The Physiological Adaptations of Strength Training for Performance During Military Loaded March

Military personnel are placed under immense physical pressure during loaded marches, which requires soldiers to carry food and water weighing up to 25kg for 8 miles. During combat operations and training exercises these loads can increase and soldiers carry these heavy loads over mixed terrain. Military personnel have a high incidence of musculoskeletal injuries (MSI) which is costly in terms of medical costs, lost training days and a reduction of combat effectiveness (Blacker, Wilkinson, Bilzon &, Rayson, 2008; Sharma, Greeves, Byres, Bennett &, Spears, 2015). Past training modalities were simplistic and involved running, loaded marches and circuit training with no emphasis on strength training. More recently the military has taken a different approach and now included strength and conditioning sessions to reduce MSI, reduced loaded marches and introduced specific tests that correspond to military specific tasks (Payne & Harvey, 2010; Tipton, Milligan &, Reilly, 2013). The aim of this paper is to discuss the benefits of strength training and critically analyse the physiological and molecular adaptations for military personnel to enhance loaded march performance and reduce MSI.

Before analysing the physiological adaptations to strength training, one must consider the physical attributes that military personnel require and the physical stressors that military personnel undergo when conducting loaded marches (Brenes, Caputo, Clark, Wehrly &, Coons, 2015; Knapik, Reynolds &, Harman, 2004; O’Leary, Saunders, McGuire &, Izard, 2017). During loaded marches, soldiers are required to walk fast using the posterior muscles to propel themselves with their weighted load and create vertical and horizontal velocity (Brenes et al., 2015; Knapik et al., 2004; O’Leary et al., 2017). At some stage in this exercise soldiers are required to run to meet the dictated timeframe allowed for the assessment (Brenes et al., 2015; Knapik et al., 2004; O’Leary et al., 2017). It is suggested from past literature that ground reaction forces (GRF) during running or jumping are increased and travel up the kinetic chain causing compressive forces and injuries in the talocural, tibiofemoral and metatarsal joints (Birrell, Hooper, Haslam, 2006; Knapik, 2001; Ortega, Rodriguez Bies &, Berral de la Rose, 2010; Polcyn, Bensel, Harman, Obusek, Pandorf &, Frykman, 2002). One needs to consider that the spine will also be placed under compressive forces and the upper body muscles will key in reducing these forces. With the increased mass of the load (25kg), the GRF and compressive forces are dramatically increased (Birrell et al., 2007; Knapik, 2001; Polycyn et al., 2002). Evidence has shown that an individual’s ability to eccentrically contract the lower limbs, can reduce GRF and ultimately reduce compressive forces on the joints of the lower limbs (Knapik et al., 2004; McNair, Prapavessis &, Callender, 2000). Birrel et al., (2007) noticed during their study that mediolateral GRF impulses were significantly increased and suggested that this was due to two factors. Firstly, instability due to the increased load and secondly a change in centre of mass (CoM) from its neutral position due to the added weight on the soldiers back. When the authors added a weapon to the soldier during gait analysis, mediolateral impulses were increased with an increased impact peak force. They suggest that the anterior carriage of the weapon with an unnatural swing during gait, is the main contributor to the increased vectors. This is a very simplistic analysis of the biomechanics during the loaded march but highlights the main physical attributes required for this exercise and the main stressors involved.

Applying the correct strength training modality to an individual will incur the following key adaptations which will be beneficial to military personnel:

·??????Increased cross section area (CSA) of the muscle, increased force production and modified force/ velocity curve (Cerretelli, Londoni, Minetti, Narici &, Roi, 1989; Dorel, Couturier, Lacour, Vandewalle, Hautier &, Hug, 2010; Santtila, Kyrolainen &, Hakkinen, 2009).

·??????Increased efficiency of the nervous system (Anderson, Dyhre-Poulsen, Magnusson, Per &, Simonsen, 2002; Cerretelli et al., 1989).

·??????Increased rate of force development (RFD) (Anderson et al., 2002; Santilla et al., 2009).

·??????Increased efficiency of mitochondria, increased work rate capacity and reduced fatigue (Porter, Reidy, Bhattarai, Sidossis &, Rasmussen, 2015)

·??????Increased hormone and enzyme activity with increased gene expression (Spiering et al., 2008; Vaara, Kokko, Isoranta &, Kyrolainen, 2015).

However, one must consider that other variables and stressors during military training, may impede on the physiological adaptations seen in other populations.

All the above adaptations will not occur unless the correct mechanical stimulus is created and the training is periodized to employ different types of modality and allow adequate rest to recover. Military personnel are required to conduct both strength training and aerobic training (Knapik, 2001; Knapik et al., 2004, Vaara et al., 2015). These training modalities use different signalling pathways, with strength training activating the mammalian target of rapamycin (mTOR) pathway, which is a cascade of signalling actions that allows muscle protein synthesis to occur during resistance training (Hall, 2008; Spiering et al., 2008). Peroxisome-proliferator-activated receptor coactivator 1 alpha (PGC -1 a) is the mitochondria biogenesis pathway, that allows oxidative and non-oxidative aerobic metabolism during aerobic and anaerobic training (Irrcher, Adhihetty, Joseph, Ljubicic &, Hood, 2003; Stepto et al., 2009). During muscle contraction (mechanical deformation), signalling pathways increase in particular Akt-mTOR pathway, Akt is an upstream positive activator of the mTOR pathway (Hahn-Windgassen, Nogueira, Chen, Skeen, Soonenberg &, Hay, 2005; Spiering et al., 2008; Stepto et al., 2009). Adenosine monophosphate-activated protein kinase (AMPK) signalling occurs when the cell has high concentrations of adenosine monophosphate (AMP) and low concentrations of glycogen. It is suggested that AMPK is an inducer of the PGC-1 a pathway, and as we can see AMPK inhibits mTOR pathway (figure 1) (Jager, Handschin, St-Pierre &, Spiegelman, 2007; Spiering et al., 2008). So, this complicated system of pathways must be considered to ensure maximum muscle protein synthesis occurs and a periodized programme will support this.?

Figure 1.?Force velocity curve and the training modalities that effect each region of the curve.

Strength training must include all modalities to modify the strength curve (Figure 1) (Gregory Haff & Nimphius, 2012; Tan, 1999). It has been suggested that conducting different modes of training such as maximum strength, strength-speed, power, speed-strength and speed within a similar timeframe is the best option to modify the individual’s strength curve and maintain the adaptations (Gregory Haff & Nimphius, 2012; Tan, 1999). From experience strength training in the military consists of blocks of training focussed on either maximum strength, muscle endurance or power development which are cycled every 6-8 weeks. It has been suggested that whilst training for power development, maximum strength training needs to be incorporated so a detriment to power development will not occur, as power is the expression of force x velocity (Haff & Nimphius, 2012; Tan, 1999).

As previously discussed, evidence has shown that resistance training can increase the CSA of limbs. There is a strong correlation between the size of CSA of lower limbs and force production. Hunter, Marshal &, McNair, 2004; Mero, 1998, have found that one of the major contributors to running gait is vertical force production which allows the individual increased flight time which in turn allows the individual time to complete the swing phase. It is suggested that military personnel during the running phase of a loaded march, will require an increased flight time and due to the extra weight imposed on the soldier, so vertical force will need to be increased (Birrel et al., 2007; Knapik, 2001). With an increased CSA, evidence has shown that an increase of the number of capillaries and their density, will increase the delivery of blood (Bell, Syrotuik, Martin, Burnham &, Quinney, 2000; McCall, Brynes, Dickinson, Pattany &, Fleck, 1996; Tan, 1999) and increase glycogen stores if sufficient carbohydrate intake is met (Haff, Lehmkuhl, Mccoy &, Stone, 2003; Tan, 1999).?

Evidence also suggest that neural drive is increased and muscle inhibition is reduced within 4 – 6 weeks of resistance training (Anderson et al., 2002; Cerretelli et al., 1989). It is inferred that with the increased neural drive there will be an improvement of co-contraction of muscles, such as the agonist, antagonist and synergistic muscle (Hashemi et al., 2011). For example, hamstring and quadriceps femoris muscle groups co-contract prior to ground contact during the running gait, which reduces shear forces at the tibiofermoral joint particularly reducing pressure on the passive restraints (collateral ligaments). It is reported that if the co-activation of these muscle groups are insufficient, then anteroposterior translation of the tibiofemoral joint will occur placing the passive restraints under immense pressure and increasing the risk of injury (Hashemi et al., 2011). It could be inferred that increasing motor control, co-contraction and neural drive will increase the individual’s ability to stabilise the lower limbs, allow the lower limb joints to articulate correctly and control the eccentric contraction of the lower limb musculature to reduce the effects of GRF.

The central nervous system is also improved with resistance training especially with plyometrics and Olympic lifting (Cormie, McGuigan &, Newton, 2011; Crewther, Cronin &, Keogh, 2005; Kraemer et al., 2001). It has been seen that plyometric exercises, increases the efficiency of the stretch reflex by two adaptations. Firstly, by improving the stiffness of the tendons and muscle fibres, and secondly by improving the mechanoreceptors ability to convey the message via the afferent nervous system. Reducing the reaction time of the nervous system to send the stretch reflex back via the efferent nervous system causing the muscle to contract autonomously (Cormie et al., 2011; Crewther et al., 2005). This action improves the stretch shortening cycle (SSC) which has been shown to improve running economy and reduce energy consumption (Stefanyshyn & Nigg, 1998; Turner & Jeffreys, 2010). Thus improving the SSC will allow the individual to maintain running velocity for longer periods (Turner, 2016).??

It has been reported that peripheral fatigue during a loaded march is caused by two factors, firstly at the sarcoplasmic reticulum with a reduced ability to release calcium (Ca2+) and in turn reducing cross-bridge cycling (Grenier et al., 2012; O’Leary et al., 2017). Secondly at the sarcomeres as the efficiency of the high force cross-bridges are reduced (Grenier et al., 2012; O’Leary et al., 2017). O’Leary et al., (2017) found that there are also differences in fatigue resistance in sexes with males having a greater reduction in maximum voluntary contraction (MVC) of the knee extensors than females. It is inferred that women have a greater percentage of type I fibres in the knee extensors, which are more fatigue resistant (Hunter 2014; Hunter, 2016). However, evidence has suggested that muscle endurance and time to fatigue can be adapted with resistance training (Campos et al., 2002). It was seen that individuals who conducted high repetitions at 60% 1 repetition maximum (RM), increased muscle endurance, time to exhaustion and maximum aerobic power, thus supporting the addition of high repetition strength training in the training programme. It has also been reported that maximal strength will cause changes in fibre type composition with resistance trained males and females seeing a reduction in type IIX fibres and an increase in type IIA fibres (Folland & Williams, 2007; Tan, 1999). This change is significant in regards to fatigue resistance as type IIA fibres have a higher oxidative capacity than type IIX fibres and it has been suggested that the change will take around 10-12 weeks to complete (Folland & Williams, 2007; Tan, 1999).

Increased CSA is achieved by strength training which activates mTOR pathway as discussed and also increases anabolic hormones as well as gene expressions at the molecular level (Spiering et al., 2008; Stepto et al., 2009). The stress hormone cortisol which is a catabolic hormone, which plays a vital role in muscle hypertrophy, as this hormone aids to the process of degrading muscle proteins, to allow the anabolic process to occur and increase the size of the muscle fibres (Kraemer et al., 1998; Kraemer & Ratamess, 2005; Spiering et al, 2008). It is reported that high intensity strength training with high volume is optimal for increasing the secretion of anabolic hormones which can last for approximately 30 minutes to an hour (Kraemer et al., 1998; Kraemer & Ratamess, 2005; Spiering et al., 2008). The key hormones that are classified as anabolic are growth hormone (GH), testosterone and insulin-like growth factor-1 (IGF-1) (Kraemer et al., 1998; Kraemer & Ratamess, 2005; Spiering et al., 2008).

Testosterone is a steroid hormone and is probably the most well-known anabolic hormone, it is vital for muscle hypertrophy. Testosterone secretion is increased following bouts of resistance training and has been seen to be greater in resistance trained athletes than endurance trained athletes (Tremblay, Copeland &, Van Helder, 2003). Testosterone not only binds with androgen receptors (AR) but it also acts together with the other anabolic hormones mentioned, to aid in the anabolic process (Schoenfeld, 2010; Spiering et al., 2008; Tremblay et al., 2003). Figure 3 shows the action of a steroid hormone and the process of androgen- specific gene expression. It is said that GH activates phosphatidylinositol-3 kinase (PI-3K) which supports Akt-mTOR pathway and promotes muscle anabolism (Schoenfeld, 2010; Spiering et al., 2008). IGF -1 also stimulates this signalling pathway and together with testosterone creates the proliferation and differentiation of stem cells (satellite cells) to bind with muscle fibres (Folland & Williams, 2007; Spiering et al., 2008). Satellite cells concentration has been found to be increased in strength trained individuals which is a positive chronic adaptation to strength training (Folland & Williams, 2007; Spiering et al., 2008). It has also been found that after a single eccentric bout of strength training, satellite cell proliferation rapidly increased within 4 days of the session (Folland & Williams, 2007; Schoenfeld, 2010). It is believed that a nucleus can only manage a certain amount of muscle tissue and an increased amount of nuclei is required for the growth of muscle tissue, satellite cells are vital for this process by adding their nuclei to the muscle tissue to increase the fibres ability for growth (Folland & Williams, 2007; Schoenfeld, 2010).?

However, it was seen during research on military training, that hormone levels varied throughout the training period with no differences in body composition measurements between the control group and no difference was seen in maximum strength measurements (Kelly, Arrington, Hrgus, Esquival &, Jameson, 2017; Vaara et al., 2015). It was suggested that due to the concurrent nature of the training, the aerobic modality had an effect on the ability to maximise strength adaptations and the stressors of the military training, effected the hormone levels, that said both groups saw improvements in their loaded march performance time (Vaara et al., 2015). Fortes, Diment, Greeves, Casey, Izard and Walsh (2011) also found a reduction in anabolic hormones during military training, albeit when a nutrition supplement was used. In this study an improvement in dynamic lift strength (power clean) and vertical jump was seen and was attributed to an increase in lean body mass. It must be noted that in this study no strength training was indicated to have taken place and changes was due to the traditional training conducted by military personnel. However, this study allows an insight into the nutritional requirements to maximise strength adaptations, increase lean body mass and increase performance.

The mRNA then carries the information from the DNA to ribosome (stage 5), where the ribosome reads the mRNA and translates the information into proteins (Folland & Williams, 2007; Spiering et al., 2008). The mTOR signalling pathway increases protein synthesis by enhancing this translational process and it has been suggested that muscle protein breakdown occurs when energy is used to create mechanical deformation during strength training and muscle breakdown surpasses muscle protein synthesis (Folland & Williams, 2007; Spiering et al., 2008; Kumar, Atherton, Smith &, Rennie, 2009). Protein synthesis is increased after resistance training with the aid of mTOR pathway which will eventually surpass muscle breakdown creating an anabolic environment (Kumar et al., 2009).

Finally, some researchers have specifically measured the performance of the military loaded march after supplementing traditional military training with resistance training. Harman et al., (2008) found that US soldiers improved their loaded march performance by 14% but it must be said that their control group also increased their loaded march performance by 15% using traditional military training. Kraemer et al., (2004) assessed different combinations of modalities for military performance outcomes, the authors found that concurrent training (resistance and endurance) improved loaded march test as well as unloaded run. However, only endurance training improved the unloaded assessment, highlighting the importance of not only the addition of strength training but the specificity of the modality.

In summary, strength training has been shown to increase the performance of the military loaded march, which in the eyes of the coach is a positive outcome measure, however this seems to be no difference from traditional military training. Literature suggests that the endocrine system can be placed under immense stress causing undulating imbalance of hormones over a period of time and in turn restricting maximum gene expression. This could be via two factors, firstly the reduction of anabolic hormones which will reduce the ability of the anabolic receptor to bind with DNA. Secondly due to the concurrent nature of military training which will affect the signalling pathways and imaginative periodization programmes are required to maximise adaptation and allow adequate rest and recovery. It could be considered that the key positive adaptation to strength training would be an increased neural drive. A high incident of lower limb injuries are sustained in training and the increased neural drive, co-activation of agonist and antagonist muscles and reduced muscle inhibition, will reduce the risk of injury. This will increase the operational effectiveness of the military, reduce medical costs and clinical time to rehabilitate injured soldiers and thus increase the longevity of a soldier’s career.

References

Anderson, J. L., Dyhre-Poulsen, P., Magnusson, P., Per, A., & Simonsen, E. B. (2002). Increased Rate of Force Development and Neural Drive of Human Skeletal Muscle Following Resistance Training.?Journal of Applied Physiology, 93, 1318-1326.

Bell, G. J., Syrotuik, D., Martin, T. P., Burnham, R., & Quinney, H. A. (2000). Effect of Concurrent Strength and Endurance Training on Skeletal Muscle Properties and Hormone Concentrations in Humans.?European Journal of Applied Physiology, 81(5), 418-427.

Birrell, S. A., Hooper, R. H., & Haslam, R. A. (2007). The Effect of Military Load Carriage on Ground Reaction Forces.?Gait and Posture, 26(4), 611-614.

Blacker, S. D., Wilkinson, D. M., Bilzon, J. L., & Rayson, M. P. (2008, March). Risk Factors for Training Injuries Among British Army Recruits.?Military Medicine, 173(3), 278 - 286.

Brenes, A. N., Caputo, J. L., Clark, C., Wehrly, L. E., & Coons, J. M. (2015). Comparisons of the Airborne Shuffle to Standard Walking While Torso Loaded.?Journal of Strength and Conditioning Research, 29(6), 1622-1626.

Campos, G. E., Luecke, T. J., Wendeln, H. K., Toma, K., Hagerman, F. C., Murray, T. F., . . . Staron, R. S. (2002). Muscular Adaptations in Response to Three Different Resistance-Training Regimes: Specificity of Repetition Maximum Training Zones.?European Journal of Applied Physiology, 88(1-2), 50-60.

Cerretelli, P., Landoni, L., Minetti, A. E., Narici, M. V., & Roi, G. S. (1989). Changes in Force, Cross-Sectional Area and Neural Activation During Strength Training and Detraining of the Human Quadriceps.?European Journal of Applied Physiology, 59, 310-319.

Cormie, P., McGuigan, M. R., & Newton, R. U. (2011). Developing Maximal Neuromuscular Power.?Sports Medicine, 41(1), 17-38.

Crewther, B., Cronin, J., & Keogh, J. (2005). Possible Stimuli for Strength and Power Adaptation.?Sports Medicine, 35(11), 967-989.

Dorel, S., Couturier, A., Lacour, J.-R., Vandewalle, H., Hautier, C., & Hug, F. (2010). Force- Velocity Relationship in cycling revisited: Benefit of Two- Dimensional Pedal Force Analysis.?Medicine and Science in Sport and Exercise, 42(6), 1174-1183.

Folland, J. P., & Williams, A. G. (2007). The Adaptations to Strength Training.?Sports Medicine, 37(2), 145-168.

Fortes, M. B., Diment, B. C., Greeves, J. P., Casey, C., Izard, R., & Walsh, N. P. (2011). Effects of a Daily Mixed Nutritional Supplement on Physical Performance, Body Composition, and Circulating Anabolic Hormones During 8 Weeks of Arduous Military Training.?Applied Physiology, Nutrition and Metabolism, 36, 967-975.

Grenier, J. G., Millet, G. Y., Peyrot, N., Samozino, P., Oullion, R., Messonnier, L., & Morin, J. B. (2013). Effects of Extreme- Duration Heavy Load Carriage on Neuromuscular Function and Locomotion: A Military Based Study.?Public Library of Science, 7(8), 1-11.

Haff, G. G., & Nimphius, S. (2012). Training Principles for Power.?Strength and Conditioning Journal, 34(6), 2-12.

Haff, G. G., Lehmkuhl, M. J., Mccoy, L. B., & Stone, M. H. (2003). Carbohydrate Supplementation and Resistance Training.?Journal of Strength and Conditioning Research, 17(1), 187-196.

Hahn-Windgassen, A., Nogueira, V., Chen, C. C., Skeen, J. E., Soonenberg, N., & Hay, N. (2005). Akt Activates the Mammalian Target of Rapamycin by Regulating Cellular ATP Level and AMPK Activity.?Journal of Biological Chemistry, 280(37), 32081-32089.

Harman, E. A., Gutekunst, D. J., Frykman, P. N., Nindl, B. C., Alemany, J. A., Mello, R. P., & Sharp, M. A. (2008). Effect of Two Different Eight-Week Training Programs on Military Physical Performance.?The Journal of Strength and Conditioning Research, 22(2), 524-534.

Hashemi, J., Breighter, R., Chandrashekar, N., Hardy, D. M., Chaudhari, A. M., Shultz, S. J., . . . Beynnon, B. D. (2011). Hip Extension, Knee Flexion Paradox: A New Mechanism for Non-Contact ACL Injury.?Journal of Biomechanics, 44(4), 577-585.

Hunter, J., Marshall, R., & McNair, P. (2004). Interaction of Step Length and Step Rate During Sprint Running.?Medicine and Science in Sport and Exercise, 36(2), 261-271.

Hunter, S. K. (2014). Sex Differences in Human fatigability: Mechanisms and Insight to Physiological Responses.?Acta Physiologica, 210(4), 768-789.

Hunter, S. K. (2016). The relevance of Sex Differences in Performance Fatigability.?Medicine and Science in Sport and Exercise, 48(11), 2241-2256.

Irrcher, I., Adhihetty, P. J., Joseph, A. M., Ljubicic, V., & Hood, D. A. (2003). Regulation of Mitochondrial Biogenesis in Muscle by Endurance Exercise.?Sport Medicine, 33(11), 783-793.

Jager, S., Handschin, C., St-Pierre, J., & Spiegelman, B. M. (2007). AMP-Activated Protein Kinase (AMPK) Action in Skeletal Muscle Via Direct Phosphoylation of PGC-1a.?Proceeding of the National Academy of Sciences, 104(29), 12017-12022.

Jornayvaz, F. R., & Shulman, G. I. (2010). Regulation of Mitochondrial Biogenesis.?Essay in Biochemistry, 47, 69-84.

Kelly, K., Arrington, L., Hargus, A., Esquival, K., & Jameson, J. (2017). Changes in Androgen Hormones During Intense Training in Elite Military Men.?Journal of Science and Medicine in Sport, 20, S61.

Knapik, J. (2001). Discharges During US Army Basic Training: Injury Rates and Risk Factors.?Military Medicine, 166, 641-647.

Knapik, J. J., Reynolds, K. L., & Harman, E. (2004). Soldier Load Carriage: Historical, physiological, Biomechanical, and Medical Aspects.?Military Medicine, 169, 45 - 56.

Kraemer, W. J., & Ratamess, N. A. (2005). Hormonal Responses and Adaptations to Resistance Exercise and Training.?Sports Medicine, 35(4), 339-361.

Kraemer, W. J., Hakkinen, K., Newton, R. U., McCormick, M., Nindl, B. C., Volek, J. S., . . . Evans, W. J. (1998). Acute Hormonal Responses to Heavy Resistance Exercise in Younger and Older Men.?European Journal of Applied Physiology and Occupational Physiology, 77(3), 206-211.

Kraemer, W. J., Mazzetti, S. A., Nindl, B. C., Gotshalk, L. A., Volek, J. S., Bush, J. A., . . . Hakkinen, K. (2001). Effect of Resistance Training on Women's Strength/ Power and Occupational Performances.?Medicine and Science in Sports and Exercise, 33(6), 1011-1025.

Kraemer, W. J., Vescovi, J. D., Volek, J. S., Nindl, B. C., Newton, R. U., Patton, J. F., . . . Hakkinen, K. (2004). Effects of Concurrent Resistance and Aerobic Training on Load- Bearing Performance and the Army Physical Fitness Test.?Military Medicine, 169(12), 994-999.

kumar, v., Atherton, P., Smith, K., & Rennie, M. J. (2009). Human Muscle Protein Synthesis and Breakdown During and After Exercise.?Journal of Applied Physiology, 106(6), 2026-2039.

McCall, G. E., Brynes, W. C., Dickinson, A., Pattany, P. M., & Fleck, S. J. (1996). Muscle Fiber Hypertrophy, Hyperplasia, and Capillary Density in College Men After Resistance Training.?Journal of Applied Science, 81(5), 2004-2012.

Mero, A. (1998). Force-Time Characteristics and Running Velocity of Male Sprinters During the Acceleration Phase of Sprinting.?Research Quarterly for Exercise and Sport, 19(3), 94-98.

O'Leary, T. J., Saunders, S. C., McGuire, S. J., & Izard, R. M. (2017). Sex Differences in Neuromuscular Fatigability in Response to Load Carriage in the Field in British Army Recruits.?Journal of Science and Medicine in Sport, 21(6), 591-595.

Ortega, D. R., Rodriguez Bies, E. C., & Berral de la Rose, F. J. (2010). Analysis of the Vertical Ground Reaction Forces and Temporal Factors in the Landing Phase of a Countermovement Jump.?Journal of Sports Science and Medicine, 9(2), 282-287.

Payne, W., & Harvey, J. (2010, July). A Framework for the Design and Development of Physical Employment Test and Standards.?Ergonomics, 53(7), 858-871.

Polcyn, A., Bensel, C., Harman, E., Obusek, J., Pandorf, C., & Frykman, P. (2002). Effects of Weight Carried by Soldiers: Combined Analysis of Four Studies on Maximal Performance, Physiology, and Biomechanics.?US Army Research Institute of Environmental Medicine, 1-64.

Porter, C., Reidy, P. T., Bhattarai, N., Sidossis, L., & Rasmussen, B. B. (2015). Resistance Training Alters Mitochondrial Function in Human Skeletal Muscle.?Medicine and Science in Sports and Exercise, 47(9), 1922-1931.

Sandri, M. (2008). Signalling in Muscle Atrophy and Hypertrophy.?Physiology, 23(3), 160-170.

Santtila, M., Kyrolainen, H., & Hakkinen, K. (2009). Changes in Maximal and Explosive Strength, Electromyography, and Muscle Thickness of Lower and Upper Extremities Induced by Combined Strength and Edurance Training in Soldiers.?Journal of Strength and Conditioning Research, 23(4), 1300-1308.

Schoenfeld, B. (2010). The Mechanisms of Muscle Hypertrophy and Their Application to Resistance Training.?Journal of Strength and Conditioning Research, 24(10), 2857-2872.

Sharma, J., Greeves, J. P., Byres, M., Bennett, A., & Spears, I. R. (2015, May). Musculoskeletal Injuries in British Army Recruits: A Prospective Study of Diagnosis-Specific Incidence and Rehabilitation Times.?BMC Musculoskeletal Disorders, 16(106).

Spiering, B. A., Kraemer, W. J., Anderson, J. M., Armstrong, L. E., Nindl, B. C., Volek, J. S., & Maresh, C. M. (2008). Resistance Exercise Biology.?Sports Medicine, 38(7), 527-540.

Stefanyshyn, D., & Nigg, B. (1998). Contribution of the Lower Extremity Joints to Mechanical Energyin Running Vertical Jumps and Running Long Jumps.?Journal of Sport Sciences, 16, 177-186.

Stepto, N. K., Coffey, V. G., Carey, A. L., Ponnampalam, A. P., Canny, B. J., Powell, D., & Hawley, J. A. (2009). Global Gene Expression in Skeletal Muscle from Well-Trained Strength and Endurance Athletes.?Medicine and Science in Sports and Exercise, 41(3), 546-565.

Tan, B. (1999). Manipulating Resistance Training Program Variables to Optimize Maximum Strength in Men: A Review.?Journal of Strength and Conditioning Research, 13(3), 289-304.

Tipton, M. J., Milligan, G. S., & Reilly, T. J. (2013, October). Physiological Employment Standards I. Occupational Fitness Standards: Objectively Subjective??European Journal of Applied Physiology, 113(10), 2435-2446.

Turner, A. (2016). Strength and Conditioning for British Soldiers.?Strength and Conditioning Journal, 38(3), 59-68.

Turner, A. N., & Jeffreys, I. (2010). The Stretch-Shortening Cycle: Proposed Mechanisms and Methods for Enhancement.?Strength and Conditioning Journal, 32(4), 87-99.

Vaara, J. P., Kokko, J., Isoranta, M., & Kyrolainen, H. (2015). Effects of Added Resistance Training on Physical Fitness, Body Composition, and Serum Hormone Concentrations During Eight Weeks of Special Military Training Period.?Journal of Strength and Conditioning Research, 29(11), 168-172.