Biomedical subjects

Shannon L Lennon

Publications and source records attributed to Shannon L Lennon.

8 recordsLinked to original sources

PubMed2004

Elevated MnSOD is not required for exercise-induced cardioprotection against myocardial stunning.

Endurance exercise provides cardioprotection against ischemia-reperfusion-induced myocardial stunning and infarction. A recent study demonstrates that an exercise-induced increase in myocardial manganese superoxide dismutase (MnSOD) activity is essential to protect the heart against infarction. It is unknown if an elevation in cardiac MnSOD is also a prerequisite to achieve exercise-induced protection against myocardial stunning. Therefore, this study determined if an exercise-induced increase in myocardial MnSOD activity is a requirement to achieve protection against myocardial stunning. Adult male rats remained sedentary or performed successive bouts of endurance exercise. Hearts were exposed to 25 min of global ischemia followed by reperfusion in an isolated working heart preparation. Postischemic recovery of cardiac external work during reperfusion was significantly higher (84 +/- 3 vs. 67 +/- 4%) in exercised animals compared with sedentary controls. Furthermore, prevention of exercise-induced expression of myocardial MnSOD via antisense oligonucleotides did not retard this exercise-induced protection against myocardial stunning. These data demonstrate that exercise-induced increases in cardiac MnSOD activity are not essential to achieve exercise-mediated protection against myocardial stunning. Therefore, we conclude that different mediators are responsible for exercise-induced cardioprotection against myocardial stunning and infarction.

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PubMed2004

Effect of exercise training on endothelial function in men with coronary artery disease.

The objective of this study was to investigate the effects of 12 weeks of standard cardiac rehabilitation on endothelial function, oxidative stress, and antioxidant defenses in patients with coronary artery disease. Twelve weeks of endurance exercise training led to an improvement in endothelial function as measured by brachial artery flow-mediated dilation (7.9% at baseline vs 11.1% at 12 weeks). Exercise training resulted in increased plasma nitrite and nitrate levels, increased plasma superoxide dismutase activity, and decreased oxidative stress.

Aged↗

PubMed2003

Loss of exercise-induced cardioprotection after cessation of exercise.

Endurance exercise provides cardioprotection against ischemia-reperfusion (I/R) injury. Exercise-induced cardioprotection is associated with increases in cytoprotective proteins, including heat shock protein 72 (HSP72) and increases in antioxidant enzyme activity. On the basis of the reported half-life of these putative cardioprotective proteins, we hypothesized that exercise-induced cardioprotection against I/R injury would be lost within days after cessation of exercise. To test this, male rats (4 mo) were randomly assigned to one of five experimental groups: 1). sedentary control, 2). exercise followed by 1 day of rest, 3). exercise followed by 3 days of rest, 4). exercise followed by 9 days of rest, and 5). exercise followed by 18 days of rest. Exercise-induced increases (P < 0.05) in left ventricular catalase activity and HSP72 were evident at 1 and 3 days postexercise. However, at 9 days postexercise, myocardial HSP72 and catalase levels declined to sedentary control values. To evaluate cardioprotection during recovery from I/R, hearts were isolated, placed in working heart mode, and subjected to 20.5 min of global ischemia followed by 30 min of reperfusion. Compared with sedentary controls, exercised animals sustained less I/R injury as evidenced by maintenance of a higher (P < 0.05) percentage of preischemia cardiac work during reperfusion at 1, 3, and 9 days postexercise. The exercise-induced cardioprotection vanished by 18 days after exercise cessation. On the basis of the time course of the loss of cardioprotection and the return of HSP72 and catalase to preexercise levels, we conclude that HSP72 and catalase are not essential for exercise-induced protection during myocardial stunning. Therefore, other cytoprotective molecules are responsible for providing protection during I/R.

Animals↗

PubMed2003

Exercise, antioxidants, and HSP72: protection against myocardial ischemia/reperfusion.

Endurance exercise is associated with protection against myocardial ischemia/reperfusion (I/R) injury and has been shown to increase heat shock protein 72 (HSP72). Dietary antioxidants have also been reported to decrease I/R-induced injury. Because exercise and antioxidants may provide cardioprotection via different mechanisms, combining these countermeasures could provide additive protection. Alternatively, because exercise-induced oxidant production may promote expression of HSP72, antioxidants could attenuate exercise-induced HSP72 expression and decrease exercise-related cardioprotection. These experiments examined the individual and combined effects of exercise and antioxidants on myocardial I/R injury (in vivo). Rats receiving a mixed antioxidant diet or control diet were assigned to exercise or sedentary groups and randomized to receive: (i) short I/R (myocardial stunning), (ii) long I/R (myocardial infarction), or (iii) sham surgery. Antioxidants significantly increased total antioxidant capacity and attenuated exercise-related HSP72 accumulation. Nonetheless, during short I/R, exercise-trained animals demonstrated improved left ventricular developed pressure (LVDP), independent of diet. Further, antioxidants alone resulted in improved LVDP. Finally, compared to control diet/sedentary animals, both exercise groups (control and antioxidant diets) and the antioxidant diet/sedentary group sustained smaller infarctions. We conclude that exercise and antioxidants can independently provide protection against myocardial contractile dysfunction and infarction, and the combination of these two strategies does not enhance or inhibit the protection observed with each individual countermeasure.

Animals↗

PubMed2002

Mechanical ventilation-induced diaphragmatic atrophy is associated with oxidative injury and increased proteolytic activity.

Prolonged mechanical ventilation (MV) results in reduced diaphragmatic maximal force production and diaphragmatic atrophy. To investigate the mechanisms responsible for MV-induced diaphragmatic atrophy, we tested the hypothesis that controlled MV results in oxidation of diaphragmatic proteins and increased diaphragmatic proteolysis due to elevated protease activity. Further, we postulated that MV would result in atrophy of all diaphragmatic muscle fiber types. Mechanically ventilated animals were anesthetized, tracheostomized, and ventilated with 21% O2 for 18 hours. MV resulted in a decrease (p < 0.05) in diaphragmatic myofibrillar protein and the cross-sectional area of all muscle fiber types (i.e., I, IIa, IId/x, and IIb). Further, MV promoted an increase (p < 0.05) in diaphragmatic protein degradation along with elevated (p < 0.05) calpain and 20S proteasome activity. Finally, MV was also associated with a rise (p < 0.05) in both protein oxidation and lipid peroxidation. These data support the hypothesis that MV is associated with atrophy of all diaphragmatic fiber types, increased diaphragmatic protease activity, and augmented diaphragmatic oxidative stress.

Animals↗

PubMed2002

Resistance exercise training attenuates exercise-induced lipid peroxidation in the elderly.

This study examined the effects of 6 months of resistance exercise (RX) on basal and post-aerobic exercise lipid peroxidation (LIPOX). Men and women [n = 62, mean (SD) age 68.4 (6) years] were divided randomly into either a control (n = 16, CON), low-intensity training [LEX n = 24; 50% one-repetition maximum (1RM), 13 repetitions/exercise], or high-intensity training (HEX n = 22, 80% 1RM, 8 repetitions/exercise) group. Pre- and post-training, subjects performed a graded aerobic exercise test (GXT). Blood samples were collected prior to and 10 min following each GXT. Subjects trained 3 times per week for 6 months using 12 RX machines. LIPOX was determined by measuring levels of thiobarbituric reactive acid substances (TBARS) and lipid hydroperoxides (PEROX). RX had no effect on resting LIPOX. Post-training, post-GXT TBARS were lower in the LEX and HEX groups by 14% and 18%, respectively, compared to CON (P < 0.05). Post-GXT PEROX levels were lower (P < 0.05) in LEX and HEX compared to CON [CON 3.51 (0.56) nmol/ml, LEX 2.89 (0.80) nmol/ml, HEX 2.99 (0.63) nmol/ml]. Serum total and non-protein (glutathione) thiols were higher in the LEX and HEX groups following training compared to CON (P < 0.05). These data suggest that RX can (1) reduce serum LIPOX, (2) provide protection against oxidizing agents in vitro, and (3) provide a "cross-protection" against the oxidative stress generated by aerobic exercise, perhaps mediated by improvements in the thiol portion of the antioxidant defense.

Aged↗

PubMed2002

Resistance exercise and physical performance in adults aged 60 to 83.

OBJECTIVES: This investigation examined the effect of 6 months of high- or low-intensity resistance exercise on muscular strength and endurance and stair climbing ability in adults aged 60 to 83. DESIGN: A randomized controlled trial. SETTING: University of Florida Center for Exercise Science. PARTICIPANTS: Sixty-two men and women completed the study protocol. Subjects were matched for strength and randomly assigned to a control (n = 16), low-intensity (LEX, n = 24), or high-intensity (HEX, n = 22) group. INTERVENTION: Six months of progressive, whole-body resistance training. Subjects trained at 50% of their one-repetition maximum (1RM) for 13 repetitions (LEX) or 80% of 1RM for eight repetitions (HEX) three times per week for 24 weeks using resistance machines. One set each of 12 exercises was performed. MEASUREMENTS: One-repetition maximum was measured for eight different exercises. Muscular endurance was measured using leg press and chest press machines. Low back strength was measured using a lumbar extension machine. Stair climbing ability was assessed as the time to ascend one flight of stairs. RESULTS: 1RM significantly increased for all exercises tested for the HEX and LEX groups (P < or =.050). The increases in total strength (sum of all eight 1RMs) were 17.2% and 17.8% for the LEX and HEX groups, respectively. Muscular endurance improved by 79.2% and 105.0% for the leg press, and 75.5% and 68.0% for the chest press for the LEX and HEX groups, respectively. The time to ascend one flight of stairs significantly decreased for both the LEX and HEX groups (P < or =.050). Lumbar extension strength increased by 62.6% and 39.5% for the LEX and HEX groups, respectively. CONCLUSIONS: These data indicate that significant and similar improvements in strength, endurance, and stair climbing time can be obtained in older adults as a consequence of high- or low-intensity resistance exercise training. These findings may have an effect on how resistance exercise is prescribed to older adults.

Aged↗

PubMed2002

Exercise and cardioprotection.

A wealth of data indicates that performing regular exercise is an important lifestyle modification to prevent cardiovascular disease. Although not fully understood, the cardioprotection by regular exercise may be exerted synergistically through improvement in many risk factors associated with cardiovascular disease. Just as important are the direct effects of exercise on the myocardium, resulting in cardioprotection against ischemia-reperfusion (I-R) injury. Cardioprotective countermeasures against myocardial I-R injury may include the development of collateral coronary arteries, induction of myocardial heat shock proteins, and improved cardiac antioxidant capacity. Improving our understanding of the molecular basis for exercise-induced cardioprotection will play an important role in developing optimal exercise interventions to protect the heart from ischemic injury.

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