Physiological Demands Of The Marathon

Mark Speedie is a national level runner, aged 25. Historically his training has involved continuous running training but he understands that interval training and/or resistance training may further enhance his performance.
The aim of the marathon is to maintain a high power output over the official 42.195km distance, a feat which requires substantial physical and psychological preparedness (John A. Hawley & Fiona J. Spargo, 2007; McLaughlin, Howley, Bassett, Thompson, & Fitzhugh, 2010). Success in the event depends upon a number of physiological, psychological and environmental factors. National level marathon running demands a high aerobic capacity and the ability to perform at a high fraction of it for a sustained period of time. A complex interplay of cardiovascular, musculoskeletal, pulmonary, and metabolic systems is necessary to achieve this. The purpose of this summary is to outline the physiological demands of the marathon, the mechanisms of performance resultant of the aforementioned characteristics and to introduce training methods documented in recent literature to enhance attributes and performance (time) of the marathon at national level.

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A.V Hill (1926) reports a high VO2Max to be the key determinant underpinning endurance performance. Astrand and Rodahl (1986) describe VO2Max as the highest rate at which the body can uptake and utilise oxygen (O2) during severe exercise at sea level; it sets the ceiling of ATP production through oxidative phosphorylation and is a key determinant of marathon performance. VO2max is traditionally increased as a result of performing high volume, low intensity (60% VO2Max) long slow distance (LSD) running.
The volume of oxygen consumed (VO2) (Berger, Campbell, Wilkerson, & Jones) at a given work rate, is more commonly termed running economy (RE) or described as the metabolic cost of running (Cr). McLaughlin et al., (2010) report a strong correlation between RE and 16km time (r =0.812), Billet et al. (2001) suggest a strong correlation between VO2Peak and Cr (r=0.65, P= 0.04), and Midgley et al. (2006) detail highly correlated (r=0.62) improvements in RE with LSD training (Midgley, McNaughton, & Wilkinson, 2006; McLaughlin, et al., 2010), similarly resistance training has been reported to derive similar improvements in RE ( Bonacci, Chapman, Blanch, & Vicenzino, 2009; Storen, Helgerud, Stoa, & Hoff, 2008a).
Research on lactate threshold (LT) suggest it is a sound predictor of marathon race velocity (Coyle, 2007). Once considered largely “a waste product of glycolysis” lactate (La-) is now considered an important metabolic fuel (Gladden, 2004). La- increases are indicative of work rates exceeding possible levels of fat oxidation required to sustain ATP production, therefore intracellular signalling stimulates glycogenolysis and glycolysis to meet ATP demands (Joyner & Coyle, 2008; Spriet, 2007).
The efficacy of alternative training protocols said to enhance physiological traits of marathon performance are emerging. Improvements of up to 7% in RE are been reported following resistance training protocols (Berryman, Maurel, & Bosquet, 2010; Paavolainen, Hakkinen, Hamalainen, Nummela, & Rusko, 1999; Saunders, et al., 2006; Spurrs, Murphy, & Watsford, 2003), primarily due to superior stretch shortening cycle (SSC) function in consequence of increased musculotendinous stiffness (A. N. M. C. Turner & Jeffreys, 2010). Similarly, SIT is purported to improve endurance performance through possible mechanisms including muscle La- buffering capacity (Laursen, 2010), enhanced enzymatic functioning, skeletal muscle remodelling (Burgomaster, et al., 2008) and metabolic adaptations such as mitochondrial biogenesis (Hawley, et al., 2007). Moreover hypothesis surrounding muscle fibre type transitions and ‘hybrid’ myosin isoforms, suggest SIT and high intensity interval training (HIIT) may elicit structural changes resulting in a greater oxidative capacity of muscle and improved endurance performance (Kubukeli, Noakes, & Dennis, 2002).
The following article will discuss these mechanisms in further and include recommendations of various training protocols, reported to improve performance.
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Athlete Profile – Mark Speedie
National athlete, Mark Speedie, has traditionally employed continuous training protocols for race preparation, 71% of total training volume comprising of low intensity training (Table 1. Athlete Profile: Mark Speedie, sub-elite marathon runner
NZ Ranking
4th
Current career goals
2016 Olympic podium contender
Age (years)
25
Weight (kg)
60
Height (cm)
172
PRM (hr:min:ss)
2:22:00
vMarathon (km.hr-1)
17.8
VO2Peak (mL.kg-1.min-1)
70
LT (%VO2Peak)
Unknown
Cr: (mL.kg-1.km-1)
Unknown
MHR (BPM)
195
Cr = Metabolic cost of running (aka running economy), LT = Lactate Threshold, MHR = Maximum heart rate, PRM = personal record for the marathon, vMarathon = velocity for marathon distance
In addition to the efficient, integrated nature of body systems required to produce elite performance, body mass and composition, as described by Pollock et.al.,(1977) reported elite marathoners ideally weigh between 59.6 and 66.2 kg with a body fat percentage of approximately 5 ± 2%. A lean stature has been reported to more economical during endurance events for movement efficiency, aerobic economy and heat dissipation (Billat, et al., 2001; Pollock, et al., 1977).
Assessments
Before recommending new training protocols, it is important to determine the current physiological status of Mark using appropriate, valid and reliable assessment strategies.
Laboratory Assessment
Intermittent or continuous treadmill protocols performed in the laboratory are used to obtain information pertaining to aerobic function, including VO2Max, RER and metabolic cost of exercise (Cr, RE). Intermittent treadmill protocol is widely used, and has the advantage of 30s recovery periods in which blood samples can be taken to measure substrate levels such as lactate (BLa-). A minimum 3 minute increment is recommended by ACSM (ACSM Guidelines for Exercise Testing and Prescription, 2010, p79) increasing velocity and/or inclination each increment until one of the following occurs; VO2 reaches a plateau despite increasing velocity or inclination; RER ≥ 1.15; (Esteve-Lanao, et al., 2005) peak HR >95% age-predicted max or RPE of >19 (ACSM p83) after which VO2Max is determined. Similarly, volitional exhaustion may end the test, the highest steady state VO2 is recorded as VO2Peak. Midgley et al. (2006) report significant differences in vVO2Max (km.hr-1) following three treadmill protocols, which demonstrates the importance of considering the methodological variations of test protocols and training intensities based upon them when prescribing exercise intensity. It should be mentioned that some articles cited within this report, use the Wingate anaerobic test (WAnT) to determine anaerobic and aerobic function in cyclists, however in a recent study, WAnT was not significantly associated with and therefore not a valid tool, for assessing aerobic function in endurance runners (Legaz-Arrese, Munguía-Izquierdo, Carranza-García, & Torres-Dávila, 2011).
BLa- is measured during intermittent treadmill test recovery stages using the Lactate Pro blood lactate analyser, a minimally invasive, fast, accurate and valid test (Pyne, Boston, Martin, & Logan, 2000) where blood (5μl) is taken from either the ear lobe or tip of the second digit after appropriate sterilisation of the area. It is important when re-testing that the same sample point is used as the ear and finger may reflect varying measures of BLa-.
Rate of perceived exertion (RPE) and heart rate (HR), as recommended by ACSM (p83) is monitored during incremental treadmill testing, a numerical scale (RPE) and heart rate monitoring device (Polar, Finland) are used during testing, respectively. ECG is used where possible to measure HR as a more accurate and intricate measure. Training intensities can then be quantified and prescribed relative to VO2Max, RER, vVO2Max and BLa-, using HR and RPE, to improve program efficacy.
Muscle Performance
Prior to recommending resistance training protocols it is essential to obtain baseline measures so as to accurately prescribed loads, and progress. Typically the leg press is recommended to assess lower body strength (ACSM p 90 – 92), however given the different kinematic variables between leg press movements and running gait; a 1RM squat test will be used as kinematics closer represent gait. The athlete must be familiarised with the movement; test protocols must be standardized using appropriate warm up, trial numbers and progressive load increments; and standardisation of squat depth, stance and bar placement are crucial. The use of a linear position transducer during the squat test provides a fast, efficient and reliable means of measuring useful information such as force, power and velocity, beneficial to program prescription and efficacy (García-Pallarés, Sánchez-Medina, Carrasco, Díaz, & Izquierdo, 2009; Harris, Cronin, Hopkins, & Hansen, 2008).
The modified reactive strength index (RSI) is a reliable and valid scientific tool for measuring SSC efficiency. Recall that improvements in RE are documented to be due to an increase in SSC function. The modified RSI replaces depth jump with the counter movement jump (CMJ), swapping ground contact time with takeoff time to calculate SSC efficiency. CMJ involves eccentric (load), amortization and concentric (unload) phases of the SSC mechanisms (Ebben & Petushek, 2010; Flanagan, Ebben, & Jensen, 2008).
Additional to baseline measures, it is important to track ongoing training status to avoid potential overtraining, and to ensure appropriate training stimulus is being prescribed. Research is currently assessing the reliability and validity of heart rate variability (HRV) and heart rate recovery time (HRRT), as assessment tools, used to indicate the readiness of the athlete’s next training bout or race. Manzi et a. (2009) suggest the HRV may indicate a high level of performance or exercise readiness (Manzi, et al., 2009), suggesting HRV to be a useful tool to determine training progression. Furthermore, Buchheit et al (2009) report HRRÏ„ to be a useful non-invasive means of measuring the athlete’s physiological status (Buchheit, et al., 2008; Manzi, et al., 2009). Further research is required to assess the reliability of HRR and HRV in elite and sub-elite athletes undertaking a combined endurance and strength training regime however may be useful for testing readiness following aerobic and anaerobic training sessions.
Field Test
In addition to laboratory based testing, it is important to assess performance measures using activities which simulate race conditions. For Mark, a 10km track run is performed to determine performance time (10PT). Coyle et al. (2007) report marathon race velocity to be ≈10% slower when compared with 10PT and to be an appropriate test to measure physiological improvements in marathon athletes.
Training Models
Training adaptations require appropriate stimulus and prescription of mode, duration, frequency, loads and intensities, while balancing accompanied stress responses to elicit performance improvements. While the dose-response relationship is gaining more ground in scientific research a previously mentioned, training models and intensities are well documented.
Training ‘Zones’ have been widely used in association with data points determined during gas and blood analysis to mark training intensity. These include percentage of, or HR at, VO2Max, LT or vVO2Max. A number of associated training models are discussed in the literature with respect to endurance running, additional to traditional training methods.
The Polarized Training Model, whereby athletes perform a high percentage (75%) of training volume in ‘Zone 1′(The Threshold Training Model, more commonly used with untrained and moderately trained individuals, involves the athlete performing a large portion of their training in ‘Zone 2 (60 – 75% VO2Max)(Esteve-Lanao et al, 2007), at or around the ventilatory threshold or maximal lactate steady state (MLSS) (Laursen, 2010). It has been documented that LT, is closely related to marathon velocity (Coyle, 2007; Roecker, S., Niess, H., Dickhuth., 1998). Prolonged training at this higher intensity, however, is shown to down-regulate the sympathetic nervous system (SNS), subsequently, due to a decrease in catecholamine secretion and sensitivity, reducing Q and blood distribution resulting in reduced performance (Esteve-Lanao, et al., 2007; Lehmann, et al., 1992). HIT is effective however, when prescribed over short duration, concomitant to reduced volume and monitoring. Acevedo and Goldfarb (1989) report improvements in 10PT of 3%, despite no change in VO2Max or ventilatory threshold, after HIT bouts in well-trained long-distance runners (Acevedo & Goldfarb, 1989). In a study on highly trained middle and long distance runners Denadai et al., (2006) report 1.2 – 4.2% improvements in vVO2max, RE (2.6-6.3%) and 1500m performance (0.8-1.9%) following four weeks HIT, twice per week, performed at 95% to 100% vVO2Max for 60% of the time that subjects were able to remain at that velocity during assessment (Denadai, de Mello, Greco, & Ortiz, 2006).
More recently, sprint interval training (SIT) performed at ‘all out’ maximal efforts has been shown to elicit similar metabolic responses in well trained endurance cyclists (Burgomaster, Heigenhauser, & Gibala, 2004; Lindsay, et al., 1996; Talanian, Macklin, Peiffer, Parker, & Quintana, 2003) and distance runners (Macpherson, Hazell, Olver, Paterson, & Lemon, 2011; Mujika, 2010), with concomitant improvements in endurance performance, metabolic control, RE (5.7 – 7.6 %) (Iaia, et al., 2009) and skeletal muscle adaptations. Alterations in aerobic power and peripheral mechanisms as documented in a study by Macpherson et.al (2011), report significant improvements in VO2Max (P = 0.001) of 11.5% (46.8 ± 1.6 to 52.2 ± 2.0 mL.kg.-1.min-1) and a(VO2)difference (7.1%) without changes in SV or Q, suggesting aerobic improvements after SIT are as a result of peripheral alterations. Moreover SIT has been shown to induce alterations in skeletal muscle mitochondrial enzymes; citrate synthase CS, 3-hydroxyacyl CoA dehydrogenase ß-HAD, suggestive of increased lipid oxidation; pyruvate dehydrogenase PDH, indicating decrease in skeletal muscle CHO oxidation, muscle glycogenolysis and PCr utilisation similar to that reported after endurance training (Burgomaster, et al., 2008). ß-HAD stimulation following SIT, is potentially the result of a rapid decrease in muscle PCr availability in conjunction with continued high work rates required to generate maximal power (Spriet, 2007). In a study by Hazell et al. (2011) authors suggest that the coupling of PCr hydrolysis and oxidative phosphorylation provide an “acute challenge to the mitochondria resulting in adaptation” and that insufficient recoveries between exercise bouts “force skeletal muscle to regenerate ATP” as anaerobic contribution decreases, may contribute to improved aerobic power following SIT (Hazell, MacPherson, Gravelle, & Lemon, 2010).
Furthermore, increases in skeletal muscle buffering capacity (ßm) (≈ 200 – 240 μatom H+ /g dry wt/pH unit), content of MCT 1 (monocarboxylate 1), found predominantly in type I fibres and required for La- transportation into muscle fibres for ATP production; and MCT 4, found in type II fibres, required for La- transport out of muscle fibres of 70% and 30% respectively (Kubukeli, et al., 2002) has been documented relative to improved anaerobic performance (Gibala, et al., 2006) following SIT. Additionally, Gibala et.al. (2009), report increases in AMP-activated protein kinase (AMPK), mitogen-activated protein kinase (MAPK) and calcium signalling mechanisms all of which are purported to be involved in the regulation of peroxisome proliferator activated receptor gamma coactivator 1 alpha (PGC-1α), which coordinates mitochondrial biogenesis. The oxidative enzyme expression regulation in skeletal muscle, suggests potential skeletal muscle remodelling (Gibala, et al., 2006) following SIT. Skeletal muscle plasticity is inconclusive however a recent publication by McCarthy (2011) indicates the coordination of fibre-type transitions through non-coding RNA (MiRNA) suggest coordination of fibre-type changes in response to altered training stimulus supporting the theory of skeletal muscle remodelling (McCarthy, 2011).
Evidence suggests that various resistance training protocols can improve long distance running performance, by enhancing biomechanical structures to reduce fatigue and injury as a result of inefficient movement. Further, resistance training has been well documented to improve RE and endurance performance (Mikkola, Rusko, Nummela, Pollari, & Hakkinen, 2007; Paavolainen, et al., 1999; Storen, et al., 2008a).
Performance improvements are indicative of neuromuscular stretch shortening cycle (SSC) adaptations (Saunders, et al., 2006) and reportedly due to an increase in α-motor neuron potentiation and subsequent increase in motor unit (MU) innervation; greater contractile force; improved neural connections at spinal level; increase MU synchronisation, and consequent rate of force development (RFD) (Wilmore, 2008 pp206; Drinkwater et al. 2009); and alterations to neural inhibitory mechanisms decreasing co-activation of antagonist muscles (Hoff & Helgerud, 2004; Millet, Jaouen, Borrani, & Candau, 2002). Hoff et.al., (2004) suggest RFD increases (52.3%) in soccer players improve overall economy; moreover, reported a positive correlation between arterial flow transit time and a(VO2) difference potentially increasing time to fatigue at submaximal velocities (Hoff & Helgerud, 2004; Storen, Helgerud, Stoa, & Hoff, 2008b). Furthermore, Turner et. al. (2010) suggest that plyometric training induces increased musculotendinous stiffness (MTS), positively correlated with improved power, force and velocity (Bosjen-Moller et. al., 2005), shorter ground contact times (Kuitunen et. al., 2002) and enhanced propulsive forces during toe off (A. M. Turner, Owings, & Schwane, 2003; A. N. M. C. Turner & Jeffreys, 2010) contribute to improved SSC function.
Exercise Prescription Recommendations
The progressive implementation of resistance training protocols for a marathon athlete such as Mark, is required to produce adaptations safely and effectively. He is advised to employ a two to three day per week model initially, graduating intensity, complexity, frequency and/or duration accordingly as performance indicators improve and tolerance levels adjust. General, functional full body exercises (low weight, high repetition) aimed at improving muscular endurance; musculoskeletal condition and motor coordination are recommended in accordance to Esteve-Lanao (2007). The athletes’ psychological state is important when altering training parameters, circuit training protocols which elicit a HR response, include eight to 10 exercises, followed by short running intervals (400m) may be beneficial to the athletes’ transition to resistance training.
Following the initial conditioning phase, a heavy strength cycle of four to eight weeks, performed two to three days per week, with low (one to five) repetitions of heavy loads as derived from strength assessments is recommended. Improvements of approximately 5% demonstrated during four to 10 week interventions (Kelly et. al., 2008, Storen et.al., 2008, Millet et.al., 2002) are detailed in Table 2. Exercises should remain functional multi-joint movements (squats, deadlifts, lunges) and aim to develop neural alterations to musculature highly involved in running gait at SSC movements.
Explosive and eccentric training protocols, including power exercises (jump squats, hang clean), gait development (single leg squat), and eccentric load (Nordic curls) should follow in the late stages of the conditioning phase. These methods have been shown to improve RFD and muscle power factors. Research suggests one to two days of explosive training, over a four to eight week period is adequate for obtaining desired power adaptations, and maintaining strength. Some low volume, low intensity plyometric training may be included during this phase also (Berryman et. al., 2010, Paavolanien et.al., 1999) aimed at condition SSC mechanisms.
Plyometric training (jumping, hopping, bounding and skipping) has been reported to produce improvements in RE and endurance performance of up to 7% and 4.8% respectively, in highly trained endurance runners when performed at high intensities, in as little as one to three sessions per week over a six to eight week period (Berryman et. al., 2010). High intensity plyometric training can be implemented leading up to competition phase and is specifically designed to improve SSC function. Functional resistance run training, including running with vests, sleds, chutes, hills, sand or mud, during this phase is recommended. Estevo-Lanao (2007) suggests this should be performed at specific competition velocity and should be coordinated with a reduced running volume leading into the late competition phase.
Mark is advised to continue with one maintenance strength session per week, at low load and intensity with adequate recovery intervals so as not to cause any muscle damage leading into his main races, allowing approximately one to two weeks taper, whereby no resistance training should be performed. Re-testing of performance and strength parameters prior to commencing a new training phase is recommended to assess and make changes accordingly for the subsequent training cycles.
During the base phase of training, HIT and SIT may be used supplementary to LSD training. Reports have shown that replacing 25% to 90% (Burgomaster, et al., 2008) of LSD volume with HIT/SIT has not changed performance times, however has produceed similar metabolic responses when compared to LSD. As the literature fails to report performance improvements, it is advised that these extreme volumes of LSD are not removed from Mark’s schedule; however a reduction a volume is recommended when implementing SIT. It is adequate to say that responses from HIT and SIT occur substantially and quickly, requiring no more than four to six weeks at high volumes (J. Esteve-Lanao, et al., 2007; Gibala, et al., 2006; Hazell, et al., 2010). Typically, SIT protocols include four to six 30-s ‘all out’ bouts of running, separated by two to four minutes of recovery (Burgomaster, et al., 2008; Gibala, et al., 2006). Training progression should also be applied to SIT, increasing the number of all out bouts from four to six repetitions over the recommended four to six week duration, after which, ATP is reduced significantly and no further metabolic or skeletal changes evident. With this in mind, HIT and SIT protocols should be introduced at approximately six weeks out from the first main priority race in the competition phase, after appropriate re-testing signifying required adaptations (Gibala, et al., 2006).
Cardiovascular, metabolic and neural alterations and also muscular improvements contribute to race performance by 2% to 8% in distance runners in a recent study by Lunden (2010). Conversely, single fibre power of MHC IIa muscle fibres appear to be a prevalent adaptation, and likely contributor to the 3% improvement in running performance reported by Luden et al. (2010) as such a taper period of one to two weeks with a load decrease of 50% in week one and a further 25% in week two, is recommended, in order to yield the physiological alterations of training (Luden, et al., 2010).
To summarise, metabolic adaptations, similar to those seen after continuous training protocols, have been reported after four to six week interventions of SIT at a substantially lower training volumes than LSD, making this an effective method of training to maintain metabolic condition while reducing training volume. MHC isoform transitions, resulting in more oxidative IIa fibres, although requiring further research, indicates that SIT/HIT be beneficial for enhancing neuromuscular parameters and also peripheral factors (O2 utilisation) associated with endurance performance at the elite level. Potentially, a greater population of IIa fibres, in conjunction with metabolic alterations resulting in more efficient lipid oxidation and CHO sparing, may contribute to greater power output from higher order fibres, with maximum metabolic efficiency, particularly in the final stages of the marathon, where lower order fibres and fuel sources are depleted. Future research is required to determine cardio-respiratory factors which may be affected as a result of reducing training volume in order to prescribe optimal volume reductions, without implicating performance. HRV and HRRT may provide useful assessment tools for this research to determine adequate training stimuli and recovery. Moreover, resistance training has been shown to improve RE and performance by up to 7%, while reducing the risk of injury and biomechanical fatigue, although some reports conflict this, there is outstanding evidence in the literature that resistance training is beneficial at the elite level.
In conclusion, it is recommended that after appropriate assessment, SIT and resistance training protocols are gradually introduced to Mark’s training regime. It is important to reduce total training volume during high intensity cycles of training, however suitable progression and test-re-test monitoring to track performance alterations is suggested in order to track any decline in cardio-respiratory or musculoskeletal condition. Additionally a one to four yearly plan is recommended in order to develop Mark safely and effectively towards his 2016 Olympic goals.
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Table 2. Resistance training, alterations to running economy and endurance performance
Study
Subjects
(total number, caliber, gender)
Training Method
Frequency and Duration
Volume
Control
RE (%)
RP km
%/sec
Turner et al., 2003
18
Moderately trained
Mixed
Plyometric Training
3d/w x 6 wks
1 set 5 – 25 reps
Regular Endurance Running
↑2.3*
Spurrs et al., 2003
8
Moderately trained
Males
Plyometric Training
2-3d/w x 6 wk
2 3 sets x 8-15 reps
Regular Endurance Running
↑5.7*
↑ 3km
2.7%
16.6 sec
Saunders et al., 2006
15
Highly trained
Plyometric Training
3d/w x 9 wk
30 mins
107 ± 43 km of running per week
↑ 4.1*
Berryman et al., 2010
35
Highly trained
Males
Plyometric
1 d/w x 8 weeks
3 – 6 sets x 8 repetitions
Endurance Running 3 x per week
↑7*
↑ 3km
4.8%
36 sec
Paavolanien et al. 1999
10
Moderately trained Males
Sport Specific Explosive Strength Training
2d/w x 9 wks
15 – 90 mins
Endurance running, circuit training
↑8.1*
↑ 5k
3.1%
Mikkola et al., 2007
25
Moderately trained
Mixed
Explosive Strength Training
3d/w x 8 wks
2 – 3 set x 6 -10 repetitions
Endurance Running
↔
↔
Guglielmo et al. 2009
16
Highly trained
Explosive Strength
2d/w x 4 wks
3,4,5 x 12 RM
Endurance training (60 – 80km.wk-1)
↔
Berryman et al., 2010
35
Highly trained
Males
Explosive Training
1 d/w x 8 weeks
3 – 6 sets x 8 repetitions
Endurance Running 3 x per week
↑ 4%
↑ 3km
4%
31 sec
Millet et al., 2002
15
Highly trained
Males (triathletes)
Strength Training
2d/w x 14 wk
3-5 sets, 3 – 5 RM
Endurance Training (Swim, Bike, Run)
↑ 5.6 – 7
Storen et al., 2008
17
Moderately trained
Mixed
Strength Training
8 wk
4sets x 4RM
Regular Endurance Running
↑5
Kelly et al., 2008
16
Recreational
Females
Strength Training
3d/w x 10 week
3 x 3 – 5 RM
Regular Endurance running
↑5.4
↑ 3km
106±91 sec
APA Style References
ACSM Guidelines for Exercise Testing and Prescription, 8th Edition, 2010. pp79, 83, 90 -92
Acevedo, E. O., & Goldfarb, A. H. (1989). Increased training intensity effects on plasma lactate, ventilatory threshold, and endurance. Medicine & Science in Sports & Exercise October, 21(5), 563-568.
Berger, N. J. A., Campbell, I. T., Wilkerson, D. P., & Jones, A. M. (2006). Influence of acute plasma volume expansion on VO2 kinetics, VO2peak, and performance during high-intensity cycle exercise. Journal of Applied Physiology, 101(3), 707-714.
Berryman, N., Maurel, D., & Bosquet, L. (2010). Effect of Plyometric vs. Dynamic Weight Training on the Energy Cost of Running. The Journal of Strength & Conditioning Research, 24(7), 1818-1825 1810.
Billat, V. L., Demarle, A., Slawinski, J., Paiva, M., & Koralsztein, J.-P. (2001). Physical and training characteristics of top-class marathon runners. Medicine