Introduction
Real-world extreme environments often combine multiple environmental stressors, thereby making their overall effects on the individuals less predictable. High altitude is characterized by this ‘extreme’ nature, as it often displays the simultaneous presence of numerous stressful factors (e.g., hypobaric hypoxia and cold) (Lloyd and Havenith
2016). However, despite the independent effect of hypoxia (Fulco et al.
1998; Robert S.Mazzeo
2006) and cold (Castellani and Tipton
2016; Oksa et al.
2004; Stensrud et al.
2007; Taylor et al.
2008; No and Kwak
2016) has been well studied in literature, scarce knowledge is present on the combined effect of the two environmental conditions on human physiology and performance, especially when considering endurance exercise (Mugele et al.
2021; Bortolan et al.
2021). In fact, currently only 2 studies (Lloyd et al.
2015,
2016) have examined the individual and combined effects of cold and hypoxia on performance at altitude, but none of them investigated physiological and mechanical work responses during whole body dynamic endurance exercises like cycling or running. To date research on single stress exposure suggests that many of the key physiological strains associated with thermal cold and hypoxia are precursors of detrimental effects on exercise capacity; it is well known that, as altitude increases, the systemic reduction in arterial O
2 content strains the cardiovascular system’s ability to meet the required O
2 delivery to active musculature (Amann et al.
2006; Fulco et al.
1998), causing a linear decrease in maximal oxygen uptake (
\(\mathop {\text{V}}\limits^{.}\)O
2max) corresponding to ≈6.3% per 1000 m increasing altitude in endurance trained athletes up to 3000 m (Wehrlin and Hallén,
2006). However, despite great differences in relative exercise intensity, submaximal oxygen uptake at a specific external workload is similar at sea level and altitude (Fulco et al.
1998; Wehrlin and Hallén,
2006). Higher controversy exists on
\(\mathop {\text{V}}\limits^{.}\)O
2max changes in the cold: Oksa et al. (
2004) and Quirion et al. (
1989) reported a 5% decrease in
\(\mathop {\text{V}}\limits^{.}\)O
2max at − 20 °C if compared to + 20 °C, whereas Renberg et al. (
2014) and Sandsund et al. (
2012) claim no changes in ambient temperatures between − 14 and + 20, and Therminaris et al. (1989) found a 13% increase in
\(\mathop {\text{V}}\limits^{.}\)O
2peak at −2 °C if compared to + 24 °C. These results suggest that V̇O
2max values may be affected in the cold for ambient temperatures lower than −15 °C, and the proposed reason for this decrease are the cold-induced local vasoconstriction that reduces venous washout of metabolic by-products in the active muscles (Oksa et al.
2004; Quirion et al.
1989), reduced ventilation due to cold-induced bronchus constriction (Kennedy et al.
2019) or cooling-induced neuromuscular changes like decreased maximal force production or slower nerve conduction and muscle contraction velocity (Oksa
2002). More agreement exists in relation to higher
\(\mathop {\text{V}}\limits^{.}\)O
2 at submaximal exercise intensities in the cold (Oksa et al.
2004; Quirion et al.
1989; Therminarias
1992; Therminarias et al.
1989) due to both a reduction in the mechanical efficiency of working muscles and to the shivering produced by muscles not involved in muscular exercise(Oksa
2002; Therminarias
1992).
As
\(\mathop {\text{V}}\limits^{.}\)O
2max, also aerobic performance is consequently affected by environmental condition. The state of art regarding maximal incremental test in hypoxia shows a 10 to 13% decrease in peak power output (PPO) or maximal aerobic velocity (VAM) at altitudes between 2500 and 3500 m if compared to sea level (Faulhaber et al.
2021; Friedmann et al.
2004,
2005; Lorenz et al.
2006; Ofner et al.
2014; Weckbach et al.
2019), and the same happens at the intensities associated with the lactate thresholds, with a reduction ranging from 12 to 19% considering different detecting methods (Faulhaber et al.
2021; Weckbach et al.
2019). Similarly, Quirion et al.
(1989) found a 22% reduction in maximal WorkLoad (WL) and Oksa et al. (
2004) a 9% decrease in running performance time when exposed to − 20 °C if compared to + 20 °C. Concerning WL at Lactate Threshold (LT), the same distinction between moderate (> − 15 °C) and severe (< −15 °C) cold previously mentioned for
\(\mathop {\text{V}}\limits^{.}\)O
2max should be considered: in fact, Morrissey et al. (
2019) found a 22% higher WL and Sandsund et al. (
2012) a 10% increase in running speed at LT within − 4 and 1 °C if compared to 20 °C (suggesting this as the optimal ambient temperature range for aerobic endurance performance), whereas Renberg and colleagues (2014) found no differences in PO at − 14 °C if compared to + 20 °C in women. However, no information on mechanical work variation at LT when exposed to severe cold (i.e., −20 °C) is available.
Both
\(\mathop {\text{V}}\limits^{.}\)O
2max and consequent aerobic performance reductions are linked to environmental induced changes in physiological responses to exercise, although the magnitude and mechanism of action for these changes are in many cases still unclear. For the purposes of this study, only responses related to acute environmental stressor exposure will be considered. HR
max has been shown to be reduced (Fornasiero et al.
2018; Grataloup et al.
2007; Mourot
2018; Ofner et al.
2014) when acutely exposed to hypoxic environments, the magnitude of this reduction being better explained by the altitude gain between normoxic and hypoxic incremental tests rather than by absolute altitude per se (i.e., 1.7 bpm per 1000 m gain in altitude (Garvican–Lewis et al.
2015), which corresponds to ≈3/4% reduction in HR
max for altitudes of 3500 m asl (Fornasiero et al.
2018; Ofner et al.
2014)). Changes in cardiac electrophysiological properties (Benoit et al.
2003; Mourot
2018) and a reduced central drive on the heart as a protective mechanism from myocardial ischemia (Noakes et al.
2001) have been addressed as possible mechanisms for HR
max reductions with acute hypoxic exposure. At submaximal exercise intensities, for the same external workload, HR in hypoxia is increased to meet exercising muscles oxygen requests (Clark et al.
2007). However, when considering workload in relative terms, HR in normoxia and hypoxia is similar (Ofner et al.
2014): this may explain why, despite absolute HR at lactate threshold seems to be reduced in hypoxia, when it is expressed as a percentage of maximal values in the respective conditions it shows no differences from sea level values (Friedmann et al.
2004,
2005). In the cold, HR
max reduction has been addressed as primarily responsible for the reduced
\(\mathop {\text{V}}\limits^{.}\)O
2max, decreasing from 10 to 30 bpm when deep body temperature is lowered by 0.5 to 2.0 °C (Castellani and Tipton
2016). Specifically, a percentage decrease ranging from − 2.5 to − 5.5% has been found for ambient temperatures between − 14 and − 20 °C if compared to + 20 °C (Oksa et al.
2004; Renberg et al.
2014; Sandsund et al.
2012). Submaximal HR changes in the cold is more controversial, with some studies showing a reduction (Sandsund et al.
2012) and other no changes (Renberg et al.
2014) for ambient temperatures lower than − 14 °C if compared to thermoneutral conditions. Cold induced peripheral vasoconstriction that results in an elevation of blood pressure, increased central blood volume and higher stroke volume (Doubt
1991; Gisolfi and Wenger
1984) seems to be responsible for a parasympathetically mediated reduction in HR (Doubt
1991; Sandsund et al.
2012; Taylor et al.
2008).
The lactate-power output/velocity curve is left shifted in hypoxia (Clark et al.
2007; Friedmann et al.
2005; Ofner et al.
2014), testifying greater reliance on anaerobic metabolism when comparing a same absolute exercise intensity. However, Ofner et al. (
2014) found completely the same pattern of the curve and no significant difference in lactate concentration between normoxia and hypoxia in relative terms (i.e., same lactate concentration per watt in both environments). Furthermore, despite anaerobic threshold concepts are very popular to prescribe intensity zones for endurance training, scientific literature dealing with this topic in hypoxia is scarce, and some authors questioned the validity of these concepts at high attitude (Faulhaber et al.
2021). Lactate production [La] and clearance at rest and during exercise is influenced also by ambient but especially muscle temperatures, and magnitude and direction of this influence depend on the entity of cold (Therminarias
1992). Blomstrand et al. (
1984) and No et al. (2016) suggested that higher levels of [La] are reached when muscle temperatures are low, due to a cold-induced change in muscle fibre recruitment from types 1 to 2 and a consequent greater reliance on anaerobic metabolism in this situation (Blomstrand & Essén‐Gustavsson, 1987), along with other factors contributing to fatigue, e.g., low levels of ATP and PCr (phosphocreatine). This would suggest that the net efficiency of exercise in the cold is lower than under normal conditions. However, Renberg et al. (
2014) found no differences in blood lactate concentration at LT between − 14 and + 20 °C and Quirion et al. (
1989) suggested that the anaerobic threshold corresponding to a lactate concentration of 4 mmol at − 20 °C is not significantly different compared to the threshold measured at + 20 °C.
Finally, also minute ventilation (Ve) is affected by acute hypoxic exposure, which results exaggerated compared to normoxia during exercise at a given absolute intensity. This allows arterial O
2 (PaO
2) to increase, despite the fact that the alveolar-to-arterial O
2 pressure difference is increased during exercise (Calbet & Lundby
2009). However, this phenomena may be muffled or reversed when considering normobaric hypoxia (NH) due to greater air viscosity if compared to hypobaric conditions, especially at maximal exercise intensities (≈2.5% decrease in Ve
max per 1000 m of altitude gain in NH (Treml et al.
2020)). However, Friedmann et al. (
2005) showed no differences in Ve at LT and Ofner et al. (
2014) found similar ventilation in relative terms between normoxia and normobaric hypoxia. Also cold seems to have an influence on Ve (Oksa et al.
2004) since ventilating heavily cold air (< − 15 °C, Kennedy et al.
2020) may induce a bronchus constriction (induced by the contraction of bronchial smooth muscles), diminishing the amount of air that can be ventilated both at maximal and submaximal exercise intensities (Anderson and Daviskas
2000).
In the complex situation of combined cold and hypoxic environments, the effect of one stressor on performance, physiological and perceptual adjustments may be subject to change, simply due to the presence of the other independent stressor. Such differential influences can occur in three basic forms: additive, antagonistic, and synergistic (Lloyd and Havenith
2016), and each term defines a fundamental concept of inter-parameter interactions. Thus, the aim of this study is to provide further information regarding maximal, submaximal and lactate threshold responses when exposed to cold and hypoxic conditions, both independently and combined, taking into account the multifactorial approach proposed by Lloyd et al. (Lloyd and Havenith
2016). This should be helpful in better understanding the characteristics of interactions as well as their role in the operation of dynamic systems. On the basis of previous research (Lloyd et al.
2015,
2016), it was hypothesized that combined environmental stressor exposure will induce additive rather than synergistic effects on several physiological and perceptual parameters.
Publisher's Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.