Joseph D. Layden

Optimising the acquisition and retention of heat acclimation

Heat acclimation (HA) often starts in a moderately hot environment to prevent thermal overload and stops immediately prior to athletic activities. The aims of this study were (1) to establish whether acclimation to a moderately hot climate is sufficient to provide full acclimation for extreme heat and (2) to investigate the physiological responses to heat stress during the HA decay period. 15 male subjects exercised for 9 consecutive days at 26° C Wet Bulb Globe Temperature (WBGT) and 3 days at 32° C WBGT on a cycle ergometer for up to 2 h per day and repeated the exercise 3, 7 and 18 days later in 26° C WBGT. Rectal temperature (T (re)) and heart rate (HR) were measured during 60 min of steady state exercise (∼45% of maximum oxygen uptake). During days 1-9, end-exercise T (re) was reduced from 38.7±0.1 to a plateau of 38.2±0.1° C (p<0.05), HR was reduced from 156±10 to 131±11 bpm (p<0.05). No changes in HR and T (re) occurred during the 3 days in the very hot environment. However, T (re) during rest and exercise were significantly lower by 0.4-0.5° C after HA compared with day 9, suggesting that heat acclimation did not decay but resulted in further favourable adaptations.

Effects of reduced ambient temperature on fat utilization during submaximal exercise.

PURPOSE The influence of cold air exposure on fuel utilization during prolonged cycle exercise was investigated. METHODS Nine male subjects cycled for 90 min in ambient temperatures of -10 degrees C, 0 degrees C, 10 degrees C, and 20 degrees C. External work performed between conditions was constant. Mean oxygen consumption (VO2) over the 90 min in the 20 degrees C trial corresponded to 64 +/- 5.8% VO2peak. RESULTS Although mean skin temperature was different between trials (P < 0.05), rectal temperatures were not different. At -10 degrees C and 0 degrees C, the respiratory exchange ratio was higher compared with 10 degrees C and 20 degrees C (0.98 +/- 0.01 and 0.97 +/- 0.01 vs 0.92 +/- 0.01 and 0.91 +/- 0.01; P < 0.05). The associated rates of fat oxidation were lower at -10 degrees C and 0 degrees C compared with 10 degrees C and 20 degrees C (0.15 +/- 0.06 and 0.17 +/- 0.06 vs 0.35 +/- 0.06 and 0.40 +/- 0.04 g.min-1; P < 0.05). Blood glycerol was lower at -10 degrees C and 0 degrees C compared with 20 degrees C (P < 0.05); mean values were 0.13 +/- 0.0, 0.13 +/- 0.0, and 0.18 +/- 0.0 mmol.L-1 for the -10 degrees C, 0 degrees C, and 20 degrees C trials, respectively. Mean VO2 was lower in the -10 degrees C trial than the 20 degrees C trial (2.53 +/- 0.06 vs 2.77 +/- 0.09. L.min-1; P < 0.05). Mean blood glucose concentrations were lower at -10 degrees C than 20 degrees C (4.9 +/- 0.2 vs 5.3 +/- 0.1 mmol.L-1; P < 0.05). Although plasma epinephrine concentrations were greater during the 20 degrees C trial compared with all other trials (P < 0.05), plasma norepinephrine did not differ between trials. CONCLUSION The diminished fat oxidation at colder temperatures potentially reflects a reduction in lipolysis and/or mobilization of FFA or impairment in the oxidative capacity of the muscle.

The impact of prolonged exercise in a cold environment upon cardiac function.

PURPOSE The purpose of the present study was to examine the impact of cold exposure coupled with prolonged exercise upon postexercise left ventricular (LV) function and markers of myocardial damage. METHODS colon; Eight highly trained male athletes (mean +/- SD; age: 28.2 +/- 8.8 yr; height: 1.78 +/- 0.07 m; body mass: 74.9 +/- 7.6 kg; VO2max: 65.6 +/- 7.0 mL x kg(-1) x min(-1)) performed two 100-mile cycle trials, the first in an ambient temperature of 0 degrees C, the second in an ambient temperature of 19 degrees C. Echocardiographic assessment was completed and blood samples drawn before, immediately postexercise, and 24-h postexercise. Left ventricular systolic (stroke volume [SV], ejection fraction [EF], and systolic blood pressure/end systolic volume ratio [SBP/ESV]) and diastolic (early [E] to late [A] filling ratio [E:A]) parameters were calculated. Serum was analyzed for creatine kinase isoenzyme MB (CK-MBmass) and cardiac troponin T (cTnT). cTnT was analyzed descriptively whereas other variables were assessed using two-way repeated-measures ANOVA. RESULTS No significant change was observed in systolic function across time or between trials. A significant difference between trials was observed in E:A immediately after exercise (1.4 +/- 0.4 [19 degrees C] vs 1.8 +/- 0.3 [0 degrees C]) (P < 0.05). CK-MBmass was significantly elevated immediately after exercise in both trials (P < 0.05). Positive cTnT concentrations were observed in two subjects immediately after the 19 degrees C trial (0.012 microg x L(-1) and 0.034 microg x L(-1)). CONCLUSIONS Cycling 100 miles in an ambient temperature of 19 degrees C is associated with an acute change in diastolic filling that is not observed after prolonged exercise at 0 degrees C. Prolonged exercise is associated with minimal cardiac damage in some individuals; it appears that this is a separate phenomenon to the change in diastolic filling.

Neuromuscular and cardiovascular responses of Royal Marine recruits to load carriage in the field.

Cardiovascular and neuromuscular responses of 12 male Royal Marine recruits (age 22 ± 3 years, body mass 80.7 ± 6.8 kg, VO(2)max 52.3 ± 2.7 ml kg(-1) min(-1)) were measured during 19.3 km of load carriage walking at 4.2 km h(-1) and carrying 31.0 kg. Heart rate during load carriage was 145 ± 10 beats·min(-1) (64 ± 5 %HRR) and showed a negative relationship with body mass (r = -0.72, P = 0.009) but no relationship with VO(2)max (ml kg(-1) min(-1); r = -0.40, P = 0.198). Load carriage caused a decrease in vertical jump height (8 ± 9%) and power (5 ± 5%) (P < 0.001). Change in vertical jump power showed a positive relationship with body mass (r(2) = 0.40, P = 0.029) but no relationship to VO(2)max (ml kg(-1) min(-1); r(2) = 0.13, P = 0.257). In conclusion, load carriage caused a reduction in vertical jump performance (i.e. decreased neuromuscular function). Lighter individuals were disadvantaged when carrying absolute loads, as they experienced higher cardiovascular strain and greater decreases in neuromuscular function.

Reply to A. D. Flouris and S. S. Cheung reply letter regarding “cold-induced vasodilation”

Flouris and Cheung (2009a) contributed to the discussion on the methodology for inducing cold-induced vasodilation (CIVD) and concluded that CIVD is a centrally originating phenomenon caused by sympathetic vasoconstrictor withdrawal. In this reply we hope to show, using the data of the recent study they refer to (Flouris and Cheung 2009b), that CIVD is of peripheral origin. First of all, there is no disagreement that CIVD is strongly inXuenced by the thermal state of the body. This is true when body heat content is modiWed by the temperature of drinks (Daanen et al. 1997) and also when the body is cooled or warmed from the outside (Daanen and Ducharme 1999). When the body is thermoneutral to slightly cold, the Wnger blood Xow is generally low. When a Wnger is immersed in cold water (<15°C) or cold air (<0°C, dependent on wind speed), the initial response is a strong vasoconstriction due to the reXexes initiated by the cold sensors in the Wngers. After about 5–10 min the paradoxical CIVD response is initiated. It is paradoxical since the body is slightly cold, the hand is very cold and still large amounts of heat are released through the extremities (generally over 30 W for one hand). The mechanisms for this response are discussed previously and, in brief, the neuromuscular junction between the sympathetic nerve and muscular wall of the arterio-venous anastomosis (AVAs) is thought to be blocked by the local cold (Daanen 2003) leading to a strong increase in peripheral blood Xow. When the body is hypothermic, it is diYcult to observe any CIVD response. Even though the AVAs open up, the arterioles leading to the AVAs are vasoconstricted, and consequently, the increase in peripheral blood Xow is negligible. When the body is hyperthermic, there is a continuous heat loss from the Wngers when immersed in cold water. This was recently conWrmed in the elegant recent study of Flouris and Cheung (2009b), who investigated the eVect of body temperature on CIVD while warming and cooling the body twice. The hand was exposed to 0°C air. The Wnger blood Xow increased substantially during body warming. During the whole-body cooling period tympanic temperature and the body heat content dropped continuously. During the cooling process, there is a period during which the body core is in the range of thermoneutrality. During this period, the Wnger blood Xow increased. This is shown in Fig. 1. The Wnger blood Xow data is derived directly from Fig. 1 of the Flouris and Cheung paper (Flouris and Cheung 2009b); the body heat content was calculated from the body heat content in Fig. 1 and follows a similar path to the tympanic temperature. Flouris and Cheung (2009b) claim that the subsequent increase in Wnger blood Xow must be attributable to sympathetic vasoconstrictor withdrawal. However, this is not visible in their data. Indeed, as sympathetic activity is negatively correlated to core temperature (Sawasaki et al. 2001), one can conclude that the sympathetic activity must have been continuously increasing during the cooling period since tympanic temperature and body heat content was continuously decreasing. Yet, despite this continuous increase in sympathetic activity, a sudden increase in Wnger blood Xow occurs. The obvious Communicated by Susan Ward.