Background and Objectives: Acute resistance exercise (RE) reduces vagal modulation and increases sympathovagal balance, which increases the risk for arrythmias. Few studies have examined sex differences in autonomic modulation after acute RE. The purpose of this investigation was to examine sex-specific responses to acute RE on autonomic modulation. Materials and Methods: Twenty-one resistance-trained individuals (men n = 11, women n = 10) between the ages of 19 and 25 y were analyzed for autonomic modulation in response to acute RE and a control (CON). Measures of autonomic modulation were collected at rest, 15 (R15), and 30 (R30) min following both conditions. Heart rate (HR), log transformed root mean square of successive differences (lnRMSSD), total power (lnTP), low-frequency power (lnLF), high-frequency power (lnHF), sample entropy (SampEn), and Lempel-Ziv entropy (LZEn) were measured at all time points. A three-way repeated analysis of variance (ANOVA) was used to analyze sex (men, women) across condition (RE, CON) and time (Rest, R15, R30). Results: The results are similar for all heart rate variability (HRV) variables at rest for both conditions (RE, CON). SampEn was significantly higher in men compared to women at rest for both conditions (p = 0.03), with no differences in LZEn (p > 0.05). There were no significant (p > 0.05) three-way interactions on any variables. Condition by time interactions demonstrated that both sexes increase in HR (p = 0.0001) and lnLF/HF ratio (p = 0.001), but decreases in lnRMSSD (p = 0.0001), lnTP (p < 0.0001), lnLF (p < 0.0001), lnHF (p = 0.0001), and LZEn (p = 0.009) at R15 and R30 compared to rest following acute RE and were different from CON. Condition by time interaction (p = 0.017) demonstrated that SampEn was attenuated at R15 compared to rest, and the CON, but not R30 following acute RE. Conclusion: Although SampEn is more complex at rest in men compared to women, autonomic modulation responses between sexes following acute RE appear to be similar.

Supramaximal interval exercise alters measures of autonomic modulation, while a cool-down may speed the recovery of vagal modulation. The purpose of this study was to compare the effects of a cool-down (pedaling a cycle ergometer at 50 rpm against a resistance of 45 W) versus passive recovery (no pedaling) after supramaximal interval exercise on autonomic modulation. Sixteen moderately active individuals (Mean ± SD: 23 ± 3 years (men: n = 10; women: n = 6) were assessed for autonomic modulation at Rest, and 15 (R15), 30 (R30), 45 (R45) and 60 (R60) min following supramaximal interval exercise. Linear measures of autonomic modulation included natural log (ln) total power (lnTP), high-frequency power (lnHF), the ratio of low frequency (LF) to HF ln(LF/HF) ratio, root mean square of successive differences between normal heartbeats (lnRMSSD), while non-linear measures included sample entropy (SampEn) and Lempel–Ziv entropy (LZEn). Two-way repeated ANOVAs were used to evaluate the main effects of condition (cool-down, passive recovery) across time (Rest, and R15, R30, R45 and R60). There were significant (p ≤ 0.05) condition by time interactions for SampEn and LZEn, such that they decreased at 15, 30, 45 and 60 min during passive recovery compared to Rest, with the recovery of SampEn and LZEn by 60 and 45 min, respectively, during cool-down. There were significant (p ≤ 0.05) main effects of time for lnTP, lnHF and lnRMSSD, such that lnTP, lnHF and lnRMSSD were attenuated, and lnLF/HF ratio was augmented, at all recovery times compared to Rest. These data demonstrate that a cool-down increases the recovery of nonlinear measures of vagal modulation within 45–60 min after supramaximal interval exercise, compared to passive recovery in moderately active individuals.

No abstract

No abstract

Cancer cachexia is a complex metabolic wasting disease that occurs in up to 80% of cancer patients and is responsible for about 20% of deaths in cancer patients. While research is growing, cancer cachexia remains a vastly underestimated and untreated condition. Current research shows that cardiac muscleis depleted during cancer cachexia but little research has been conducted examining the effects of sex on this phenomenon. PURPOSE: The purpose of this study was to examine the effects of sex on cardiac dysfunction during cancer cachexia and determine the underlying mechanisms responsible for this phenomenon. METHODS: Male and female LC3 Tg+ mice underwent a 3-week Lewis Lung Carcinoma (LLC; 1x10 6 in flank) protocol. Cardiac function was assessed via conscious echocardiography, and autophagic and inflammatory proteins were investigated for their possible role in cancer-mediated cardiac wasting. RESULTS: Echocardiography revealed that there was a significant (p<0.05) reduction in the fractional shortening in both males and females when comparing pre-and post-inoculation values. Furthermore, males exhibited a significantly greater degree of cardiac dysfunction compared to females after 3 weeks of tumor bearing (fractional shortening: males, -29% vs. female, -8%; P< 0.01). Autophagic flux analysis showed both male and female hearts exhibited a significant increase in late phase autolysosomes, with females exhibiting significantly (P< 0.05) more late phase puncta (P< 0.05). Similarly, tumor bearing females expressed significantly more cardiac LC3-II and FoxO3a compared to male tumor bearing mice. Interestingly, while both male and female tumor bearing groups showed increased NF-kB expression (not significant), only female tumor bearing mice exhibited a significant (P< 0.05) increase in IL-1beta expression. No significant difference in TNF-alpha levels was found when comparing tumor bearing males and females. CONCLUSION: Our data supports the idea that cardiac dysfunction is mediated by cancer cachexia and that certain autophagy and inflammatory pathways respond differently based on sex. This data can serve an important role in understanding how cancer cachexia presents and progresses differently based off sex and helps identify sex specific targets for therapeutic intervention.