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The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 60:1111-1117 (2005)
© 2005 The Gerontological Society of America

Triceps Surae Muscle Power, Volume, and Quality in Older Versus Younger Healthy Men

Jeanette M. Thom1,, Chris I. Morse1, Karen M. Birch2 and Marco V. Narici1

1 Institute for Biophysical and Clinical Research into Human Movement (IRM), Manchester Metropolitan University, Cheshire, United Kingdom.
2 School of Sport and Exercise Science, University of Leeds, United Kingdom.

Address correspondence to Dr. Jeanette Thom, Institute for Biophysical and Clinical Research into Human Movement, MMU Cheshire, Alsager Campus, Hassall Road, Alsager, Cheshire, ST7 2HL, U.K. E-mail: j.thom{at}mmu.ac.uk


   Abstract
Top
 Abstract
Methods
 Results
 Discussion
 References
 
This study investigated whether loss of power with aging is fully accounted for by a decrease in muscle volume. Triceps surae power and volume (VOL) were measured in 18 older (OM: 69–82 years) and 12 younger men (YM: 19–35 years). Isokinetic peak torque was measured to determine torque–velocity and power–velocity relationships. Both peak power observed (PPobs) and peak power estimated from Hill's equation (PPest) were markedly reduced in the OM (PPobs was 45% and PPest was 43% of those of the YM). VOL was 81% of that of the YM (p <.001). Specific power (PPest/VOL) of the OM was 55.2% of that of the YM (p <.001). Torque at PPest accounted for a greater proportion of the decline in PPest in the OM than did optimum velocity (50% vs 13%, respectively). Hence, the present results showed that only approximately half of the loss in triceps surae peak power in old age is due to decreases in muscle VOL.

THE age-related loss of muscle mass, or sarcopenia, combined with the loss of muscle strength contribute significantly to the decline in functional ability and independence in old age (1). The loss of muscle strength is nevertheless disproportionate with respect to sarcopenia so that a decrease in strength normalized to muscle cross-sectional area has been found by several authors (2–6). This phenomenon has been referred to as a loss in "muscle quality" (defined as isometric strength per muscle cross-sectional area) (7,8).

However, when one considers functional performance, it is muscle power more than isometric strength that is required for the accomplishment of most activities of daily living (7,9). Despite this, most studies have focused on isometric muscle strength, but fewer investigated the effect of aging on muscle power (9–21). Also, several of these studies reported muscle power developed in bilateral contractions (12–14,16,19,20) while some in unilateral contractions (9,11,17,21). Problems exist, however, when comparing muscle power (and force) generated during bilateral as against to unilateral movements because of the reduced neural drive associated with bilateral deficit (22–26). This comparison is rendered difficult by the finding that bilateral deficit is present in young adults but is reduced/absent in older individuals (22,25)—an effect that would reduce differences in muscle power between elderly and young persons. Hence caution should be taken when comparing studies reporting power measured using unilateral with those using bilateral movements.

Generally, muscle power has been shown to decline at a faster rate than isometric muscle strength with age (10,20,27), for it decreases at a rate of approximately 3.5% per annum, compared to a rate of strength decline of approximately 1.5% per annum (10). Thus the decrease in muscle power in elderly persons seems only partly accounted for by the loss in muscle strength, and other factors such as a loss of in series sarcomere number, myosin heavy chain composition, intrinsic shortening speed of the myosin molecules, and motor unit recruitment are also likely involved.

Muscle power is known to be proportional to the volume (or muscle mass, because muscle density is 1.050 g·cm–3) of the contracting muscle (28–30). Thus one would expect older individuals, with a smaller muscle volume in comparison to younger counterparts, to have a reduced maximal power. Hence, if with age muscle power were scaled in proportion to muscle volume, then no difference in "specific power" (power normalized to muscle volume) should be observed. However, only a few studies investigated the differences in specific muscle power between young and older adults (16,31,32), while some have reported specific power values only in older individuals (13,19). In these studies, power output was measured either during vertical jumps (hence a bilateral movement) (16) and during maximum isoinertial cycling (31,32). In all cases, specific muscle power was obtained by normalizing peak muscle power for leg muscle volume obtained either anthropometrically (16,19,32) or by magnetic resonance imaging (MRI) (32). The calculated muscle volume, however, comprised all the muscles of the lower limb and was not restricted to that of the muscles involved in producing the power output, i.e., the extensor muscles, in the above cases. For this reason, it seems plausible to expect that this procedure may have introduced an underestimation of the actual specific power of both young and elderly individuals.

As power is a product of force and velocity, factors that cause a decrease in either force or velocity, or both, will contribute to the loss of maximal power. Although it is well established that the loss of muscle force in old age is caused partly by sarcopenia, partly by a reduction in single fiber specific tension (33,34), and often, in vivo, by a reduction in neural drive (4,6,35,36), confounding evidence exists on the effect of aging on maximum shortening velocity (Vmax) of single fibers. As a matter of fact, some studies report a decrease in estimated Vmax (37,38), whereas others (39–42) reported no change. Hence it seems difficult to predict the contribution of changes in force and velocity to the loss of muscle power in old age, but by normalizing muscle power to muscle volume it should be possible at least to eliminate those factors related to changes in muscle "quantity" from those factors related to changes in muscle "quality." The purposes of this study were to investigate whether specific muscle power of young and older men differ and to discuss the origins of any possible difference.


   METHODS
Top
 Abstract
 Methods
Results
 Discussion
 References
 
Participants
Thirty healthy, recreationally active men volunteered to participate in this study. The participants were divided into two groups: (1) older men (OM: n = 18, age: 73.9 ± 3.8 years [range 69–82 years], height: 171.4 ± 4.9 cm, mass: 78.0 ± 8.2 kg, mean ± SD) and (2) young men (YM: n = 12, age: 26.5 ± 4.1 years [range 19–35 years], height: 178.1 ± 7.1 cm, mass: 76.9 ± 10.7 kg). The OM were medically screened for cardiovascular, myopathic, neurological, and inflammatory diseases and gained consent from their general practitioner prior to inclusion in the study. YM were also screened, but through a health status questionnaire. All participants gave informed written consent prior to commencement of the study, and were familiarized with the proceedings on a separate test session prior to data collection. The study was approved by the local ethics committee.

Study Procedure
Each participant visited the laboratory on three occasions. Following the familiarization session, participants returned twice, once for an MRI scan and once for an examination of muscle torque, power, and twitch characteristics.

Muscle Volume
MRI was used to assess muscle volume of the three components of the triceps surae (TS) of the left leg (soleus, and the medial and lateral gastrocnemii muscles). Serial axial plane scans were performed along the length of the TS using an extremity coil-fixed 0.2-T MRI scanner (E-Scan; ESAOTE Biomedica, Genova, Italy). A representative scan of an OM and a YM is shown in Figure 1. Scans were performed using a T1 weighted 3D isotropic profile with the following scanning parameters: time to echo: 16 ms; repetition time: 38 ms; field of view: 180 mm x 180 mm; matrix: 256 x 192 pixels. Throughout the scanning process and for 15 minutes prior, the participants were supine to adjust for fluid shifts. The initial scan was centered over the knee to include the origin of both heads of the gastrocnemius muscle, with subsequent scans performed distally. A total of four scans were obtained, with each scan containing seven axial images 1 cm apart (slice thickness 8 mm and gap 2 mm). Cod liver oil markers were placed on the skin to align each scan with the previous one. In total, the distance covered by the four axial packages was 280 mm.



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  		Figure 1. Representative magnetic resonance imaging of the lower leg for a young man (A) and an older man (B). The muscles of the triceps surae are highlighted. S = soleus; GL = gastrocnemius lateralis; GM = gastrocnemius medialis muscle

 
For each slice, the anatomical cross sectional area (ACSA) of the TS was calculated from the sum of the three muscles (the soleus and the medial and lateral gastrocnemius muscles) using imaging software (NIH Image, version 1.61/ppc; National Institutes of Health, Bethesda, MD). Muscle ACSA was obtained after subtraction of all visible fat and connective tissue distributed subcutaneously and between the septa using routine procedures in place in our laboratory. The sum of the ACSAs by the number of scans (1 cm thickness) was used to estimate the muscle volume of the TS. Due to limitations of the positioning of participants and coil size, it was necessary to estimate the distal portion of the soleus using polynomial regressions from the measured portion of the soleus and its length estimated from ultrasonography, as described by Morse and colleagues (4). However, the error introduced by this estimation was judged to be negligible if one considers that the cross-sectional areas of the soleus in its distal portion are very small and hence would contribute minimally to the total volume (61).

Muscle Isometric and Concentric Torque
Maximal isometric plantar flexor torque produced during maximal voluntary contraction (MVC) was measured using a Cybex dynamometer (Cybex Norm; Cybex International Inc., Medway, MA), with the participant lying prone, the ankle at 0° (neutral), and the knee extended. The left foot was positioned on the foot plate so that the lateral malleolus was aligned to the dynamometer's axis of rotation and tightly secured to the footplate with straps to minimize heel displacement during contractions. Two MVCs were performed at 0°, with at least 1 minute of rest in between each contraction. Maximal isokinetic concentric torque of the TS was measured at 0.87, 1.75, 2.62, 3.49, and 4.36 rad·s–1 (50, 100, 150, 200, and 250 degree·s–1) to assess the torque–velocity relationship. At each velocity, four concentric contractions were attempted in succession, with the foot placed at –20° to begin each movement, with the range of motion from –20° to 30°, with at least 1 minute of rest in between each velocity. Data were sampled with a Macintosh G4 computer using a data acquisition system (Biopac Systems Inc., Goleta, CA). Maximal isokinetic torque was determined from the peak torque at 0° for each velocity. As previous measurements of moment arm length in the same participant group showed similarities between OM and YM (5.08 and 5.11 cm, respectively; 62), it was decided not to convert torque measurements (Nm) into force (N); therefore, torque values, not forces values, are reported in this study.

The order of the tests conducted during this session was: three warm-up MVCs, followed by resting twitches, two MVCs at 0°, and the isokinetic contractions. The angular velocities of the isokinetic contractions were distributed in a randomized order. Verbal encouragement was given for all contractions, with at least 1 minute of rest between contractions and 5 minutes of rest between the different types of contractions.

Muscle Power
Concentric torque–velocity and power–velocity relationships were determined from the torque values obtained above. Observed peak power (PPobs) was determined from the torque–velocity data (PPobs = torque x angular velocity) across the range of velocities measured. The torque–velocity relationship and peak power was also estimated by fitting the experimental values with Hill's equation: (P + a)(V + b) = (Po + a)b (43), where a and b are constants with the dimension of force and velocity, respectively. These constants were determined from the intercept a/b and slope 1/b of the linearized Hill's plot of (Po –V)/V versus P, where Po is the maximal isometric torque (MVC), P is the torque developed at different velocities of shortening, and V is the velocity of shortening. Peak power was then estimated (PPest) from the equation: PPest = Topt x Vopt, where Topt is the optimum torque (Topt = (a2 + a x Po)1/2 – a) and Vopt the optimum velocity at Topt (44). Specific power of the TS was calculated as the ratio between PPobs and PPest to TS muscle volume.

Twitch Characteristics
Supramaximal single twitches were applied to the TS percutaneously using rubber stimulation pads (38 mm x 89 mm and 76 mm x 127 mm; Versastim; Conmed, Utica, NY) from a DSV Digitimer Stimulator (Digitmer, Hertfordshire, U.K.) during the last testing session. The anode was placed distal to the popliteal crease and the cathode over the distal myotendinous junction of the soleus. Supramaximal percutaneous electrical stimulation was used, as previously it has been shown to provide results similar to those of direct nerve stimulation (45,46). To obtain the supramaximal level for each participant, the twitches were administered with increasing current intensity from 100 mA in 50- to 100-mA intervals prior to data collection until a plateau in twitch torque was exceeded. The four resting supramaximal twitches were elicited 5 seconds apart to determine peak torque (Pt), half relaxation time (1/2RT), and time to Pt (TPT). Analysis was performed on the last three twitches for each participant.

Statistical Analyses
Independent variables between YM and OM were compared using independent two-tailed t tests. Data were expressed as means ± SE unless otherwise stated. Differences were considered significant at p <.05.


   RESULTS
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 Abstract
 Methods
 Results
Discussion
 References
 
Maximal Muscle Torque and Power
The isokinetic torque of the OM was significantly lower than that of the YM at all concentric velocities (40.5%–56.2% of YM, p <.001) and in isometric (62.6%) contractions. Table 1 shows the observed and the estimated torque–velocity data from Hill's equation. It is noteworthy that, within the investigated range of angular velocities, good agreement was found between the observed and estimated torque values, indicating a robust fit of the experimental points with Hill's equation.


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  		Table 1. Observed and Estimated Torque–Velocity Data.

 
TS PPest of the OM was only 43.3% that of the YM (p <.001), and PPobs was similarly affected, being 45.5% that of the YM (p <.001), as shown in Table 2. Figure 2 shows the estimated torque–velocity and power–velocity relationships in both YM and OM. The calculated Topt and Vopt from Hill's equation showed that the OM had a 50.1% lower Topt than the YM (28.5 Nm and 57.1 Nm, respectively), whereas the Vopt was 86.8% that of the OM (3.6 rad·s–1) compared with the YM (4.1 rad·s–1). The velocity at which maximal PPobs occurred was not statistically different between the OM and YM (3.73 ± 0.21 and 4.15 ± 0.16 rad·s–1, respectively).


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  		Table 2. Absolute and Scaled Peak Power in Young and Older Men.

 


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  		Figure 2. Torque–velocity and power–velocity curves for young (YM) and older men (OM) derived using Hill's equation. The young men were significantly stronger and more powerful at all velocities than the older men (**p <.01). Values are means ± SE.

 
Muscle Volume
TS muscle volume of the OM was 19% smaller than that of the YM (7.41 ± 0.19 x 10–4 m3 and 9.16 ± 0.47 x 10–4 m3, respectively, p <.001).

Normalized Power
Power normalized to body mass and to muscle volume (specific power) results are presented in Table 2. The maximum specific power (PPest/muscle volume) of the OM was 55.2% lower than that of the YM (p <.001). The estimated specific power–velocity relationship between YM and OM is shown in Figure 3.



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  		Figure 3. Specific power–velocity curves for young (YM) and older men (OM). Specific power calculated from power derived using Hill's equation/triceps surae muscle volume. The young men were significantly more powerful at all velocities than the older men (**p <.01). Values are means ± SE.

 
Twitch Characteristics
OM had a 28% lower Pt than did YM (12.9 ± 0.6 Nm compared to 16.6 ± 1.5 Nm respectively, p <.05). A typical twitch recording of an OM and a YM is depicted in Figure 4. The OM had a 23% longer TPT (114.7 ± 7.6 ms vs 87.8 ± 3.7 ms, p <.01), but showed no difference in 1/2RT (107.2 ± 6.2 ms vs 100.5 ± 4.7 ms, not significant) compared with the YM. When TPT and 1/2RT were normalized to Pt, both were found to be slower in the OM group than in the YM group (TPT/Pt: 9.4 ± 0.8 ms·Nm–1 vs 5.7 ± 0.5 ms·Nm–1, p <.01, and 1/2RT/Pt: 8.6 ± 0.6 ms·Nm–1 vs 6.6 ± 0.7 ms·Nm–1, p <.05, in OM and YM, respectively).



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  		Figure 4. A typical electrically stimulated twitch recording of an old man (OM) and a young man (YM). Pt = peak torque; TPT = time to peak tension; 1/2RT = half relaxation time

 

   DISCUSSION
Top
 Abstract
 Methods
 Results
 Discussion
References
 
The main finding of the current study is that a reduction in muscle volume accounts for only approximately half of the loss of muscle power, indicating a remarkable decrease in specific power (–55%) in old age. The loss of muscle power was found to be due to a greater decrease in optimum torque (–50%) than in optimum velocity (–13%).

Maximum Muscle Power and Specific Power
In the current study the maximal power of the TS was found to be 57% lower in the OM than in the YM. This finding is in line with a previous report of Harridge and Young (7) in the plantar flexors of older men (with maximal power values ~45% lower than in those of young men). In the present investigation the lower power produced by the OM was only partly accounted for by the smaller (19%) muscle volume. As a consequence, TS specific power was substantially lower (55%) in the older males. Although great caution is expressed when comparing human with animal data, it is interesting to note that maximal power normalized to muscle mass has been found to be 20% lower in older mice extensor digitorum longus muscle (30). Surprisingly, however, in single muscle fibers of older humans no age-related decline in power normalized to cell size has been found (47).

Several previous studies have investigated specific power between young and older adults (16,31,32), also finding that the lower muscle power in older individuals could not be explained by the loss in muscle volume alone, although the loss in muscle volume was a significant contributor. These studies measured muscle power during motor activities different from that of the present study, as power was assessed either during vertical jumping (16) or during isoinertial cycling (31,32), and power was normalized either to total limb volume or to lean limb volume measured by anthropometry. Although normalization of muscle power to anthropometrically derived muscle volume is practical and easily applicable to the testing of large populations, the volume so obtained includes all muscles within a certain segment and does not differentiate, for instance, between the extensors and the flexors. Hence this technique will inevitably underestimate the actual normalized power pertaining to those muscles considered "prime movers" in a particular motor task. Martin and colleagues (32), however, also measured thigh muscle volume using MRI in a subgroup of persons and found a high correlation to lean thigh volume (R2 = 0.914).

Several other studies have investigated specific power in older individuals only (13,19) or have compared muscle power per ACSA and/or body mass. Given the lack of measurements in younger individuals, the different muscles investigated, and the different power normalization procedure followed by the authors, comparison of the present data with those of the above studies seems difficult. When normalizing muscle power to volume, one takes into account the decrease in muscle size with age due to the loss of sarcomeres in series (fascicle length) as well as in parallel (physiological cross-sectional area). One must do this because muscle power is partly determined by the number of force-generating units both in series and parallel (28,48), and is thus proportional to muscle volume. The present investigation showed that only about half of the loss of TS muscle power in old age was accounted for by a decrease in muscle volume (Figure 3). This finding suggests that the following additional factors must account for the remaining ~50%: a) slowing of muscle contractile speed, reflected by longer TPT and 1/2RT, due to changes in myosin heavy chain (MHC) composition and myosin molecule intrinsic speed; b) lower fiber-specific tension; and c) decreased neural drive.

Maximal muscle power is the product of optimal force and optimal velocity and thus it is affected by those factors exerting an influence on both of these determinants. These are discussed hereafter.

Factors Affecting Optimum Torque
In the current study the decrease in maximal power with age was mainly accounted for by a decrease in muscle torque. Topt was calculated to be 50% lower in the OM than in the YM, whereas Vopt was only 13% lower. Hence the loss of peak power was due to a greater loss of force than velocity with age.

An age-related decrease in Topt is mainly related to the corresponding decrease in muscle size (sarcopenia) (1). However, even when accounting for differences in muscle size, a greater loss of force is still apparent with age (2,4–6). Thus additional factors must contribute to the observed force loss. These factors are probably represented by a decrease in fiber-specific tension (2,33,34), alterations in neural drive (4,42), and changes in MHC isoform composition (49).

Factors Affecting Optimum Velocity
In the present investigation the lower estimated Vopt (13%) in the OM was associated with slower (23%–39%) twitch contraction times normalized for Pt in the OM. This finding is in line with previous observations of prolonged twitch contraction and 1/2RTs in the plantar flexors of older individuals (50–52) and of ~20% lower optimal speed at peak power during a single leg press in older women (17).

The lower Vopt observed in older men could be due to either a difference in MHC composition or to differences in motor unit recruitment between young and old persons. A reduced motor unit recruitment, frequently reported in older individuals (4,6,35,36), could potentially contribute to the lower Vopt, because it is known that each motor unit population has its own Vopt (53).

The primary determinant of Vmax, and thus Vopt, is the MHC expression of the contractile proteins (48). The difference in Vmax between human fast and slow fibers has been found to be six and two fiber lengths per second, respectively (54), which is similar to the 2.5-fold greater Vmax observed in mouse extensor digitorum longus muscle than in the soleus (55). Larsson and colleagues (34) showed that maximal unloaded shortening velocity was highly dependent on MHC isoform composition of the quadriceps. The unloaded shortening velocity of human muscle is ~10 times greater for the IIX fibers than for the slow fibers (56), and aging has been associated with a change in the MHC composition, with an increased coexpression of MHC I and MHC IIA (49). Also, an age-related reduction in both number and size of mainly Type II muscle fibers (57–59) may contribute to the decrease in Vmax and thus Vopt. Percent muscle fiber type composition may be maintained in very old persons; however, alterations in muscle morphology (e.g., fiber grouping and changes in shape, especially in Type II fibers) and greater increase in MHC coexpression occur (49). Bottinelli and colleagues (60) showed that Type I fibers produce less power and at lower contraction velocities than do Type IIA and IIB fibers. Type I fibers also show a greater curvature of the force–velocity curve than do Type II fibers (54). Thus if aging is associated with a greater percentage of Type 1 fibers and MHC I expression (49,57,59), it would be expected that contraction times and thus Vopt and peak power would be reduced.

One additional reason that may account for the smaller decline in optimum velocity than in optimum torque is the confounding effect of disuse and aging in elderly populations. Disuse results in a shift towards faster myosin isoforms, whereas aging, leading to partial denervation of muscle fibers, results in a shift towards a slower phenotype (33). In fact, older individuals tend to have a more sedentary lifestyle than do young people, and this lifestyle may result in a conflicting effect of aging and disuse on muscle contraction speed. Although "active older" men were used in this study, the participants were found to be ~20% less active at higher energy expenditure levels than were their young counterparts, though overall there was no significant difference in energy expenditure between the groups (4). This decrease in intense activity may have counteracted a greater decline in Vopt than that observed.

A limitation of the present study, as of many cross-sectional studies, is that it is difficult to infer the effects of aging from the comparison of data obtained in different individuals because different individuals may show different declines in biological functions. Such individual variability between chronological and biological aging is indeed of great interest because it may cast light on some of the regulatory mechanisms underlying the ageing process.

Conclusion
The maximal muscle power in older men was found to be ~50% that of young men. About half of this difference in power was accounted for by a reduction in muscle volume indicating that other factors, such as MHC composition, myosin molecule intrinsic speed, specific tension, and neural drive may account for the remaining half of the power loss. The observation that a reduction in torque is the major determinant of the loss in power output underlines the importance of resistance training programs for recovering power output and functional performance in old age.


   Acknowledgments
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 Abstract
 Methods
 Results
 Discussion
 References
 
This study was supported by the European Commission Framework V funding (‘Better-Ageing’ Project, No. QLRT-2001-00323).

We thank Ian Rothwell for his technical assistance.


   Footnotes
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 Methods
 Results
 Discussion
 References
 
Decision Editor: James R. Smith, PhD

Received December 15, 2004

Accepted April 21, 2005


   References
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 Abstract
 Methods
 Results
 Discussion
 References
 

  1. Doherty TJ. Invited review: aging and sarcopenia. J Appl Physiol. 2003;95:1717-1727.[Abstract/Free Full Text]
  2. Frontera WR, Suh D, Krivickas LS, Hughes VA, Goldstein R, Roubenoff R. Skeletal muscle fiber quality in older men and women. Am J Physiol Cell Physiol. 2000;279:C611-C618.[Abstract/Free Full Text]
  3. Macaluso A, Nimmo MA, Foster JE, Cockburn M, McMillan NC, De Vito G. Contractile muscle volume and agonist-antagonist coactivation account for differences in torque between young and older women. Muscle Nerve. 2002;25:858-863.[Medline]
  4. Morse CI, Thom JM, Davis MG, Fox KR, Birch KM, Narici MV. Reduced plantarflexor specific torque in the elderly is associated with a lower activation capacity. Eur J Appl Physiol. 2004;92:219-226.[Medline]
  5. Narici MV, Maganaris CN, Reeves ND, Capodaglio P. Effect of aging on human muscle architecture. J Appl Physiol. 2003;95:2229-2234.[Abstract/Free Full Text]
  6. Yue GH, Ranganathan VK, Siemionow V, Liu JZ, Sahgal V. Older adults exhibit a reduced ability to fully activate their biceps brachii muscle. J Gerontol A Biol Sci Med Sci. 1999;54:M249-M253.
  7. Harridge SD, Young A. Skeletal muscle. In: Pathy MSJ, ed. Principles and Practice of Geriatric Medicine. 3rd ed. Hoboken, New Jersey: John Wiley & Sons Ltd; 1998.
  8. Kent-Braun JA, Ng AV. Specific strength and voluntary muscle activation in young and elderly women and men. J Appl Physiol. 1999;87:22-29.[Abstract/Free Full Text]
  9. Skelton DA, Kennedy J, Rutherford OM. Explosive power and asymmetry in leg muscle function in frequent fallers and non-fallers aged over 65. Age Ageing. 2002;31:119-125.[Abstract/Free Full Text]
  10. Skelton DA, Greig CA, Davies JM, Young A. Strength, power and related functional ability of healthy people aged 65–89 years. Age Ageing. 1994;23:371-377.[Abstract/Free Full Text]
  11. Bassey EJ, Fiatarone MA, O'Neill EF, Kelly M, Evans WJ, Lipsitz LA. Leg extensor power and functional performance in very old men and women. Clin Sci. 1992;82:321-327.[Medline]
  12. Bosco C, Komi PV. Influence of aging on the mechanical behavior of leg extensor muscles. Eur J Appl Physiol Occup Physiol. 1980;45:209-219.[Medline]
  13. Caserotti P, Aagaard P, Simonsen EB, Puggaard L. Contraction-specific differences in maximal muscle power during stretch-shortening cycle movements in elderly males and females. Eur J Appl Physiol. 2001;84:206-212.[Medline]
  14. Ferretti G, Narici MV, Binzoni T, et al. Determinants of peak muscle power: effects of age and physical conditioning. Eur J Appl Physiol Occup Physiol. 1994;68:111-115.[Medline]
  15. Foldvari M, Clark M, Laviolette LC, et al. Association of muscle power with functional status in community-dwelling elderly women. J Gerontol A Biol Sci Med Sci. 2000;55:M192-M199.[Abstract/Free Full Text]
  16. Grassi B, Cerretelli P, Narici MV, Marconi C. Peak anaerobic power in master athletes. Eur J Appl Physiol Occup Physiol. 1991;62:394-399.[Medline]
  17. Macaluso A, De Vito G. Comparison between young and older women in explosive power output and its determinants during a single leg-press action after optimisation of load. Eur J Appl Physiol. 2003;90:458-463.[Medline]
  18. Young A, Skelton DA. Applied physiology of strength and power in old age. Int J Sports Med. 1994;15:149-151.[Medline]
  19. De Vito G, Bernardi M, Forte R, Pulejo C, Macaluso A, Figura F. Determinants of maximal instantaneous muscle power in women aged 50–75 years. Eur J Appl Physiol Occup Physiol. 1998;78:59-64.[Medline]
  20. Izquierdo M, Ibanez J, Gorostiaga E, et al. Maximal strength and power characteristics in isometric and dynamic actions of the upper and lower extremities in middle-aged and older men. Acta Physiol Scand. 1999;167:57-68.[Medline]
  21. Lanza IR, Towse TF, Caldwell GE, Wigmore DM, Kent-Braun JA. Effects of age on human muscle torque, velocity, and power in two muscle groups. J Appl Physiol. 2003;95:2361-2369.[Abstract/Free Full Text]
  22. Hakkinen K, Kraemer WJ, Newton RU. Muscle activation and force production during bilateral and unilateral concentric and isometric contractions of the knee extensors in men and women at different ages. Electromyogr Clin Neurophysiol. 1997;37:131-142.[Medline]
  23. Howard JD, Enoka RM. Maximum bilateral contractions are modified by neurally mediated interlimb effects. J Appl Physiol. 1991;70:306-316.[Abstract/Free Full Text]
  24. Ohtsuki T. Decrease in human voluntary isometric arm strength induced by simultaneous bilateral exertion. Behav Brain Res. 1983;7:165-178.[Medline]
  25. Owings TM, Grabiner MD. Normally aging older adults demonstrate the bilateral deficit during ramp and hold contractions. J Gerontol A Biol Sci Med Sci. 1998;53:B425-B429.[Abstract]
  26. Secher NH, Rube N, Elers J. Strength of two- and one-leg extension in man. Acta Physiol Scand. 1988;134:333-339.[Medline]
  27. Pearson SJ, Young A, Macaluso A, et al. Muscle function in elite master weightlifters. Med Sci Sports Exerc. 2002;34:1199-1206.[Medline]
  28. Woledge RC, Curtin NA, Homsher E. Energetic Aspects of Muscle Contraction. London: Academic Press; 1985.
  29. Sargeant AJ, Hoinville E, Young A. Maximum leg force and power output during short-term dynamic exercise. J Appl Physiol. 1981;51:1175-1182.[Abstract/Free Full Text]
  30. Brooks SV, Faulkner JA. Maximum and sustained power of extensor digitorum longus muscles from young, adult, and old mice. J Gerontol. 1991;46:B28-B33.[Abstract]
  31. Marsh GD, Paterson DH, Govindasamy D, Cunningham DA. Anaerobic power of the arms and legs of young and older men. Exp Physiol. 1999;84:589-597.[Abstract]
  32. Martin JC, Farrar RP, Wagner BM, Spirduso WW. Maximal power across the lifespan. J Gerontol A Biol Sci Med Sci. 2000;55:M311-M316.[Abstract/Free Full Text]
  33. D'Antona G, Pellegrino MA, Adami R, et al. The effect of ageing and immobilization on structure and function of human skeletal muscle fibres. J Physiol. 2003;552:(Pt 2): 499-511.[Abstract/Free Full Text]
  34. Larsson L, Li X, Frontera WR. Effects of aging on shortening velocity and myosin isoform composition in single human skeletal muscle cells. Am J Physiol. 1997;272:(2 Pt 1): C638-C649.
  35. Harridge SD, Kryger A, Stensgaard A. Knee extensor strength, activation, and size in very elderly people following strength training. Muscle Nerve. 1999;22:831-839.[Medline]
  36. Kamen G, Sison SV, Du CC, Patten C. Motor unit discharge behavior in older adults during maximal-effort contractions. J Appl Physiol. 1995;79:1908-1913.[Abstract/Free Full Text]
  37. Alway SE. Slowing of contractile properties in quail skeletal muscle with aging. J Gerontol A Biol Sci Med Sci. 1995;50A:B26-B33.[Abstract]
  38. Valour D, Ochala J, Ballay Y, Pousson M. The influence of ageing on the force-velocity-power characteristics of human elbow flexor muscles. Exp Gerontol. 2003;38:387-395.[Medline]
  39. Fitts RH, Troup JP, Witzmann FA, Holloszy JO. The effect of ageing and exercise on skeletal muscle function. Mech Ageing Dev. 1984;27:161-172.[Medline]
  40. Eddinger TJ, Cassens RG, Moss RL. Mechanical and histochemical characterization of skeletal muscles from senescent rats. Am J Physiol. 1986;251:(3 Pt 1): C421-C430.
  41. Brooks SV, Faulkner JA. Contractile properties of skeletal muscles from young, adult and aged mice. J Physiol. 1988;404:71-82.[Abstract/Free Full Text]
  42. Larsson L, Ansved T. Effects of ageing on the motor unit. Prog Neurobiol. 1995;45:397-458.[Medline]
  43. Hill AV. The heat of shortening and the dynamic constants of muscle. Proc R Soc Lond B Biol Sci. 1938;126:136-195.[Free Full Text]
  44. Josephson RK. Contraction dynamics and power output of skeletal muscle. Annu Rev Physiol. 1993;55:527-546.[Medline]
  45. Newman SA, Jones G, Newham DJ. Quadriceps voluntary activation at different joint angles measured by two stimulation techniques. Eur J Appl Physiol. 2003;89:496-499.[Medline]
  46. Rutherford OM, Jones DA, Newham DJ. Clinical and experimental application of the percutaneous twitch superimposition technique for the study of human muscle activation. J Neurol Neurosurg Psychiatry. 1986;49:1288-1291.[Abstract/Free Full Text]
  47. Trappe S, Gallagher P, Harber M, Carrithers J, Fluckey J, Trappe T. Single muscle fibre contractile properties in young and old men and women. J Physiol. 2003;552:(Pt 1): 47-58.[Abstract/Free Full Text]
  48. Sargeant AJ. Neuromuscular determinants of human performance. In: Whipp BJ, Sargeant AJ, eds. Physiological Determinants of Exercise Tolerance in Humans. London: Portland Press; 1999.
  49. Andersen JL. Muscle fibre type adaptation in the elderly human muscle. Scand J Med Sci Sports. 2003;13:40-47.[Medline]
  50. Vandervoort AA, McComas AJ. Contractile changes in opposing muscles of the human ankle joint with aging. J Appl Physiol. 1986;61:361-367.[Abstract/Free Full Text]
  51. Narici MV, Bordini M, Cerretelli P. Effect of aging on human adductor pollicis muscle function. J Appl Physiol. 1991;71:1277-1281.[Abstract/Free Full Text]
  52. Davies CT, White MJ. Contractile properties of elderly human triceps surae. Gerontology. 1983;29:19-25.[Medline]
  53. Rome LC, Funke RP, Alexander RM, et al. Why animals have different muscle fiber types. Nature. 1988;335:824-827.[Medline]
  54. Faulkner JA, Claflin DR, McCully KK. Power output of fast and slow fibers from human skeletal muscles. In: Jones NL, McCartney N, McComas AJ, eds. Human Muscle Power. Champaign, IL: Human Kinetics; 1986.
  55. Barclay CJ, Constable JK, Gibbs CL. Energetics of fast- and slow-twitch muscles of the mouse. J Physiol. 1993;472:61-80.[Abstract/Free Full Text]
  56. Bottinelli R, Reggiani C. Human skeletal muscle fibres: molecular and functional diversity. Prog Biophys Mol Biol. 2000;73:195-262.[Medline]
  57. Lexell J. Human aging, muscle mass, and fiber type composition. J Gerontol A Biol Sci Med Sci. 1995;50:(Spec No): 11-16.
  58. Hunter SK, Thompson MW, Ruell PA, et al. Human skeletal sarcoplasmic reticulum Ca2+ uptake and muscle function with aging and strength training. J Appl Physiol. 1999;86:1858-1865.[Abstract/Free Full Text]
  59. Staron RS. Human skeletal muscle fiber types: delineation, development, and distribution. Can J Appl Physiol. 1997;22:307-327.[Medline]
  60. Bottinelli R, Pellegrino MA, Rossi R, Canepari M, Reggiani C. Contractile properties of human skeletal muscle fibres in disuse and disease. In: Capodaglio P, Narici MV, eds Muscle Atrophy: Disuse and Disease, Advances in Occupational Medicine and Rehabilitation. Vol. 4. Pavia: PI-ME Press 1998;17-36.
  61. Morse CI, Thom JM, Birch KM, Narici MV. Changes in triceps surae muscle architecture with sarcopenia. Acta Physiol Scand. 2005;183:291-298.[Medline]
  62. Morse CI, Thom JM, Reeves ND, Birch KM, Narici M. In vivo physiological cross sectional area and specific force are reduced in the gastrocnemius of elderly males. J Appl Physiol. 2005; 10.1152/japplphysiol.01186.2004.



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