Influence of Inspiratory Muscle Training on Changes in Fasting Hyperglycemia in the Older Adult

Fasting hyperglycemia is often observed in the older adult population, showing that after the age of 50, fasting blood glucose levels increase by 0.06 mmol/decade. Therefore, many authors embrace the hypothesis that with aging and progressive fasting blood sugar disorders can lead to glucose intolerance and type 2 diabetes.¹ Fasting hyperglycemia (100-125 mg/dl or 5.6 to 6.9 mmol/L) is defined as an intermediate state type 2 diabetes and normal levels.²

Older people are often faced with limitations when it comes to regular physical activity, in these cases, inspiratory muscle training with Threshold® can be an effective alternative to overcome these barriers. A study carried out in older adult with insulin resistance revealed significant improvements after inspiratory training with the Threshold device. These results support the use of intervention in fasting hyperglycemia.³

For this research, 38 older adults over 60 years with fasting hyperglycemia from the Center for the Study of Aging at UNIFESP were divided into 2 groups: a control group (n = 20) that trained with the Threshold device with minimal load and an experimental group (n = 18) that performed respiratory muscular training during the first session of each week at inspiratory loads of 40% of the maximal inspiratory pressure (PImax). The training program was performed over 8 weeks in 30-minute daily sessions.

Data were analyzed and the comparison between groups was done using SPSS version 19.0, and means were analyzed using ANOVA.

The 2 groups were homogeneous, showing a mean age of 74.10 years, BMI of 27 kg/m². After intervention, the individuals presented a significant increase of the inspiratory and expiratory pressure values, maximum threshold pressure sustained, and charging times in both groups. The laboratory evaluation results showed the interaction effects for blood glucose variable and HOMA-β. Others variables presented no significant differences and remained within the normal range (see Table 1).

Table 1.

Laboratory Characteristics After Intervention.

Variable	Control (n = 20)		Experimental (n = 18)		P group	P time	P interaction
	Before	After	Before	After
Cholesterol (mg/dL)	203.85 ± 7.81	194.15 ± 8.89	195.22 ± 8.23	195.72 ± 9.38	.752	.363	.314
HDL (mg/dL)	49.50 ± 2.77	54.10 ± 3.29	49.88 ± 2.92	52.83 ± 3.47	.915	.32	.627
LDL (mg/dL)	127.53 ± 8.77	120.70 ± 9.16	123.04 ± 9.24	120.11 ± 9.65	.835	.31	.686
Triglyc (mg/dL)	166.40 ± 16.01	146.80 ± 16.55	133.55 ± 16.88	133.66 ± 17.44	.322	.108	.104
Glucose (mg/dL)	108.0 ± 7.37	108.20 ± 9.35	108.78 ± 8.70	96.33 ± 8.05	.052	.001*	.001*
Insulin (uIU/mL)	9.80 ± 7.14	9.87 ± 8.17	9.63 ± 8.66	9.05 ± 9.71	.853	.716	.648
HOMA IR	2.66 ± 2.08	2.64 ± 2.59	2.54 ± 2.36	2.39 ± 2.79	.812	.702	.78
HOMA β	77.27 ± 50.01	76.18 ± 52.80	73.24 ± 58.08	89.62 ± 71.79	.843	.222	.015*
HbA1C (%)	5.97 ± 0.31	5.92 ± 0.31	5.94 ± 0.46	5.72 ± 0.47	.335	.034	1.57
Cortisol (ug/dL)	15.49 ± 1.10	15.39 ± 1.20	14.54 ± 1.22	13.89 ± 1.33	.794	.214	.776

HbA1C, glycated hemoglobin; Triglyc, triglycerides. Data are means ± SD.

^*P < .005.

Intervention increased inspiratory and expiratory pressure values, and the result was expected to the extent that the recruitment of motor units promoted increased muscle strength in muscles working in the thoracoabdominal region.⁴

Inspiratory muscle training induced a reduction in fasting glucose levels and improved the secretory capacity of pancreatic β cells. These results support a previous study in which inspiratory muscle training effectively improved insulin resistance, where the respiratory training may strengthen the skeletal musculature improving diaphragmatic respiratory capacity and increasing mobilization of GLUT4 with subsequent increase in glucose uptake and a reduction in HOMA-IR parameters.³ Another hypothesis is that the reduction of impaired fasting glucose in the older adult population may be due to an improvement in mitochondrial oxidative metabolism and a decreased reactive oxygen species (ROS) production, increased antioxidant capacity, or increased mitochondrial density.⁵ Moreover, the mitochondrial theory of aging proposes that mitochondrial DNA mutations, associated with increased ROS generation, can cause alterations in protein synthesis involved in the mitochondrial respiratory chain, which consequently can induce pancreatic β cell dysfunction.⁶

Our study points to a novel strategy aimed to ameliorate changes in glucose metabolism and delay a possible evolution to diabetes in older adults, besides being an important approach for older adult patients who cannot perform physical activity.