The effect of ambient temperature on gross-efficiency in cycling

GE during sub-maximal cycling exercise in the heat was significantly reduced compared to exercise in N by 0.9%. Values for GE corresponded to values found in literature, between 17 and 22% (Foster et al. 2003; Moseley et al. 2001). It has to be kept in mind that in calculating GE at 60% \( P_{V{\text{O}}_{{\text{2max}}} } ,\) anaerobic contribution was assumed to be negligible. But it might have been influenced by the different climates. Gonzalez-Alonso et al. (1999) reported that exercise in a hot environment results in a higher anaerobic contribution and found an increase in carbohydrate utilization and lactate accumulation during exercise. Though not significant, BLC in the present study was higher in H. According to di Prampero et al. (1999), an increase of BLC of 1 mmol l⁻¹ of blood is equivalent to an O₂ consumption of 3 ml kg⁻¹ body weight. Differences in BLC in the present study between climates (2.6 mmol l⁻¹ in N vs. 3.9 mmol l⁻¹ in H) thus correspond with a difference in O₂ consumption equivalent of ∼14.1 ml min⁻¹. Accordingly, differences in GE between climates might be even larger then reported in the present study. If one adds this ‘anaerobic O₂ equivalent’ to the VO₂, then GE decreases about ∼0.19% in N compared to ∼0.27% in H, which means that the difference in GE between N and H increases with ∼0.07%.

Mean T _re was about 0.3°C higher in H compared to N. Mean T _sk was about 5.7°C higher in H than in N. Comparable differences of 0.2–0.4°C in T _re (Tatterson et al. 2000; Tucker et al. 2004) and ∼6.0°C in T _sk (Tatterson et al. 2000) were reported during cycling bouts of ∼30 min in climates comparable to the present study. Although the difference in rectal temperature between H and N was significant, it was not a large difference compared to literature. The measured absolute values for T _re were somewhat low, presumably due to the relatively short period of exercise in our protocol and the use of a fan to optimize losing heat to the environment, as was done in the studies of Tatterson et al. (2000) and Tucker et al. (2004). The fan was used to simulate competitive circumstances, and although wind velocity in this study was not as high as the cycling speed, combined with the relatively low RH, the effect would have been considerable (Saunders et al. 2005).

The differences in ambient temperature between H and N represent a considerable difference in thermal stress. Thermal strain is mainly visible in the increased skin temperature, but although the difference of 0.3°C in core temperature is small, it is significant. Rectal and skin temperature changes combined, the difference in body heat content between N and H amounts to 138.5 ± 35.1 kJ, which is considerable. Further, the differences between climates have been shown to be large enough to evoke a difference in GE of 0.9%, the main purpose of the present study.

A possible explanation for the lower GE in the heat may be the higher core temperature. Daanen et al. (2006) found a strong linear relationship between body temperature, mainly determined by T _re, and GE at 60% \( P_{V{\text{O}}_{{\text{2max}}} }\) in 30°C. Their study showed that our difference in T _re of 0.3°C could account for a reduction in GE of ∼0.2%, and thus was not large enough to explain the entire reduction in GE of 0.9%. In the study of Daanen et al. (2006), the skin temperature however was almost unchanged, while in the present study skin temperature in the H condition was about 5.6°C higher, indicating an increased blood flow to the skin. The present study did not find a strong correlation in heat (r ² = of 0.36) between T _re and GE. Further, remarkably, in the N-condition, no correlation between T _re and GE was found at all, even though T _re reached values which are also observed in the H-condition, only later in time (see Fig. 3). Apparently, T _re does not seem to be the main cause of the reduced GE. This is supported by the observation that even though T _re rose significantly during the time trial with about 1°C, GE did not increase significantly comparing the first half with the second half within the trials.

Two other explanations for the reduced GE in heat can be given. Firstly, an explanation for the temperature-induced reduction in GE might be a metabolic disruption that is known to occur at elevated muscle temperatures (Brooks et al. 1971; Willis and Jackman 1994). Though Ferguson et al. (2006) found no effect of increasing muscle temperature on energy turnover in dynamic exercise in a range of 34.2–38.3°C, ADP:O ratio has been shown to decrease at higher muscle temperatures (Brooks et al. 1971; Willis and Jackman 1994). During heavy exercise in the heat, non-specific proton leakage across the inner mitochondrial membrane is increased, resulting in a decrease in the efficiency of oxidative phosphorylation and increasing the resting metabolic rate (Willis and Jackman 1994). This will result in a reduction in GE. Willis and Jackman (1994) found a decrease of 10–20% in ADP:O ratio at muscle temperatures of 40°C and higher compared to 37°C. They found that this decrease resulted in a 400–800 ml min⁻¹ increase in VO₂. In the present study, a smaller but significant increase in VO₂ of 124 ml min⁻¹ was found. Mean T _mmax in heat was 38.7°C, lower than the 40°C as found in Willis and Jackman (1994), but higher than 34.2–38.3°C, the T _m range in which Ferguson et al. (2006) found no effect of increasing T _m on energy turnover in dynamic exercise. Since T _m was not measured in both climates, it cannot be confirmed if muscle temperature was significantly different. T _sk and T _re were significantly different but did not approach 40°C in either condition. It seems that, as suggested by Brooks (1971), the core of the body functions as a heat sink for the skeletal musculature helping to maintain T _m below the point where significant reductions in the ADP:O ratio occur.

Another potential cause for the decrease of GE in a hot ambient temperature was the larger vasodilatation of the skin to lose heat, as was shown by the significantly higher T _sk in H compared to N. The resulting decreased blood flow to exercising and respiratory muscles may be compensated by increasing cardiac output (Nielsen et al. 1990; Rowell et al. 1966), since a significant increase in heart rate was found in heat. The extra VO₂ in the H condition is at least partially attributable to the extra myocardial VO₂, since a higher cardiac output has to exist to continue supplying the muscles with the same blood flow, but have to send extra blood to the skin for cooling. Additionally, ventilation was increased, which may also lead to a reduction in GE. Assuming that the mechanical work per breath is 80–125 J (Milic-Amili et al. 2001), it can be estimated that the higher V _E in this study can account for maximally 10% of the increase in VO₂.

Lastly, it has to be noticed, that GE decreases if the proportion of energy expenditure that is used to maintain homeostasis is increased. Thus, the lower GE in H could have been solely due to an increase in resting metabolic rate, while net efficiency remained unchanged. This would be consistent with the hypothesis that muscle temperature in the hot conditions was not high enough to make mitochondrial leakage a likely explanation for the observed reduced GE. Unfortunately, resting metabolic rate has not been measured.

To determine the potential importance of the measured decrease in GE on time trial performance, a 20-km time trial, which was also studied by Tucker et al. (2004), was modeled by the use of the energy flow model (De Koning et al. 1999). A time trial of this distance can be seen as a mainly aerobic exercise bout. Tucker et al. (2004) found a difference in final time of 48 s between exercise in 35°C compared to 15°C. Using the energy flow model of De Koning et al. (1999), it was calculated that the measured difference in GE of 0.9% would lead to a difference in final time between H and N of 25.6 s. This explains about half of the 48 s found by Tucker et al. (2004). For the entire reduction in final time of 48 s, a decrease in GE of 2% would be necessary, which was not found. It can be concluded that about half of the decrease in time trial performance can be accounted for by the reduction in GE. It has to be noted that in this simulation, it is assumed that the difference in GE between H and N at higher intensities will not change. Although it has been shown that GE increases with exercise intensity, since the relative share of resting metabolism diminishes at higher sub-maximal intensities (Mosely and Jeukendrup 2001), this effect seems to be equal for both conditions and will at most have only a minor effect on the difference between conditions.