The Effects of Acute Anaerobic Exercise on the Cardiovascular and Metabolic Response to the Cold Pressor Test in Healthy Adult Males

International Journal of Exercise Science 13(3): 1729-1740, 2020. Little is known about the physiological response to the cold pressor test (CPT) when in a clinically-induced state of autonomic nervous system (ANS) imbalance, despite its utility in various disease- and injury-states. To date, research in this area is limited to acute aerobic and isometric exercise, with a paucity of research investigating the effects of anaerobic exercise on the physiological response to the CPT. Therefore, the purpose of our study was to assess the effects of the Wingate anaerobic cycle test (WAT) on cardiovascular (CV) and metabolic recovery following the CPT in a group of healthy adult males. A pre-post intervention study was conducted, whereby 10 healthy adult males (age = 29 ± 4 years, height = 182 ± 7 cm, mass = 83 ± 9 kg) completed a baseline cold pressor test (CPT-only) and a follow-up cold pressor test preceded by a Wingate anaerobic exercise test (WAT+CPT). Recovery slopes for various CV and metabolic variables, including heart rate (HR), blood pressure (BP), and relative oxygen consumption (O2) were analyzed using single-subject analysis, with celeration line slopes calculated for all participants in the CPT-only and WAT+CPT testing sessions. Celeration line slopes were compared between testing sessions using paired t-tests. No differences were identified for recovery slopes for HR (p = .295), diastolic BP (p = .300), and relative O2 (p= .176) when comparing CPT-only and WAT+CPT testing sessions. Our results suggest that the CPT elicits a CV and metabolic response beyond that elicited solely by an acute bout of anaerobic exercise. As such, the CPT may be able to serve as a surrogate test for anaerobic exercise for individuals where high-intensity exercise may be contraindicated. Future research is warranted however, as the specific physiological mechanisms governing the observed responses have yet to be elucidated

Molecular pathways leading to loss of skeletal muscle mass in cancer cachexia can findings from animal models be translated to humans?

Background: Cachexia is a multi-factorial, systemic syndrome that especially affects patients with cancer of the gastrointestinal tract, and leads to reduced treatment response, survival and quality of life. The most important clinical feature of cachexia is the excessive wasting of skeletal muscle mass. Currently, an effective treatment is still lacking and the search for therapeutic targets continues. Even though a substantial number of animal studies have contributed to a better understanding of the underlying mechanisms of the loss of skeletal muscle mass, subsequent clinical trials of potential new drugs have not yet yielded any effective treatment for cancer cachexia. Therefore, we questioned to which degree findings from animal studies can be translated to humans in clinical practice and research. Discussion: A substantial amount of animal studies on the molecular mechanisms of muscle wasting in cancer cachexia has been conducted in recent years. This extensive review of the literature showed that most of their observations could not be consistently reproduced in studies on human skeletal muscle samples. However, studies on human material are scarce and limited in patient numbers and homogeneity. Therefore, their results have to be interpreted critically. Summary: More research is needed on human tissue samples to clarify the signaling pathways that lead to skeletal muscle loss, and to confirm pre-selected drug targets from animal models in clinical trials. In addition, improved diagnostic tools and standardized clinical criteria for cancer cachexia are needed to conduct standardized, randomized controlled trials of potential drug candidates in the future

Exercise-induced increases in the expression and activity of cardiac sarcoplasmic reticulum calcium-ATPase 2 (SERCA2) is attenuated in AMPKα2 kinase-dead mice

Exercise enhances cardiac sarcoplasmic reticulum Ca2+-ATPase 2a (SERCA2a) function through unknown mechanisms. The present study tested the hypothesis that the positive effects of exercise on SERCA2a expression and function in the left ventricle is dependent on adenosine-monophosphate-activated protein kinase (AMPK) α2 function. AMPKα2 kinase-dead (KD) transgenic mice, which overexpress inactivated AMPKα2 subunit, and wild-type C57Bl/6 (WT) mice were randomized into sedentary groups or groups with access to running wheels. After 5 months, exercised KD mice exhibited shortened deceleration time compared with sedentary KD mice. In left ventricular tissue, the ratio of phosphorylated AMPKαThr172:total AMPKα was 65% lower (P < 0.05) in KD mice compared with WT mice. The left ventricle of KD mice had 37% lower levels of SERCA2a compared with WT mice. Although exercise increased SERCA2a protein levels in WT mice by 53%, this response of exercise was abolished in exercised KD mice. Exercise training reduced total phospholamban protein content by 23% in both the WT and KD mice but remained 20% higher overall in KD mice. Collectively, these data suggest that AMPKα influences SERCA2a and phospholamban protein content in the sedentary and exercised heart, and that exercise-induced changes in SERCA2a protein are dependent on AMPKα function.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author