Perceptions of academic preparedness of first-gen freshmen in a physiology major inform recommendations for program-level academic development initiatives.

Many factors contribute to students' academic success, and some, including first-generation (FG) college student status and academic preparation, are especially relevant in physiology programs. The purpose of this qualitative study was to examine FG college students' perceptions of academic preparedness and intended success strategies with the goal of informing program-level strategies to support FG students in similar undergraduate physiology-related programs. FG freshmen completed short surveys and reflections at the start and end of the semester. Qualitative responses from written reflections were compiled, and content was analyzed. Students were high achievers in high school; 98% expected As and Bs in college, but only 53% had achieved this by the end of the first semester. At the start of the semester, FG students reported feeling prepared academically but were hoping to improve their academic readiness skills, and academic success plans focused on organizational strategies. At the end of the semester, some thought they were as prepared as they expected, but most found they were not as academically prepared for college as they had expected. Several minor themes were identified as areas to address with future cohorts. This study proposes several potential avenues by which to support FG freshmen's academic success in similar physiology programs, including early identification of at-risk students, setting realistic expectations, educating students early and often about evidence-based strategies, and developing academic recovery strategies as needed.NEW & NOTEWORTHY A qualitative investigation of first-generation (FG) college freshmen's perceptions of academic preparedness and intended success strategies informs the development of potential avenues by which to support FG freshmen in physiology programs.

Resveratrol Enhances Exercise-Induced Cellular and Functional Adaptations of Skeletal Muscle in Older Men and Women.

Older men (n = 12) and women (n = 18) 65-80 years of age completed 12 weeks of exercise and took either a placebo or resveratrol (RSV) (500 mg/d) to test the hypothesis that RSV treatment combined with exercise would increase mitochondrial density, muscle fatigue resistance, and cardiovascular function more than exercise alone. Contrary to our hypothesis, aerobic and resistance exercise coupled with RSV treatment did not reduce cardiovascular risk further than exercise alone. However, exercise added to RSV treatment improved the indices of mitochondrial density, and muscle fatigue resistance more than placebo and exercise treatments. In addition, subjects that were treated with RSV had an increase in knee extensor muscle peak torque (8%), average peak torque (14%), and power (14%) after training, whereas exercise did not increase these parameters in the placebo-treated older subjects. Furthermore, exercise combined with RSV significantly improved mean fiber area and total myonuclei by 45.3% and 20%, respectively, in muscle fibers from the vastus lateralis of older subjects. Together, these data indicate a novel anabolic role of RSV in exercise-induced adaptations of older persons and this suggests that RSV combined with exercise might provide a better approach for reversing sarcopenia than exercise alone.

Improved arterial-ventricular coupling in metabolic syndrome after exercise training: a pilot study.

PURPOSE: The metabolic syndrome (MetS) is associated with threefold increased risk of cardiovascular (CV) morbidity and mortality, which is partly due to a blunted CV reserve capacity, reflected by a reduced peak exercise left ventricular (LV) contractility and aerobic capacity and a blunted peak arterial-ventricular coupling. To date, no study has examined whether aerobic exercise training in MetS can reverse peak exercise CV dysfunction. Furthermore, examining how exercise training alters CV function in a group of individuals with MetS before the development of diabetes and/or overt CV disease can provide insights into whether some of the pathophysiological CV changes can be delayed/reversed, lowering their CV risk. The objective of this study was to examine the effects of 8 wk of aerobic exercise training in individuals with MetS on resting and peak exercise CV function. METHODS: Twenty participants with MetS underwent either 8 wk of aerobic exercise training (MetS-ExT, n = 10) or remained sedentary (MetS-NonT, n = 10) during this period. Resting and peak exercise CV function was characterized using Doppler echocardiography and gas exchange. RESULTS: Exercise training did not alter resting LV diastolic or systolic function and arterial-ventricular coupling in MetS. In contrast, at peak exercise, an increase in LV contractility (40%, P < 0.01), cardiac output (28%, P < 0.05), and aerobic capacity (20%, P < 0.01), but a reduction in vascular resistance (30%, P < 0.05) and arterial-ventricular coupling (27%, P < 0.01), were noted in the MetS-ExT but not in the MetS-NonT group. Furthermore, an improvement in lifetime risk score was also noted in the MetS-ExT group. CONCLUSIONS: These findings have clinical importance because they provide insight that some of the pathophysiological changes associated with MetS can be improved and can lower the risk of CV disease.

Aerobic exercise training reduces arterial stiffness in metabolic syndrome.

The metabolic syndrome (MetS) is associated with a threefold increase risk of cardiovascular disease (CVD) mortality partly due to increased arterial stiffening. We compared the effects of aerobic exercise training on arterial stiffening/mechanics in MetS subjects without overt CVD or type 2 diabetes. MetS and healthy control (Con) subjects underwent 8 wk of exercise training (ExT; 11 MetS and 11 Con) or remained inactive (11 MetS and 10 Con). The following measures were performed pre- and postintervention: radial pulse wave analysis (applanation tonometry) was used to measure augmentation pressure and index, central pressures, and an estimate of myocardial efficiency; arterial stiffness was assessed from carotid-femoral pulse-wave velocity (cfPWV, applanation tonometry); carotid thickness was assessed from B-mode ultrasound; and peak aerobic capacity (gas exchange) was performed in the seated position. Plasma matrix metalloproteinases (MMP) and CVD risk (Framingham risk score) were also assessed. cfPWV was reduced (P < 0.05) in MetS-ExT subjects (7.9 ± 0.6 to 7.2 ± 0.4 m/s) and Con-ExT (6.6 ± 1.8 to 5.6 ± 1.6 m/s). Exercise training reduced (P < 0.05) central systolic pressure (116 ± 5 to 110 ± 4 mmHg), augmentation pressure (9 ± 1 to 7 ± 1 mmHg), augmentation index (19 ± 3 to 15 ± 4%), and improved myocardial efficiency (155 ± 8 to 168 ± 9), but only in the MetS group. Aerobic capacity increased (P < 0.05) in MetS-ExT (16.6 ± 1.0 to 19.9 ± 1.0) and Con-ExT subjects (23.8 ± 1.6 to 26.3 ± 1.6). MMP-1 and -7 were correlated with cfPWV, and both MMP-1 and -7 were reduced post-ExT in MetS subjects. These findings suggest that some of the pathophysiological changes associated with MetS can be improved after aerobic exercise training, thereby lowering their cardiovascular risk.

Exercise reveals impairments in left ventricular systolic function in patients with metabolic syndrome.

Metabolic syndrome (MetS) is the manifestation of a cluster of cardiovascular risk factors and is associated with a threefold increase in the risk of cardiovascular morbidity and mortality, which is suggested to be mediated, in part, by resting left ventricular (LV) systolic dysfunction. However, to what extent resting LV systolic function is impaired in MetS is controversial, and there are no data indicating whether LV systolic function is impaired during exercise. Accordingly, the objective of this study was to examine comprehensively the LV and arterial responses to exercise in individuals with MetS without diabetes and/or overt cardiovascular disease in comparison to a healthy control population. Cardiovascular function was characterized using Doppler echocardiography and gas exchange in individuals with MetS (n = 27) versus healthy control subjects (n = 20) at rest and during peak exercise. At rest, individuals with MetS displayed normal LV systolic function but reduced LV diastolic function compared with healthy control subjects. During peak exercise, individuals with MetS had impaired contractility, pump performance and vasodilator reserve capacity versus control subjects. A blunted contractile reserve response resulted in diminished arterial-ventricular coupling reserve and limited aerobic capacity in individuals with MetS versus control subjects. These findings are of clinical importance, because they provide insight into the pathophysiological changes in MetS that may predispose this population of individuals to an increased risk of cardiovascular morbidity and mortality.

Resistance exercise reduces skeletal muscle cachexia and improves muscle function in rheumatoid arthritis.

Rheumatoid arthritis (RA) is a chronic, systemic, autoimmune, inflammatory disease associated with cachexia (reduced muscle and increased fat). Although strength-training exercise has been used in persons with RA, it is not clear if it is effective for reducing cachexia. A 46-year-old woman was studied to determine: (i) if resistance exercise could reverse cachexia by improving muscle mass, fiber cross-sectional area, and muscle function; and (2) if elevated apoptotic signaling was involved in cachexia with RA and could be reduced by resistance training. A needle biopsy was obtained from the vastus lateralis muscle of the RA subject before and after 16 weeks of resistance training. Knee extensor strength increased by 13.6% and fatigue decreased by 2.8% Muscle mass increased by 2.1%. Average muscle fiber cross-sectional area increased by 49.7%, and muscle nuclei increased slightly after strength training from 0.08 to 0.12 nuclei/µm(2). In addition, there was a slight decrease (1.6%) in the number of apoptotic muscle nuclei after resistance training. This case study suggests that resistance training may be a good tool for increasing the number of nuclei per fiber area, decreasing apoptotic nuclei, and inducing fiber hypertrophy in persons with RA, thereby slowing or reversing rheumatoid cachexia.

Myogenin and oxidative enzyme gene expression levels are elevated in rat soleus muscles after endurance training.

The intent of this study was to determine whether endurance exercise training regulates increases in metabolic enzymes, which parallel modulations of myogenin and MyoD in skeletal muscle of rats. Adult Sprague-Dawley rats were endurance trained (TR) 5 days weekly for 8 wk on a motorized treadmill. They were killed 48 h after their last bout of exercise. Sedentary control (Con) rats were killed at the same time as TR animals. Myogenin, MyoD, citrate synthase (CS), cytochrome-c oxidase (COX) subunits II and VI, lactate dehydrogenase (LDH), and myosin light chain mRNA contents were determined in soleus muscles by using RT-PCR. Myogenin mRNA content was also estimated by using dot-blot hybridization. Protein expression levels of myogenin and MyoD were measured by Western blots. CS enzymatic activity was also measured. RT-PCR measurements showed that the mRNA contents of myogenin, CS, COX II, COX VI, and LDH were 25, 20, 17, 16, and 18% greater, respectively, in TR animals compared with Con animals (P < 0.05). The ratio of myogenin to MyoD mRNA content estimated by RT-PCR in TR animals was 28% higher than that in Con animals (P < 0.05). Myosin light chain expression was similar in Con and TR muscles. Results from dot-blot hybridization to a riboprobe further confirmed the increase in myogenin mRNA level in TR group. Western blot analysis indicated a 24% greater level of myogenin protein in TR animals compared with Con animals (P < 0.01). The soleus muscles from TR animals had a 25% greater CS enzymatic activity than the Con animals (P < 0.01). Moreover, myogenin mRNA and protein contents were positively correlated to CS activity and mRNA contents of CS, COX II, and COX VI (P < 0.05). These data are consistent with the hypothesis that myogenin is in the pathway for exercise-induced changes in mitochondrial enzymes.

Citrate synthase expression and enzyme activity after endurance training in cardiac and skeletal muscles.

The present study was designed to examine the acute and chronic effects of endurance treadmill training on citrate synthase (CS) gene expression and enzymatic activity in rat skeletal and cardiac muscles. Adult rats were endurance trained for 8 wk on a treadmill. They were killed 1 h (T(1), n = 8) or 48 h (T(48), n = 8) after their last bout of exercise training. Eight rats were sedentary controls (C) during the training period. CS mRNA levels and enzymatic activities of the soleus and ventricle muscles were determined. Training resulted in higher CS mRNA levels in both the soleus muscles (21% increase in T(1); 18% increase in T(48), P < 0.05) and ventricle muscles (23% increase in T(1); 17% increase in T(48), P < 0.05) when compared with the C group. The CS enzyme activities were 42 (P < 0.01) and 25% (P < 0.01) greater in the soleus muscles of T(1) and T(48) groups, respectively, when compared with that of the C group. Soleus CS enzyme activity was significantly greater in the T(1) vs. T(48) groups (P < 0.05). However, no appreciable alterations in CS enzyme activities were observed in the ventricle muscles in both training groups. These findings suggest differential responses of skeletal and cardiac muscles in CS enzymatic activity but similar responses in CS gene expression at 1 and 48 h after the last session of endurance training. Moreover, our data support the existence of an acute effect of exercise on the training-induced elevation in CS activity in rat soleus but not ventricle muscles.