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Background/Objectives: Glucose metabolism and hormonal responses are largely affected by exercise intensity, which exhibits an alternating pattern in many sports activities. The aim of this study was to investigate and compare glycemic and hormonal responses during and after exercise of constant (CON) and alternating (ALT) intensity with the same duration and total work. Methods: Ten healthy male volunteers performed two, 60 min cycling exercise bouts in random order: the ALT bout, where exercise intensity alternated between 46.5 ± 1.9% of VO2max for 40 s and 120% of VO2max for 20 s, so the mean intensity was at 105% of the lactate threshold (LT), and the CON exercise bout, where the intensity was constant at 105% of LT (70 ± 4.7% of VO2max). Results: No significant differences were observed in blood glucose concentrations between the two exercise protocols (p = 0.22) or over time at any time point measured, i.e., before, at 30 and 60 min of each exercise bout, and 60 min post-exercise (p > 0.05). Circulating insulin levels decreased significantly over time in both protocols (p < 0.01 and p < 0.05 in ALT and CON, respectively); nevertheless, they did not differ between the exercise protocols (p = 0.45). Similarly, there were no significant differences in serum leptin and prolactin levels between the two protocols (p = 0.77 and p = 0.80 in ALT and CON, respectively); however, circulating levels of leptin decreased at 30 and 60 min of exercise only in CON (p < 0.05) and those of prolactin at 60 min of exercise only in ALT (p < 0.05) compared to pre-exercise values. Conclusions: Cycling exercise of constant or alternating moderate intensity (~70% of VO2max) with the same duration induces similar glycemic but differential over time hormonal responses in healthy males. [ABSTRACT FROM AUTHOR]

Background/Objectives: There is a growing interest in the research of wound healing mechanisms worldwide. Particular attention has been paid to the expression of tissue remodeling- and inflammation-related factors. Herein, we investigate the expression patterns of TGF-β1, IL-6, TNF-a, uPA, uPA receptors, MMP-2, and MMP-9 through the four phases of the normal wound-healing process in humans. Methods: Twenty-two individuals presenting with a first episode of pilonidal sinus underwent surgical excision and the wound was left to heal by secondary intention. Sequential biopsies were collected on day 0 (operation), day 2 (inflammatory phase), day 9 (proliferative phase), and day 14 (tissue remodeling phase). The expression levels of the proteins were evaluated using reverse transcription–quantitative PCR. Statistical analyses were performed using GraphPad Prism software. One-way analysis of variance (ANOVA) with Dunn's Multiple Comparison post hoc test was used. Results: The results showed statistically significant differences in the expressions of the factors during wound healing (p < 0.05). TGF-b1 increased on days 2 and 9. TNF-a increased on day 2 and then decreased on day 9. Il-6 was increased on day 2 and decreased on days 9 and 14. uPa mRNA increased up to day 9 but its receptor exhibited high expression throughout the observation time. Finally, MMP-2 mRNA expression increased on day 2 and declined on days 9 and 14, while MMP-9 was highly expressed until the 14th postoperative day. Conclusions: Each factor investigated in this study has an important and distinct role in the normal wound repair procedure. Further investigation is required to evaluate the tissue-specific regulation of these factors and their potential use as therapeutic targets or prognostic biomarkers in wound healing. [ABSTRACT FROM AUTHOR]

Background/Objectives: Mitochondria are the main organelles for ATP synthesis able to produce energy for several different cellular activities. Cardiac cells require high amounts of energy and, thus, they contain a high number of mitochondria. Consequently, mitochondrial dysfunction in these cells is a crucial factor for the development of cardiovascular diseases. Mitochondria constitute central regulators of cellular metabolism and energy production, producing approximately 90% of the cells' energy needs in the form of ATP via oxidative phosphorylation. The mitochondria have their own circular, double-stranded DNA encoding 37 genes. Any mitochondrial DNA sequence anomaly may result in defective oxidative phosphorylation and lead to cardiac dysfunction. Methods: In this study, we investigated the potential association between mitochondrial DNA mutation and cardiovascular disease. Cardiac tissue and serum samples were collected from seven patients undergoing coronary artery bypass grafting. Total DNA was extracted from cardiac muscle tissue specimens and serum and each sample was subjected to polymerase chain reaction (PCR) to amplify the NADH dehydrogenase 1 (ND1) gene, which is part of the mitochondrial complex I enzyme complex and was screened for mutations. Results: We identified one patient with a homoplasmic A to G substitution mutation in cardiac tissue DNA and two patients with heteroplasmic A3397G mutation in serum DNA. Specifically, amplicon sequence analysis revealed a homoplasmic A3397G substitution in the ND1 gene in a tissue sample of the patient with ID number 1 and a heteroplasmic mutation in A3397G in serum samples of patients with ID numbers 3 and 6, respectively. The A to G substitution changes the amino acid from methionine (ATA) to valine (GTA) at position 31 of the ND1 gene. Conclusions: The detection of this novel mutation in patients with coronary artery disease may contribute to our understanding of the association between mitochondrial dysfunction and the disease, implying that mitochondria may be key players in the pathogenesis of cardiovascular diseases. [ABSTRACT FROM AUTHOR]

Skeletal muscle and bone rely on a number of growth factors to undergo development, modulate growth, and maintain physiological strength. A major player in these actions is insulin-like growth factor I (IGF-I). However, because this growth factor can directly enhance muscle mass and bone density, it alters the state of the musculoskeletal system indirectly through mechanical crosstalk between these two organ systems. Thus, there are clearly synergistic actions of IGF-I that extend beyond the direct activity through its receptor. This review will cover the production and signaling of IGF-I as it pertains to muscle and bone, the chemical and mechanical influences that arise from IGF-I activity, and the potential for therapeutic strategies based on IGF-I. This article is part of a Special Issue entitled "Muscle Bone Interactions".