Biomedical subjects

John Quindry

Publications and source records attributed to John Quindry.

6 recordsLinked to original sources

PubMed2005

Exercise training provides cardioprotection against ischemia-reperfusion induced apoptosis in young and old animals.

Endurance exercise provides cardioprotection against ischemia-reperfusion (IR)-induced necrotic cell death in young animals. However, whether exercise-induced cardioprotection prevents IR-induced apoptosis in young and old animals is unknown. We tested the hypothesis that endurance exercise training will attenuate IR-induced myocardial apoptosis in young (4 months) and old (24 months) male F344 rats. Young and old rats remained sedentary or performed multiple bouts of moderate intensity running exercise. To induce apoptosis, isolated working hearts were exposed to 45 min of ischemia followed by 90 min of reperfusion. Assessment of myocardial levels of caspase-3 cleaved alpha-spectrin and TUNEL labeled nuclei revealed that IR resulted in apoptosis in hearts from both young and old animals. Importantly, independent of age, exercise attenuated the IR-induced apoptosis of cardiac myocytes. Moreover, exercise attenuated IR-induced calpain activation in the hearts of both young and old animals. These experiments for the first time demonstrate that exercise attenuates IR-induced myocardial apoptosis in both young and old animals. Potential mechanisms for this exercise-induced cardioprotection against IR-induced apoptosis include improved myocardial antioxidant capacity and prevention of calpain and caspase-3 activation.

Aging↗

PubMed2004

Dietary antioxidants and exercise.

Muscular exercise promotes the production of radicals and other reactive oxygen species in the working muscle. Growing evidence indicates that reactive oxygen species are responsible for exercise-induced protein oxidation and contribute to muscle fatigue. To protect against exercise-induced oxidative injury, muscle cells contain complex endogenous cellular defence mechanisms (enzymatic and non-enzymatic antioxidants) to eliminate reactive oxygen species. Furthermore, exogenous dietary antioxidants interact with endogenous antioxidants to form a cooperative network of cellular antioxidants. Knowledge that exercise-induced oxidant formation can contribute to muscle fatigue has resulted in numerous investigations examining the effects of antioxidant supplementation on human exercise performance. To date, there is limited evidence that dietary supplementation with antioxidants will improve human performance. Furthermore, it is currently unclear whether regular vigorous exercise increases the need for dietary intake of antioxidants. Clearly, additional research that analyses the antioxidant requirements of individual athletes is needed.

Antioxidants↗

PubMed2004

Aging, exercise, and cardioprotection.

Myocardial ischemia-reperfusion (I-R) injury is a major contributor to the morbidity and mortality associated with coronary artery disease. The incidence of I-R events is greatest in older persons, and studies also indicate that the magnitude of myocardial I-R injury is greater in senescent individuals compared to younger adults. Regular exercise has been confirmed as a pragmatic countermeasure to protect against I-R-induced cardiac injury. Specifically, endurance exercise has been proven to provide cardioprotection against an I-R insult in both young and old animals. Proposed mechanisms to explain the cardioprotective effect of exercise include the induction of myocardial heat shock proteins (HSPs), improved cardiac antioxidant capacity, and/or elevation of other cardioprotective proteins. Of these potential mechanisms, evidence indicates that elevated myocardial levels of heat shock proteins or antioxidants can provide myocardial protection against I-R injury. At present, which of these protective mechanisms is essential for exercise-induced cardioprotection remains unclear. Understanding the molecular basis for exercise-induced cardioprotection is important in developing exercise paradigms to protect the heart during an I-R insult.

Aging↗

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

The effects of endurance exercise and vitamin E on oxidative stress in the elderly.

To examine the effects of exercise and vitamin E supplementation on oxidative stress in older adults, 59 participants, age 76.3 +/- 4.2 years, were randomly assigned to 1 of 4 groups: an exercise group taking placebos (EGP) or vitamin E (EGE) or a sedentary group taking placebos (SGP) or vitamin E (SGE). Measures included weight, VO2max, blood pressure (BP), and serum concentrations of vitamin E and lipid hydroperoxide (LOOH). At the end of the 16-week trial, the EGP and EGE had significant increases in VO2max and significant decreases in resting BP, weight, and LOOH concentrations (P < 0.05). The SGE had significant decreases in LOOH and BP (P < 0.05). There were no significant changes in the SGP (P > 0.05). The results suggest that endurance exercise in combination with vitamin E reduces oxidative stress, improves aerobic fitness, and reduces BP and weight in older adults. Even sedentary participants who take vitamin E may reduce oxidative stress and lower BP.

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.

Blood Pressure↗