Browsing by Subject "Resistance training"

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Aging, habitual exercise, and vascular ischemia-reperfusion injury
(2009-12) DeVan, Allison Elizabeth; Tanaka, Hirofumi, Ph. D.
Ischemia-reperfusion (IR) injury occurs during myocardial infarction and during some cardiovascular surgeries. Animal studies support the role of endurance exercise training in preventing myocardial IR injury and coronary endothelial dysfunction. In human and animal studies, habitual exercise has been shown to attenuate endothelial dysfunction caused by aging and disease. It is unknown; however, if exercise can protect against vascular IR injury in humans and if so, whether these effects persist with advancing age. Using 20 minutes of forearm ischemia and the response of the brachial artery as a noninvasive surrogate model for the heart, the association between the mode of exercise training (endurance versus resistance) and vascular IR injury was examined in young healthy adults in the first study. Endothelial function, as measured by flow-mediated dilation (FMD) in the brachial artery, decreased significantly after forearm ischemia, suggesting that this noninvasive model of the heart produces significant and measureable vascular injury. These measures returned to baseline levels within 30 minutes following ischemia, illustrating the transient nature of this form of IR injury. The magnitude of injury and recovery from ischemia were not significantly different among young sedentary, endurance-trained, and resistance-trained subjects, suggesting that exercise training is not associated with protection from vascular IR injury in a young, healthy population. In the second study, the association between aging, endurance exercise training, and vascular IR injury was studied. Twenty minutes of forearm ischemia was associated with a transient fall in brachial FMD in young and older sedentary and endurance-trained subjects. Young subjects recovered more quickly from IR injury than older subjects. Within 30 minutes of injury, the endothelial function of the young group was back to baseline while blunted endothelial function persisted in older subjects for greater than 45 minutes after injury. There was no association between endurance exercise training and enhanced recovery from IR injury. These findings suggest that aging is associated with delayed recovery from vascular IR injury and that endurance training does not appear to modulate the vascular IR injury responses.
Mechanical overload induces muscle hypertrophy in mice with lowered serum IGF-1
(2004-05-22) Zannikos, Symeon Vasilios; Farrar, Roger P.
Decreased serum levels of IGF-1 result in lower muscle and body weights. Muscular autocrine/paracrine IGF-I may be stimulated in response to mechanical overload. Purpose: to determine whether normal levels of serum IGF-I are required for the increased muscle mass tha occurs in habitual mechanical overload. Design: The Liver IGF-I Deficient (LID) mouse has selective disruption of the liver IGF-I alleles, resulting in 20-25% of normal serum IGF-1 levels. Wildtype, LL, mice have normal circulating levels of IGF-1. LID and LL mice, 15-16 mos of age, were divided into resistance trained (LID-TR n=11, LL-TR n = 10) and sedentary groups (LID-NT n = 9, LL-NT n = 8). The resistance training protocol consisted of ladder climbing (85°, 1.5cm spacing), utilizing progressive overload. Initially weights, 50% of body weight (BW) were attached to the base of their tail, and the resistance was progressively increased. The training protocol was performed twice a day, every third day for 16-18 weeks, with the mice pulling over 3X their body weight during their last bouts. The in situ physiological parameters of the Plantaris muscle were determined. Results: SP[subscript o],SP[subscript t], as well as TPT & 1/2 RT were the same among groups. The Plantaris muscle was the most responsive to the weight training, exhibiting a 12 % (p < 0.05) increase in absolute weight in both training groups vs. their sedentary counterparts. Other hindlimb muscles increased by 7-9% (p <0.05). Hematoxylin-Eosin staining revealed cellular damage in both training groups. The LID-TR group sustained damage in 1.4% of myofibers, while the LL-TR only showed damage in 0.5% of myofibers (p <0.05). No cellular damage was evident in either sedentary group. Central nuclei were visualized utilizing laminin antibody staining. In the LID-TR group 1.8% of myofibers showed central nuclei vs. 0.5% in the LL-TR (p <0.05). The central nuclei were mostly localized around the areas of cellular damage. Conclusion: The degree of hypertrophy was the greatest in the plantaris and FHL muscle, as expected from this type of training. In this experiment, decreased serum IGF-1Ea levels did not attenuate the muscular hypertrophy induced by habitual mechanical overload. The LID-TR group was able to hypertrophy to the same degree as the LL-TR animals. Even though they weighed significantly less than their sedentary counterparts, their muscle weights in the FHL and Plantaris were greater. Satellite activation was not hindered either as evidenced by the significantly higher levels of central nuclei in the LID-TR group. The increased number of central nuclei found in the LID-TR group is likely due in part to the increased levels of damage, as the majority was localized around the areas of damage. Neverthless, the data shows that satellite activation is not hindered in the presence of reduced IGF-1Ea. The compensatory mechanisms for the adaptation evidenced in this study need to be elucidated. Release of IGF-1Eb can be a likely reason, as IGF-1Eb has been shown to be more potent in inducing muscle hypertrophy, and thus may be able to compensate for the reduced serum levels of IGF-1Ea (Goldspink 2002). Individual steps among the cascade of intracellular signals activated by IGF-1Ea may also be amplified to allow normal hypertrophy during muscle overload
Resistance training as a modality to enhance muscle regeneration in a rat skeletal muscle defect
(2009-12) Taylor, Daniel Ryan; Farrar, Roger P.; Suggs, Laura
Traumatic skeletal muscle injuries that include loss of large amounts of muscle mass are becoming more common in today’s warfare. Traditional treatments often do not prevent long term functional impairments. Using a decellularized extracellular matrix (ECM) as scaffolding to replace lost muscle tissue allows for transmission of force through the injury site, and provides a suitable microenvironment receptive to myofiber growth. Seeding the ECM with progenitor cells improves cellular content in the defect area. Exercise exposes the muscle to improved blood flow as well as higher than normal loading. This results in increased blood vessel density as well as higher levels of cellular content, and near complete restoration of function.
Signaling cascades downstream IGF-I receptor in response to resistance exercise relevant to skeletal muscle hypertrophy in rats
(2007-05) Kim, Il-young, 1973-; Farrar, Roger P.
Mechanical loading of a muscle induces stimulation of IGF-I receptor and its signaling cascades within the muscle. This study evaluated the effect of mechanical loading through resistance training utilizing the ladder climbing paradigm of Hornberger and Farrar. Rats were trained for up to 5 weeks and then muscles were evaluated either 12 or 40 hours after their last bout of exercise. The resistance exercise resulted in progressive increases in body mass, FHL muscle mass and maximal load as the exercise was accumulated over 5 weeks. 12 hours following the last bout of the exercise, phosphorylation of ERK1/2 was elevated while that of p70S6K declined. There were no differences in phosphorylation of other representable proteins: Akt, mTOR, and GSK-3β. Furthermore, 40 hours following the last bout of the exercise, there were no significant changes in phosphorylation of selective pathways within either the ERK or PI3Kinase pathways. The early phase of recovery was associated with an increase in phosphorylation of ERK1/2 and a decrease in phosphorylation of p70S6K. While the resistance training induced a significant increase in muscle mass, the relationship between IGF-I signaling and increases in protein accretion need to be evaluated in relationship to the time of evaluation of the last bout of exercise.
The effects of carbohydrate and protein supplementation on signaling pathways regulating protein turnover and muscle mass following chronic resistance training
(2016-12) Huang, Lu, M. S. in Kinesiology; Farrar, Roger P.; Stone, Audrey
Skeletal muscle is important for physical activity and regulation of metabolism. Increase or maintenance of muscle mass is pursued by different populations ranging from athletes to people suffering from severe muscular diseases causing muscle atrophy/wasting. In this study, four animal groups were generated: sedentary group (No supplements or exercise) (SED); resistance training (RE) and whey supplements (WP); RE and combo (Carbohydrate and whey) supplements (CP); RE and placebo (DI water) (PLA). Flexor hallucis longus (FHL) muscles were collected after 8 weeks of training. Expression of several key proteins controlling muscle mass and protein turnover were measured in order to compare how different combinations affect muscle growth. It was found that resistance training induced reductions in myostatin protein expression compared with sedentary controls (p<0.05) and that MuRF was elevated in the CP group compared with sedentary group (p<0.05). We conclude that resistance training may upregulate protein synthesis through suppressing myostatin and that resistance training may increase muscle protein breakdown.