A comparison of the genetic and clinical profile of men that respond and do not respond to the immediate antihypertensive effects of aerobic exercise

Figures & data

Table 3 Logistic regression model of genetic and clinical correlates of exercise responders (n = 34) and nonresponders (n = 8) to the immediate antihypertensive effects of aerobic exercisea

Determinant	β	Standard error β	X^2	df	p	e^β odds ratio
C-reactive protein	−16.396	8.721	3.535	1	0.060	0.000
High-density lipoprotein	−0.532	0.273	3.798	1	0.051	0.587
Metabolic syndromeb	−2.612	2.369	1.215	1	0.270	0.073
Family historyc	−6.987	3.564	3.842	1	0.050	0.001
RAS
polymorphismsd	0.910	2.022	0.203	1	0.653	2.485
α-adducin Gly460Trpe	−0.947	1.592	0.354	1	0.552	0.388
ENOS 786 T > Cf	−2.569	2.056	1.562	1	0.211	0.077
Test
Likelihood ratio	14.770			7	0.000
Goodness-of-fit	0.397			8	1.000

Notes:

a Responders (Referent Group); the average change in blood pressure from baseline ≥1 mmHg less after LIGHT and/or MODERATE compared to nonexercise control over 9 hr; all else were classified as nonresponders; LIGHT, 40% VO₂ peak; MODERATE, 60% VO₂ peak;

b Metabolic Syndrome, absent (n = 26) or present (n = 16) by National Cholesterol Education Adult Treatment Panel III Criteria (NCEP 2002);

c Family History, self disclosed family history of hypertension among first degree relatives no (n = 21) or yes (n = 21);

d RAS SNPs, 0–2 risk alleles (n = 20) or ≥3 risk alleles (n = 22) from three polymporhisms of the RAS. Polymorphisms were angiotensin-converting enzyme insertion deletion polymorphism, an adenine/cytosine substitution at position 1166 of the angiotensin II type 1 receptor gene, and a gene conversion in intron 2 of the aldosterone synthase gene;

e α-adducin Gly460Trp, GlyGly (n = 32) or GlyTrp (n = 10);

f ENOS 786 T > C, a threonine/cysteine substitution at position 786 of the endothelial nitric oxide synthase gene; TT (n = 23) vs TC/CC (n = 19).

Table 5 Logistic regression model of genetic and clinical correlates of MODERATE responders (n = 31) and ronresponders (n = 13) to the immediate antihypertensive effects of aerobic exercisea

Determinant	β	Standard error β	X^2	df	p	e^β odds ratio
Baseline blood pressure	−0.068	0.048	2.016	1	0.156	0.935
High-density lipoprotein	−0.269	0.113	5.709	1	0.017	0.764
Metabolic syndromeb	−2.853	1.516	3.541	1	0.060	0.058
Family historyc	−3.100	1.388	4.992	1	0.025	0.045
RAS polymorphismsd	1.662	1.159	2.057	1	0.152	5.269
α-adducin Gly460Trpe	1.491	1.281	1.355	1	0.244	4.442
ENOS 786 T > Cf	−2.666	1.491	3.198	1	0.074	0.069
Test
Likelihood ratio	29.903			7	0.001
Goodness-of-fit	7.077			8	0.528

Notes:

a MODERATE, 60% VO₂ peak; Responders (Referent Group), the average change in blood pressure from baseline ≥1 mmHg less after MODERATE compared to nonexercise control over 9 hr; all else were classified as nonresponders;

b Metabolic Syndrome, absent (n = 27) or present (n = 17) by National Cholesterol Education Adult Treatment Panel III Criteria (NCEP 2002);

c Family history, self-disclosed family history of hypertension among first degree relatives: no (n = 22) or yes (n = 22);

d RAS SNPs, 0–2 risk alleles (n = 21) or ≥3 risk alleles (n = 23) from three polymporhisms of the RAS. Polymorphisms were angiotensin-converting enzyme insertion deletion polymorphism, an adenine/cytosine substitution at position 1166 of the angiotensin II type 1 receptor gene, and a gene conversion in intron 2 of the aldosterone synthase gene;

e α-adducin Gly460Trp, Gly/Gly (n = 33) or Gly/Trp (n = 11);

f ENOS 786 T > C, a threonine/cysteine substitution at position 786 of the endothelial nitric oxide synthase gene; TT (n = 23) vs TC/CC (n = 21).

Table 1 Mean (± SEM) fasting clinical characteristics of the total sample and among exercise responders and nonrespondersa

Clinical characteristic	Total sample (n = 45)	Exercise responders (n = 36)	Exercise nonresponders (n = 9)
Age (yr)	43.5 ± 1.5	44.0 ± 1.7	41.4 ± 3.4
Peak oxygen consumption (ml.kg^−1.min^−1)	30.8 ± 1.0	30.4 ± 1.1	32.4 ± 2.4
Body mass index (kg/m^2)	29.7 ± 0.7	29.6 ± 0.9	30.0 ± 0.8
Waist circumference (cm)	102.6 ± 2.2	102.1 ± 2.5	104.7 ± 4.0
Orientation awake systolic blood pressure (mmHg)b	145.7 ± 15	145.0 ± 1.8	148.8 ± 2.6
Orientation awake diastolic blood pressure (mmHg)	85.7 ± 1.1	85.2 ± 1.3	87.7 ± 1.8
C-reactive protein (mg.L^−1)	1.6 ± 0.2	1.7 ± 0.2	1.2 ± 0.2
Insulin (pmol.L^−1)	76.7 ± 8.0	74.6 ± 8.5	85.3 ± 8.0
Glucose (mmol.L^−1)	4.5 ± 0.1	4.5 ± 0.1	4.6 ± 0.2
Homeostasis model assessment	2.2 ± 1.6	2.2 ± 1.6	2.3 ± 0.6
Total cholesterol (TCHOL) (mmol.L^−1)	4.9 ± 0.2	5.0 ± 0.2	4.6 ± 0.3
High-density lipoproteincholesterol (mmol.L^−1)	1.1 ± 0.0	1.1 ± 0.0	1.0 ± 0.0
Low-density lipoproteincholesterol (mmol.L^−1)	3.1 ± 0.2	3.1 ± 0.2	2.8 ± 0.2
Total cholesterol/high-density lipoprotein ratio (U)	4.7 ± 0.2	4.6 ± 0.2	4.9 ± 0.2
Triglycerides (mmol.L^−1)	1.6 ± 0.3	1.6 ± 0.2	2.0 ± 0.4

Notes:

a Exercise responders; the average change in blood pressure from baseline ≥1 mmHg less after LIGHT and/or MODERATE compared to nonexercise control over 9 hr; all else were classified as nonresponders;

b Orientation awake blood pressure; ambulatory blood pressure averaged over the time period following the orientation session when men were awake, ie, day time blood pressure.

Abbreviations: LIGHT, 40% VO₂ peak; MODERATE, 60% VO₂ peak.

Figure 1 The average adjusted systolic blood pressure change from baseline after LIGHT and MODERATE compared to nonexercise control at hourly intervals over 9 hr among exercise responders^a.

Notes:^aExercise responders; the average change in blood pressure from baseline ≥1 mmHg less after LIGHT and/or MODERATE compared to nonexercise control over 9 hr; all else were classified as nonresponders.
Abbreviations: LIGHT, 40% VO₂ peak; MODERATE, 60% VO₂ peak.

Figure 2 The average adjusted diastolic blood pressure change from baseline after LIGHT and MODERATE compared to nonexercise control at hourly intervals over 9 hr among exercise nonresponders^a.

Notes:^aExercise responders; the average change in blood pressure from baseline ≥1 mmHg less after LIGHT and/or MODERATE compared to nonexercise control over 9 hr; all else were classified as nonresponders.
Abbreviations: LIGHT, 40% VO₂ peak; MODERATE, 60% VO₂ peak.

Table 2 Blood pressure difference {mean ± SEM (95% confidence interval)} from baseline after exercise versus nonexercise control over 9 hr among EXERCISE, LIGHT, and MODERATE responders and nonrespondersa

	SBP difference (mmHg)			DBP difference (mmHg)
	LIGHT MODERATE			LIGHT MODERATE
EXERCISE	Responder	−5.2 ± 1.3dg	−7.8 ± 1.4dg	−3.9 ± 1.1cg	−3.6 ± 1.1cg
(n = 42)	(n = 34)	(−7.9, −2.5)	(−10.5, −5.0)	(−6.0, −1.7)	(−5.8, −1.5)
	Nonresponder	11.3 + 3.5b	5.1 + 1.9b	10.0 ± 2.4b	5.1 ± 1.5b
	(n = 8)	(3.1,19.6)	(1.2,10.0)	(−4.3, 15.7)	(1.5, 8.6)
LIGHT	Responder	−6.7 ± 1.2dg	−7.4 ± 1.3df	−5.0 ± 1.0dg	−3.3 ± 1.1ce
(n = 43)	(n = 30)	(−9.2, −4.2)	(−10.1, −4.6)	(−6.9, −3.0)	(−5.6, −1.1)
	Nonresponder	9.5 ± 2.2c	0.4 ± 3.0	8.0 ± 1.9c	1.6 ± 2.0
	(n = 13)	(4.6, 14.3)	(−6.2, 6.7)	(3.8, 12.2)	(−2.8, 6.0)
MODERATE	Responder	−5.9 ± 1.5dg	−9.5 ± 1.3df	−4.5 ± 1.1dg	−4.8 ± 1.1dg
(n = 44)	(n = 31)	(−8.9, −2.9)	(−12.1, −6.9)	(−6.7, −2.2)	(−7.0, −2.6)
	Nonresponder	4.6 ± 3.5	4.9 ± 1.2c	6.4 ± 2.1b	5.1 ± 1.2c
	(n = 13)	(−3.0, 12.2)	(2.3, 7.4)	(1.8,11.0)	(2.4,7.8)

Notes:

a Exercise responders; the average change in blood pressure from baseline ≥1 mmHg less after LIGHT and/or MODERATE minus nonexercise control over 9 hr; all else were classified as nonresponders; LIGHT, 40% VO₂ peak; MODERATE, 60% VO₂ peak;

b p < 0.05,

c p < 0.01,

d p < 0.001 blood pressure difference exercise vs nonexercise control;

e p < 0.05,

f p < 0.01,

g p < 0.001 responders vs nonresponders.

Table 4 Logistic regression model of genetic and clinical correlates of LIGHT responders (n = 30) and nonresponders (n = 13) to the immediate antihypertensive effects of aerobic exercisea

Determinant	β	Standard error β	X^2	df	p	e^β odds ratio
C-reactive protein	−21.543	10.413	4.280	1	0.039	0.000
High-density lipoprotein	−0.090	0.074	1.496	1	0.221	0.914
Metabolic dyndromeb	1.540	1.588	0.940	1	0.332	4.664
Family historyc	−1.866	1.301	2.057	1	0.151	0.155
RAS
polymorphismsd	0.729	1.080	0.456	1	0.499	2.074
α-adducin Gly460Trpe	−2.692	1.492	3.254	1	0.071	0.068
GNAS 393 T > Cf	1.453	1.197	1.472	1	0.225	4.274
Test
Likelihood ratio	30.011			7	0.002
Goodness-of-fit	7.872			8	0.446

Notes:

a LIGHT, 40% VO₂ peak; Responders (Referent Group), the average change in blood pressure from baseline ≥1 mmHg less after LIGHT compared to nonexercise control over 9 hr; all else were as nonresponders;

b Metabolic syndrome, absent (n = 26) or present (n = 17) by National Cholesterol Education Adult Treatment Panel III Criteria (NCEP 2002);

c Family history, self-disclosed family history of hypertension among first degree relatives: no (n = 22) or yes (n = 21);

d RAS SNPs, 0–2 risk alleles (n = 20) or ≥3 risk alleles (n = 23) from three polymporhisms of the RAS. Polymorphisms were angiotensin-converting enzyme insertion deletion polymorphism, an adenine/cytosine substitution at position 1166 of the angiotensin II type 1 receptor gene, and a gene conversion in intron 2 of the aldosterone synthase gene;

e α-adducin Gly460Trp, Gly/Gly (n = 33) or Gly/Trp (n = 10);

f GNAS 393 T > C, a threonine/cysteine substitution at position 393 of the alpha subunit of the guanine binding system protein gene; TT/TC (n = 33) vs CC (n = 10).

[NCEP] National Cholesterol Education Program2002Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on the Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III)NIH Publication No. 02-5215

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