1.0 Introduction

This article provides an overview of the physiologic adaptations to resistance training.

It outlines the adaptations associated with strength and power followed by endurance.

2.0 Strength and Power

The benefits of resistive exercise extend beyond the obvious improvements in muscle performance to include positive effects on the cardiovascular system, connective tissue, and bone.

Moreover, these effects translate into function.

Individuals perform their daily activities with more ease because they are functioning at a lower percentage of their maximum capacity.

Improved functioning also enhances the individual’s sense of well-being and independence.

Additionally, strength training has shown crossover effects, where training one limb translates into muscle performance improvements in the contralateral limb (Munn et al., 2005; Seger & Thorstensson, 2005).

2.1 Muscle

The most obvious benefits of resistive training are for the muscular system.

Regular resistive exercise is associated with several positive adaptations, most of which are dosage dependent (see Table 1 below).

Table 1: Physiologic Adaptations to Resistance Training
Variable	Result after Resistance Training
Performance
Muscle strength	Increases
Muscle endurance	Increases for higher output
Aerobic capacity	No change or increases slightly
Maximal rate of force production	Increases
Vertical jump	Increases
Anaerobic power	Increases
Sprint speed	Improves
Muscle Fibers
Fiber size	Increases
Capillary density	No change or decreases
Mitochondrial density	Decreases
Enzyme Activity
Creatine phosphokinase	Increases
Myokinase	Increases
Phosphofructokinase	Increases
Lactate dehydrogenase	No change or variable
Metabolic Energy Stores
Stored ATP	Increases
Stored creatine phosphate	Increases
Stored glycogen	Increases
Stored triglycerides	May increase
Connective tissue
Ligament length	May increase
Tendon strength	May increase
Collagen content	May increase
Bone density	Increases
Body Composition
Percentage of body fat	Decreases
Fat-free mass	Increases

The cross-sectional area of the muscle increases as a result of an increase in the myofibril volume of individual muscle fibers, fiber splitting, and potentially an increase in the number of muscle fibers.

This cross-sectional area increase primarily results from preferential hypertrophy of type II fibers. Changes in the muscle depend on fiber type and the stimulus.

Hypertrophy of fast-twitch fibers occurs when all or most of the fibers are being recruited and is considered an adaptation for increased power output.

Slow-twitch fibers hypertrophy in response to frequent recruitment. In repetitive, low-intensity activity, fast-twitch fibers are rarely recruited, and these fibers may atrophy while the slow-twitch fibers hypertrophy.

A study by Staron et al. (1994) examined the differences in the proportion of muscle fiber types in distance runners, weight lifters, and sedentary controls. The investigators found the weight lifters had a greater proportion of type IIA fibers and had a greater type IIA fiber area than the controls or distance runners (Staron et al., 1984). Specificity of resistive training exists and must be considered when designing a training programme.

Other changes occur on cellular and systemic levels. The capillary density is unchanged or decreases, and the mitochondrial density decreases. Some of these changes result from their number relative to total muscle volume. Although protein volume and cross-sectional area increase in response to resistive training, some of the cellular or systemic factors may remain unchanged, giving the perception of a decrease, although the decrease is only relative.

Energy sources necessary to fuel muscle contraction increase after resistive training. In general, levels of creatine phosphate, ATP, myokinase, and phosphofructokinase increase in response to a resistive exercise programme (Thorstensson et al., 1975; Costill et al., 1976; MacDougall et al., 1979; Tesch et al., 1987). Lactate dehydrogenase is variably changed (Tesch et al., 1987).

Neural adaptations occur with resistive training. Studies have shown increases in the muscle’s ability to produce torque and increased neural activation, as measured by EMG (Hakkinen & Komi, 1983). Increases in muscle activity were also seen after resistive training that consisted of explosive jumping. Increased EMG values associated with greater power and maximal contraction were attributed to a combination of increased motor unit recruitment and increased firing rate of each unit (Hakkinen, Komi & Alen, 1985).

2.2 Connective Tissue

Although disuse and inactivity cause atrophy and weakening of connective tissues such as tendon and ligament, physical training can increase the maximum tensile strength and the amount of energy absorbed before failure (Stone, 1988).

Physical activity returns damaged tendons and ligaments to normal tensile strength values faster than complete rest (Tipton et al., 1975). Physical training, particularly resistive exercise, may alter tendon and ligament structures to make them larger, stronger, and more resistant to injury.

2.3 Bone

Weightlessness (Vogel & Whittle, 1976) and immobilisation (Hanson, Roos & Nachemson, 1975) can cause profound loss of bone density and mass. Weight-bearing activities that recruit anti-gravity muscles can maintain or enhance bone density and mass (White et al., 1984).

Weight training, particularly with a weight-bearing component, can substantially alter bone mineral density. Individuals in sports requiring repeated high-force movements such as weight lifting and throwing events have higher bone densities than distance runners and soccer players or swimmers (Nilsson & Westlin, 1971).

Those who play tennis regularly have higher bone density in their dominant forearms, and professional pitchers have greater bone density in the dominant humerus (Jones et al., 1977).

A 5-month study of weight training compared with jogging found that weight training produced significantly better increases in lumbar bone density than the aerobic exercise (Lane et al., 1988).

These studies suggest that regular exercise, specifically exercise such as resistive training, can maintain or improve bone density. Resistive training to improve bone density is important for women of all ages.

A study of adolescent female athletes found runners to have higher total body and site-specific bone mineral density than swimmers or cyclists, and that knee extension strength was an independent predictor of bone mineral density in this population (Duncan et al., 2002).

Finally, a study of bone mass and exercise dosage found that daily loading regimens broken down into four sessions with recovery time in between improved bone mass significantly over a loading schedule that performed the training in a single, uninterrupted session (Robling et al., 2002).

Thus smaller exercise sessions separated by recovery periods may be a better prescription when increased bone mass is the goal.

2.4 Cardiovascular System

Resistive training benefits the cardiovascular system. The idea that strength training causes hypertension is erroneous. Most reports show that highly strength-trained athletes have average or lower than average systolic and diastolic blood pressures (Fleck, 1988). When performed properly and heeding the proper precautions, strength training can have a positive effect on the cardiovascular system.

Increased intrathoracic or intra-abdominal pressures may affect cardiac output and blood pressure during resistive exercise. In the classic model, increased intrathoracic pressures are thought to decrease venous return to the heart and decrease cardiac output. Intrathoracic pressure is inversely related to cardiac output and stroke volume and directly related to systolic and diastolic blood pressure during resistive exercise. Increased intrathoracic pressures may limit venous return and decrease cardiac output while causing an accumulation of blood in the systemic circulation that may increase blood pressure. Performing resistive exercises with a Valsalva manoeuvre, which elevates intrathoracic pressure, leads to a greater blood pressure response than performance of the exercise without a Valsalva manoeuvre (Fleck, Henke & Wilson, 1989). Instructing an individual to breathe properly during exercise may reduce the increase in blood pressure sometimes seen during exercise.

Increased intramuscular pressure during resistive exercise may result in increased total peripheral resistance and increased blood pressure. Mechanically induced increases in peripheral resistance probably are the cause of higher blood pressures during isometric and concentric exercise compared with pressures during eccentric exercise (Miles & Gotshall, 1989). Isometric or concentric exercise combined with a Valsalva manoeuvre can produce the greatest increase in blood pressure. This combination should be avoided, especially by individuals at risk for elevated blood pressure.

Resistive exercise does result in a pressor response that affects the cardiovascular system by causing hypertension through exciting the vasoconstrictor centre, which leads to increased peripheral resistance. If precautions are taken to ensure proper breathing and avoid isometric contractions in persons at risk for a pressor response, resistive exercise’s benefits outweigh the risks. Long-term performance of resistive exercise can result in positive adaptations of the cardiovascular system at rest and during work. Cardiovascular adaptations to resistive training are summarised in Table 2 below.

Table 2

Benefits of Strength Training on the Cardiovascular System

Decreased heart rate

Decreased or unchanged systolic blood pressure

Decreased or unchanged diastolic blood pressure

Increased or unchanged cardiac output

Increased or unchanged stroke volume

Increased or unchanged maximal oxygen consumption

Decreased or unchanged total cholesterol

3.0 Endurance

The muscle’s response to endurance training is different from its response to strength or power training. This response is expected because of the differences in training dosage.

Muscular endurance depends on oxidative capacity, and training increases the muscle’s metabolic capacity. Muscular endurance is often limited by a local accumulation of lactate, with glycolysis inhibition and a failure to regenerate ATP in the working muscle (Shepard, 1992).

During prolonged activities, depletion of intramuscular glycogen reserves may contribute to impaired muscular endurance.

Muscles trained for endurance demonstrate cells with increased mitochondrial size, number, and enzymatic activity, as well as increased perfusion (Lash & Sherman, 1993). Increased enzymatic activity allows the muscle to better use the oxygen delivered, encouraging use of fats as a fuel and sparing glycogen.

Muscles that are stronger use a smaller portion of the maximum voluntary contraction force with activity, thereby delaying the onset of muscular fatigue.

Muscles trained for endurance also demonstrate increased local fuel storage. Glycogen stores may be increased twofold, and when endurance training is combined with appropriate carbohydrate intake, stores may increase as much as threefold (Lash & Sherman, 1993).

In addition to increasing fuel stores, the endurance-trained muscle also increases fatty acid use and decreases the use of glycogen as a fuel. This alteration allows more exercise before fatigue.

Endurance muscle training improves the oxygen delivery system by increasing the local capillary network, producing more capillaries per muscle fiber (Lash & Sherman, 1993).

Increased perfusion slows the accumulation of lactate in the working muscles.

4.0 References

Costill, D.C., Daniels, J., Evans, et al. (1976) Skeletal muscle enzymes and fiber composition in male and female track athletes. Journal of Applied Physiology. 40, pp.149–154.

Duncan, C.S., Blimkie, C.J., Cowell, C., et al. (2002) Bone mineral density in adolescent female athletes: relationship to exercise type and muscle strength. Medicine and Science in Sports and Exercise. 34, pp.286–294.

Fleck, S.J. (1988) Cardiovascular adaptations to resistance training. Medicine and Science in Sports and Exercise. 20, pp.S146–S151.

Fleck, S.J., Henke, C. & Wilson, W. (1989) Cardiac MRI of elite junior Olympic weight lifters. International Journal of Sports Medicine. 10, pp.329–333.

Hakkinen, K., Komi, P.V. & Alen, M. (1985) Effect of explosive type strength training on isometric force and relaxation time, electromyographic and muscle fibre characteristics of leg extensor muscles. Acta Physiol Scand. 125, pp.587–600.

Hakkinen. K. & Komi, P.V. (1983) Electromyographic changes during strength training and detraining. Medicine and Science in Sports and Exercise. 15, pp.455–460.

Hanson, T.H., Roos, B.O. & Nachemson, A. (1975) Development of osteopenia in the fourth lumbar vertebrae during prolonged bed rest after operation for scoliosis. Acta Orthop Scand. 46, pp.621–630.

Jones, H.H., Priest, J.S, Hayes, W.C., et al. (1977) Humeral hypertrophy in response to exercise. J Bone Joint Surg Am. 59, pp.204–208.

Lane, N., Bevier, W., Bouxsein, M., et al. (1988) Effect of exercise intensity on bone mineral. Medicine and Science in Sports and Exercise. 20, pp.S51.

Lash, J.M. & Sherman, W.M. (1993) Skeletal muscle function and adaptations to training. In: American College of Sports Medicine: Resource Manual for Guidelines for Exercise Testing and Prescription. 2nd Ed. Philadelphia, PA: Lea & Febiger.

MacDougall, J.D., Sale, D.G., Moroz, J.R., et al. (1979) Mitochondrial volume density in human skeletal muscle following heavy resistance training. Medicine and Science in Sports. 11:164–166.

Miles, D.S. & Gotshall, R.W. (1989) Impedance cardiography: noninvasive assessment of human central hemodynamics at rest and during exercise. Exerc Sports Sci Rev. 17, p.231–264.

Munn, J., Herbert, R.D., Hancock, M.J., et al. (2005) Resistance training for strength: effect of number of sets and contraction speed. Medicine and Science in Sports and Exercise. 37(9), pp.1622–1666.

Nilsson, B.E. & Westlin, N.E. (1971) Bone density in athletes. Clin Orthop. 77, pp.179–182.

Robling, A.G., Hinant, F.M., Burr, D.B., et al. (2002) Shorter, more frequent mechanical loading sessions enhance bone mass. Medicine and Science in Sports and Exercise. 34, pp.196–202.

Seger, J.Y. & Thorstensson, A. (2005) Effects of eccentric versus concentric training on thigh muscle strength and EMG. International Journal of Sports Medicine. 26(1), pp.45–52.

Shephard, R.J. Muscular endurance and blood lactate. In: Shephard RM, Astrand P-O, eds. Endurance in Sport. Oxford: Blackwell Scientific Publications, 1992.

Staron, R., Hikida, R.S., Hagerman, F.C., et al. (1984) Human muscle skeletal muscle fiber type adaptability to various workloads. J Histochem Cytochem. 32, pp.146–152.

Staron, R.S., Karapondo, D.L., Kraemer WJ, et al. (1994) Skeletal muscle adaptations during early phase of heavy-resistance training in men and women. Journal of Applied Physiology. 76, pp.1247–1255.

Stone, M.H. (1988) Implications for connective tissue and bone alterations resulting from resistance exercise training. Medicine and Science in Sports and Exercise. 20, pp.S162–S168.

Tesch, P.A., Komi, P.V., Hakkinen, K. (1987) Enzymatic adaptations consequent to long term strength training. International Journal of Sports Medicine. 8(Suppl), pp.66–69.

Thorstensson, A., Spokin, B. & Karlsson, J. (1975) Enzyme activities and muscle strength after “sprint training” in man. Acta Physiol Scand. 94, pp.313–316.

Tipton, C.M., Mattes, R.D., Maynard, J.A., et al. (1975) The influence of physical activity on ligaments and tendons. Medicine and Science in Sports. 7, pp.165–175.

Vogel, J.M. & Whittle, M.W. (1976) Proceedings: bone mineral content changes in the Skylab astronauts. Am J Roentgenol. 126, pp.1296–1297.

White, M.K., Martin, R.B., Yeater, R.A., et al. (1984) The effects of exercise on postmenopausal women. Int Orthop. 7, pp.209–214.