The effect of 48?weeks of aerobic exercise training on cutaneous vasodilator function in post-menopausal females

Skin blood flow (SkBF) and endothelial-dependent vasodilatation decline with ageing and can be reversed with exercise training. We tested whether 48 weeks of training could improve SkBF and endothelial function in post-menopausal females; 20 post-menopausal subjects completed the study. SkBF was measured by laser-Doppler flowmetry (LDF). Cutaneous vascular conductance (CVC) was calculated as LDF/blood pressure. Resting CVC was measured at 32°C and peak CVC at 42°C. Cutaneous endothelial-dependent and -independent vasodilatations were determined by the iontophoresis of acetylcholine (ACh) and sodium nitroprusside (SNP), respectively. All assessments described were performed at entry (week 0), and after 6, 12, 24, 36, and 48 weeks of training. Resting CVC measures did not change (P > 0.05) throughout the study. Peak CVC increased (P < 0.05) after 24 weeks (7.2 ± 1.2 vs. 11.6 ± 1.4 AU mmHg⁻¹) and at the 36- and 48-week assessments (13.0 ± 1.7 and 14.9 ± 2.1 AU mmHg⁻¹, respectively). Responses to ACh also increased (P < 0.05) at the 24-week assessment (5.1 ± 2.1 vs. 8.55 ± 2.3 AU mmHg⁻¹) and increased further at the 36 and 48-week assessments (11.6 ± 3.7 and 13.2 ± 3.9 AU mmHg⁻¹, respectively). Cutaneous responses to SNP increased (P < 0.05) after 36 weeks (8.7 ± 2.1 vs. 13.02 ± 2.23 AU mmHg⁻¹ at 36 weeks). VO_2max increased after 12 weeks (23.5 ± 0.7 vs. 25.4 ± 0.9 ml kg⁻¹ min⁻¹) and improved (P < 0.05) further throughout the study (31.6 ± 1.8 ml kg⁻¹ min⁻¹ at week 48). Aerobic exercise produces positive adaptations in the cutaneous vasodilator function to local heating as well as in cutaneous endothelial and endothelial-independent vasodilator mechanisms. Aerobic capacity was also significantly improved. These adaptations were further enhanced with progressive increases in exercise intensity.     

Exercise modality modulates body temperature regulation during exercise in uncompensable heat stress

This study evaluated exercise modality [i.e. self-paced (SP) or fixed-intensity (FI) exercise] as a modulator of body temperature regulation under uncompensable heat stress. Eight well-trained male cyclists completed (work-matched) FI and SP cycling exercise bouts in a hot (40.6 ± 0.2°C) and dry (relative humidity 23 ± 3%) environment estimated to elicit 70% of [(V)\dot] \dot{V} O₂max. Exercise intensity (i.e. power output) decreased over time in SP, which resulted in longer exercise duration (FI 20.3 ± 3.4 min, SP 23.2 ± 4.1 min). According to the heat strain index, the modification of exercise intensity in SP improved the compensability of the thermal environment which, relative to FI, was likely a result of the reductions in metabolic heat production (i.e. [(V)\dot] \dot{V} O₂). Consequently, the rate of rise in core body temperature was higher in FI (0.108 ± 0.020°C/min) than in SP (0.082 ± 0.016°C/min). Interestingly, cardiac output, stroke volume, and heart rate during exercise were independent of exercise modality. However, core body temperature (FI 39.4 ± 0.3°C, SP 39.1 ± 0.4°C), blood lactate (FI 2.9 ± 0.8 mmol/L, SP 2.3 ± 0.7 mmol/L), perceived exertion (FI 18 ± 2, SP 16 ± 2), and physiological strain (FI 9.1 ± 0.9, SP 8.3 ± 1.1) were all higher in FI compared to SP at exhaustion/completion. These findings indicate that, when exercise is SP, behavioral modification of metabolic heat production improves the compensability of the thermal environment and reduces thermoregulatory strain. Therefore, under uncompensable heat stress, exercise modality modulates body temperature regulation.     

The effect of the rate of heat storage on serum heat shock protein 72 in humans

Hsp72 concentration has been shown to be higher in the serum (eHsp72) of runners with symptoms of heat illness than in non-ill runners. Recently, it has been suggested that the rate of heat storage during exercise in the heat may be an important factor in the development of heat stroke. Therefore, we compared the effect of two rates of heat storage on eHsp72 concentration during exercise in which subjects reached the same final core temperature. We hypothesized that with a lower rate of heat storage the increase in eHsp72 would be attenuated compared to a higher rate of heat storage. Nine heat acclimated subjects performed two exercise trials in a counterbalanced order in the heat (42°C, 30% relative humidity). The trials consisted of walking on a treadmill (~50% VO ₂ peak) dressed in military summer fatigues until rectal temperature reached 38.5°C. A high rate of heat storage (HS, 1.04 ± 0.10 W m⁻² min⁻¹, mean ± SE) occurred when subjects walked without cooling. To produce a lower rate of heat storage (LS, 0.54 ± 0.09 W m⁻² min⁻¹) subjects walked while wearing a water-perfused cooling vest underneath clothing. eHsp72 increased pre- to post-exercise (P < 0.05) but there was no difference (P > 0.05) in eHSP between the two rates of heat storage (LS 1.25 ± 0.73 to 2.23 ± 0.70 ng ml⁻¹, HS 1.04 ± 0.57 to 2.02 ± 0.60 ng ml⁻¹). This result suggests that eHsp72 is a function of the core temperature attained rather than the rate of heat storage.     

Thermoregulatory responses to ice-slush beverage ingestion and exercise in the heat

We compared the effects of an ice-slush beverage (ISB) and a cool liquid beverage (CLB) on cycling performance, changes in rectal temperature (T _re) and stress responses in hot, humid conditions. Ten trained male cyclists/triathletes completed two exercise trials (75 min cycling at ~60% peak power output + 50 min seated recovery + 75% peak power output × 30 min performance trial) on separate occasions in 34°C, 60% relative humidity. During the recovery phase before the performance trial, the athletes consumed either the ISB (mean ± SD −0.8 ± 0.1°C) or the CLB (18.4 ± 0.5°C). Performance time was not significantly different after consuming the ISB compared with the CLB (29.42 ± 2.07 min for ISB vs. 29.98 ± 3.07 min for CLB, P = 0.263). T _re (37.0 ± 0.3°C for ISB vs. 37.4 ± 0.2°C for CLB, P = 0.001) and physiological strain index (0.2 ± 0.6 for ISB vs. 1.1 ± 0.9 for CLB, P = 0.009) were lower at the end of recovery and before the performance trial after ingestion of the ISB compared with the CLB. Mean thermal sensation was lower (P < 0.001) during recovery with the ISB compared with the CLB. Changes in plasma volume and the concentrations of blood variables (i.e., glucose, lactate, electrolytes, cortisol and catecholamines) were similar between the two trials. In conclusion, ingestion of ISB did not significantly alter exercise performance even though it significantly reduced pre-exercise T _re compared with CLB. Irrespective of exercise performance outcomes, ingestion of ISB during recovery from exercise in hot humid environments is a practical and effective method for cooling athletes following exercise in hot environments.     

Whole-body pre-cooling does not alter human muscle metabolism during sub-maximal exercise in the heat

Muscle metabolism was investigated in seven men during two 35 min cycling trials at 60% peak oxygen uptake, at 35°C and 50% relative humidity. On one occasion, exercise was preceded by whole-body cooling achieved by immersion in water during a reduction in temperature from 29 to 24°C, and, for the other trial, by immersion in water at a thermoneutral temperature (control, 34.8°C). Pre-cooling did not alter oxygen uptake during exercise (P>0.05), whilst the change in cardiac frequency and body mass both tended to be lower following pre-cooling (0.05< P<0.10). When averaged over the exercise period, muscle and oesophageal temperatures after pre-cooling were reduced by 1.5 and 0.6°C respectively, compared with control (P<0.05). Pre-cooling had a limited effect on muscle metabolism, with no differences between the two conditions in muscle glycogen, triglyceride, adenosine triphosphate, creatine phosphate, creatine or lactate contents at rest, or following exercise. These data indicate that whole-body pre-cooling does not alter muscle metabolism during submaximal exercise in the heat. It is more likely that thermoregulatory and cardiovascular strain are reduced, through lower muscle and core temperatures. Electronic Publication     

The effect of arm training on thermoregulatory responses and calf volume during upper body exercise

Purpose

The smaller muscle mass of the upper body compared to the lower body may elicit a smaller thermoregulatory stimulus during exercise and thus produce novel training-induced thermoregulatory adaptations. Therefore, the principal aim of the study was to examine the effect of arm training on thermoregulatory responses during submaximal exercise.

Methods

Thirteen healthy male participants (Mean ± SD age 27.8 ± 5.0 years, body mass 74.8 ± 9.5 kg) took part in 8 weeks of arm crank ergometry training. Thermoregulatory and calf blood flow responses were measured during 30 min of arm cranking at 60 % peak power (W _peak) pre-, and post-training and post-training at the same absolute intensity as pre-training. Core temperature and skin temperatures were measured, along with heat flow at the calf, thigh, upper arm and chest. Calf blood flow using venous occlusion plethysmography was performed pre- and post-exercise and calf volume was determined during exercise.

Results

The upper body training reduced aural temperature (0.1 ± 0.3 °C) and heat storage (0.3 ± 0.2 J g^?1) at a given power output as a result of increased whole body sweating and heat flow. Arm crank training produced a smaller change in calf volume post-training at the same absolute exercise intensity (?1.2 ± 0.8 % compared to ?2.2 ± 0.9 % pre-training; P < 0.05) suggesting reduced leg vasoconstriction.

Conclusion

Training improved the main markers of aerobic fitness. However, the results of this study suggest arm crank training additionally elicits physiological responses specific to the lower body which may aid thermoregulation.     

Aerobically trained individuals have greater increases in rectal temperature than untrained ones during exercise in the heat at similar relative intensities

To determine if the increases in rectal temperature (T _REC) during exercise in the heat at a given percent of [(V)\dot]O_2 \textpeak \dot{V}\hbox{O}_{{2\,{\text{peak}}}} depend on a subject’s aerobic fitness level. On three occasions, 10 endurance-trained (Tr) and 10 untrained (UTr) subjects ([(V)\dot]O_2 peak \dot{V}\hbox{O}_{2\,{\rm peak}} : 60 ± 6 vs. 44 ± 3 mL kg⁻¹ min⁻¹, P < 0.05) cycled in a hot-dry environment (36 ± 1°C; 25 ± 2% humidity, airflow 2.5 m s⁻¹) at three workloads (40, 60, and 80% [(V)\dot]O_2 peak \dot{V}\hbox{O}_{2\,{\rm peak}} ). At the same percent of [(V)\dot]O_2 peak \dot{V}\hbox{O}_{2\,{\rm peak}} , on average, Tr had 28 ± 5% higher heat production but also higher skin blood flow (29 ± 3%) and sweat rate (20 ± 7%; P = 0.07) and lower skin temperature (0.5°C; P < 0.05). Pre-exercise T _REC was lower in the Tr subjects (37.4 ± 0.2 vs. 37.6 ± 0.2; P < 0.05) but similar to the UTr at the end of 40 and 60% [(V)\dot]O_2 peak \dot{V}\hbox{O}_{2\,{\rm peak}} trials. Thus, exercise T _REC increased more in the Tr group than in the UTr group (0.6 ± 0.1 vs. 0.3 ± 0.1°C at 40% [(V)\dot]O_2 peak \dot{V}\hbox{O}_{2\,{\rm peak}} and 1.0 ± 0.1 vs. 0.6 ± 0.3°C at 60% [(V)\dot]O_2 peak \dot{V}\hbox{O}_{2\,{\rm peak}} ; P < 0.05). At 80% [(V)\dot]O_2 peak \dot{V}\hbox{O}_{2\,{\rm peak}} not only the increase in T _REC (1.7 ± 0.1 vs. 1.3 ± 0.3°C) but also the final T _REC was larger in Tr than in UTr subjects (39.15 ± 0.1 vs. 38.85 ± 0.1°C; P < 0.05). During exercise in the heat at the same relative intensity, aerobically trained individuals have a larger rise in T _REC than do the untrained ones which renders them more hyperthermic after high-intensity exercise.     

Oral tyrosine supplementation improves exercise capacity in the heat

Increased brain dopamine availability improves prolonged exercise tolerance in the heat. It is unclear whether supplementing the amino-acid precursor of dopamine increases exercise capacity in the heat. Eight healthy male volunteers [mean age 32 ± 11 (SD) years; body mass 75.3 ± 8.1 kg; peak oxygen uptake ([(V)\dot]O_2peak \dot{V}O_{{2peak}} ) 3.5 ± 0.3 L min⁻¹] performed two exercise trials separated by at least 7 days in a randomised, crossover design. Subjects consumed 500 mL of a flavoured sugar-free drink (PLA), or the same drink with 150 mg kg body mass⁻¹ tyrosine (TYR) in a double-blind manner 1 h before cycling to exhaustion at a constant exercise intensity equivalent to 68 ± 5% [(V)\dot]O_2peak \dot{V}O_{{2peak}} in 30°C and 60% relative humidity. Pre-exercise plasma tyrosine:large neutral amino acids increased 2.9-fold in TYR (P < 0.01), while there was no change in PLA (P > 0.05). Subjects cycled longer in TYR compared to PLA (80.3 ± 19.7 min vs. 69.2 ± 14.0 min; P < 0.01). Core temperature, mean weighted skin temperature, heart rate, ratings of perceived exertion and thermal sensation were similar in TYR and PLA during exercise and at exhaustion (P > 0.05) despite longer exercise time in TYR. The results show that acute tyrosine supplementation is associated with increased endurance capacity in the heat in moderately trained subjects. The results also suggest for the first time that the availability of tyrosine, a nutritional dopamine precursor, can influence the ability to subjectively tolerate prolonged submaximal constant-load exercise in the heat.     

Heat balance and cumulative heat storage during exercise performed in the heat in physically active younger and middle-aged men

On separate days, eight physically active younger (22 ± 2 years) and eight highly trained middle-aged (45 ± 4 years) men matched for physical fitness and body composition performed 90 min of semi-recumbent cycling at a constant rate of heat production (290 W) followed by 60 min of seated recovery in either a temperate (T, 30°C), warm (W, 35°C) or hot (H, 40°C) ambient condition. Rectal temperature (T _re) was measured continuously, while the rate of whole-body heat loss (H _L), as well as changes in body heat content (∆H _b) was measured simultaneously using direct whole-body and indirect calorimetry. No difference in H _L was observed between age groups for all ambient conditions. Accordingly, the average ∆H _b during the 90-min exercise was similar for the younger (+193 ± 52, 212 ± 82 and +211 ± 44 kJ for T, W and H, respectively) and middle-aged men (+192 ± 119, +225 ± 76 and +217 ± 130 kJ for T, W and H, respectively). This was paralleled by a similar increase in T _re of 0.40 ± 0.20, 0.36 ± 0.14 and 0.34 ± 0.23°C for T, W and H, respectively in the younger men and 0.37 ± 0.23, 0.32 ± 0.19 and 0.28 ± 0.14°C for T, W and H, respectively in the middle-aged men. After 60 min of recovery, ∆H _b was similar for the younger and the middle-aged men, respectively (−45 ± 52 and −38 ± 31 kJ for T; −57 ± 78 and −40 ± 25 kJ for W; and −32 ± 71 and 11 ± 96 kJ for H). End recovery T _re remained elevated to similar levels in both the younger and middle-aged men, respectively, for each of the ambient conditions (0.24 ± 019 and 0.18 ± 0.18°C for T; 0.25 ± 0.11 and 0.24 ± 0.14°C for W and 0.33 ± 0.21 and 0.33 ± 0.13°C for H). We conclude that highly trained middle-aged men demonstrate a similar capacity for heat dissipation when compared with physically active younger men.     

Sex-related differences in evaporative heat loss: the importance of metabolic heat production

We evaluated the hypothesis that different rates of metabolic heat production between sexes, during exercise at the same percentage of maximum oxygen consumption give proportional differences in evaporative heat loss. Seven males and seven females, exercised at 41.3 ± 2.7% for 60-min at 40°C and 30% relative humidity. Whole-body direct air calorimetry measured rate of whole-body evaporative heat loss while metabolic heat production was measured by indirect calorimetry. was greater in males (243 ± 18 W m⁻²) relative to females (201 ± 4 W m⁻²) (P ≤ 0.05) throughout exercise. This was paralleled by a greater at end-exercise in males (207 ± 51 W m⁻²) relative to females (180 ± 3 W m⁻²) (P ≤ 0.05). Differences in metabolic heat production between sexes during exercise at a fixed percentage of give differences in evaporative heat loss. To compare thermoregulatory function between sexes, differences in metabolic heat production must therefore be accounted for.     

Performance and thermoregulatory effects of chronic bupropion administration in the heat

The combination of acute dopamine/noradrenaline reuptake inhibition (bupropion; BUP) and heat stress (30°C) significantly improves performance (9%). Furthermore the maintenance of a higher power output resulted in the attainment of significantly higher heart rates and rectal temperatures—above 40°C—in the BUP trial compared to the placebo trial. Since BUP is an aid to cease smoking that is taken for longer periods, question remains if similar performance and thermoregulatory effects are found following administration of BUP over several days (10 days). The purpose of the present study was to examine the effects of chronic BUP on exercise performance, thermoregulation and hormonal variables in the heat. Eight trained male cyclists participated in the study. Subjects completed two trials consisting of 60 min fixed intensity exercise (55% W _max) followed by a time trial (TT) in a double-blind randomized crossover design. Exercise was performed in 30°C. Subjects took either placebo (PLAC) or BUP (Zyban™) for 3 days (150 mg), followed by 300 mg for 7 days. Chronic BUP did not influence TT performance (BUP 40′42″ ± 4′18″; PLAC 41′36″ ± 5′12″), but significantly increased core temperature (P = 0.030). BUP significantly increased circulating growth hormone levels (PLAC: 9.8 ± 5.8 ng L⁻¹; BUP: 13 ± 6.8 ng L⁻¹; P < 0.008). Discussion/conclusion: Chronic BUP did not influence TT performance in 30°C and subjects did not reach core temperature values as high as observed during the acute BUP study. It seems that chronic administration results in an adaptation of central neurotransmitter homeostasis, resulting in a different response to the drug.     

Safe cooling limits from exercise-induced hyperthermia

We evaluated the cooling rate of hyperthermic subjects, as measured by three estimates of deep core temperatures (esophageal, rectal and aural canal temperatures), during immersion in a range of water temperatures. The objective of the study was to compare the three indices of core temperature and define safe cooling limits when using rectal temperature to avoid the development of hypothermia. On 4 separate days, seven subjects (four males, three females) exercised for 45.4±4.1 min at 65% at an ambient temperature of 39°C, RH: 36.5%, until rectal temperature (T _re) increased to 40.0°C (39.5°C for two subjects). Following exercise, the subjects were immersed in a circulated water bath controlled at 2, 8, 14 and 20°C until T _re returned to 37.5°C. When T _re reached normothermia during the cooling period (37.5±0.05°C), both esophageal (T _es) (35.6±1.3°C) and aural canal (T _ac) (35.9±0.9°C) temperatures were approaching or reaching hypothermia, particularly during immersion in 2°C water (T _es=34.5±1.2°C). On the basis of the heat loss data, the heat gained during the exercise was fully eliminated after 5.4±1.5, 7.9±2.9, 10.4±3.8 and 13.1±2.8 min of immersion in 2, 8, 14 and 20°C water, respectively, with the coldest water showing a significantly faster cooling rate. During the immersion in 2°C water, a decrease of only 1.5°C in T _re resulted in the elimination of 100% of the heat gained during exercise without causing hypothermia. This study would therefore support cooling the core temperature of hyperthermic subjects to a rectal temperature between 37.8°C (during immersion in water >10°C) and 38.6°C (during immersion in water <10°C) to eliminate the heat gained during exercise without causing hypothermia.     

Core temperature differences between males and females during intermittent exercise: physical considerations

We examined differences in dynamic heat balance between males and females during intermittent exercise. Six males (M) and six females (F) performed three 30-min bouts of exercise (Ex1, Ex2, Ex3) at a constant rate of metabolic heat production () of ~500 W separated by three 15-min periods of inactive recovery. Rate of total heat loss () was measured by direct calorimetry, while was determined by indirect calorimetry. Esophageal (T _es) was measured continuously. Exercise at a constant of ~500 W, was paralleled by a similar between sexes at the end of Ex1 (M: 462 ± 30 W, F: 442 ± 9 W, p = 0.117), Ex2 (M: 468 ± 28 W, F: 508 ± 18 W, p = 0.343), and Ex3 (M: 469 ± 17 W, F: 465 ± 13 W, p = 0.657). Consequently, changes in body heat content were comparable after Ex1 (M: 218 ± 21 kJ, F: 287 ± 35 kJ, p = 0.134), Ex2 (M: 109 ± 18 kJ, F: 158 ± 29 kJ, p = 0.179), and Ex3 (M: 92 ± 19 kJ, F: 156 ± 35 kJ, p = 0.136). However, females had greater overall increases in T _es at the end of Ex3 (M: 0.55 ± 0.25°C, F: 0.97 ± 0.26°C, p ≤ 0.05). Differences in core temperature between sexes appear to be solely related to differences in physical characteristics, and not due to concurrent differences in whole-body thermoregulatory responses.     

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.     

Induction and decay of short-term heat acclimation

The purpose of this work was to investigate adaptation and decay from short-term (5-day) heat acclimation (STHA). Ten moderately trained males (mean ± SD age 28 ± 7 years; body mass 74.6 ± 4.4 kg; [(V)\dot]_{\textO 2\textpeak} \dot{V}_{{{\text{O}}_{ 2{\text{peak}}} }} 4.26 ± 0.37 l min⁻¹) underwent heat acclimation (Acc) for 90-min on 5-days consecutively (T _a = 39.5°C, 60% RH), under controlled hyperthermia (rectal temperature 38.5°C). Participants completed a heat stress test (HST) 1 week before acclimation (Acc), then on the 2nd and 8th day (1 week) following Acc (T _a = 35°C, 60% RH). Seven participants completed HSTs 2 and 3 weeks after Acc. HST consisted of 90-min cycling at 40% peak power output before an incremental performance test. Rectal temperature at rest (37.1 ± 0.4°C) was not lowered by Acc (95% CI −0.3 to 0.2°C), after 90-min exercise (38.6 ± 0.5°C) it reduced 0.3°C (−0.5 to −0.1°C) and remained at this level 1 week later (−0.5 to −0.1°C), but not two (0.1°C −0.4 to 0.5°C; n = 7) or 3 weeks. Similarly, heart rate after 90-min exercise (146 ± 21 b min⁻¹) was reduced (−13: −6 to −20 b min⁻¹) and remained at this level after 1 week (−13: −6 to −20 b min⁻¹) but not two (−9: 6 to −23 b min⁻¹; n = 7) or 3 weeks. Performance (746 s) increased 106 s: 59 to 152 s after Acc and remained higher after one (76 s: 31 to 122) but not two (15 s: −88 to 142 s; n = 7) or 3 weeks. Therefore, STHA (5-day) induced adaptations permitting increased heat loss and this persisted 1 week but not 2 weeks following Acc.     

Body regional heat pain thresholds using the method of limit and level: a comparative study

Purpose

The purpose of this study was to compare cutaneous heat pain thresholds using the method of limit and level.

Methods

Sixteen young males (23.2 ± 3.2 year, 174.9 ± 4.9 cm, and 70.1 ± 8.6 kg) participated in this study. The thermode temperature increased at a constant rate of 0.1 °C s⁻¹ from 33 °C for the method of limit, whereas the method of level consisted of 3 s heat pulses increasing from 44 °C to 50 °C in 100 s separated by 5 s intervals. All measurements were conducted on 14 body regions (the forehead, neck, chest, abdomen, upper back, upper arm, forearm, waist, hand, palm, thigh, calf, foot, and sole) in 28 °C, 35% relative humidity.

Results

The results are as follows. Heat pain thresholds were on average 3.2 ± 2.1 °C higher for the method of level than for the method of limit (P < 0.05). Second, the correlation coefficient between values by two methods was 0.819 (P < 0.01). Third, lower body regions (thigh, calf, and sole) had higher heat pain thresholds than upper body regions (chest) by the method of level only (P < 0.05). Fourth, body regional subcutaneous fat thickness showed no relationship with heat pain thresholds except the upper arm.

Conclusion

These results indicated that cutaneous heat pain thresholds vary based on the type of heat stimuli and body regions. The method of limit could be applied for predicting accumulated thermal pain starting from moderate heat, whereas the method of level may be applicable for predicting acute heat pain to flames or high heat.

     

Effect of low-intensity resistance training on arterial function

Although high-intensity resistance training increases central arterial stiffness, moderate-intensity resistance training does not. However, the effects of low-intensity resistance training on arterial stiffness are unknown. The aim of this study was to investigate the effect of low-intensity resistance training with short inter-set rest period (LSR) on arterial stiffness. Twenty-six young healthy subjects were randomly assigned to training (10 males, 3 females) and control groups (9 males, 4 females). The subjects performed LSR twice a week at 50% of one repetition maximum for 10 weeks. Training consisted of five sets of ten repetitions with an inter-set rest period of 30 s. Changes in brachial-ankle pulse wave velocity (baPWV) and brachial flow-mediated dilation (FMD) were assessed before and after the intervention period. After the intervention period, one repetition maximum strength increased (by 9–38%, P < 0.05 to <0.001; increases varied among the exercise types), baPWV decreased (from 1,093 ± 148 to 1,020 ± 128 cm/s, P < 0.05), and brachial FMD increased (from 9.7 ± 1.3 to 11.8 ± 1.9%, P < 0.05). These values did not change in the control group. These results suggest that LSR reduced arterial stiffness and improved vascular endothelial function.     

Combined carbohydrate-protein supplementation improves competitive endurance exercise performance in the heat

Laboratory-based studies have demonstrated that adding protein (PRO) to a carbohydrate (CHO) supplement can improve thermoregulatory capacity, exercise performance and recovery. However, no study has investigated these effects in a competitive sporting context. This study assessed the effects of combined CHO–PRO supplementation on physiological responses and exercise performance during 8 days of strenuous competition in a hot environment. Twenty-eight cyclists participating in the TransAlp mountain bike race were randomly assigned to fitness-matched placebo (PLA 76 g L⁻¹ CHO) or CHO–PRO (18 g L⁻¹ PRO, 72 g L⁻¹ CHO) groups. Participants were given enough supplements to allow ad libitum consumption. Physiological and anthropometric variables were recorded pre- and post-exercise. Body mass decreased significantly from race stage 1 to 8 in the PLA group (−0.75 ± 0.22 kg, P = 0.01) but did not change in the CHO–PRO group (0.42 ± 0.42 kg, P = 0.35). Creatine kinase concentration and muscle soreness were substantially elevated during the race, but were not different between groups (P = 0.82, P = 0.44, respectively). Urine osmolality was significantly higher in the CHO–PRO versus the PLA group (P = 0.04) and the rise in tympanic temperature from pre- to post-exercise was significantly less in CHO–PRO versus PLA (P = 0.01). The CHO–PRO group also completed the 8 stages significantly quicker than the PLA group (2,277 ± 127 vs. 2,592 ± 68 min, respectively, P = 0.02). CHO–PRO supplementation therefore appears to prevent body mass loss, enhance thermoregulatory capacity and improve competitive exercise performance despite no effect on muscle damage.     

Carbohydrate ingestion and pre-cooling improves exercise capacity following soccer-specific intermittent exercise performed in the heat

Ingestion of carbohydrate and reducing core body temperature pre-exercise, either separately or combined, may have ergogenic effects during prolonged intermittent exercise in hot conditions. The aim of this investigation was to examine the effect of carbohydrate ingestion and pre-cooling on the physiological responses to soccer-specific intermittent exercise and the impact on subsequent high-intensity exercise performance in the heat. Twelve male soccer players performed a soccer-specific intermittent protocol for 90 min in the heat (30.5°C and 42.2% r.h.) on four occasions. On two occasions, the participants underwent a pre-cooling manoeuvre. During these sessions either a carbohydrate–electrolyte solution (CHOc) or a placebo was consumed at (PLAc). During the remaining sessions either the carbohydrate–electrolyte solution (CHO) or placebo (PLA) was consumed. At 15-min intervals throughout the protocol participants performed a mental concentration test. Following the soccer-specific protocol participants performed a self-chosen pace test and a test of high-intensity exercise capacity. The period of pre-cooling significantly reduced core temperature, muscle temperature and thermal sensation (P < 0.05). Self-chosen pace was greater with CHOc (12.5 ± 0.5 km h⁻¹) compared with CHO (11.3 ± 0.4 km h⁻¹), PLA (11.3 ± 0.4 km h⁻¹) and PLAc (11.6 ± 0.5 km h⁻¹) (P < 0.05). High-intensity exercise capacity was improved with CHOc and CHO when compared with PLA (CHOc; 79.8 ± 7 s, CHO; 72.1 ± 5 s, PLAc; 70.1 ± 8 s, PLA; 57.1 ± 5 s; P < 0.05). Mental concentration during the protocol was also enhanced during CHOc compared with PLA (P < 0.05). These results suggest pre-cooling in conjunction with the ingestion of carbohydrate during exercise enhances exercise capacity and helps maintain mental performance during intermittent exercise in hot conditions.     

Heat stress attenuates the increase in arterial blood pressure during isometric handgrip exercise

The purpose of this study was to examine arterial blood pressure responses during isometric handgrip (IHG) exercise performed at increasing levels of heat stress. Ten male subjects performed 1 min of IHG exercise at 60 % of maximal voluntary contraction under no heat stress (NHS), moderate heat stress [MHS, 0.6 °C increase in esophageal temperature (T _es)] and high heat stress (HHS, 1.4 °C increase in T _es). For all conditions, IHG exercise significantly elevated mean arterial pressure (MAP) (NHS: 124 ± 6 vs. 90 ± 4 mmHg, MHS: 112 ± 6 vs. 89 ± 6 mmHg, HHS: 107 ± 7 vs. 91 ± 5 mmHg, P ≤ 0.05) and cardiac output (CO) (NHS: 9.0 ± 1.5 vs. 6.1 ± 0.6 L/min, MHS: 9.8 ± 1.8 vs. 7.6 ± 1.3 L/min, HHS: 10.0 ± 2.0 vs. 8.5 ± 1.9 L/min, P ≤ 0.05) relative to baseline, whereas no differences in total peripheral resistance (TPR) were observed (P > 0.05). However, the relative increases in MAP and CO were significantly reduced during MHS (MAP: 23 ± 6 mmHg, CO: 2.1 ± 0.9 L/min) and HHS (MAP: 16 ± 7 mmHg, CO: 1.5 ± 0.8 L/min) compared to NHS (34 ± 5 mmHg, CO: 2.9 ± 1.1 L/min, P ≤ 0.05). Furthermore, these elevations were significantly attenuated during HHS compared to MHS (P ≤ 0.05). Our findings show that heat stress attenuates the increase in arterial blood pressure during isometric handgrip exercise and this attenuation is cardiac output dependent, since TPR did not change during exercise for all heat stress conditions.