Cardiorespiratory Fitness Changes Following an Unsupervised Exercise Prescription in an Executive Health Program

Heart failure (HF) is a cardiovascular disease (CVD) outcome that is associated with high morbidity and mortality as well as high healthcare costs.1 Given that HF is the end stage of most CVDs, both conditions share common risk factors such as type 2 diabetes (T2D), hypertension, smoking and obesity.2 Socioeconomic status (SES) has been recognized to have a measurable and significant effect on cardiovascular health. It has been reported that low SES may confer a cardiovascular risk that is equivalent to conventional risk factors.3 Low SES has been shown to be a powerful and independent predictor of HF development and adverse outcomes.4 Biological, behavioural and psychosocial risk factors prevalent in socioeconomically deprived individuals are known to accentuate the relationship between low SES and cardiovascular outcomes such as HF.3 These include lower levels of education, unhealthy lifestyles such as excessive alcohol consumption, limited access to health care and higher prevalence of comorbid conditions. The beneficial effects of regular physical activity (PA) and exercise in preventing vascular disease and promoting overall health are well established and documented. These benefits also extend to HF prevention.5 Though cardiorespiratory fitness (CRF) reflects habitual aerobic PA, it is a separate measure that captures the capacity of the cardiovascular and respiratory systems to supply oxygen to skeletal muscles during progressive PA or incremental exercise to volitional fatigue.6 The gold standard for CRF assessment is direct measurement of the highest attained oxygen consumption (VO2) during cardiopulmonary exercise testing. Similar to PA, high levels of CRF are strongly and independently associated with lower risk of vascular outcomes including HF.7, 8 The inverse associations between CRF and vascular outcomes have been reported to be stronger than that of traditional risk factors such as T2D and smoking; this has led to CRF being proposed as a vital sign.9 There is increasing evidence showing that higher levels of CRF can attenuate the adverse impact of other risk factors; for instance, we and others have previously shown that high CRF levels can attenuate the impact of risk factors associated with mortality,10 pneumonia11 and COVID-19 hospitalization.12 Given the evidence, we hypothesized that high CRF levels would attenuate the increased risk of HF due to low SES. To explore this, we aimed to evaluate the joint effects of SES and CRF on the risk of incident HF using a population-based prospective cohort of 1831 middle-aged Finnish men without a history of HF at baseline. We also evaluated the separate associations of SES and CRF with the risk of HF to confirm previous evidence of these associations. Reporting of the study conforms to broad EQUATOR guidelines13 and was conducted according to STROBE (STrengthening the Reporting of OBservational studies in Epidemiology) guidelines for reporting observational studies in epidemiology (Appendix S1). The current analysis is based on the Kuopio Ischaemic Heart Disease (KIHD) risk factor study, a general population-based prospective cohort study comprising of a representative sample of men aged 42–61 years recruited in eastern Finland. A detailed description of the study design, recruitment methods, risk marker assessment and physical examinations have been described previously.8 Baseline measurements were performed between 01 March 1984 and 31 December 1989. The research protocol was approved by the Research Ethics Committee of the University of Eastern Finland and written informed consent was obtained from all the participants. A self-reported questionnaire was used to assess SES, which involved a summary index that combined factors such as income, education, occupational prestige, material standard of living and housing conditions. The composite SES index ranged from 0 to 25, with higher values indicating lower SES. Maximal oxygen uptake (VO2max) was used as a measure of CRF, which was assessed using a respiratory gas exchange analyser (Medical Graphics, MCG, St. Paul, Minnesota) during cycle ergometer exercise testing.14 We excluded men with a prevalent history of HF for the current analysis. We included all HF events that occurred from study entry through to 2018. The diagnostic classification of HF cases was coded according to the ICD-10 codes. Hazard ratios (HRs) with 95% confidence intervals (CIs) for HF were calculated using Cox proportional hazard models and these were adjusted for in three models: (Model 1) age; (Model 2) Model 1 plus systolic blood pressure (SBP), body mass index (BMI), heart rate, smoking status, history of T2D, history of coronary heart disease (CHD), total cholesterol, high-density lipoprotein cholesterol (HDL-C) and PA; and (Model 3) Model 2 plus mutual adjustment for each exposure. For consistency with previous reports,10, 15 the exposures (SES and CRF) were categorized into low and high levels based on their median cutoffs. The exposures were also modelled as continuous variables given evidence of linear relationships with HF risk using multivariable restricted cubic spline curves. Evaluation of the joint association of SES and CRF with HF risk was based on the following four combinations: high SES-low CRF; low SES- low CRF; high SES-high CRF and low SES-high CRF. Tests of interaction were used to formally assess if the risk of HF due to one exposure is modified by the other exposure and vice versa. To put our findings into clinical context, we also calculated the number needed to treat (NNT) associated with high SES-high CRF using the formula proposed by Altman and Anderson16: NNT (t) =1/[SB(t))HR – SB(t)], where SB(t) denotes the Kaplan–Meir survival probability in the reference group (High SES-Low CRF) at time t and HR refers to the Cox regression estimate comparing the exposure group with the reference group. Stata version MP 16 (Stata Corp, College Station) was employed for all analyses. The overall mean (standard deviation, SD) age, SES and CRF of study participants at baseline was 52 (5) years, 8.26 (4.24) and 30.8 (7.9) ml/kg/min, respectively (Table 1). There were significant differences in baseline characteristics between low and high CRF groups. Overall Mean (SD) or median (IQR) or n (%) High CRF Mean (SD) or median (IQR) or n (%) Low CRF Mean (SD) or median (IQR) or n (%) During a median (interquartile range) follow-up of 27.3 (18.6–31.2) years, 364 incident HF cases occurred. In an analysis adjusted for age, SBP, BMI, heart rate, smoking status, history of T2D, history of CHD, total cholesterol, HDL-C and PA, low compared with high SES was associated with an increased risk of HF 1.43 (95% CI: 1.15–1.79), which remained similar on further adjustment for CRF. On adjustment for the confounders as above, high CRF was associated with a decreased risk of HF compared with low CRF 0.70 (95% CI: 0.55–0.89), which remained similar on additional adjustment for SES. There was evidence of significant associations when both exposures were modelled as continuous variables (Table 2). Restricted cubic spline curves with adjustment for age, SBP, BMI, heart rate, smoking status, history of T2D, history of CHD, total cholesterol, HDL-C and PA showed that HF risk increased continuously with decreasing SES across the range 7–19 (p-value for nonlinearity =.83) (Figure 1A), whereas HF risk decreased continuously with increasing CRF across the range 18–58 ml/kg/min (p-value for nonlinearity =.79) (Figure 1B). The spline curves were qualitatively similar in subgroups of CRF and SES (Figure 2). In multivariable analysis, low SES-low CRF was associated with an increased HF risk 1.32 (95% CI: 1.01–1.74), high SES-high CRF with a decreased HF risk 0.62 (95% CI: 0.43–0.89), with no evidence of an association for low SES-high CRF and HF risk 1.01 (95% CI: 0.73–1.39) when compared with men with high SES-low CRF (Table 2). The association of SES with HF risk was not modified by CRF (p-value for interactions >.10) and neither was the association between CRF and HF risk modified by SES (p-value for interactions >.10), when both exposures were modelled as continuous or categorical variables (Figure 3). The absolute risk reduction of HF associated with high SES-high CRF was 0.21 during the entire duration of follow-up, which translated into a NNT of 10 (95% CI: 6–35) to prevent one HF. Our results based on a general population-based prospective cohort study of middle-aged to older Finnish men confirms the previously reported independent associations of low SES with increased HF risk and high CRF levels with lowered risk of HF. The associations were also potentially consistent with graded dose-response relationships. Evaluation of the joint associations of SES and CRF with HF risk showed that increased CRF levels appeared to attenuate the increased risk of HF associated with low SES. However, formal tests showed no significant evidence of interactive effects of SES and CRF on the long-term risk of HF, suggesting the effect of each exposure on HF risk may be independent of the other. Given the low sample size and event rates in the exposure categories, studies with larger samples are needed to confirm or refute potential interactive effects of SES and CRF on HF risk. Finally, our findings suggest that the NNT for high aerobic fitness levels and high SES to prevent a HF event over long-term follow-up ranged from 6 to 35 in approximately healthy middle-aged to older men. The interaction between SES and HF has been reported to be complex and the precise mechanisms accounting for the association between low SES and increased HF risk remain elusive.4 Socioeconomic differences in potential aetiological risk factors such as alcohol consumption, hypertension and systemic inflammation, have been reported to contribute to the risk. Social deprivation is also associated with lower rates of treatment, dose and adherence to therapy for, and delayed presentation of hypertension, diabetes and CHD,4 which consequently lead to HF. Psychosocial factors such as stress and depression, which are strongly associated with cardiovascular outcomes, also disproportionately affect individuals of low SES.3 Though CRF is determined by many non-modifiable factors such as age, sex and heritability, it remains a modifiable risk factor. The most established methods of increasing CRF are via exercise training and increased PA.9 Greater PA and exercise reduce HF risk through various mechanisms including (i) reducing the prevalence of standard and novel cardiovascular risk factors such as hypertension, obesity, blood glucose and coronary artery disease; (ii) preventing adverse changes in cardiac structure and function; (iii) promoting physiologic remodelling and (iv) improving cardiac, neurohormonal, skeletal muscle, pulmonary, renal and vascular performance.5 These findings may have important clinical implications. They add to the overwhelming evidence on the benefits of high CRF levels (via regular aerobic PA) on chronic diseases and their potential ability to attenuate the adverse effects of traditional risk factors. Despite guideline recommendations and population-wide strategies to promote PA levels, most populations do not achieve general PA recommendations. Populations at high cardiovascular risk including the socioeconomically deprived need more education on the substantial benefits of PA. Furthermore, there should be widened access to PA resources that are both feasible and attractive for these populations. This is the first evaluation of the separate and joint associations of SES and CRF with HF risk. We also assessed the nature of the dose-response relationships of the exposures with HF risk. Other strengths of this analysis included the use of a prospective cohort design with exclusion of men with pre-existing HF, the long-term follow-up duration of the cohort and the use of a gold standard measure of CRF. Limitations deserving consideration included the relatively low sample size due to the categorization of exposures, use of self-administered questionnaires in assessing SES, findings may only be generalizable to middle-aged and older northern European men and potential for biases such as residual confounding and regression dilution bias. In a general male Finnish population, both SES and CRF were each independently associated with HF risk, potentially consistent with graded dose-response relationships. High levels of CRF may attenuate the increased risk of HF due to low SES, but further study is needed to confirm if there are true interactive effects of SES and CRF on the long-term risk of HF. The authors thank the staff of the Kuopio Research Institute of Exercise Medicine and the Research Institute of Public Health and University of Eastern Finland, Kuopio, Finland for the data collection in the study. J.A.L. acknowledges support from The Finnish Foundation for Cardiovascular Research, Helsinki, Finland. These sources had no role in design and conduct of the study; collection, management, analysis and interpretation of the data; and preparation, review or approval of the manuscript. No potential conflict of interest was reported by the authors. S.K.K.: Study design, data analysis and interpretation, drafting manuscript, and revising manuscript content and approving final version of manuscript; S.Y.J.: Study design and revising manuscript content and approving final version of manuscript; T.H.M: Study design and revising manuscript content and approving final version of manuscript; J.A.L.: Study design and conduct, responsibility for the patients and data collection, and revising manuscript content and approving final version of manuscript. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

Are We There Yet? Pediatric Screening for Inflammatory Biomarkers and Low Cardiorespiratory Fitness to Identify Youth at Increased Risk of Cardiovascular Disease

The Interplay of Type 2 Diabetes Status, Cardiorespiratory Fitness Level, and Sudden Cardiac Death: A Prospective Cohort Study

Association of Increased Cardiorespiratory Fitness with Low Risk for Clustering of Metabolic Syndrome Components in Asymptomatic Men

Both baseline cardiorespiratory fitness and adiposity predict the risk of cancer mortality. However, the effects of changes in these two factors over time have not been evaluated thoroughly. The aim of this study was to examine the independent and joint associations of changes in cardiorespiratory fitness and body composition on cancer mortality. The cohort consisted of 13,930 men (initially cancer-free) with two or more medical examinations from 1974 to 2002. Cardiorespiratory fitness was assessed by a maximal treadmill exercise test, and body composition was expressed by body mass index (BMI) and percent body fat. Changes in cardiorespiratory fitness and body composition between the baseline and the last examination were classified into loss, stable, and gain groups. There were 386 deaths from cancer during an average of 12.5 yr of follow-up. After adjusting for possible confounders and BMI, change hazard ratios (95% confidence intervals) of cancer mortality were 0.74 (0.57-0.96) for stable fitness and 0.74 (0.56-0.98) for fitness gain. Inverse dose-response relationships were observed between changes in maximal METs and cancer mortality (P for linear trend = 0.05). Neither BMI change nor percent body fat change was associated with cancer mortality after adjusting for possible confounders and maximal METs change. In the joint analyses, men who became less fit had a higher risk of cancer mortality (P for linear trend = 0.03) compared with those who became more fit, regardless of BMI change levels. Being unfit or losing cardiorespiratory fitness over time was found to predict cancer mortality in men. Improving or maintaining adequate levels of cardiorespiratory fitness appears to be important for decreasing cancer mortality in men.

Both excess visceral adipose tissue (VAT) and low cardiorespiratory fitness (CRF) levels are associated with a deteriorated cardiometabolic risk profile. The aim of the study was to examine the respective contributions of changes in VAT accumulation vs. changes in CRF to 6-yr longitudinal changes in cardiometabolic risk markers. We conducted a prospective, population-based study with an average follow-up of 5.9 ± 0.8 yr. We followed 132 middle-aged participants from the Quebec Family Study (mean age, 35.3 ± 13.9 yr). VAT was measured by computed tomography, whereas the level of CRF was assessed by a submaximal physical working capacity test at baseline and at follow-up. A complete cardiometabolic risk profile, including systolic and diastolic blood pressure, fasting glucose and insulin levels, C-reactive protein (n = 72), as well as a standard lipoprotein-lipid profile, was obtained at baseline and at follow-up. We measured changes in CRF, VAT, and cardiometabolic risk profile over 6 yr. After adjusting for age and sex, 6-yr changes in VAT were negatively correlated with changes in CRF (r = -0.38; P < 0.001). In a multivariate model that included age, sex, changes in VAT, changes in CRF, as well as baseline levels of the above cardiometabolic risk factors, 6-yr changes in VAT were the most important predictor of the change in the metabolic syndrome score (R(2) = 13.2%; P < 0.001). Adding 6-yr changes in CRF levels significantly improved the predictability of the model (R(2) = 19.7%; P = 0.002). Changes in both VAT and CRF levels observed over 6 yr are associated with changes in parameters of the lipoprotein-lipid profile, glucose-insulin homeostasis, and inflammatory markers. Thus, maintaining a low level of VAT and a high level of CRF are important targets for maintenance of cardiometabolic health.

Competing Impact of Excess Weight Versus Cardiorespiratory Fitness on Cardiovascular Risk

Evaluation of Metabolic Risk in Prepubertal Girls Versus Boys in Relation to Fitness and Physical Activity

Introduction: There is a strong inverse association between cardiorespiratory fitness (CRF) and mortality outcomes. This relationship has predominantly been assessed cross-sectionally, however low CRF is a modifiable risk factor, thus assessing this association using a single baseline measure may be sub-optimal. The primary purpose of this research was to examine the association of the long-term change in CRF, measured using cardiopulmonary exercise testing (CPX) with all-cause and disease-specific mortality. Methods: Participants included 833 apparently healthy men and women (42.9±10.8 y) who underwent two maximal CPXs, the second CPX being ≥ 1 year following the baseline assessment. Participants were followed for 17.7 ± 11.8 years for all-cause, cardiovascular disease (CVD), and cancer mortality. Cox-proportional hazard models were performed to determine the association between the change in CRF, computed as visit 1 (V1) peak oxygen consumption (VO 2peak (ml·kg -1· min -1 )) - visit 2 (V2) VO 2peak , and mortality outcomes. Results: During follow-up, 172 participants died. Overall, the change in CPX-derived CRF was inversely related to all-cause, CVD, and cancer mortality (p&lt;0.05). Each 1 ml·kg -1· min -1 increase was associated with a 10.8, 14.7, and 15.9% reductions in all-cause, CVD, and cancer mortality, respectively. The inverse relationship between CRF and all-cause mortality remained significant (p&lt;0.05) when men and women were examined independently, after adjusting for years since first CPX, baseline VO 2peak , and age. Conclusions: Long-term changes in CRF were inversely related to mortality outcomes, and mortality was better predicted by CRF measured at subsequent examination than baseline CRF. These findings support the recent American Heart Association scientific statement advocating CRF as a clinical vital sign that should be assessed routinely in clinical practice, as well as support regular participation in physical activity to maintain adequate CRF levels across the lifespan.

ObjectivesThis individual participant data meta-analysis investigates the association between occupational physical activity (OPA) and both cardiovascular mortality and all-cause mortality across different cardio-respiratory fitness (CRF) groups among male workers.MethodsData were pooled from five European cohort studies. OPA was categorized into three levels and CRF into low, moderate, and high tertiles. OPA was assessed using self-reports and CRF through objective measurements. Two-stage meta-analyses were conducted. First, we analyzed each cohort using Cox-regression models then we pooled results with random effects model to evaluate the associations between OPA and both cardiovascular and all-cause mortality, stratified by CRF. Models were adjusted for age, body mass index, smoking status, leisure-time physical activity, and educational level.ResultsAmong 9922 men (mean age 46.8, standard deviation 6.7, years), 55.7% died during an average 25.6-year follow-up, of which 29.3% died from cardiovascular causes. Individuals with low CRF and high levels of OPA showed increased risks of cardiovascular [hazard ratio (HR) 1.27, 95% confidence interval (CI) 1.04–1.55] and all-cause mortality (HR 1.22, 95% CI 1.07–1.40) compared to those with low CRF and low levels of OPA. High CRF mitigated cardiovascular mortality risk (HR 1.08, 95% CI 0.79–1.48) but not all-cause mortality (HR 1.27, 95% CI 0.98–1.83) for those with high OPA.ConclusionsOur findings for cardiovascular mortality suggest that high CRF levels may protect workers with physically demanding jobs from adverse cardiovascular outcomes, supporting the ‘fit for work’ principle. However, this protective effect was not observed for all-cause mortality.

Increased glucose levels above a threshold of 4.9 mmol/L are associated with a greater risk of cardiovascular disease (CVD). The menopause has been associated with impaired glucose control, including poor glucose tolerance, increased glycosylated haemoglobin (HbA1C) and fasting insulin concentration. The positive effect of increased cardio-respiratory fitness (CRF) upon glucose control in postmenopausal women (PM-women) is unclear. PURPOSE: To determine the effects of CRF upon glucose control in PM-women. METHODS: CRF was assessed via Bruce treadmill test in 79 sedentary-to-moderately active and 10 marathon running (MR) PM-women. Sedentary-to-moderately active women were classified into low, medium or high CRF levels according to VO2 peak, MR were a separate group. Assessment of glucose control included analysis of fasting venous glucose and insulin (thus the homeostasis model assessment (HOMA)) and HbA1c concentrations The following additional CVD risk factors were assessed: body composition (skinfold analysis/waist and hip circumferences, BMI and body mass), flow mediated dilation (reactive hyperaemia) as an index of endothelial function, total cholesterol, high and low density lipoproteins, triglycerides and high sensitivity C-reactive protein (hsCRP). CRF level differences in glucose control variables were analysed via ANCOVA (all other variables as covariates), and multiple regression assessed which variables best predicted glucose control variables. RESULTS: Fasting plasma glucose concentration was the only glucose control variable to differ between CRF levels with the MR group having significantly lower concentrations (4.1mmol/L) than all other CRF levels (low CRF 5.7; medium CRF 5.5; high CRF 5.5 mmol/L). Additionally, MR women were the only group to have a glucose concentration less that 4.9 mmol/L (threshold for CVD risk). CRF was found to be the strongest predictor for glucose concentration. Conversely, body mass, waist circumference and hsCRP were the strongest predictors of insulin concentration and HOMA, whereas CRF had little predictive influence. CONCLUSION: Very high levels of CRF similar to marathon runners may be required to lower glucose concentration in PM-women to levels below the threshold for increased risk of CVD. Supported by a Heart Research UK grant 2508/06/08

The United States is unfit for optimal health with its low level of cardiorespiratory fitness (CRF). Low CRF clinically translates to markedly higher rates of type 2 diabetes (T2D). While the percentages of obesity (13%) and type 2 diabetes (T2D) (1.6%) were too large in 1960, they have both increased manyfold in the past half century to 36% and 7%, respectively, in 2013 in the United States. Historically, type 2 diabetes (T2D) was rare in youth. In contrast, T2D was an adult disease, appearing after 30 years of age. Around 1990, T2D accounted for less than 3% of adolescent diabetes. Ten years later, it accounted for 45% of youth cases. Physical inactivity decreases CRF, and decreases in CRF increase mortality in T2D. This chapter considers (a) CRF’s association with morbidity and mortality, (b) factors determining CRF, and (c) clinical implications associated with low CRF. Also discussed are associations of low CRF with (a) glucose metabolism, (b) metabolic syndrome, (c) increased prevalence with cardiovascular diseases, and (d) increases in multiple risk factors for increased mortality. The relationship of changes in CRF on changes in the relative risk of death is presented. CRF’s inverse relationships are given with various pathological mechanisms (insulin resistance, hyperlipidemia, body composition, obesity, and inflammation). CRF is not fixed at an inheritable level but can be modulated up (by increased physical activity) or down (by physical inactivity, such as sedentary lifestyle). However, genes fix a decline in CRF beginning as early as adolescence.

The Health Risks of Obesity Have Been Exaggerated.

Sang-Koo Woo, Soo-Hyun Park, Tae-Kyung Han, Hyun-Sik Kang. Andong National University, Andong, Sungkyunkwan University, Suwon, Republic of Korea Substantial evidence supports the use of CRF and physical activity as powerful predictors of health outcomes, including metabolic syndrome, among western populations. No such studies have been conducted in Asians including Koreans. PURPOSE: To investigate the relationship between cardio/respiratory fitness (CRF) and metabolic syndrome (MS) in young Korean men. METHODS: In a cross-sectional study, we examined 909 young Korean men (mean±SD age, 24.0±2 years) who were healthy and not taking any medications affecting blood pressure, glucose, or lipids concentrations. Body fatness, resting blood pressures, and fasting blood levels of lipids, glucose, and insulin were measured with our standardized laboratory protocols. CRF was quantified as the maximum volume of minute oxygen consumption measured during a graded treadmill test. RESULTS: Group analyses showed significant and inverse dose-response trends between the metabolic risk factors and CRF levels such that men with high and moderate CRF levels had more favorable profiles in body fatness, resting blood pressures, mean values in fasting lipids, glucose, and insulin, and homeostasis model of assessment-insulin resistance than men with low CRF level. After adjusting for several potential confounders such as age, smoking, and body fatness variables, the low and moderate CRF groups had odds of 4.64 (95% CI, 2.00 to 10.79) and 2.57 (95% CI, 1.04 to 6.34) for having MS than the high CRF group. CONCLUSION: These findings suggest that low CRF is significantly associated with elevated risk of MS independent of body fatness in young Korean men. Supported by the Korean Research Foundation funded by the Korean Government (KRF-2005-042-G00025)

Frequent sauna bathing and higher cardiorespiratory fitness (CRF) levels may play a role in reducing the risk of mental disorders such as psychosis, however, data on their joint contributions is scanty. We aimed to investigate the interplay between sauna bathing, CRF and psychosis risk using a population-based prospective study. Self-reported frequency of sauna bathing (FSB) and CRF measured by respiratory gas analyses were assessed at baseline in 2221 men aged 42–61 years who had no history of psychosis. Frequency of sauna bathing was categorized as low and high (≤2 and 3–7 sessions/week, respectively) and CRF as tertiles (low, medium and high). Hazard ratios (HRs) with 95% CIs were estimated. During a median follow-up of 25.2 years, 215 psychotic disorders were recorded. Comparing high vs low FSB, the multivariable-adjusted HRs (95% CIs) for psychosis was 0.49 (0.32–0.74), which persisted on further adjustment for CRF 0.50 (0.33–0.75). Compared to low CRF, the multivariable-adjusted HRs (95% CIs) for medium and high CRF levels were 0.65 (0.46–0.90) and 0.75 (0.52–1.07) respectively. Compared to low FSB & low CRF, the HRs (95% CIs) for low FSB & medium-high CRF, high FSB & low CRF, and high FSB & medium-high CRF were 0.62 (0.45–0.84), 0.26 (0.11–0.60), and 0.41 (0.25–0.68) respectively. Frequent sauna baths and medium-high CRF levels appear to each independently decrease psychosis risk. However, frequent sauna bathing may be related to a reduced risk of psychosis irrespective of fitness levels and might be a stronger risk indicator for psychosis than CRF.