periods and subsequent 1-min cycling bouts at 125% [(V)\dot] \textO_{2 max} \dot{V} {\text{O}}_{{2{ \max }}} (with 1-min rest periods) until exhaustion, in order to deplete muscle glycogen. A diet providing 10% (CHO_low) or 65% (CHO_control) of energy as carbohydrates was consumed for the following 2 days until the experimental test. The Poicaré plots (standard deviations 1 and 2: SD1 and SD2, respectively) and spectral autoregressive model (low frequency LF, and high frequency HF) were applied to obtain HRV parameters. The CHO availability had no effect on the HRV parameters or ventilation during moderate-intensity exercise. However, the SD1 and SD2 parameters were significantly higher in CHO_low than in CHO_control, as taken at exhaustion during the severe-intensity exercise (P < 0.05). The HF and LF frequencies (ms²) were also significantly higher in CHO_low than in CHO_control (P < 0.05). In addition, ventilation measured at the 5 and 10-min was higher in CHO_low (62.5 ± 4.4 and 74.8 ± 6.5 L min⁻¹, respectively, P < 0.05) than in CHO_control (70.0 ± 3.6 and 79.6 ± 5.1 L min⁻¹, respectively; P < 0.05) during the severe-intensity exercise. These results suggest that the CHO availability alters the HRV parameters during severe-, but not moderate-, intensity exercise, and this was associated with an increase in ventilation volume.     

Combining heat stress and moderate hypoxia reduces cycling time to exhaustion without modifying neuromuscular fatigue characteristics

Purpose

This study investigated the isolated and combined effects of heat [temperate (22 °C/30 % rH) vs. hot (35 °C/40 % rH)] and hypoxia [sea level (FiO₂ 0.21) vs. moderate altitude (FiO₂ 0.15)] on exercise capacity and neuromuscular fatigue characteristics.

Methods

Eleven physically active subjects cycled to exhaustion at constant workload (66 % of the power output associated with their maximal oxygen uptake in temperate conditions) in four different environmental conditions [temperate/sea level (control), hot/sea level (hot), temperate/moderate altitude (hypoxia) and hot/moderate altitude (hot + hypoxia)]. Torque and electromyography (EMG) responses following electrical stimulation of the tibial nerve (plantar-flexion; soleus) were recorded before and 5 min after exercise.

Results

Time to exhaustion was reduced (P < 0.05) in hot (?35 ± 15 %) or hypoxia (?36 ± 14 %) compared to control (61 ± 28 min), while hot + hypoxia (?51 ± 20 %) further compromised exercise capacity (P < 0.05). However, the effect of temperature or altitude on end-exercise core temperature (P = 0.089 and P = 0.070, respectively) and rating of perceived exertion (P > 0.05) did not reach significance. Maximal voluntary contraction torque, voluntary activation (twitch interpolation) and peak twitch torque decreased from pre- to post-exercise (?9 ± 1, ?4 ± 1 and ?6 ± 1 % all trials compounded, respectively; P < 0.05), with no effect of the temperature or altitude. M-wave amplitude and root mean square activity were reduced (P < 0.05) in hot compared to temperate conditions, while normalized maximal EMG activity did not change. Altitude had no effect on any measured parameters.

Conclusion

Moderate hypoxia in combination with heat stress reduces cycling time to exhaustion without modifying neuromuscular fatigue characteristics. Impaired oxygen delivery or increased cardiovascular strain, increasing relative exercise intensity, may have also contributed to earlier exercise cessation.