Effects of Life-Long Wheel Running Behavior on Plantar Flexor Contractile Properties is a well-researched Life Sciences Thesis/Dissertation topic, it is to be used as a guide or framework for your Academic Research.
Aging in skeletal muscle is characterized by a loss in muscular performance. This is in part related to the direct loss of muscle mass due to senescence, known as sarcopenia. With age, skeletal muscles lose force production, contractile speed, and power production.
The force-velocity relationship of muscle is a product of force production and contraction speed, both of which decline with age; however, the mechanisms and trajectory of this decline are not well understood.
Exercise has positive effects on muscle and thus may assist in maintaining performance in old age. However, few long-term studies have been performed to examine the effects of life-long exercise on muscle contractile performance.
In order to test the potential for life-long exercise to reduce the effects of again on muscle contractile performance, muscle performance was determined in control mice and mice selected for high voluntary wheel running at baseline, adult, and old ages. Peak isometric force declined with age in control (C) mice without exercise (P<0.05), but high runner mice (HR) mice without wheels did not differ significantly with age.
With age pooled, He mice had significantly greater muscle quality (N/g) than C mice, regardless of wheel access (P<0.05). Mass specific peak power production (W/g) was significantly greater in old mice that had access to wheels compared to those that did not, regardless of selection (P<0.05). The findings of this study support the hypothesis that voluntary lifelong exercise behavior attenuates losses in important performance metrics, such as mass-specific power production and
Aging of Muscle Tissue
Biological tissues degrade via senescence. Aged skeletal muscle tissue
experiences sarcopenia, the loss of muscle mass during senescence (Narici et al., 2003). Significant reductions in muscle mass begin in humans near the fifth decade of life (Janssen et al., 2000), coinciding with a significant reduction in force (Narici et al., 1991).
By the seventh decade, quadriceps cross-sectional area (CSA) is 25-33% smaller than that of individuals in their second to the third decade of life (Lexell et al., 1988; Young et al., 1984). While skeletal muscle loses its capacity to generate force with aging (Doherty, 2003; Porter et al., 1995), the magnitude of this deficit is directly correlated with the activity of the muscle during its lifetime.
Unused fibers degrade due to disuse atrophy or sarcopenia, while regularly recruited muscle fibers preserve force production via hypertrophy of existing fibers (E.P. Widmaier et al., 2004; Hill et al., 2004; Lieber, 1992).
However, studies report that even well into the eighth decade of life, short term exercise in the form of sprint training results in isometric force production to be comparable with that of individuals in their fifth decade of life (Korhonen et al., 2006). Studies like these highlight the plastic nature of skeletal muscle and their ability to remodel themselves through active loading, even in the end stages of
The load and total activity muscle experience determine the nature and
extent of homeostatic response due to exercise (i.e. muscle adaptation). The number of fibers recruited during exercise is also an important factor in determining the extent of adaptation (e.g. sprint training compared to endurance running) (Lieber, 1992).
For example after endurance training, skeletal muscles can experience as much as two-fold increases in mitochondrial enzyme activity, indicative of increased aerobic capacity (Baldwin et al., 1972). Post strength training, muscles may increase their cross-sectional area via hypertrophy of existing fibers, thereby also enhancing force production (Bell et al., 2000).
Muscles connect to the tendon to impose movement on the skeleton, and therefore changes in tendon mechanics with aging may also alter muscle-tendon unit (MTU), mechanics. Increases in MTU stiffness associated with aging show adverse effects on normal locomotor function (Kovanen et al. 1987; Kragstrup et al. 2011; Shadwick 1990).
Alterations in either muscle or tendon can affect the functionality of the entire MTU and impact locomotor performance (Brainerd and Azizi 2005, Azizi 2008, Randhawa 2013, Azizi and Roberts 2014, Carrier 1998). Thus, understanding how aging affects the muscle-tendon unit is important in considering the mechanisms of declining locomotor performance with age.
Force-Velocity Relationship, Aging, and Endurance Training
The force-velocity relationship of muscles is dependent on many factors,
including fiber length, muscle mass, and fiber type composition.
With age, there is typically a reduction in both shortening velocity and
maximal force production, caused by loss of mass and a general shift towards a predominant type I fiber composition, which has a greater oxidative capacity, small in cross-sectional area, and relatively slow contractile speed (Close, 1972; Laughlin et al., 1990).
Interestingly, eccentric (active lengthening) strength is preserved rather than concentric (active shortening) strength (Porter et al. 1995), suggesting non-contractile elements like extracellular matrix (ECM), tendon, and collagen cross-linkages may have a significant role in preserving force (Pousson et al., 2001).
Reduction in motor unit activation capacity and decreases in a single fiber specific tension contributes to reduced muscle function with late-stage aging (Narici et al., 2003). Though there are many compounding effects that contribute to late-life muscle decline, alterations in maximal shortening velocity (Vmax), peak isometric force production (Po), peak power (Pmax), and MTU stiffness are likely to impact mobility the most.
With aged muscle, Vmax reductions can be attributed to a reduction in sarcomeres in series (Narici et al. 2003; Raj et al. 2010). Several studies consistently report a range of 20-40% reduction in Vmax with age (Morse et al., 2005; Raj et al., 2010; Thom et al., 2005; Valour et al., 2003) compared to younger, healthy adults.
This reduction in shortening velocity impacts other aspects of muscle function, such as a muscle’s architectural gear ratio (Azeri et al., 2008; Holt et al., 2016). Longitudinal human studies using I so kinetic dynamometers to test contractile velocities between 30o /s and 300o /s show strength declines with age, with patients experiencing 10-22% loss in vast us lateral strength by the sixth decade of life (Aniansson et al., 1986; Frontera et al., 2000; Gajdosik et al., 1999; Grimby, 1995; Winegard et al., 1996).
Reductions in peak power production (along with contractile velocity) are indicative of declining muscle performance with age and are reported to be at minimum 30% less than those of healthy young adults and can be as great as 80% less (Narici et al. 2005; Thom et al. 2005; Toji and Kaneko 2007; Valour et al. 2003). Non-contractile elements play a significant role in declining muscle function with age (Gajdosik et al., 1999).
Alterations in series elastic elements (tendons and aponeuroses) from an aging result in stiffer muscle-tendon units due to increases in tendon collagen content and changes in the microstructure of collagen fibers (Kovanen et al. 1987; Kragstrup et al. 2011; Lieber and Ward 2013; Mays et al. 1988)
Effects of Endurance Training on Age and Musculoskeletal Performance
Endurance training has been shown to reduce the decline of musculoskeletal performance with age as well as recoup lost muscle mass in late-stage aging (Aagaard et al., 2010; Chamari, K. et al., 1995; Gollnick et al., 1973; Gosselin et al., 1998; Kirkendall and Garrett, 1998; Kovanen et al., 1984; Lieber, 1992).
Force production can be preserved based on a training regimen that
utilizes endurance-based cardiovascular training (Aagaard et al., 2010; Gollnick et al., 1973), while strength training elicits hypertrophy of existing muscle fibers along with increased muscle fiber recruitment (Kraemer et al., 1995). Traditional resistance training, power training, and eccentric loading training are deemed the most effective at preserving strength and contractile speed (Ferri et al. 2003;
Suetta et al. 2008; Fronterra et al. 1988; Reeves et al. 2005; Labarque et al. 2002; Morse et al. 2007; Petrella et al. 2007).
Endurance training is an effective combination of each of these effects for preserving not only overall muscular health (Chamari et al. 1995; Kirkendall and Garrett 1998), but cardiovascular health, cellular health, and collagen fiber content in mice and rats (Allen et al. 2001; Hambrecht et al. 1997; Kovanen et al 1984; Kovanen et al. 1987).
Endurance training staves off declines in aerobic power production, showing a significantly smaller reduction compared to anaerobic power production (Chamari et al., 1995). Therefore, endurance training may be used as an effective way to maintain muscle force and power production throughout the process of aging.