Endurance exercise training inhibits activity of plasma GOT and liver caspase-3 of rats exposed to stress by induction of heat shock protein 70

A single bout of exercise increases production of heat shock protein 70 (HSP70), which protects cells against various stresses. In this study, we investigated whether endurance exercise training enhances liver level of HSP70 and, if so, whether HSP70 contributes to hepatic protection against stress in vivo. Mice of an exercise-training group performed 60 min of treadmill running 5 days/wk for 4 wk. The resting level of liver HSP70 was 4.5 times higher in the trained than in sedentary mice. After 4 wk of exercise training, both groups of mice were exposed to the following stresses: 1) heat stress, 2) cold stress, 3) oxidative stress, 4) ethanol stress, and 5) exercise stress by compelling the mice to run on a treadmill until exhausted. After exposure to the stresses, the liver was immediately isolated. Elevation of liver HSP70 in the trained mice was evident, whereas no elevation was found in the sedentary mice. On exposure to heat, diethyldithiocarbamate and ethanol, activities of glutanic oxalacetic transaminase in plasma, and liver caspase-3, a key enzyme of apoptotic processing, were elevated in the sedentary mice but not in the trained mice. These results suggest that exercise training enhanced the resting level of liver HSP70 and hepatic protection against various stresses, at least partly attributing to the suppression of caspase-3 activity by the increase in HSP70.

Download Full-text

Higher mitochondrial fatty acid oxidation following intermittent versus continuous endurance exercise training

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y98-094 ◽

1998 ◽

Vol 76 (9) ◽

pp. 891-894 ◽

Cited By ~ 23

Author(s):

P D Chilibeck ◽

G J Bell ◽

R P Farrar ◽

T P Martin

Keyword(s):

Fatty Acid ◽

Exercise Training ◽

Fatty Acid Oxidation ◽

Endurance Exercise ◽

High Intensity ◽

Treadmill Running ◽

Acid Oxidation ◽

Interval Exercise ◽

Endurance Exercise Training ◽

Mitochondrial Fatty Acid

It has been well documented that skeletal muscle fatty acid oxidation can be elevated by continuous endurance exercise training. However, it remains questionable whether similar adaptations can be induced with intermittent interval exercise training. This study was undertaken to directly compare the rates of fatty acid oxidation in isolated subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria following these different exercise training regimes. Mitochondria were isolated from the gastrocnemius-plantaris muscles of male Sprague-Dawley rats following exercise training 6 days per week for 12 weeks. Exercise training consisted of either continuous, submaximal, endurance treadmill running (n = 10) or intermittent, high intensity, interval running (n = 10). Both modes of training enhanced the oxidation of palmityl-carnitine-malate in both mitochondrial populations (p < 0.05). However, the increase associated with the intermittent, high intensity exercise training was significantly greater than that achieved with the continuous exercise training (p < 0.05). Also, the increases associated with the IMF mitochondria were greater than the SS mitochondria (p < 0.05). These data suggest that high intensity, intermittent interval exercise training is more effective for stimulation of fatty acid oxidation than continuous submaximal exercise training and that this adaptation occurs preferentially within IMF mitochondria.Key words: muscle, subsarcolemmal mitochondria, intermyofibrillar mitochondria.

Download Full-text

Myocardial hypoperfusion/reperfusion tolerance with exercise training in hypertension

Journal of Applied Physiology ◽

10.1152/japplphysiol.00350.2005 ◽

2006 ◽

Vol 100 (2) ◽

pp. 541-547 ◽

Cited By ~ 17

Author(s):

Patricia O. Reger ◽

Mary F. Barbe ◽

Mamta Amin ◽

Brian F. Renna ◽

Leigh Ann Hewston ◽

...

Keyword(s):

Blood Pressure ◽

Heat Shock ◽

Exercise Training ◽

Heat Shock Protein ◽

Endurance Training ◽

Left Ventricular ◽

Treadmill Running ◽

Rate Pressure Product ◽

Protein Abundance ◽

Myocardial Hypoperfusion

The purpose of this study was to examine whether exercise training, superimposed on compensated-concentric hypertrophy, could increase myocardial hypoperfusion-reperfusion (H/R) tolerance. Female Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) (age: 4 mo; N = 40) were placed into a sedentary (SED) or exercise training (TRD) group (treadmill running; 25 m/min, 1 h/day, 5 days/wk for 16 wk). Four groups were studied: WKY-SED ( n = 10), WKY-TRD ( n = 10), SHR-SED ( n = 10), and SHR-TRD ( n = 10). Blood pressure and heart rate were determined, and in vitro isolated heart performance was measured with a retrogradely perfused, Langendorff isovolumic preparation. The H/R protocol consisted of a 75% reduction in coronary flow for 17 min followed by 30 min of reperfusion. Although the rate-pressure product was significantly elevated in SHR relative to WKY, training-induced bradycardia reduced the rate-pressure product in SHR-TRD ( P < 0.05) without an attenuation in systolic blood pressure. Heart-to-body weight ratio was greater in both groups of SHR vs. WKY-SED ( P < 0.001). Absolute and relative myocardial tolerance to H/R was greater in WKY-TRD and both groups of SHR relative to WKY-SED ( P < 0.05). Endurance training superimposed on hypertension-induced compensated hypertrophy conferred no further cardioprotection to H/R. Postreperfusion 72-kDa heat shock protein abundance was enhanced in WKY-TRD and both groups of SHR relative to WKY-SED ( P < 0.05) and was highly correlated with absolute left ventricular functional recovery during reperfusion ( R2= 0.86, P < 0.0001). These data suggest that both compensated hypertrophy associated with short-term hypertension and endurance training individually improved H/R and that increased postreperfusion 72-kDa heat shock protein abundance was, in part, associated with the cardioprotective phenotype observed in this study.

Download Full-text

Skeletal muscle biochemical adaptations to exercise training in miniature swine

Journal of Applied Physiology ◽

10.1152/jappl.1997.82.6.1862 ◽

1997 ◽

Vol 82 (6) ◽

pp. 1862-1868 ◽

Cited By ~ 23

Author(s):

Richard M. McAllister ◽

Brian L. Reiter ◽

John F. Amann ◽

M. Harold Laughlin

Keyword(s):

Skeletal Muscle ◽

Antioxidant Enzymes ◽

Lactate Dehydrogenase ◽

Exercise Training ◽

Endurance Exercise ◽

Oxidative Capacity ◽

Treadmill Running ◽

Miniature Swine ◽

Endurance Exercise Training ◽

Hydroxyacyl Coa Dehydrogenase

McAllister, Richard M., Brian L. Reiter, John F. Amann, and M. Harold Laughlin. Skeletal muscle biochemical adaptations to exercise training in miniature swine. J. Appl. Physiol. 82(6): 1862–1868, 1997.—The primary purpose of this study was to test the hypothesis that endurance exercise training induces increased oxidative capacity in porcine skeletal muscle. To test this hypothesis, female miniature swine were either trained by treadmill running 5 days/wk over 16–20 wk (Trn; n = 35) or pen confined (Sed; n = 33). Myocardial hypertrophy, lower heart rates during submaximal stages of a maximal treadmill running test, and increased running time to exhaustion during that test were indicative of training efficacy. A variety of skeletal muscles were sampled and subsequently assayed for the enzymes citrate synthase (CS), 3-hydroxyacyl-CoA dehydrogenase, and lactate dehydrogenase and for antioxidant enzymes. Fiber type composition of a representative muscle was also determined histochemically. The largest increase in CS activity (62%) was found in the gluteus maximus muscle (Sed, 14.7 ± 1.1 μmol ⋅ min−1 ⋅ g−1; Trn, 23.9 ± 1.0; P < 0.0005). Muscles exhibiting increased CS activity, however, were located primarily in the forelimb; ankle and knee extensor and respiratory muscles were unchanged with training. Only two muscles exhibited higher 3-hydroxyacyl-CoA dehydrogenase activity in Trn compared with Sed. Lactate dehydrogenase activity was unchanged with training, as were activities of antioxidant enzymes. Histochemical analysis of the triceps brachii muscle (long head) revealed lower type IIB fiber numbers in Trn (Sed, 42 ± 6%; Trn, 10 ± 4; P < 0.01) and greater type IID/X fiber numbers (Sed, 11 ± 2; Trn, 22 ± 3; P < 0.025). These findings indicate that porcine skeletal muscle adapts to endurance exercise training in a manner similar to muscle of humans and other animal models, with increased oxidative capacity. Specific muscles exhibiting these adaptations, however, differ between the miniature swine and other species.

Download Full-text

Commentary to: ‘A comparison of two commercially available ELISA methods for the quantification of human plasma heat shock protein 70 during rest and exercise stress’ by Lee et al. 2015

Cell Stress and Chaperones ◽

10.1007/s12192-015-0626-8 ◽

2015 ◽

Vol 20 (6) ◽

pp. 865-866 ◽

Cited By ~ 3

Author(s):

Janina Schwarzer ◽

Gabriele Multhoff

Keyword(s):

Heat Shock ◽

Heat Shock Protein ◽

Human Plasma ◽

Heat Shock Protein 70 ◽

Exercise Stress ◽

Rest And Exercise

Download Full-text

Effect of endurance exercise training on heart rate onset and heart rate recovery responses to submaximal exercise in animals susceptible to ventricular fibrillation

Journal of Applied Physiology ◽

10.1152/japplphysiol.00793.2006 ◽

2007 ◽

Vol 102 (1) ◽

pp. 231-240 ◽

Cited By ~ 42

Author(s):

George E. Billman ◽

Monica Kukielka

Keyword(s):

Heart Rate ◽

Ventricular Fibrillation ◽

Exercise Training ◽

Endurance Exercise ◽

Submaximal Exercise ◽

Treadmill Running ◽

Vagal Activity ◽

Endurance Exercise Training ◽

Increased Risk ◽

Exercise Onset

Both a large heart rate (HR) increase at exercise onset and a slow heart rate (HR) recovery following the termination of exercise have been linked to an increased risk for ventricular fibrillation (VF) in patients with coronary artery disease. Endurance exercise training can alter cardiac autonomic regulation. Therefore, it is possible that this intervention could restore a more normal HR regulation in high-risk individuals. To test this hypothesis, HR and HR variability (HRV, 0.24- to 1.04-Hz frequency component; an index of cardiac vagal activity) responses to submaximal exercise were measured 30, 60, and 120 s after exercise onset and 30, 60, and 120 s following the termination of exercise in dogs with healed myocardial infarctions known to be susceptible ( n = 19) to VF (induced by a 2-min coronary occlusion during the last minute of a submaximal exercise test). These studies were then repeated after either a 10-wk exercise program (treadmill running, n = 10) or an equivalent sedentary period ( n = 9). After 10 wk, the response to exercise was not altered in the sedentary animals. In contrast, endurance exercise increased indexes of cardiac vagal activity such that HR at exercise onset was reduced (30 s after exercise onset: HR pretraining 179 ± 8.4 vs. posttraining 151.4 ± 6.6 beats/min; HRV pretraining 4.0 ± 0.4 vs. posttraining 5.8 ± 0.4 ln ms2), whereas HR recovery 30 s after the termination of exercise increased (HR pretraining 186 ± 7.8 vs. posttraining 159.4 ± 7.7 beats/min; HRV pretraining 2.4 ± 0.3 vs. posttraining 4.0 ± 0.6 ln ms2). Thus endurance exercise training restored a more normal HR regulation in dogs susceptible to VF.

Download Full-text