Though my form still needs a lot of work, I am considering starting strength training in the near future, since I have read about how it can help swimming speed, form, etc.
However, I am still struggling with the idea of why strength training is needed. Lets assume that lifting a certain weight in a certain way improves a core muscle, which will help steady my posture (?).
Now assuming I don't weight lift, but instead try to hold the proper posture (high elbow, etc.) for a long period of time, and gradually increase the time I do that over weeks and months, won't those muscle(s) automatically improve?
It seems to me that intuitively the proper muscles would gradually get stronger in order to adjust to the frequent usage - that way the exact muscles I need would get stronger, instead of having to train a large array of muscles that have a relation to swimming.
What am I missing?
A few cites and summaries:
Narici M.V., Maganaris C.N. Adaptability of elderly human muscles and tendons to increased loading. J. Anat. 2006;208:433–443
Senile sarcopenia, the loss of muscle mass associated with aging, is one of the main causes of muscle weakness and reduced locomotor ability in old age. Although this condition is mainly driven by neuropathic processes, nutritional, hormonal and immunological factors, as well as a reduction in physical activity, contribute to this phenomenon. Sarcopenia alone, however, does not fully account for the observed muscle weakness, as the loss of force is greater than that accounted for by the decrease in muscle size. As a consequence, a reduction in the force per unit area, both at single fibre and at whole muscle level, is observed. We recently suggested that at whole muscle level, this reduction in intrinsic force is the result of the combined effect of changes in (1) muscle architecture, (2) tendon mechanical properties, (3) neural drive (reduced agonist and increased antagonist muscle activity) and (4) single fibre-specific tension. Whereas several studies support the role of the last two factors in the loss of intrinsic muscle force with aging, alterations in muscle architecture and in tendon mechanical properties have also been shown to contribute to the above phenomenon
Runge M., Rittweger J., Russo C.R., Schiessl H., Felsenberg D. Is muscle power output a key factor in the age-related decline in physical performance? A comparison of muscle cross section, chair-rising test and jumping power. Clin. Physiol. Funct. Imaging. 2004;24:335–340.
Ageing compromises locomotor capacity and is associated with an increased risk of falls. Several lines of evidence indicate that both changes in muscle mass and performance are causative. Most studies, however, do not discern between effects of ageing, sedentarism and comorbidity. The present study compares the age effects in muscle cross section, force and power in physically competent self-selected subjects of different age groups. A total of 169 women and 89 men between 18 and 88 years, without any disease, impairment or medication affecting the musculoskeletal system were enrolled in this study. Calf muscle cross-sectional area was assessed by computed tomography. Muscle force and power were assessed by jumping mechanography. No significant correlation between muscle cross section and age was found in the men. A weak correlation in the women disappeared after correction for height. Close correlations with age, however, were found for peak force and peak power. Correction for muscle cross section or body weight further increased these correlation coefficients, particularly for peak power specific to body weight (r = 0.81 in women and r = 0.86 in men). The non-sedentarian population investigated here depicted a reduction of >50% between the age of 20 and 80 without a reduction in muscle cross section. This suggests a crucial role for muscular power in the ageing process. Possibly, the jumping mechanography as a measurement of anti-gravitational power output is a promising extension of the chair-rising test, known to be predictive for immobilization and the risk of falls.
Kirkendall, D., Garrett, W. The Effects of Aging and Training on Skeletal Muscle? Am J Sports Med July 1998 vol. 26 no. 4 598-602
With age the number and area of fast twitch fibres decreases. The loss of muscle mass with age is secondary to age-related denervation of muscle fibres, particularly the denervation of Type II fibres. With age large numbers of type II motor neurons become nonfunctional; the neural input is disrupted. With reduced demand on skeletal muscle it adapts to the new lower requirement, but with increased demand the declines due to aging can be minimized
A few cites and summaries:
Narici M.V., Maganaris C.N. Adaptability of elderly human muscles and tendons to increased loading. J. Anat. 2006;208:433–443
Senile sarcopenia, the loss of muscle mass associated with aging, is one of the main causes of muscle weakness and reduced locomotor ability in old age. Although this condition is mainly driven by neuropathic processes, nutritional, hormonal and immunological factors, as well as a reduction in physical activity, contribute to this phenomenon. Sarcopenia alone, however, does not fully account for the observed muscle weakness, as the loss of force is greater than that accounted for by the decrease in muscle size. As a consequence, a reduction in the force per unit area, both at single fibre and at whole muscle level, is observed. We recently suggested that at whole muscle level, this reduction in intrinsic force is the result of the combined effect of changes in (1) muscle architecture, (2) tendon mechanical properties, (3) neural drive (reduced agonist and increased antagonist muscle activity) and (4) single fibre-specific tension. Whereas several studies support the role of the last two factors in the loss of intrinsic muscle force with aging, alterations in muscle architecture and in tendon mechanical properties have also been shown to contribute to the above phenomenon
Runge M., Rittweger J., Russo C.R., Schiessl H., Felsenberg D. Is muscle power output a key factor in the age-related decline in physical performance? A comparison of muscle cross section, chair-rising test and jumping power. Clin. Physiol. Funct. Imaging. 2004;24:335–340.
Ageing compromises locomotor capacity and is associated with an increased risk of falls. Several lines of evidence indicate that both changes in muscle mass and performance are causative. Most studies, however, do not discern between effects of ageing, sedentarism and comorbidity. The present study compares the age effects in muscle cross section, force and power in physically competent self-selected subjects of different age groups. A total of 169 women and 89 men between 18 and 88 years, without any disease, impairment or medication affecting the musculoskeletal system were enrolled in this study. Calf muscle cross-sectional area was assessed by computed tomography. Muscle force and power were assessed by jumping mechanography. No significant correlation between muscle cross section and age was found in the men. A weak correlation in the women disappeared after correction for height. Close correlations with age, however, were found for peak force and peak power. Correction for muscle cross section or body weight further increased these correlation coefficients, particularly for peak power specific to body weight (r = 0.81 in women and r = 0.86 in men). The non-sedentarian population investigated here depicted a reduction of >50% between the age of 20 and 80 without a reduction in muscle cross section. This suggests a crucial role for muscular power in the ageing process. Possibly, the jumping mechanography as a measurement of anti-gravitational power output is a promising extension of the chair-rising test, known to be predictive for immobilization and the risk of falls.
Kirkendall, D., Garrett, W. The Effects of Aging and Training on Skeletal Muscle? Am J Sports Med July 1998 vol. 26 no. 4 598-602
With age the number and area of fast twitch fibres decreases. The loss of muscle mass with age is secondary to age-related denervation of muscle fibres, particularly the denervation of Type II fibres. With age large numbers of type II motor neurons become nonfunctional; the neural input is disrupted. With reduced demand on skeletal muscle it adapts to the new lower requirement, but with increased demand the declines due to aging can be minimized
