Heat training increases exercise capacity in hot but not in temperate conditions: a mechanistic counter-balanced cross-over study

Abstract

The aim was to determine the mechanisms facilitating exercise performance in hot conditions following heat training. In a counter-balanced order, seven males (V̇o2max 61.2 ± 4.4 ml·min(-1)·kg(-1)) were assigned to either 10 days of 90-min exercise training in 18 or 38°C ambient temperature (30% relative humidity) applying a cross-over design. Participants were tested for V̇o2max and 30-min time trial performance in 18 (T18) and 38°C (T38) before and after training. Blood volume parameters, sweat output, cardiac output (Q̇), cerebral perfusion (i.e., middle cerebral artery velocity [MCAvmean]), and other variables were determined. Before one set of exercise tests in T38, blood volume was acutely expanded by 538 ± 16 ml with an albumin solution (T38A) to determine the role of acclimatization induced hypervolemia on exercise performance. We furthermore hypothesized that heat training would restore MCAvmean and thereby limit centrally mediated fatigue. V̇o2max and time trial performance were equally reduced in T38 and T38A (7.2 ± 1.6 and 9.3 ± 2.5% for V̇o2max; 12.8 ± 2.8 and 12.9 ± 2.8% for time trial). Following heat training both were increased in T38 (9.6 ± 2.1 and 10.4 ± 3.1%, respectively), whereas both V̇o2max and time trial performance remained unchanged in T18. As expected, heat training augmented plasma volume (6 ± 2%) and mean sweat output (26 ± 6%), whereas sweat [Na(+)] became reduced by 19 ± 7%. In T38 Q̇max remained unchanged before (21.3 ± 0.6 l/min) to after (21.7 ± 0.5 l/min) training, whereas MCAvmean was increased by 13 ± 10%. However, none of the observed adaptations correlated with the concomitant observed changes in exercise performance.

Effect of Permissive Dehydration on Induction and Decay of Heat Acclimation, and Temperate Exercise Performance

“…Although pronounced PV expansion was evident in both drinking conditions, there was no evidence of any change in VO 2max . This is in contrast to Lorenzo et al (2010), who demonstrated increased VO 2max concomitant with HA induced PV expansion, but is consistent with recent work showing no effect of HA induced PV expansion on VO 2max (Karlsen et al, 2015; Keiser et al, 2015). The reason for these equivocal findings is not entirely clear, although in Lorenzo et al (2010) the relative intensity of training sessions in the heat was higher than for a control group undertaking training under cool conditions and the possibility of an additional training stimulus cannot be excluded.…”

“…The reason for these equivocal findings is not entirely clear, although in Lorenzo et al (2010) the relative intensity of training sessions in the heat was higher than for a control group undertaking training under cool conditions and the possibility of an additional training stimulus cannot be excluded. Cardiovascular strain was matched between control and experimental groups in Keiser et al (2015), although it may have been higher in the experimental group of Karlsen et al (2015). Alternatively, while the effect of PV expansion on VO 2max appears unfavorable at the population level for trained individuals, there appears to be substantial inter-individual variation (Keiser et al, 2015), possibly due to individuality in the balance between increased cardiac output and the haemodilution effect on O 2 -carrying capacity.…”

“…Moreover, the influence of PV expansion on VO 2max depends on the balance between increased cardiac output and the haemodilution effect on O 2 -carrying capacity, which may be unfavorable in an already hypervolemic population. Recently, Keiser et al (2015) showed no effect of PV expansion on VO 2max or exercise performance among a well-trained cohort, whether induced through HA, or by albumin-solution infusion, although there was considerable inter-individual variation. Given that dehydration may augment the hypervolemic aspect of HA (Garrett et al, 2014), understanding the resultant effects on VO 2max and exercise performance is important, particularly as these programmes are often used by athletes and individuals undertaking heavy physical work.…”

“…Typically, heat acclimation (HA) is acquired by frequently and repeatedly elevating both core ( T C ) and skin ( T Sk ) temperature (Regan et al, 1996) to a level challenging sudomotor and vasomotor thermoeffector responses for a sufficient duration (Fox et al, 1963). Although passive approaches have sometimes been employed (Beaudin et al, 2009), the increased thermal strain is often achieved through a combination of environmental heat-stress and increased metabolic heat-production through exercise (e.g., Lorenzo et al, 2010; Gibson et al, 2014, 2015; Keiser et al, 2015). More recently, it has been suggested that dehydration, the process of losing fluid and achieving a state of hypohydration (lower-than-normal body water volume), may also represent an important stimulus for facilitating HA (Garrett et al, 2012, 2014; Périard et al, 2015; Akerman et al, 2016), although this may be controversial (Horowitz et al, 1999; Schwimmer et al, 2006) and in contrast to traditional guidelines for maintaining fluid and electrolyte balance (Armstrong and Maresh, 1991; Bergeron et al, 2012).…”

“…Studies also provide indication that HA elicits improvements in VO 2max (Sawka et al, 1985; Lorenzo et al, 2010), exercise economy (Sawka et al, 1983) and lactate threshold (Lorenzo et al, 2010) in temperate conditions; together these are key determinants of endurance performance (Joyner and Coyle, 2008). However, many of these studies have been criticized for inadequate control (Corbett et al, 2014) and this ergogenic effect has not been replicated in recent experiments employing more appropriate controls (Karlsen et al, 2015; Keiser et al, 2015). Moreover, the influence of PV expansion on VO 2max depends on the balance between increased cardiac output and the haemodilution effect on O 2 -carrying capacity, which may be unfavorable in an already hypervolemic population.…”