Investigating a psychological model of mental conditions and coping during the COVID-19 pandemic driven by participatory methods.

BACKGROUND: There is evidence of increased mental health problems during the early stages of the COVID-19 pandemic. We aimed to identify the factors that put certain groups of people at greater risk of mental health problems. METHODS: We took a participatory approach, involving people with lived experience of mental health problems and/or carers, to generate a set of risk factors and potential moderators of the effects of COVID on mental health. An online cross-sectional survey was completed by 1464 United Kingdom residents between 24th April and 27th June 2020. The survey had questions on whether respondents were existing mental health service users and or carers, level of depression (PHQ9) and anxiety (GAD7), demographics, threat and coping appraisals, perceived resilience (BRS), and specific coping behaviours (validated as part of this study). The relationship between responses and coping strategies was measured using tetrachoric correlations. Structural equation modelling was used to test the model. RESULTS: A model significantly fit our data (rel χ2 = 2.05, RMSEA = 0.029 95%, CI (0.016, 0.042), CFI = 0.99, TLI = 0.98, SRMR = 0.014). Age and coping appraisal predicted anxiety and depression. Whereas, threat appraisal and ethnicity only predicted anxiety, and resilience only predicted depression. Additionally, specific coping behaviours predicted anxiety and depression, with overlap on distraction. CONCLUSIONS: Some, but not all, risk factors significantly predict anxiety and depression. While there is a relationship between anxiety and depression, different factors may put people at greater risk of one or the other during the pandemic.

Exercise training improves left ventricular systolic function in older men.

To determine whether endurance exercise training can improve left ventricular systolic function in older men, 10 healthy sedentary men (64 +/- 3 years old; mean +/- SD) were studied. Training consisted of endurance exercise 4 +/- 0.3 days per week for 11.8 +/- 2.5 months at a progressively increasing intensity of 60-80% of maximal O2 uptake (Vo2max) with additional brief bouts of exercise equal to 93 +/- 13% of Vo2max. Vo2max increased from 29.6 +/- 4.1 to 37.2 +/- 5.7 ml/kg/min (p less than 0.001). Percent body fat was decreased (17.8 +/- 3.6% versus 15.6 +/- 3.6%; p less than 0.001). Before training, left ventricular ejection fraction, determined by electrocardiographic-gated equilibrium blood pool imaging, increased only modestly during exercise (from 66.3 +/- 6.7% at rest to 70.6 +/- 6.9% at peak exercise). After training, the increase in ejection fraction during exercise was significantly greater (from 67 +/- 4.8% at rest to 77.6 +/- 7.5% at peak exercise) than that observed before training and was similar to that in young sedentary men (64 +/- 7% at rest versus 74 +/- 9% at peak exercise). Although the changes in systolic pressure from rest to exercise were similar, end-systolic volume decreased significantly at peak exercise after (51 +/- 12 versus 38 +/- 13 ml; p less than 0.005) but not before (46 +/- 8 versus 43 +/- 13 ml; p = NS) training with a shift in the end-systolic volume-systolic blood pressure relation to the left compatible with enhanced inotropic state.(ABSTRACT TRUNCATED AT 250 WORDS)

Exercise and recovery ventilatory and VO2 responses of patients with McArdle's disease.

This study was designed to determine whether patients with McArdle's disease, who do not increase their blood lactate levels during and after maximal exercise, have a slow "lactacid" component to their recovery O2 consumption (VO2) response after high-intensity exercise. VO2 was measured breath by breath during 6 min of rest before exercise, a progressive maximal cycle ergometer test, and 15 min of recovery in five McArdle's patients, six age-matched control subjects, and six maximal O2 consumption- (VO2 max) matched control subjects. The McArdle's patients' ventilatory threshold occurred at the same relative exercise intensity [71 +/- 7% (SD) VO2max] as in the control groups (60 +/- 13 and 70 +/- 10% VO2max) despite no increase and a 20% decrease in the McArdle's patients' arterialized blood lactate and H+ levels, respectively. The recovery VO2 responses of all three groups were better fit by a two-, than a one-, component exponential model, and the parameters of the slow component of the recovery VO2 response were the same in the three groups. The presence of the same slow component of the recovery VO2 response in the McArdle's patients and the control subjects, despite the lack of an increase in blood lactate or H+ levels during maximal exercise and recovery in the patients, provides evidence that this portion of the recovery VO2 response is not the result of a lactacid mechanism. In addition, it appears that the hyperventilation that accompanies high-intensity exercise may be the result of some mechanism other than acidosis or lung CO2 flux.

Alterations in plasma lipids consequent to endurance training and beta-blockade.

Alterations in plasma lipids consequent to endurance training and beta-blockade. Med. Sci. Sports Exerc., Vol. 21, No. 3, pp. 288-292, 1989. The chronic use of beta adrenergic blockers (BAB) has been associated with reductions in HDL-cholesterol (HDL-C) and increases in triglycerides (TG). This study evaluated the impact of concurrent endurance exercise training and chronic medication with BAB on plasma lipid and lipoprotein profiles in healthy young adult males. Changes in plasma lipids and lipoproteins were investigated while exercise training under the influence of one of two nonselective BAB [sotalol (320 mg.d-1) and propranolol (160 mg.d-1)], one beta 1 selective BAB [atenolol (100 mg.d-1)], or a placebo control. Total cholesterol (TC), HDL-C, LDL-cholesterol (LDL-C), TG, and the ratios of TC/HDL and LDL/HDL were determined before and after endurance training programs of either 14 (N = 27, sotalol) or 15 (N = 47, propranolol/atenolol) wk duration. The subjects exhibited increases in maximal oxygen uptake of 12-20%. Despite increased endurance capacity, the subjects in both BAB and placebo control groups failed to demonstrate the expected increase in HDL-C and decrease in TG. In fact, HDL-C was significantly decreased post-training in the propranolol group. The placebo groups did decrease TC, LDL-C and the TC/HDL and LDL/HDL ratios, improving their CHD risk profile. Similar changes were not observed in the groups on BAB. Thus, with respect to the present population, BAB does appear to interfere with the usual training-induced improvements in the lipid profile. Endurance training may, however, reduce the deterioration in the lipid profile known to occur with BAB.

Maximal exercise responses to acute and chronic beta-adrenergic blockade in healthy male subjects.

Conflicting data on the alterations in the maximal exercise response to beta blockade (BB) may be the result of differences in the length of time the subject has been on medication, i.e., hours vs days. The purpose of this study was to examine maximal exercise responses during acute and chronic administration of BB. Twenty-eight healthy males, 14 untrained (UT) and 14 involved in a personal training regimen (TR), performed maximal treadmill tests after 1 d and 9 d under three double-blind, randomized conditions: a placebo (PLAC), propranolol (PROP) 80 mg b.i.d., and atenolol (ATEN) 100 mg o.d. Maximal heart rate (HR), oxygen consumption (VO2), ventilation (VE), and treadmill time were significantly reduced by PROP and ATEN after an acute and chronic dose when compared to PLAC (P less than 0.05) in both groups of subjects. Maximal HR was decreased more after 1 d of BB than after 9 d of BB with both PROP and ATEN in the UT subjects and with PROP only in the TR group. VO2max, VEmax, and treadmill time were also less attenuated after 9 d of BB; however, this trend did not reach statistical significance. The nonselective beta blocker, PROP, caused greater reductions in VO2max compared to the selective beta blocker, ATEN, in both groups of subjects. These data indicate that, other than a small change in maximal HR, there is no difference in the exercise response to acute and chronic BB in normal and highly conditioned individuals.

Altered hemodynamics during exercise in older essential hypertensive subjects.

This study was designed to compare the resting and exercise hemodynamics of older adults with moderate hypertension with those of age-matched normotensive controls. Thirty-one hypertensive (20 men, 11 women; mean age, 63.9 +/- 2.8 years) and 28 normotensive subjects (15 men, 13 women; mean age, 62.6 +/- 2.4 years) were studied. There were no differences between the groups in terms of body weight, body composition, and maximal O2 consumption (VO2). At rest, there were no differences in VO2, cardiac output, stroke volume, or heart rate between the two groups, although systolic (158 +/- 13 vs 121 +/- 12 mm Hg) and diastolic blood pressures (94 +/- 7 vs 79 +/- 8 mm Hg) were higher in the hypertensive subjects. The hypertensive subjects' elevated blood pressure at rest was the result of a higher total peripheral resistance. During exercise, the hypertensive subjects had a lower cardiac output and stroke volume, no difference in heart rate and VO2, higher systolic, diastolic, and mean blood pressures, and a higher total peripheral resistance compared with their normotensive peers. The results indicate that older hypertensive persons have an altered cardiovascular response to exercise as compared with age-matched normotensive subjects. The responses also indicate that older essential hypertensive persons do not undergo excessive myocardial demands during exercise of the intensity usually prescribed in rehabilitation programs.

Effect of beta-blockade on the drift in O2 consumption during prolonged exercise.

The effect of beta-adrenergic blockade on the drift in O2 consumption (VO2 drift) typically observed during prolonged constant-rate exercise was studied in 14 healthy males in moderate heat at 40% of maximal O2 consumption (VO2max). After an initial maximum cycle ergometer test to determine the subjects' control VO2max, subjects were administered each of three medications: placebo, atenolol (100 mg once daily), and propranolol (80 mg twice daily), in a randomized double-blind fashion. Each medication period was 5 days in length and was followed by a 4-day washout period. On the 3rd day of each medication period, subjects performed a maximal cycle ergometer test. On the final day of each medication period, subjects exercised at 40% of their control VO2max for 90 min on a cycle ergometer in a warm (31.7 +/- 0.3 degrees C) moderately humid (44.7 +/- 4.7%) environment. beta-Blockade caused significant (P less than 0.05) reductions in VO2max, maximal minute ventilation (VEmax), maximal heart rate (HRmax), and maximal exercise time. Significantly greater decreases in VO2max, VEmax, and HRmax were associated with the propranolol compared with the atenolol treatment. During the 90-min submaximal rides, beta-blockade significantly reduced heart rate. Substantially lower values for O2 consumption (VO2) and minute ventilation (VE) were observed with propranolol compared with atenolol or placebo. Furthermore, VO2 drift and HR drift were observed under atenolol and placebo conditions but not with propranolol. Respiratory exchange ratio decreased significantly over time during the placebo and atenolol trials but did not change during the propranolol trial.(ABSTRACT TRUNCATED AT 250 WORDS)

Thermoregulation during prolonged exercise in heat: alterations with beta-adrenergic blockade.

Thermoregulation and cardiovascular drift were studied under conditions of prolonged exercise in a warm environment (dry bulb temperature 31.7 +/- 0.3 degrees C, rh 44.7 +/- 4.7%) during beta-adrenergic blockade. Fourteen subjects performed 90-min rides on a cycle ergometer at a work rate equivalent to 40% of their control maximal O2 uptake under each of three treatments provided in a randomized double-blind manner: atenolol (100 mg/day), propranolol (160 mg/day), and a placebo. Exercise during the propranolol trial resulted in significantly higher forearm vascular resistance values and significantly lower forearm blood flows (FBF) compared with the placebo trial. However, the significantly lower FBF during propranolol did not significantly alter the rectal temperature (Tre) response to prolonged exercise. In addition, both beta-blockers produced lower FBF for any given Tre, suggesting that beta-adrenergic blockade affects FBF through nonthermal factors. The slight differences in Tre, despite the large differences in FBF between the various treatments, are apparently the result of an enhanced sweat loss and a lower mean skin temperature during exercise with beta-blockade. The uncoupling of FBF and sweat loss provides evidence of independent regulation. The reduction in FBF at any given Tre was concomitant to lower blood pressure values during beta-blockade and suggests that baroreflexes provide significant input to the control of skin blood flow when both pressure and temperature maintenance are simultaneously challenged.

Beta-blockade reduces tidal volume during heavy exercise in trained and untrained men.

The effects of beta-blockade on tidal volume (VT), breath cycle timing, and respiratory drive were evaluated in 14 endurance-trained [maximum O2 uptake (VO2max) approximately 65 ml X kg-1 X min-1] and 14 untrained (VO2max approximately 50 ml X kg-1 X min-1) male subjects at 45, 60, and 75% of unblocked VO2max and at VO2max. Propranolol (PROP, 80 mg twice daily), atenolol (ATEN, 100 mg once a day) and placebo (PLAC) were administered in a randomized double-blind design. In both subject groups both drugs attenuated the increases in VT associated with increasing work rate. CO2 production (VCO2) was not changed by either drug during submaximal exercise but was reduced in both subject groups by both drugs during maximal exercise. The relationship between minute ventilation (VE) and VCO2 was unaltered by either drug in both subject groups due to increases in breathing frequency. In trained subjects VT was reduced during maximal exercise from 2.58 l/breath on PLAC to 2.21 l/breath on PROP and to 2.44 l/breath on ATEN. In untrained subjects VT at maximal exercise was reduced from 2.30 l/breath on PLAC to 1.99 on PROP and 2.12 on ATEN. These observations indicate that 1) since VE vs. VCO2 was not altered by beta-adrenergic blockade, the changes in VT and f did not result from a general blunting of the ventilatory response to exercise during beta-adrenergic blockade; and 2) blockade of beta 1- and beta 2-receptors with PROP caused larger reductions in VT compared with blockade of beta 1-receptors only (ATEN), suggesting that beta 2-mediated bronchodilation plays a role in the VT response to heavy exercise.

Effects of beta-blockade on exercise capacity of trained and untrained men: a hemodynamic comparison.

To study the effects of cardiovascular fitness on hemodynamic responses to exercise during beta-adrenergic blockade (BAB), submaximal [60% of maximum O2 uptake (VO2max)] and maximal treadmill exercise data were collected in 11 trained (T, VO2max 63.3 ml X kg-1 X min-1, 26.8 yr) and 11 untrained (UT, VO2max 44.5 ml X kg-1 X min-1, 25.0 yr) male subjects. Subjects completed two maximal control tests followed by a randomized, double-blind series of maximal tests after 1-wk treatments with placebo (PLAC), propranolol (PROP, 160 mg/day, beta 1- and beta 2-blockade), and atenolol (ATEN, 100 mg/day, beta 1-blockade). Treatments were separated by 1-wk washout periods. At 60% of control VO2max T and UT subjects experienced no reductions in O2 uptake (VO2) with either drug. Submaximal heart rate (HR, beats/min) was 134.8 PLAC, 107.0 PROP, 107.9 ATEN (P less than 0.05 both drugs vs. PLAC) in T subjects and 141.1 PLAC, 106.1 PROP, and 105.0 ATEN (P less than 0.05 both drugs vs. PLAC) in UT subjects. Cardiac output (1/min) for T was 17.3 PLAC, 16.9 PROP, 16.5 ATEN (P less than 0.05 ATEN vs. PLAC in T only) and for UT it was 12.2 (PLAC), 11.7 (PROP), 11.5 (ATEN) (P less than 0.05 both drugs vs. PLAC in UT). Stroke volume increased from 129.8 ml (PLAC) to 158.6 (PROP) and 156.2 (ATEN) in T (P less than 0.05 both drugs vs. PLAC) and from 86.8 (PLAC) to 110.0 (PROP) and 109.8 (ATEN) (P less than 0.05 both drugs vs. PLAC) in UT. The increases in stroke volume (SV) were similar in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiorespiratory alterations consequent to endurance exercise training during chronic beta-adrenergic blockade with atenolol and propranolol.

A study was undertaken to determine if normal healthy subjects can increase their endurance capacity consequent to endurance training during chronic beta-adrenergic blockade. Forty-seven subjects, 17 to 34 years of age, were randomly assigned to 1 of 3 treatments (placebo, propranolol, 160 mg/day, and atenolol, 100 mg/day) and then completed a 15-week aerobic exercise training program. All groups reduced their submaximal steady-state heart rates consequent to training; submaximal oxygen uptake was slightly reduced; submaximal stroke volume was increased only in the placebo and atenolol groups; submaximal cardiac output was generally lower; and arterial-mixed venous oxygen difference was increased after training in all 3 groups, suggesting decreased muscle blood flow and increased oxidative capacity. Maximal oxygen uptake and maximal treadmill time were increased in all 3 groups after training. However, while still on medication the atenolol group had significantly greater increases in maximal oxygen uptake and maximal treadmill time compared with the propranolol group. Because most patients will remain on medication, these results suggest a distinct advantage for cardioselective blocking agents. It is concluded that beta-adrenergic blockade does not reduce the ability of normal healthy subjects to gain the benefits associated with cardiorespiratory endurance training.