Physical exercise (PE) improves physical performance, mental status, general health, and well-being. It does so by affecting many mechanisms at the cellular and molecular level. PE is beneficial for people suffering from neuro-degenerative diseases because it improves the production of neurotrophic factors, neurotransmitters, and hormones. PE promotes neuronal survival and neuroplasticity and also optimizes neuroendocrine and physiological responses to psychosocial and physical stress. PE sensitizes the parasympathetic nervous system (PNS), Autonomic Nervous System (ANS) and central nervous system (CNS) by promoting many processes such as synaptic plasticity, neurogenesis, angiogenesis, and autophagy. Overall, it carries out many protective and preventive activities such as improvements in memory, cognition, sleep and mood; growth of new blood vessels in nervous system; and the reduction of stress, anxiety, neuro-inflammation, and insulin resistance. In the present work, the protective effects of PE were overviewed. Suitable examples from the current research work in this context are also given in the article.

Heart rate variability (HRV) and parasympathetic power are closely related to the well-being and health status in humans. The main goal of the study was to determine whether these measures can reflect recovery status after weight training. After a 10-day detraining period, 7 weightlifters were challenged with a 2-hour weight training which elicited approximately fourfold increases in circulating muscle creatine kinase level and protracted pain feeling (p < 0.05). Weightlifting performance was then evaluated 3, 24, 48, and 72 hours after training to determine the degree of recovery from fatigue. Heart rate variability, circulating dehydroepiandrostendione sulfate (DHEA-S), and muscle damage markers were measured before each performance test. An electrocardiogram was recorded for 5 minutes continuously at rest in seated positions. After training, weightlifting performance of the subjects decreased below baseline in paralleled with suppressed parasympathetic power (high-frequency [HF] HRV), whereas sympathetic power (normalized low-frequency HRV) was slightly elevated at 3 hours of recovery (p < 0.05). Both weightlifting performances and parasympathetic power returned to baseline values in 24 hours and further increased above baseline during 48-72 hours of recovery in a similar fashion (p < 0.05). Circulating DHEA-S level dropped at 24 hours (p < 0.05) and returned to normal values by 48 hours. Muscle pain increased at 3 hours after training and remained higher than baseline values for the 72-hour recovery period (p < 0.05). Our data suggest that parasympathetic power, indicated by HF HRV, is able to reflect the recovery status of weightlifters after training.

Although IGF-II activating the IGF-II receptor signaling pathway has been found to stimulate cardiomyocyte hypertrophy, the role of IGF-II in cardiac cell apoptosis remains unclear. This study aimed to identify the roles of IGF-II and/or IGF-II receptors (IGF-II/IIR) in cardiomyoblast apoptosis and in hypertensive rat hearts with abdominal aorta ligation. Cultured rat heart-derived H9c2 cardiomyoblasts and excised hearts from Sprague-Dawley rats with 0- to 20-day complete abdominal aorta ligation, a model of ANG II elevation and hypertension, were used. IGF-II/IIR expression, caspase activity, DNA fragmentation, and apoptotic cells were measured by RT-PCR, Western blot, agarose gel electrophoresis, and TUNEL assay following various combinations of ANG II, IGF-II/IIR antibody, CsA (calcineurin inhibitor), SP-600125 (JNK inhibitor), SB-203580 (p38 inhibitor), U-0126 (MEK inhibitor), or Staurosporine (PKC inhibitor) in H9c2 cells. ANG II-induced DNA fragmentation and TUNEL-positive cells were blocked by IGF-II/IIR antibodies and antisense IGF-II, but not by IGF-II sense. IGF-II-induced apoptosis was blocked by IGF-IIR antibody and CsA. The increased gene expressions of IGF-II and -IIR induced by ANG II were reversed by U-0126 and Sp600125, respectively. Caspase 8 activities induced by ANG II were attenuated by U-0126, SP-600125, and CsA. DNA fragmentation induced by ANG II was totally blocked by SP-600125, and CsA and was attenuated by U-0126. In rats with 0- to 20-day complete abdominal aorta ligation, the increases in IGF-II/IIR levels in the left ventricle were accompanied by hypertension as well as increases in caspase 9 activities and TUNEL-positive cardiac myocytes. ANG II-induced apoptosis was reversed by IGF-II/IIR blockade and coexisted with increased transactivation of IGF-II and -IIR, which are mediated by ERK and JNK pathways, respectively, both of which further contributed to cardiomyoblast apoptosis via calcineurin signaling. The increased cardiac IGF-II, IGF-IIR, caspase 9, and cellular apoptosis were also found in hypertensive rats with abdominal aorta ligation.