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Abstract

Background

Mechanisms underlying the association between grip strength and cardiovascular mortality are poorly understood. We aimed to assess the association of grip strength with a panel of cardiovascular risk markers.

Design

The study was based on a cross-sectional analysis of 3468 adults aged 50–75 years (1891 women) from a population-based sample in Lausanne, Switzerland.

Methods

Grip strength was measured using a hydraulic hand dynamometer. Cardiovascular risk markers included anthropometry, blood pressure, lipids, glucose, adiposity, inflammatory and other metabolic markers.

Results

In both genders, grip strength was negatively associated with fat mass (Pearson correlation coefficient: women: −0.170, men: −0.198), systolic blood pressure (women: −0.096, men: −0.074), fasting glucose (women: −0.048, men: −0.071), log-transformed leptin (women: −0.074, men: −0.065), log-transformed high-sensitivity C-reactive protein (women: −0.101, men: −0.079) and log-transformed homocysteine (women: −0.109, men: −0.060). In men, grip strength was also positively associated with diastolic blood pressure (0.068), total (0.106) and low density lipoprotein-cholesterol (0.082), and negatively associated with interleukin-6 (–0.071); in women, grip strength was negatively associated with triglycerides (–0.064) and uric acid (–0.059). After multivariate adjustment, grip strength was negatively associated with waist circumference (change per 5 kg increase in grip strength: −0.82 cm in women and −0.77 cm in men), fat mass (–0.56% in women; −0.27% in men) and high-sensitivity C-reactive protein (–6.8% in women; −3.2% in men) in both genders, and with body mass index (0.22 kg/m2) and leptin (–2.7%) in men.

Conclusion

Grip strength shows only moderate associations with cardiovascular risk markers. The effect of muscle strength as measured by grip strength on cardiovascular disease does not seem to be mediated by cardiovascular risk markers.

Grip strength, anthropometry, blood pressure, lipids, glucose, inflammation, Switzerland, population-based study

Introduction

Muscle strength is an important predictor of health,1 partly explained by the beneficial effect of muscle resistance activities on physical fitness.2 Compared with other muscular tests such as trunk and knee extension or flexion, grip strength is the most appropriate marker of muscle strength3 and has also been related to fitness.4 Therefore, it remains the simplest and most widely recommended technique to assess muscle strength in clinical practice.5 Grip strength has been shown to be inversely associated with overall and cardiovascular mortality in all age groups,6,7 but the mechanisms involved have been less well established. Several cross-sectional studies assessed the associations between grip strength and cardiovascular (CV) risk factors, metabolic syndrome or inflammatory markers, but have been limited by the fact that they assessed a small set of variables,8,9 relied on a small sample size10 or were based only on elderly participants.9,10 Further, several studies have suggested that fitness can exert its effects independently of physical activity levels,11 and that not all types of physical activity are beneficial for health.12 For instance, leisure-time physical activity (LTPA) has been shown to be beneficial while occupational physical activity (OPA) has been shown to be deleterious regarding all-cause mortality.13 Still, no previous study took into account this finding.

Thus, the aim of this study was to assess the associations between grip strength and 19 CV risk markers using a large population-based sample aged 50–75 years from the city of Lausanne, Switzerland (CoLaus study), taking into account the effects of LTPA and OPA.

Materials and methods

Recruitment

A detailed description of the recruitment of the CoLaus study has been published previously.14 Briefly, the CoLaus study assesses the prevalence and determinants of CV disease in the city of Lausanne, Switzerland. A non-stratified, representative sample of the Lausanne population aged 35–75 years was drawn from the population register of the city. A letter was sent to these individuals, and subjects who volunteered to participate were then contacted by phone to set up an appointment. The baseline CoLaus study was conducted between 2003–2006 and included 6733 participants.

Grip strength

Participants of the CoLaus study aged over 50 years were invited to participate in a sub-study on frailty, which included grip strength. Grip strength was assessed using the Baseline Hydraulic Hand Dynamometer and positioning of the participants was done according to the American Society of Hand Therapists’s guidelines:5 subject seated, shoulders adducted and neutrally rotated, elbow flexed at 90°, forearm in neutral and wrist between 0° and 30° of dorsiflexion. Three measurements were performed consecutively at the right hand and the highest value (expressed in kg) was included in the analyses. Participants were also asked about their handedness.

Exclusion criteria

Participants were excluded if they presented any condition precluding adequate measurement of grip strength, i.e. pain, injury, recent surgery, osteoarthritis and rheumatoid arthritis, among others.

Other data

A self-administered questionnaire collected demographic data. Information on educational level, job and on several lifestyle factors, including tobacco and LTPA (weekly number of ≥20 min bouts of exercise) were also collected. OPA was categorised as non-physical (when sitting or standing) and physical (carrying light or heavy load). History of CV disease and CV risk factor was elicited with a standardised interview-based questionnaire filled in by a trained recruiter. Participants indicated if they have been diagnosed with hypertension, dyslipidaemia, diabetes, and if they were treated for these conditions.

Body weight and height were measured to the nearest 0.1 kg and 5 mm (Seca scale, Seca height gauge, Hamburg, Germany), with participants in light indoor clothes standing without shoes. Body mass index (BMI) was computed as weight/height2. Waist circumference (WC) was measured at mid-way between the lowest rib and the iliac crest as recommended.15 Body composition was assessed by bioimpedance (Bodystat 1500 analyser, Isle of Man, UK) and expressed as percentage of fat. Blood pressure (BP) was measured using an Omron HEM-907 automated oscillometric sphygmomanometer after at least 10 min rest in a seated position and the average of the last two measurements was used. Hypertension was defined as a systolic BP ≥ 140 mm Hg and/or a diastolic BP ≥ 90 mm Hg and/or presence of an anti-hypertensive treatment.

A fasting venous blood sample was drawn and most measurements performed by the clinical laboratory of the Lausanne university hospital. Lipid markers included total and high density lipoprotein (HDL)-cholesterol, triglycerides and apolipoprotein B, low density lipoprotein (LDL)-cholesterol was calculated using the Friedewald formula if triglycerides were <4.6 mmol/l. Dyslipidaemia was defined either by the presence of a lipid-lowering drug or using the LDL-cholesterol thresholds according to the PROspective CArdiovascular Münster (PROCAM) risk score adapted for Switzerland.16 Glucometabolic markers included glucose and insulin; diabetes was defined by a fasting glucose ≥7.0 and/or presence of antidiabetic drug treatment. Inflammatory markers included high-sensitivity C-reactive protein (hs-CRP), interleukin 6 (IL-6) and tumour necrosis factor alpha (TNF-α). Other markers included leptin, adiponectin, homocysteine and uric acid.

CV absolute risk was calculated using the European Society of Cardiology Systematic COronary Risk Evaluation (SCORE) recalibrated and validated for the Swiss population.17 This risk equation uses age, gender, smoking, systolic BP and total cholesterol to compute the 10-year absolute risk of fatal CV disease. No CV absolute risk was calculated for participants with history of CV disease.

Statistical analysis

Statistical analyses were stratified by gender and conducted using Stata version 14.0 for windows (Stata Corp, College Station, Texas, USA). Descriptive results were expressed as number of participants (percentage) or as average ± standard deviation. Between-group comparisons were performed using chi-square or Student t-test for categorical and continuous variables, respectively. Natural log transformation was applied to variables with a skewed distribution: triglycerides, insulin, leptin, adiponectin, hs-CRP, IL-6, TNF-α and homocysteine. Bivariate associations were assessed by Pearson correlation. Multivariate associations were assessed using linear regression and the results were expressed as multivariate-adjusted standardized coefficients, which can be interpreted as multivariate-adjusted correlation coefficients.

The effect of a 5 kg increase in grip strength on the different CV risk markers was assessed by linear regression, and the results were expressed as coefficient and (95% confidence interval). For log-transformed dependent variables, results were expressed as percentage change of the untransformed dependent variable and (95% confidence interval), as recommended.18 Multivariate analyses were conducted using linear or quadratic regression models and the adequacy of the linear model relative to the quadratic one was tested by likelihood ratio test. Multicollinearity of the dependent variables was assessed by computing the variance inflation factor; values ranged from 1.02–1.21, suggesting lack of collinearity.

All multivariate models were adjusted for age (continuous), smoking status (current/other), LTPA (three categories), OPA (physical/non-physical) and BMI (except for anthropometry). Further adjustments were performed on: weight (continuous) for WC; hypertensive drug treatment (yes/no) for BP; lipid-lowering drug treatment (yes/no) for lipid markers and antidiabetic drug treatment (yes/no) for glucometabolic markers. Sensitivity analyses were performed by further stratifying on tertiles of age. Statistical significance was assessed for a two-sided test with p < 0.05.

Ethical statement

The CoLaus study was approved by the Ethics Committee of the University of Lausanne and all participants gave their signed informed consent before entering the study.

Results

Characteristics of excluded participants

Of the initial 3704 participants invited to the sub-study on frailty, 3550 (95.8%) accepted. A further 82 (2.3%) participants were excluded because of issues related to grip strength measurement. Included and excluded participants’ characteristics are presented in Supplementary Material, Table 1. Included participants were more likely right-handed than the excluded ones, while no significant differences were found for all other variables analysed.

The final sample consisted of 3468 participants; their characteristics overall and according to gender are summarized in Supplementary Material, Table 2. Men had higher grip strength, were more likely to be current or former smoker, to have a university level of education, to be full-time worker, to perform a physical job, and to have a higher 10-year CV absolute risk than women.

Association of grip strength with CV risk markers

The bivariate and multivariate-adjusted associations using linear regression between grip strength and CV risk markers are described in Table 1; the corresponding changes in CV risk markers due to a 5 kg increase in grip strength are described in Table 2. Bivariate analysis showed that grip strength was negatively associated with fat mass, systolic BP, fasting glucose, leptin, hs-CRP and homocysteine in both genders. In men, grip strength was positively associated with diastolic BP, total and LDL-cholesterol, and negatively associated with IL-6; in women, grip strength was negatively associated with triglycerides and uric acid. Finally, grip strength was negatively associated with 10-year CV absolute risk as assessed by the SCORE equation in both genders (Pearson correlation coefficient: women: −0.245, p < 0.001, men: −0.264, p < 0.001). Most of the previous associations were no longer significant after multivariate adjustment. In both genders, grip strength was negatively associated with WC, fat mass and hs-CRP; in men, grip strength was positively associated with BMI and negatively associated with leptin (Tables 1 and 2).

Table 1.
Open in new tab

Bi- and multivariate associations between grip strength and cardiovascular risk markers.

Pearson correlation coefficient
Multivariate-adjusted standardised coefficient
WomenMenWomenMen
Anthropometry
 Body mass index (kg/m2)−0.0340.022−0.0000.092***
 Waist circumference (cm)−0.0050.039−0.069***,a−0.114***,a
 Fat mass (%)−0.170***−0.198***−0.078*−0.084*
Blood pressure (mm Hg)
 Systolic−0.096***−0.074*0.038b0.003b
 Diastolic0.0070.068*0.015b0.045b
Lipid markers (mmol/l)
 Total cholesterol−0.0280.106***0.004c0.082*,c
 HDL-cholesterol0.0150.002−0.001c0.029c
 LDL-cholesterol−0.0250.082*0.001c0.055*,c
 Triglycerides§−0.064*0.048−0.003c0.026c
 Apolipoprotein B (mg/dl)−0.0070.0100.003c−0.006c
Glucometabolic markers
 Fasting glucose (mmol/l)−0.048*−0.071*−0.006d−0.036d
 Insulin (µU/ml)§−0.031−0.0490.007d−0.032d
Adipokines (µU/ml)
 Leptin§−0.074*−0.065*−0.026e−0.059*,e
 Adiponectin§−0.036−0.014−0.024e0.012e
Inflammatory markers
 hs-CRP (mg/l)§−0.101***−0.079*−0.071*,e−0.052*,e
 IL-6 (pg/ml)§−0.009−0.071*−0.009e−0.054e
 TNF-α (pg/ml)§−0.005−0.0430.016e−0.024e
Homocysteine (µmol/l)§−0.109***−0.060*−0.022e0.032e
Uric acid (µmol/l)−0.059*0.0120.017e0.018e
Pearson correlation coefficient
Multivariate-adjusted standardised coefficient
WomenMenWomenMen
Anthropometry
 Body mass index (kg/m2)−0.0340.022−0.0000.092***
 Waist circumference (cm)−0.0050.039−0.069***,a−0.114***,a
 Fat mass (%)−0.170***−0.198***−0.078*−0.084*
Blood pressure (mm Hg)
 Systolic−0.096***−0.074*0.038b0.003b
 Diastolic0.0070.068*0.015b0.045b
Lipid markers (mmol/l)
 Total cholesterol−0.0280.106***0.004c0.082*,c
 HDL-cholesterol0.0150.002−0.001c0.029c
 LDL-cholesterol−0.0250.082*0.001c0.055*,c
 Triglycerides§−0.064*0.048−0.003c0.026c
 Apolipoprotein B (mg/dl)−0.0070.0100.003c−0.006c
Glucometabolic markers
 Fasting glucose (mmol/l)−0.048*−0.071*−0.006d−0.036d
 Insulin (µU/ml)§−0.031−0.0490.007d−0.032d
Adipokines (µU/ml)
 Leptin§−0.074*−0.065*−0.026e−0.059*,e
 Adiponectin§−0.036−0.014−0.024e0.012e
Inflammatory markers
 hs-CRP (mg/l)§−0.101***−0.079*−0.071*,e−0.052*,e
 IL-6 (pg/ml)§−0.009−0.071*−0.009e−0.054e
 TNF-α (pg/ml)§−0.005−0.0430.016e−0.024e
Homocysteine (µmol/l)§−0.109***−0.060*−0.022e0.032e
Uric acid (µmol/l)−0.059*0.0120.017e0.018e

HDL: high density lipoprotein: hs-CRP: high sensitivity C-reactive protein; IL-6: interleukin 6; LDL: low density lipoprotein; TNF-α: tumour necrosis factor alpha.

Bivariate associations assessed using Pearson correlation or multivariable linear regression; results are expressed as Pearson correlation coefficient or as multivariate-adjusted standardized coefficient.

***

p < 0.001; *p < 0.05; §log-transformed; multivariable linear model was adjusted for age, current smoking, leisure-time physical activity and occupational physical activity, with a further adjustment on aweight; bbody mass index and antihypertensive drug treatment; cbody mass index and lipid lowering drug treatment; dbody mass index and antidiabetic drug treatment; ebody mass index.

Table 1.
Open in new tab

Bi- and multivariate associations between grip strength and cardiovascular risk markers.

Pearson correlation coefficient
Multivariate-adjusted standardised coefficient
WomenMenWomenMen
Anthropometry
 Body mass index (kg/m2)−0.0340.022−0.0000.092***
 Waist circumference (cm)−0.0050.039−0.069***,a−0.114***,a
 Fat mass (%)−0.170***−0.198***−0.078*−0.084*
Blood pressure (mm Hg)
 Systolic−0.096***−0.074*0.038b0.003b
 Diastolic0.0070.068*0.015b0.045b
Lipid markers (mmol/l)
 Total cholesterol−0.0280.106***0.004c0.082*,c
 HDL-cholesterol0.0150.002−0.001c0.029c
 LDL-cholesterol−0.0250.082*0.001c0.055*,c
 Triglycerides§−0.064*0.048−0.003c0.026c
 Apolipoprotein B (mg/dl)−0.0070.0100.003c−0.006c
Glucometabolic markers
 Fasting glucose (mmol/l)−0.048*−0.071*−0.006d−0.036d
 Insulin (µU/ml)§−0.031−0.0490.007d−0.032d
Adipokines (µU/ml)
 Leptin§−0.074*−0.065*−0.026e−0.059*,e
 Adiponectin§−0.036−0.014−0.024e0.012e
Inflammatory markers
 hs-CRP (mg/l)§−0.101***−0.079*−0.071*,e−0.052*,e
 IL-6 (pg/ml)§−0.009−0.071*−0.009e−0.054e
 TNF-α (pg/ml)§−0.005−0.0430.016e−0.024e
Homocysteine (µmol/l)§−0.109***−0.060*−0.022e0.032e
Uric acid (µmol/l)−0.059*0.0120.017e0.018e
Pearson correlation coefficient
Multivariate-adjusted standardised coefficient
WomenMenWomenMen
Anthropometry
 Body mass index (kg/m2)−0.0340.022−0.0000.092***
 Waist circumference (cm)−0.0050.039−0.069***,a−0.114***,a
 Fat mass (%)−0.170***−0.198***−0.078*−0.084*
Blood pressure (mm Hg)
 Systolic−0.096***−0.074*0.038b0.003b
 Diastolic0.0070.068*0.015b0.045b
Lipid markers (mmol/l)
 Total cholesterol−0.0280.106***0.004c0.082*,c
 HDL-cholesterol0.0150.002−0.001c0.029c
 LDL-cholesterol−0.0250.082*0.001c0.055*,c
 Triglycerides§−0.064*0.048−0.003c0.026c
 Apolipoprotein B (mg/dl)−0.0070.0100.003c−0.006c
Glucometabolic markers
 Fasting glucose (mmol/l)−0.048*−0.071*−0.006d−0.036d
 Insulin (µU/ml)§−0.031−0.0490.007d−0.032d
Adipokines (µU/ml)
 Leptin§−0.074*−0.065*−0.026e−0.059*,e
 Adiponectin§−0.036−0.014−0.024e0.012e
Inflammatory markers
 hs-CRP (mg/l)§−0.101***−0.079*−0.071*,e−0.052*,e
 IL-6 (pg/ml)§−0.009−0.071*−0.009e−0.054e
 TNF-α (pg/ml)§−0.005−0.0430.016e−0.024e
Homocysteine (µmol/l)§−0.109***−0.060*−0.022e0.032e
Uric acid (µmol/l)−0.059*0.0120.017e0.018e

HDL: high density lipoprotein: hs-CRP: high sensitivity C-reactive protein; IL-6: interleukin 6; LDL: low density lipoprotein; TNF-α: tumour necrosis factor alpha.

Bivariate associations assessed using Pearson correlation or multivariable linear regression; results are expressed as Pearson correlation coefficient or as multivariate-adjusted standardized coefficient.

***

p < 0.001; *p < 0.05; §log-transformed; multivariable linear model was adjusted for age, current smoking, leisure-time physical activity and occupational physical activity, with a further adjustment on aweight; bbody mass index and antihypertensive drug treatment; cbody mass index and lipid lowering drug treatment; dbody mass index and antidiabetic drug treatment; ebody mass index.

Table 2.
Open in new tab

Unadjusted and multivariate-adjusted changes in cardiovascular risk marker levels per 5 kg increase in grip strength, stratified by gender.

Women
Men
Unadjustedp-ValueMultivariate-adjustedp-ValueUnadjustedp-ValueMultivariate-adjustedp-Value
Anthropometry
 Body mass index (kg/m2)−0.16 (−0.37–0.05)0.1430.00 (−0.22–0.22)0.9850.05 (−0.07–0.17)0.3840.22 (0.10–0.35)<0.001
 Waist circumference (cm)−0.06 (−0.60–0.49)0.839−0.82 (−1.13– −0.52)a<0.0010.26 (−0.07–0.59)0.121−0.77 (−0.93– −0.61)a<0.001
 Fat mass (%)−1.23 (−1.55– −0.90)<0.001−0.56 (−0.89– −0.22)0.001−0.63 (−0.78– −0.47)<0.001−0.27 (−0.43– −0.11)0.001
Blood pressure (mm Hg)
 Systolic−1.67 (−2.46–−0.89)<0.0010.66 (−0.12–1.43)b0.098−0.77 (−1.28– −0.26)0.0030.04 (−0.48–0.56)b0.892
 Diastolic0.07 (−0.38–0.52)0.7620.15 (−0.31–0.61)b0.5220.44 (0.12–0.76)0.0070.29 (−0.05– 0.63)b0.090
Lipid markers (mmol/l)
 Total cholesterol−0.03 (−0.07–0.02)0.2300.00 (−0.04–0.05)c0.8630.06 (0.03–0.09)<0.0010.05 (0.02–0.08)c0.002
 HDL-cholesterol0.01 (−0.01–0.03)0.5050.00 (−0.02–0.02)c0.9690.00 (−0.01–0.01)0.9390.01 (0.00–0.02)c0.257
 LDL-cholesterol−0.02 (−0.06–0.02)0.2730.00 (−0.04–0.04)c0.9610.04 (0.02–0.07)0.0010.03 (0.00–0.06)c0.036
 Triglycerides §−2.7 (−4.5– −0.8)0.006−0.1 (−2.0–1.7)c0.8841.6 (−0.1–3.2)0.0580.8 (−0.8–2.5)c0.312
 Apolipoprotein B (mg/dl)−0.91 (−7.02–5.20)0.7700.35 (−6.21–6.90)c0.9180.83 (−3.34–5.01)0.695−0.52 (−5.01–3.97)c0.820
Glucometabolic markers
 Fasting glucose (mmol/l)−0.05 (−0.10–0.00)0.036−0.01 (−0.05–0.04)d0.777−0.06 (−0.10– −0.02)0.005−0.03 (−0.07–0.01)d0.116
 Insulin (µU/ml)§−1.6 (−4.0–0.9)0.2150.4 (−2.0–2.7)d0.764−1.7 (−3.4–0.1)0.069−1.1 (−2.7–0.6)d0.201
Adipokines (µU/ml)
 Leptin§−4.9 (−8.0– −1.7)0.003−1.8 (−4.4–0.9)e0.198−2.9 (−5.2– −0.5)0.016−2.7 (−4.6– −0.6)e0.010
 Adiponectin§−2.1 (−4.8–0.6)0.129−1.4 (−4.2–1.5)e0.337−0.5 (−2.4–1.4)0.5980.4 (−1.6–2.5)e0.671
Inflammatory markers
 hs-CRP (mg/l)§−9.6 (−13.5– −5.5)<0.001−6.8 (−10.7– −2.8)e0.001−4.7 (−7.6– −1.8)0.002−3.2 (−6.1– −0.2)e0.039
 IL-6 (pg/ml)§−1.1 (−6.6–4.8)0.713−1.1 (−7.0–5.2)e0.730−5.4 (−9.1– −1.5)0.007−4.1 (−8.2–0.1)e0.055
 TNF-α (pg/ml)§−0.4 (−4.0–3.3)0.8281.2 (−2.6–5.3)e0.534−2.1 (−4.5–0.4)0.094−1.2 (−3.8–1.5)e0.392
Homocysteine (µmol/l)§−2.9 (−4.0– −1.7)<0.001−0.6 (−1.8–0.7)e0.359−1.1 (−2.0– −0.2)0.0190.6 (−0.4–1.6)e0.212
Uric acid (µmol/l)−3.93 (−6.92– −0.94)0.0101.12 (−1.79–4.04)e0.4490.53 (−1.75–2.80)0.6500.84 (−1.52–3.21)e0.485
Women
Men
Unadjustedp-ValueMultivariate-adjustedp-ValueUnadjustedp-ValueMultivariate-adjustedp-Value
Anthropometry
 Body mass index (kg/m2)−0.16 (−0.37–0.05)0.1430.00 (−0.22–0.22)0.9850.05 (−0.07–0.17)0.3840.22 (0.10–0.35)<0.001
 Waist circumference (cm)−0.06 (−0.60–0.49)0.839−0.82 (−1.13– −0.52)a<0.0010.26 (−0.07–0.59)0.121−0.77 (−0.93– −0.61)a<0.001
 Fat mass (%)−1.23 (−1.55– −0.90)<0.001−0.56 (−0.89– −0.22)0.001−0.63 (−0.78– −0.47)<0.001−0.27 (−0.43– −0.11)0.001
Blood pressure (mm Hg)
 Systolic−1.67 (−2.46–−0.89)<0.0010.66 (−0.12–1.43)b0.098−0.77 (−1.28– −0.26)0.0030.04 (−0.48–0.56)b0.892
 Diastolic0.07 (−0.38–0.52)0.7620.15 (−0.31–0.61)b0.5220.44 (0.12–0.76)0.0070.29 (−0.05– 0.63)b0.090
Lipid markers (mmol/l)
 Total cholesterol−0.03 (−0.07–0.02)0.2300.00 (−0.04–0.05)c0.8630.06 (0.03–0.09)<0.0010.05 (0.02–0.08)c0.002
 HDL-cholesterol0.01 (−0.01–0.03)0.5050.00 (−0.02–0.02)c0.9690.00 (−0.01–0.01)0.9390.01 (0.00–0.02)c0.257
 LDL-cholesterol−0.02 (−0.06–0.02)0.2730.00 (−0.04–0.04)c0.9610.04 (0.02–0.07)0.0010.03 (0.00–0.06)c0.036
 Triglycerides §−2.7 (−4.5– −0.8)0.006−0.1 (−2.0–1.7)c0.8841.6 (−0.1–3.2)0.0580.8 (−0.8–2.5)c0.312
 Apolipoprotein B (mg/dl)−0.91 (−7.02–5.20)0.7700.35 (−6.21–6.90)c0.9180.83 (−3.34–5.01)0.695−0.52 (−5.01–3.97)c0.820
Glucometabolic markers
 Fasting glucose (mmol/l)−0.05 (−0.10–0.00)0.036−0.01 (−0.05–0.04)d0.777−0.06 (−0.10– −0.02)0.005−0.03 (−0.07–0.01)d0.116
 Insulin (µU/ml)§−1.6 (−4.0–0.9)0.2150.4 (−2.0–2.7)d0.764−1.7 (−3.4–0.1)0.069−1.1 (−2.7–0.6)d0.201
Adipokines (µU/ml)
 Leptin§−4.9 (−8.0– −1.7)0.003−1.8 (−4.4–0.9)e0.198−2.9 (−5.2– −0.5)0.016−2.7 (−4.6– −0.6)e0.010
 Adiponectin§−2.1 (−4.8–0.6)0.129−1.4 (−4.2–1.5)e0.337−0.5 (−2.4–1.4)0.5980.4 (−1.6–2.5)e0.671
Inflammatory markers
 hs-CRP (mg/l)§−9.6 (−13.5– −5.5)<0.001−6.8 (−10.7– −2.8)e0.001−4.7 (−7.6– −1.8)0.002−3.2 (−6.1– −0.2)e0.039
 IL-6 (pg/ml)§−1.1 (−6.6–4.8)0.713−1.1 (−7.0–5.2)e0.730−5.4 (−9.1– −1.5)0.007−4.1 (−8.2–0.1)e0.055
 TNF-α (pg/ml)§−0.4 (−4.0–3.3)0.8281.2 (−2.6–5.3)e0.534−2.1 (−4.5–0.4)0.094−1.2 (−3.8–1.5)e0.392
Homocysteine (µmol/l)§−2.9 (−4.0– −1.7)<0.001−0.6 (−1.8–0.7)e0.359−1.1 (−2.0– −0.2)0.0190.6 (−0.4–1.6)e0.212
Uric acid (µmol/l)−3.93 (−6.92– −0.94)0.0101.12 (−1.79–4.04)e0.4490.53 (−1.75–2.80)0.6500.84 (−1.52–3.21)e0.485

HDL: high density lipoprotein: hs-CRP: high sensitivity C-reactive protein; IL-6: interleukin 6; LDL: low density lipoprotein; TNF-α: tumour necrosis factor alpha.

Statistical analyses performed using linear regression. Results are expressed as effect of a 5 kg increase in grip strength and (95% confidence interval). Multivariate adjustment for age, current smoking, leisure-time physical activity and occupational physical activity, with a further adjustment on aweight; bbody mass index and antihypertensive drug treatment; cbody mass index and lipid lowering drug treatment; dbody mass index and antidiabetic drug treatment; ebody mass index.

§

On log-transformed data results are expressed as % change of the risk marker related to a 5 kg increase in grip strength.

Table 2.
Open in new tab

Unadjusted and multivariate-adjusted changes in cardiovascular risk marker levels per 5 kg increase in grip strength, stratified by gender.

Women
Men
Unadjustedp-ValueMultivariate-adjustedp-ValueUnadjustedp-ValueMultivariate-adjustedp-Value
Anthropometry
 Body mass index (kg/m2)−0.16 (−0.37–0.05)0.1430.00 (−0.22–0.22)0.9850.05 (−0.07–0.17)0.3840.22 (0.10–0.35)<0.001
 Waist circumference (cm)−0.06 (−0.60–0.49)0.839−0.82 (−1.13– −0.52)a<0.0010.26 (−0.07–0.59)0.121−0.77 (−0.93– −0.61)a<0.001
 Fat mass (%)−1.23 (−1.55– −0.90)<0.001−0.56 (−0.89– −0.22)0.001−0.63 (−0.78– −0.47)<0.001−0.27 (−0.43– −0.11)0.001
Blood pressure (mm Hg)
 Systolic−1.67 (−2.46–−0.89)<0.0010.66 (−0.12–1.43)b0.098−0.77 (−1.28– −0.26)0.0030.04 (−0.48–0.56)b0.892
 Diastolic0.07 (−0.38–0.52)0.7620.15 (−0.31–0.61)b0.5220.44 (0.12–0.76)0.0070.29 (−0.05– 0.63)b0.090
Lipid markers (mmol/l)
 Total cholesterol−0.03 (−0.07–0.02)0.2300.00 (−0.04–0.05)c0.8630.06 (0.03–0.09)<0.0010.05 (0.02–0.08)c0.002
 HDL-cholesterol0.01 (−0.01–0.03)0.5050.00 (−0.02–0.02)c0.9690.00 (−0.01–0.01)0.9390.01 (0.00–0.02)c0.257
 LDL-cholesterol−0.02 (−0.06–0.02)0.2730.00 (−0.04–0.04)c0.9610.04 (0.02–0.07)0.0010.03 (0.00–0.06)c0.036
 Triglycerides §−2.7 (−4.5– −0.8)0.006−0.1 (−2.0–1.7)c0.8841.6 (−0.1–3.2)0.0580.8 (−0.8–2.5)c0.312
 Apolipoprotein B (mg/dl)−0.91 (−7.02–5.20)0.7700.35 (−6.21–6.90)c0.9180.83 (−3.34–5.01)0.695−0.52 (−5.01–3.97)c0.820
Glucometabolic markers
 Fasting glucose (mmol/l)−0.05 (−0.10–0.00)0.036−0.01 (−0.05–0.04)d0.777−0.06 (−0.10– −0.02)0.005−0.03 (−0.07–0.01)d0.116
 Insulin (µU/ml)§−1.6 (−4.0–0.9)0.2150.4 (−2.0–2.7)d0.764−1.7 (−3.4–0.1)0.069−1.1 (−2.7–0.6)d0.201
Adipokines (µU/ml)
 Leptin§−4.9 (−8.0– −1.7)0.003−1.8 (−4.4–0.9)e0.198−2.9 (−5.2– −0.5)0.016−2.7 (−4.6– −0.6)e0.010
 Adiponectin§−2.1 (−4.8–0.6)0.129−1.4 (−4.2–1.5)e0.337−0.5 (−2.4–1.4)0.5980.4 (−1.6–2.5)e0.671
Inflammatory markers
 hs-CRP (mg/l)§−9.6 (−13.5– −5.5)<0.001−6.8 (−10.7– −2.8)e0.001−4.7 (−7.6– −1.8)0.002−3.2 (−6.1– −0.2)e0.039
 IL-6 (pg/ml)§−1.1 (−6.6–4.8)0.713−1.1 (−7.0–5.2)e0.730−5.4 (−9.1– −1.5)0.007−4.1 (−8.2–0.1)e0.055
 TNF-α (pg/ml)§−0.4 (−4.0–3.3)0.8281.2 (−2.6–5.3)e0.534−2.1 (−4.5–0.4)0.094−1.2 (−3.8–1.5)e0.392
Homocysteine (µmol/l)§−2.9 (−4.0– −1.7)<0.001−0.6 (−1.8–0.7)e0.359−1.1 (−2.0– −0.2)0.0190.6 (−0.4–1.6)e0.212
Uric acid (µmol/l)−3.93 (−6.92– −0.94)0.0101.12 (−1.79–4.04)e0.4490.53 (−1.75–2.80)0.6500.84 (−1.52–3.21)e0.485
Women
Men
Unadjustedp-ValueMultivariate-adjustedp-ValueUnadjustedp-ValueMultivariate-adjustedp-Value
Anthropometry
 Body mass index (kg/m2)−0.16 (−0.37–0.05)0.1430.00 (−0.22–0.22)0.9850.05 (−0.07–0.17)0.3840.22 (0.10–0.35)<0.001
 Waist circumference (cm)−0.06 (−0.60–0.49)0.839−0.82 (−1.13– −0.52)a<0.0010.26 (−0.07–0.59)0.121−0.77 (−0.93– −0.61)a<0.001
 Fat mass (%)−1.23 (−1.55– −0.90)<0.001−0.56 (−0.89– −0.22)0.001−0.63 (−0.78– −0.47)<0.001−0.27 (−0.43– −0.11)0.001
Blood pressure (mm Hg)
 Systolic−1.67 (−2.46–−0.89)<0.0010.66 (−0.12–1.43)b0.098−0.77 (−1.28– −0.26)0.0030.04 (−0.48–0.56)b0.892
 Diastolic0.07 (−0.38–0.52)0.7620.15 (−0.31–0.61)b0.5220.44 (0.12–0.76)0.0070.29 (−0.05– 0.63)b0.090
Lipid markers (mmol/l)
 Total cholesterol−0.03 (−0.07–0.02)0.2300.00 (−0.04–0.05)c0.8630.06 (0.03–0.09)<0.0010.05 (0.02–0.08)c0.002
 HDL-cholesterol0.01 (−0.01–0.03)0.5050.00 (−0.02–0.02)c0.9690.00 (−0.01–0.01)0.9390.01 (0.00–0.02)c0.257
 LDL-cholesterol−0.02 (−0.06–0.02)0.2730.00 (−0.04–0.04)c0.9610.04 (0.02–0.07)0.0010.03 (0.00–0.06)c0.036
 Triglycerides §−2.7 (−4.5– −0.8)0.006−0.1 (−2.0–1.7)c0.8841.6 (−0.1–3.2)0.0580.8 (−0.8–2.5)c0.312
 Apolipoprotein B (mg/dl)−0.91 (−7.02–5.20)0.7700.35 (−6.21–6.90)c0.9180.83 (−3.34–5.01)0.695−0.52 (−5.01–3.97)c0.820
Glucometabolic markers
 Fasting glucose (mmol/l)−0.05 (−0.10–0.00)0.036−0.01 (−0.05–0.04)d0.777−0.06 (−0.10– −0.02)0.005−0.03 (−0.07–0.01)d0.116
 Insulin (µU/ml)§−1.6 (−4.0–0.9)0.2150.4 (−2.0–2.7)d0.764−1.7 (−3.4–0.1)0.069−1.1 (−2.7–0.6)d0.201
Adipokines (µU/ml)
 Leptin§−4.9 (−8.0– −1.7)0.003−1.8 (−4.4–0.9)e0.198−2.9 (−5.2– −0.5)0.016−2.7 (−4.6– −0.6)e0.010
 Adiponectin§−2.1 (−4.8–0.6)0.129−1.4 (−4.2–1.5)e0.337−0.5 (−2.4–1.4)0.5980.4 (−1.6–2.5)e0.671
Inflammatory markers
 hs-CRP (mg/l)§−9.6 (−13.5– −5.5)<0.001−6.8 (−10.7– −2.8)e0.001−4.7 (−7.6– −1.8)0.002−3.2 (−6.1– −0.2)e0.039
 IL-6 (pg/ml)§−1.1 (−6.6–4.8)0.713−1.1 (−7.0–5.2)e0.730−5.4 (−9.1– −1.5)0.007−4.1 (−8.2–0.1)e0.055
 TNF-α (pg/ml)§−0.4 (−4.0–3.3)0.8281.2 (−2.6–5.3)e0.534−2.1 (−4.5–0.4)0.094−1.2 (−3.8–1.5)e0.392
Homocysteine (µmol/l)§−2.9 (−4.0– −1.7)<0.001−0.6 (−1.8–0.7)e0.359−1.1 (−2.0– −0.2)0.0190.6 (−0.4–1.6)e0.212
Uric acid (µmol/l)−3.93 (−6.92– −0.94)0.0101.12 (−1.79–4.04)e0.4490.53 (−1.75–2.80)0.6500.84 (−1.52–3.21)e0.485

HDL: high density lipoprotein: hs-CRP: high sensitivity C-reactive protein; IL-6: interleukin 6; LDL: low density lipoprotein; TNF-α: tumour necrosis factor alpha.

Statistical analyses performed using linear regression. Results are expressed as effect of a 5 kg increase in grip strength and (95% confidence interval). Multivariate adjustment for age, current smoking, leisure-time physical activity and occupational physical activity, with a further adjustment on aweight; bbody mass index and antihypertensive drug treatment; cbody mass index and lipid lowering drug treatment; dbody mass index and antidiabetic drug treatment; ebody mass index.

§

On log-transformed data results are expressed as % change of the risk marker related to a 5 kg increase in grip strength.

Comparison between linear and quadratic models for homocysteine, total and LDL-cholesterol are expressed in Supplementary Material, Table 3. For log-transformed homocysteine, total and LDL-cholesterol, the quadratic regression model showed a better fit than the linear one. An inverse U-shaped association between grip strength and total and LDL-cholesterol was found in women. A U-shaped association between grip strength and homocysteine was found in men.

The linear associations between grip strength and CV risk markers stratified by tertiles of age are represented in Supplementary Material, Table 4 (women) and Table 5 (men), and the quadratic associations for homocysteine, total and LDL-cholesterol in Supplementary Material, Table 6. Most associations remained identical through tertiles of age.

Discussion

This study assessed the associations between grip strength and a large panel of CV risk markers in a population-based setting. Our results suggest that grip strength is only moderately associated with CV risk markers and CV absolute risk. Thus, the reported associations between grip strength and CV disease might not be mediated via those CV risk markers.

Grip strength, anthropometric and adiposity-related markers

Grip strength was negatively associated with WC and fat mass in both genders, and positively with BMI in men. The negative association with WC is consistent with a large cross-sectional population-based study8 but not with another including older participants.10 Fitness and regular exercise have been shown to improve body composition by reducing fat mass,19,20 but the effect of grip strength on CV mortality has also been suggested to be independent of body composition.21 According to a large 8.3-year follow-up study,22 muscle strength (measured using bench and leg press tests) showed a strong inverse prediction of excessive WC and fat mass after adjusting for fitness. The results suggest that grip strength is negatively related to body fat and positively to BMI, possibly due to the larger muscle mass of overweight and obese subjects. Still, the changes in WC, fat mass and BMI induced by 5 kg change in grip strength were modest (1.2 cm, 1.2% and 0.30 kg/m2, respectively) at the individual level.

A negative association between grip strength and leptin was found in men but not in women, and no association was observed for adiponectin. These findings are partly in agreement with a cross-sectional study10 where no association was found between grip strength and adiposity-related hormones. Exercise has been shown to decrease leptin levels 23 but not adiponectin levels.23 Overall, our results suggest that grip strength is moderately associated with leptin levels in men, but further studies should be conducted to confirm this association.

Grip strength, BP, lipids and glucometabolic markers

On multivariate analysis, no significant association was found between grip strength and BP levels. These findings are in agreement with a recent cross-sectional study10 but not with another.8 Fitness and regular exercise have been shown to decrease BP levels,24 while muscle strength (measured using bench and leg press tests) showed no effect on 19-year incidence of hypertension after adjustment for fitness.25 Overall, our results suggest that grip strength is not associated with BP levels, or that the association is too small to be detected using our sample size.

In both genders, an inverse U-shaped association between grip strength and total and LDL-cholesterol was found, this association being more prominent in women. Conversely, no association was found between grip strength and HDL-cholesterol, triglycerides and apolipoprotein B. These findings are partly in agreement with a cross-sectional study10 which found no association between grip strength and triglycerides, total and HDL-cholesterol. The inverse U-shaped association between grip strength and total and LDL cholesterol might be explained by two differing phenomena: first, increased fitness is associated with an improved lipids profile,19 which would explain the negative association between high grip strength values and lipid levels on the right hand side of the curve. Second, low lipid levels have been associated with mortality in an elderly cohort;26 as low grip strength is also associated with increased mortality, this would explain the positive association between grip strength and lipid levels on the left hand side of the curve. Thus, our results suggest that grip strength has a complex association with the lipid profile, high values of grip strength being associated with a ‘beneficial’ low lipid profile, while low values of grip strength are associated with a ‘deleterious’ low lipid profile. Nevertheless, these findings should be further confirmed in other studies.

No association was found between grip strength and fasting glucose and insulin, a finding in agreement with two cross-sectional studies.8,10 Fitness and regular exercise have been shown to improve glucose profile19,27 while muscle strength showed no beneficial effect on glucose levels after adjustment for fitness.28 The results suggest that grip strength is not associated with glucose metabolism or that the association is too small to be detected using the current sample size.

Grip strength and inflammation

Grip strength was negatively associated with hs-CRP levels, a finding in agreement with the literature.9,10 Fitness and regular exercise decrease CRP levels,29 probably by a decrease in adiposity levels and adiposity-related inflammation. Indeed, a previous study30 showed an association between poor muscle quantity and quality (i.e. fat deposition in skeletal muscle) and adiposity-related inflammation. Conversely, the association between grip strength and IL-6 or TNF-α is still a matter of debate: some studies reported a negative association9,31 while others reported no association.10 Thus, our findings confirm that grip strength is negatively associated with hs-CRP levels, but not with IL-6 or TNF-α. Still, the change in CRP levels was moderate (8.5% decrease per 5 kg increase in grip strength) compared for example to the reduction induced by statin treatment.32 Thus, whether decrease in CRP levels due to grip strength is clinically significant remains to be assessed.

Grip strength, homocysteine and uric acid

A U-shaped association between grip strength and homocysteine was found in men. Low grip strength was associated with high homocysteine levels, a finding also reported in a recent review,33 while the high homocysteine levels found among subjects with high grip strength deserve further clarification. Finally, no clear association was found between grip strength and uric acid levels, a finding in agreement with the literature.34

Grip strength and CV absolute risk

Grip strength was negatively associated with CV absolute risk in both genders, a finding in agreement with the beneficial effects of fitness11 and muscle strength7 on CV mortality.

Study strengths and limitations

This is one of the largest studies assessing the associations between grip strength and a wide panel of CV risk markers. Importantly, the specific effects of grip strength were separated from those of LTPA and OPA.

This study also has several limitations worth acknowledging. Firstly, grip strength was assessed on the right hand whereas approximately 8% of our participants were left-handed. However, it has been shown that grip strength does not differ between dominant and non-dominant hands in left-handed people.5 Secondly, the cross-sectional design of our study precludes the assessment of any causal effect of grip strength on CV risk markers; the ongoing follow-up of the CoLaus participants will enable assessing the prospective effects of grip strength on CV risk markers. Thirdly, only participants aged between 50–75 years were included, so our findings cannot be extrapolated to younger or older ages. Finally, most of the associations between grip strength and CV risk markers were weak, suggesting that grip strength might exert its effect on CV disease via other pathways, such as changes in endothelial function or autonomic nervous system.

Conclusion

In a population-based sample aged between 50–75 years, grip strength was only moderately associated with some CV risk markers. Thus, the reported associations between grip strength and CV disease might not be mediated via CV risk markers.

Author contribution

CG made part of the statistical analyses and wrote most of the article; PMV made part of the statistical analysis and wrote part of the article; PV revised the article.

Declaration of conflicting interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: The CoLaus study was and is supported by research grants from GlaxoSmithKline, the Faculty of Biology and Medicine of Lausanne, and the Swiss National Science Foundation (grant numbers 33CSCO-122661, 33CS30-139468 and 33CS30-148401). The funding sources had no role in study design; in the collection, analysis and interpretation of data; in the writing of the report; and in the decision to submit the article for publication.

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© The European Society of Cardiology 2017
This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://dbpia.nl.go.kr/journals/pages/open_access/funder_policies/chorus/standard_publication_model)
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CVD Risk Factors > Original scientific papers
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    CPR680695_Supplementary_Material - pdf file

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