Physiological effects of Altitude - Part 2

Traditionally, athletes attend altitude training camps where they both live and train at moderate altitude (1800-2500 m, LHTH) for typically 2-4 weeks, 2-3 times a year (Wilber, 2007; Millet et al., 2010). This method involves generous time and financial commitment while also brings questionable sea-level performance benefits as there are large variations in individual responses (McLean et al., 2013). The well-known, live high-train low (LHTL) philosophy is considered as the ‘Gold-standard’ method for altitude training (Levine and Stray-Gundersen, 1997), though it is debated for its efficacy in elite endurance athletes (Siebenmann et al., 2012), underlying mechanisms (Gore and Hopkins, 2005; Levine and Stray-Gundersen, 2005), and the degree and type of the hypoxic stimulus (hypobaric vs normobaric) (Millet et al., 2012a; 2013b). There is a difference between 'real' altitude (hypobaric hypoxia) and simulated altitude (normobaric hypoxia) and research suggests that simulated altitude is not quite as effective as real altitude (Saugy et al., 2016). But, in any case, the simulation of altitude can be quite beneficial for athletes. This type of altitude training intervention is based on the principle that chronic exposure to an altitude environment stresses the body to make adaptations in your blood, increasing the erythropoietic effect (production of more red blood cells) and hemoglobin mass (oxygen carrying molecule in the blood) and thus allows the blood to deliver more oxygen to working muscles (Wehrlin et al., 2006). It has been well documented that hemoglobin mass increases at approximately 1% for every 100 hours of altitude exposure regardless of the exposure method, meaning living in real (hypobaric) or simulated (normobaric) hypoxia and whether training was performed in hypoxia or normoxia [i.e., live high train high, LHTH (> 2100 m) or live high train low, LHTL (~3000 m)] (Gore et al., 2013). 

An important consideration of these training methods is the altitude dose (how much exposure is needed), as it has been suggested that reaching an altitude of 2200-2500 m for at least 4 weeks with ideally 20-22 hours of hypoxic exposure/day is optimal for improved hematological changes and sea-level performance where longer exposure is better (Millet et al., 2010). It has been shown that benefits still occur in the blood adaptation while spending ideally 16 hours/day and minimum 12 hours/day (Millet et al., 2010) (especially important when considering sleeping in an altitude tent). When using simulated altitude (chamber, sleeping tent, hypoxic generator system for training, etc.), it is generally recommended to use slightly higher altitudes to better stimulate similarly to real altitude.

We need to be careful of how your body reacts to this additional stress of the altitude environment. I recommend monitoring your body with oxygen saturation (fingertip measurement) and morning heart rate recovery testing (See Physiological Effects of Altitude Part 1). This is especially important when using altitude training methods (particularly living high), as you should still be able to perform your training as suggested by your coach/team. Sleep is of extreme importance - make sure you get extra sleep, longer at night, or take a short nap in the afternoon if possible. It is also important to hydrate and eat well to maintain your capacities and help your body handle the extra stress of altitude exposure. Special attention should be given to your training upon return to sea-level after an altitude training camp, as the body needs time to recover from the extra stimulus of altitude exposure and training and fatigue levels should be monitored closely to optimize the performance benefits upon return to sea-level competition (Chapman et al., 2014).

While living at altitude elicits hematological adaptations to hypoxia and allows for subsequential improvement of oxygen supply to the tissues, living low and training in hypoxia (LLTH) challenges the efficiency of the cardiovascular system to transport and perfuse the muscles with oxygenated blood to stimulate vessel adaptation and improve performance (see above panorama of altitude training methods). Even though LLTH studies have reported improved oxygen utilization within the muscle (Vogt et al., 2001; Ponsot et al., 2006; Zoll et al., 2006) through advantages for aerobic and anaerobic performance, which depends on the exercise mode, duration, and intensity, the amount of hypoxic exposure is inconclusive (Millet et al., 2010). Furthermore, it has been demonstrated that athletic performance is likely improved with intermittent hypoxic training (IHT) at high intensity by increased mitochondrial efficiency and improved pH/lactate regulation (Katayama et al., 2003; Ponsot et al., 2006; Zoll et al., 2006).

The physiological challenge associated with exercise in hypoxia is evident as mentioned above. However, the additional influence of high-intensity exercise must be considered as there are several advantageous adaptations to the cardiovascular and muscle systems that occur including: increased skeletal muscle oxidative capacity, increased resting glycogen content, increased capacity for muscle lipid oxidation, enhanced peripheral vascular structure and function, and improved time-trial and maximal performance test results (Burgomaster et al., 2005; Gibala et al., 2006; Burgomaster et al., 2008; Rakobowchuk et al., 2008). Generally, exercise leads to increases in blood flow and thereby increases laminar shear stress in the vessel, which leading to upregulation of endothelial nitric oxide synthase (an enzyme which allows smooth muscle relaxation, vasodilation, and increased blood flow) (Gielen et al., 2001; Tinken et al., 2009). This response is proportional to exercise intensity and therefore, the demand should increase with high-intensity exercise (such as repeated sprint performance) as previously suggested (Mortensen et al., 2008; Casey and Joyner, 2012). Similar vasodilation mechanisms exist during conditions of systemic hypoxia (at altitude) but to a greater extent due to the reduced oxygen availability (Casey and Joyner, 2012). 

An innovative training method was developed involving demanding repeated bursts of high intensity exercise (≤ 30s) in hypoxia (repeated sprint training in hypoxia, RSH) to maximize the metabolic stress and has demonstrated improved maximal performance and delayed fatigue when compared to the same training but in normoxia (RSN) (Faiss et al., 2013). Performing this repeated high-intensity sprint exercise in hypoxia places a great physiological and metabolic demand on the body in short periods of time with primarily reliance on anaerobic glycolysis and a shift towards aerobic energy metabolism as sprinting is repeated (Gaitanos et al., 1993; Bogdanis et al., 1995). This then allowed the combination of the known principles of LHTL methods with RSH, meaning living high while training low while including sessions of the  RSH intervention (LHTLH). Among the specific responses associated to LHTLH, there are increased mRNA levels involved in oxygen signaling, oxygen transport, mitochondrial biogenesis, and metabolism (Brocherie et al., 2018), as well as positive functional adaptations as shown by the improved oxidative capacity in type I and type II fibers, while maintaining fiber size (van der Zwaard et al., 2018). From these investigations, it becomes clear that high intensity training provides an important metabolic stress when combined with hypoxia to stimulate peripheral adaptations. 

Since 2013, repeated sprint training in hypoxia has been successful across several exercise modes [leg cycling (Faiss et al., 2013), cross-country skiing (Faiss, Willis et al., 2014), running (Galvin et al., 2013), and team sports (Brocherie et al., 2014), with a meta-analysis (Brocherie et al., 2017)], demonstrating an increase in power output and number of sprints. It has been indicated that RSH is a beneficial mode of altitude/hypoxic training demonstrating improvements in performance (Millet et al., 2013b).

This has led to new methods which combine repeated sprint training with novel ways of creating a hypoxic environment either systemically (whole body exposure to lower oxygen environment) or locally (creating a hypoxic environment by limiting blood flow to tissues, i.e., blood flow restriction). 

It has been shown that severe hypoxia can be created locally in the muscle tissue (ischemia) by applying a blood flow restriction (BFR, also known as vascular occlusion) to the limbs during exercise (Scott et al., 2014). This external application of pressure sufficiently allows the maintenance of arterial blood inflow (partial vascular occlusion as a percentage of resting total occlusion pressure) while completely (or almost completely) occluding the venous outflow (Kaijser et al., 1990), thus increasing blood in the tissues distal (away from the heart) to the occlusion. 

When compared to systemic hypoxia, using BFR that induces both ischemia and local hypoxia likely has a different effect on vascular/endothelial function due to specific vascular resistance and vessel diameter adjustments, accumulation of metabolites (nitric oxide, adenosine, prostaglandins, hydrogen ions, etc.) and/or indirect sympathetic activation. In these BFR conditions with restricted vasodilation, the demand for increased blood flow cannot be met with similar mechanisms as during systemic hypoxia (hypoxia-induced vasodilation). Thus, there are both different methods (systemic, via lower fraction of inspired oxygen; and local, via greater vessel resistance and lower blood flow) and intrinsic mechanisms (systemic, metabolic vasodilation to increase blood flow for oxygen delivery, and local, greater vascular challenge for blood flow regulation) by which a hypoxic environment may exist, and in which alterations of vascular conductance and blood flow are present.

Implementing these methods into training programs is likely beneficial for increasing the capacity and reactivity of blood and oxygen transport, possibly improving the diffusion capacity along with vessel adaptations which may altogether enhance endothelial function leading to improved tissue oxygenation and performance. The implementation of short training blocks with these methods can be valuable to induce a rapid and robust stimulus in a short time frame, thus providing a time-saving strategy and effective method for adaptations to occur. It is interesting to pursue this training across different sports, as this type of repeated sprint training may be applicable for not only team-sport athletes, but also endurance athletes (i.e., pacing surges and increases in tempo). The concept of using BFR in training can provide a greater stimulus and an increased workload while presenting a new stimulus for adaptations. Different training programs should be designed with special attention placed on limb differences, as arms seem to have a greater and more reactive vascular response than legs. 

While the optimal stimulus depends on the population of interest, suggested training recommendations are as follows and supported by a recent meta-analysis (Brocherie et al., 2017). The high-intensity exercise protocol (whether in hypoxia or normoxia and whether with or without BFR) should last approximately 60 min including the warm-up and cool-down periods and be performed 2-3 times a week during blocks of training (2-5 weeks duration as part of a periodized training program. During each session, the athlete performs a series of 3-4 sets of 4-7 maximal ‘all-out’ sprints (4-15 s duration) in hypoxia (3000-3800 m and 14.2-12.8% FiO2) and/or with BFR of about 45% of total occlusion pressure. It is important to achieve a specific sprint-to-rest ratio of 1:2 to 1:4 with inter-set recovery about 3-5 min without occlusion. This specific training should be performed in alteration with low-intensity exercise to maintain and develop basic fitness along with aerobic metabolism.