Psychosocial Functioning in Women with Symptoms of Persistent Genital Arousal

Persistent genital arousal disorder (PGAD) is characterized by physiological sexual arousal (vasocongestion, sensitivity of the genitals and nipples) that is described as distressing, and sometimes painful. Although awareness of PGAD is growing, there continues to be a lack of systematic research on this condition. The vast majority of published reports are case studies. Little is known about the symptom characteristics, biological factors, or psychosocial functioning associated with the experience of persistent genital arousal (PGA) symptoms. This study sought to characterize a sample of women with PGA (Study One); compare women with and without PGA symptoms on a series of biopsychosocial factors (Study Two); and undertake an exploratory comparison of women with PGA, painful PGA, and genital pain (Study Three)—all within a biopsychosocial framework. Symptom-free women, women with PGA symptoms, painful PGA, and genital pain, completed an online survey of biological factors (medical history, symptom profiles), psychological factors (depression, anxiety) and social factors (sexual function, relationship satisfaction). Study One found that women report diverse symptoms associated with PGA, with almost half reporting painful symptoms. In Study Two, women with symptoms of PGA reported significantly greater impairment in most domains of psychosocial functioning as compared to symptom-free women. In particular, catastrophizing of vulvar sensations was related to symptom ratings (i.e., greater severity, distress) and psychosocial outcomes (i.e., greater depression and anxiety). Finally, Study Three found that women with PGA symptoms reported some overlap in medical comorbidities and symptom expression as those with combined PGA and vulvodynia and those with vulvodynia symptoms alone; however, there were also a number of significant differences in their associated physical symptoms. These studies indicate that PGA symptoms have negative consequences for the psychosocial functioning of affected women. As such, future research and clinical care may benefit from a biopsychosocial approach to PGA symptoms. These studies highlight areas for more targeted research, including the role of catastrophizing in PGA symptom development and maintenance, and the potential conceptualization of both PGA and vulvodynia (and potentially other conditions) under a general umbrella of ‘genital paraesthesias’ (i.e., disorders characterized by abnormal sensations, such as tingling and burning).

The relationship between changes in cardiovascular function and changes in VO2peak following SIT

Background: It is well known that sprint interval training (SIT), induces significant increases in peak oxygen uptake (VO2peak) at the group level. However, there have been only a few studies that have addressed the variability of VO2peak response following SIT, and precise mechanism(s) that may explain individual magnitude of response are unknown. Purpose: Therefore, the purpose of this thesis was to: 1) examine the inter-individual variability of the VO2peak response following SIT, 2) to inspect the relationship between changes in both central and peripheral measures and changes in VO2peak, and 3) to assess if peripheral or central adaptations play a role in whether an individual is a high or low responder with respect to VO2peak. Subjects: Twenty-two young, recreationally active males (age: 20.4 1.7 years; weight: 78.4 10.2 kg; VO2peak: 3.7 0.62 L/min) Methods: VO2peak (L/min), peak cardiac output (Qpeak [L/min]), and peak deoxygenated hemoglobin (HHbpeak [mM]) were measured before and after 16 sessions of SIT (Tabata Protocol) over four weeks. Peak a-vO2diff was calculated using a derivation of the Fick equation. Results: Due to a systematic error, HHbpeak could not be used to differentiate between individual responses. There was a large range of VO2peak response from pre to post testing (-4.75 to 32.18% change) and there was a significant difference between the Low Response Group (LRG) (n=8) and the High Response Group (HRG) (n=8) [f(1, 14)= 64.27, p<0.001]. Furthermore, there was no correlation between delta () VO2peak and Qpeak (r=-0.18, p=0.46) for all participants, nor was there an interaction effect between the Low and High Response Groups [f(1,11)=0.572, p=0.47]. Lastly, there was a significant correlation between VO2peak and peak a-vO2diff [r=0.692, p<0.001], and a significant interaction effect with peak a-vO2diff [f(1, 14)= 13.27, p<0.004] when comparing the HRG to the LRG. Conclusions: There was inter-individual variability of VO2peak response following 4 weeks of SIT, but central adaptations did not influence this variation. This suggests that peripheral adaptations may be responsible for VO2peak adaptation.