Effects of Sodium Bicarbonate Supplementation on Physical Performance and Cardiovascular Variables in Middle-Aged and Elderly Adults with Type 2 Diabetes Mellitus

Abstract

The global epidemic of diabetes mellitus (DM) presents a significant health challenge, and physical exercise is crucial in managing type 2 DM (T2DM). Sodium bicarbonate (SB) supplementation may enhance high-intensity exercise performance. This study aimed to analyze acute physical performance, blood glucose, and cardiovascular responses following SB or placebo supplementation in middle-aged and elderly adults with T2DM. Thirteen T2DM participants (62.15 ± 6.90 years; body mass index 29.14 ± 4.49 kg/m²) performed a maximal incremental treadmill test after ingesting SB (0.3 g/kg) or placebo in a triple-blind, randomized crossover design. Blood pressure (BP), heart rate (HR), and capillary blood glucose were measured preand post-test. SB significantly increased exercise performance (481 ± 116.97 s vs. 439 ± 99.92 s with placebo; p = 0.005) and was associated with a greater reduction in post-exercise blood glucose (p = 0.0001), which was attributed to the longer exercise duration. However, it did not potentiate the acute reduction in blood glucose typically induced by exercise. No significant differences were found between SB and placebo conditions for BP, HR, or other cardiovascular measures (p > 0.05). Acute SB supplementation improved exercise tolerance and reduced blood glucose in individuals with T2DM, indicating a potential ergogenic strategy to improve exercise performance. However, it had no observable acute impact on cardiovascular variables. These preliminary findings suggest that SB may be a safe, short-term aid to enhance high-intensity exercise performance in T2DM, but confirmation in larger studies is needed.

Keywords:
buffers; physical performance; fatigue; performance-enhancing substances; safety.

HIGHLIGHTS

Acute sodium bicarbonate (SB) supplementation increased exercise test duration by ~9.6%.

No significant changes in blood pressure or heart rate were observed with SB.

Both SB and placebo conditions showed ~15% reductions in blood glucose after exercise.

SB was safe, well tolerated, and effective, with no significant adverse effects reported.

INTRODUCTION

The epidemic of diabetes mellitus (DM) is a global health problem. Estimates indicate that over 537 million individuals worldwide have been diagnosed with the disease, and this number may increase to 783 million by 2045 [¹]. Type 2 diabetes (T2DM), accounting for approximately 90-95% of cases, results from progressive insulin secretory dysfunction combined with insulin resistance and predominantly affects middle-aged and elderly individuals [²]. It is common to observe changes in the cardiovascular autonomic response in T2DM, such as chronotropic incompetence (CI) and slower post-exercise heart rate recovery (HRR) [³,⁴]. Since the autonomic nervous system plays a crucial role in HRR after exercise, a delay in this response may indicate autonomic dysfunction and predict disease progression [⁵]. CI has multifactorial origins, but adopting an active lifestyle is a safe and effective approach to prevent or reduce insulin resistance and cardiac autonomic neuropathy in T2DM [⁶-⁸], leading to significant improvements in quality of life.

Additionally, individuals with T2DM may experience acid-base imbalances when glycemic control is poor. Diabetic ketoacidosis (DKA), characterized by hyperglycemia, metabolic acidosis, and ketosis, is a common emergency in type 1 DM, but it can also occur in poorly controlled T2DM [⁹]. Regular physical exercise plays a crucial role in mitigating risks associated with acid-base imbalances in T2DM [⁸]. It is important to note that both acute and chronic sodium bicarbonate supplementation do not substantially affect DKA parameters. However, supplementation may improve physical performance, providing additional benefits to exercise in this population [⁸,⁹].

Physical exercise is recognized as a key non-pharmacological pillar in preventing and treating T2DM [¹⁰,¹¹]. It confers acute and chronic benefits, such as improved metabolic control, enhanced physical capacity, and better cardiovascular health [¹²,¹³]. However, disease-related factors (e.g. muscle fatigue) can limit exercise performance. Thus, using additional strategies like sodium bicarbonate (SB) supplementation could help improve physical performance.

There is strong evidence that SB can delay muscle fatigue and enhance performance via physicochemical buffering mechanisms [¹⁴-¹⁶]. Extracellular buffering is the primary mechanism by which SB supplementation influences high-intensity exercise performance, preventing excessive accumulation of hydrogen ions (H⁺) and reducing metabolic acidosis, one of the main contributors to muscle fatigue [¹⁴,¹⁷]. Studies in athletic populations have shown that SB supplementation yields positive effects on performance [¹⁸], particularly in high-intensity training, which also provides numerous benefits in T2DM patients [¹⁹,²⁰]. Although previous studies observed performance improvements with SB supplementation in other populations, there is no data on the effects of SB effects on physical performance in individuals with T2DM. Thus, the hypothesis of the present paper was to observe improvements in physical performance and biochemical and cardiovascular parameters after SB supplementation in middle-aged and elderly adults with T2DM. This study addresses an underexplored intersection of exercise physiology and metabolic disease management, potentially contributing to novel supportive strategies in T2DM care.

MATERIAL AND METHODS

Participants

The sample consisted of 13 individuals with T2DM, a sample size like previous supplementation studies [²¹-²³]. Participants were recruited via convenience sampling from clinics, hospitals, and the community. Inclusion criteria were: (1) confirmed diagnosis of T2DM; (2) age 45-74 years. Exclusion criteria included: (1) proliferative diabetic retinopathy or autonomic/peripheral neuropathy; (2) any health conditions that could affect physical performance; (3) recurrent or recent hospitalizations in the past six months; (4) resting systolic BP ≥ 160 mmHg or diastolic BP ≥ 105 mmHg; (5) smoking; (6) pregnancy or lactation; (7) insulin dependence. Their anthropometric and clinical characteristics are detailed in Table 1.

Table 1
Anthropometric and clinical characteristics of participants (n = 13)

Variable	Results
Women (%)	11 (84.61)
Age (y)	62.15 ± 6.90
Body weight (kg)	73.39 ± 14.19
Height (m)	1.58 ± 0.09
Body mass index (kg/m2)	29.14 ± 4.49
Fat-free mass (%)	63.14 ± 7.60
Body fat (%)	36.88 ± 7.59
Resting HR (bpm)	70.23 ± 11.94
Disease diagnosis (y)	5.03 ± 6.64
Comorbidities
Systemic arterial hypertension (%)	69.23 (9)
Hypothyroidism (%)	23.08 (3)
Hypercholesterolemia (%)	7.69 (1)
Hypertriglyceridemia (%)	7.69 (1)

Experimental Design

This clinical trial was a triple-blind, randomized, placebo-controlled crossover study comparing acute SB intervention and placebo (Figure 1). The study received approval from the Ethics Committee on Human Research at the State University of Ponta Grossa (UEPG) (Approval No. 62650422.9.0000.0105, October 10, 2022). Data collection took place at the Laboratory of Physical Assessment and Health of the Department of Physical Education at UEPG.

Figure 1
Experimental Design of the Clinical Study. This figure illustrates the experimental protocol, which followed a randomized, triple-blind, crossover design. Participants underwent a physical assessment and test familiarization on Day 1, followed by two experimental sessions (Days 2 and 3), during which they received either SB or placebo in a counterbalanced order. Blood glucose levels, blood pressure, and heart rate during recovery were assessed before and after the maximal incremental test on both intervention days.

The experimental protocol was divided into two stages. In the first stage, participants underwent anthropometric measurements and a familiarization session with the exercise test. In the second stage, participants performed the maximal incremental treadmill test under the two supplementations (SB or placebo) as reported below. HR was recorded before, during, and after the tests. Key exercise response parameters assessed included: (a) percentage of chronotropic reserve (CR); (b) heart rate recovery (HRR). To evaluate the effectiveness of the blinding procedure, participants were asked which substance they believed they had ingested in each experimental condition.

Participants ingested the supplement 60 minutes before each exercise session, under blind conditions (neither evaluators nor participants knew the substance administered). They were instructed to avoid strenuous exercise and refrain from consuming caffeine or other stimulants 24 hours prior to each test to standardize pre-test conditions.

Sodium Bicarbonate and Placebo Supplementation

For the SB condition, a dose of 0.3 g/kg was administered 60 minutes before the test to ensure sufficient absorption [¹⁸,²⁴]. This dosage was chosen because higher doses do not provide additional benefits and are associated with more adverse effects [¹⁸]. The active solution (SB) consisted of 92.78% sodium bicarbonate, 2.4% stevioside, 0.016% green dye, 4% lemon flavoring, and 0.8% micronized silica gel, with a correction factor of 1.077 for the preparation of each participant's individual dose. The isotonic placebo solution was composed of 0.9% sodium chloride, 0.3% stevioside, 0.025% green dye, 1% lemon flavoring, and 0.5% micronized silica gel. The solutions were carefully prepared to ensure uniformity in appearance, taste, smell, and viscosity. To evaluate potential gastrointestinal discomfort from the supplementation, participants rated symptoms on a 0-10 scale, where 0 = no symptoms and 10 = extreme discomfort [²⁵]. Each dose (SB or placebo) was prepared in 200 mL of chilled, carbonated water by an independent researcher to ensure blinding and enhance palatability [²⁶], and participants were instructed to drink the entire dose within 1 minute.

Glucose Measurement

Capillary blood glucose was measured at rest and 3 minutes after finishing of the exercise test, following standard finger-prick procedures (including site antisepsis with 70% alcohol and use of disposable lancets) [²⁷]. Measurements were obtained using a glucometer (G-Tech Free, Brazil; measurement range 10-600 mg/dL) with compatible reagent strips. These samples were taken at least 2 hours after the last meal.

Anthropometry, Blood Pressure, and Body Composition

Measurement followed the recommendations of Guedes (2006) [²⁸]. Body weight and height were measured using a calibrated digital scale with a stadiometer (Welmy W200A, Brazil; capacity 200 kg, precision 0.1 kg). Body mass index (BMI) was calculated as body mass (kg) / [height (m)]². Resting blood pressure was measured on the upper arm (Omron HEM-7122 digital sphygmomanometer, Brazil) after 5 minutes of seated rest. Two measurements were taken with a 1-minute interval between them, and the average of these readings was used, following standard procedures. Body composition (lean mass and body fat percentage) was assessed via tetrapolar bioimpedance (Maltron 906, UK), according to the manufacturer’s protocol. These measurements characterized the participants and screened for any conditions (e.g., marked obesity or neuropathy) that might influence exercise responses.

Maximal Incremental Test

Participants then performed a maximal incremental treadmill test consisting of an initial speed of 2.5 km/h with increments of 0.5 km/h every minute, at a constant incline of 3%. HR was continuously monitored during exercise using a chest strap heart rate sensor (Polar, Finland). The test used in our investigation was developed based on a modification of the protocol proposed by Puga and coauthors (2012) [²⁹]. Maximal HR was estimated by the formula 208 - (0.7 × age) [³⁰]. Perceived exertion was recorded at the end of each stage using the Borg 6-20 scale [³¹]. The test was terminated upon volitional exhaustion or if the participant met failure criteria 4 (unable to continue running, or any safety concern). The highest HR achieved was recorded as peak HR, and time to exhaustion (test duration in seconds) was noted.

Heart Rate Response

The calculation of the percentage of CR was performed considering three parameters: resting HR, reserve HR, and maximum HR. The equation used for CR calculation was CR = (reserve HR / [maximum HR - resting HR]) x 100. CR values below 80% are indicative of chronotropic incompetence [³²], and recovery HR values less than 18 beats per minute (bpm) after 60 seconds are indicative of altered chronotropic response [³³]. HRR was measured by observing the difference between HR at 30, 60, 90, and 120 seconds into recovery compared to HR at the point of exhaustion. HR monitoring was conducted using a heart rate monitor (Polar V800, Kempele, Finland).

Statistical Analysis

To minimize bias, the trial adopted a triple-blind design, in which the participants, outcome assessors, and the statistician were unaware of the intervention groups. Data normality was checked with the Shapiro-Wilk test. For within-condition comparisons (prevs post-test), variables were analyzed by paired t-tests or Wilcoxon tests as appropriate. For between-condition comparisons (SB vs placebo), paired t-tests were used for normally distributed variables (e.g., test duration, %CR) and Wilcoxon or chi-square/Fisher’s exact tests for non-parametric or categorical data (e.g., peak HR, incidence of GI discomfort, participants’ guess of supplement). Blood pressure and blood glucose over time (pre vs post between conditions) were analyzed with two-way repeated measures ANOVA (condition × time). Significance was set at p < 0.05 for all analyses.

RESULTS

Performance outcomes for chronotropic reserve and exercise test duration are shown in Table 2 and individual exercise test duration in Figure 2. The exercise test time was significantly longer in the SB condition compared to placebo (481 ± 116.97 s vs 439 ± 99.92 s, p = 0.005). The reported gastrointestinal discomfort was low in both conditions (SB: 2.8 ± 4.1; placebo: 0.1 ± 0.3 on the 0-10 scale) with no significant difference (p = 0.07). Fisher’s exact test revealed no significant association between the supplement given and the participant’s guess of which supplement they received (x²(1) = 1.815, p = 0.371), indicating the blinding was effective.

Table 2
Exercise test duration and gastrointestinal discomfort with SB vs placebo (n = 13)

Variable	SB	Placebo	p
Test time (s)	481.00 ± 116.97	439.00 ± 99.92	0.005*
Gastrointestinal discomfort (0-10)	2.8 ± 4.1	0.1 ± 0.3	0.07

• Data are depicted as mean ± SD.
• ^*
  There was a statistically significant difference between groups.

Figure 2
Individual exercise test duration responses with SB and placebo (n = 13).

As shown in Table 3, no statistically significant differences were observed in systolic (SBP) and diastolic (DBP) blood pressure values between conditions (p = 0.84 and p = 0.34, respectively) or across time (p = 0.40 and p = 0.47, respectively), with no significant interaction effects (p = 0.19 and p = 0.34, respectively). However, significant differences were observed in blood glucose levels between preand post-exercise measurements (p = 0.0001), although no significant differences were observed between the supplementation conditions (SB or placebo) (p = 0.88).

Table 3
Blood pressure and capillary blood glucose values preand post-exercise with SB and placebo supplementation (n = 13)

Variable	SB		Placebo		p
	Pre	Post	Pre	Post	Condition	Time	Interaction
SBP (mmHg)	126.2 ± 15.47	124.8 ± 15.87	123.6 ± 16.51	129.5 ± 16.48	0.84	0.40	0.19
DBP (mmHg)	76.2 ± 9.58	75.8 ± 5.31	71.8 ± 6.97	74.6 ± 10.35	0.34	0.47	0.34
Blood glucose (mg/dL)	151.31 ± 60.33	127.85 ± 57.37	155.85 ± 76.97	131.15 ± 79.78	0.88	0.0001*	0.88

• The data are presented as mean ± SD. SBP: systolic blood pressure; DBP: diastolic blood pressure.
• ^*
  There was a statistically significant difference between groups.

Heart rate responses at peak exercise, chronotropic reserve and during recovery are shown in Table 4. Chronotropic reserve (% of HR reserve achieved) was slightly higher with SB (86.45 ± 20.47%) than placebo (82.93 ± 17.63%) but did not reach statistical significance (p = 0.13). Peak HR was similar between SB and placebo conditions (151.08 ± 20.77 vs 147.92 ± 18.10 bpm, p = 0.169). HR values at 30, 60, 90, and 120 seconds into recovery did not differ significantly between SB and placebo (all p > 0.1). Both conditions showed a robust drop in HR after exercise, with no significant condition effect at any time point (30 s: p = 0.472; 60 s: p = 0.238; 90 s: p = 0.194; 120 s: p = 0.147). This indicates that SB supplementation did not affect the immediate post-exercise HRR pattern compared to placebo.

Table 4
Peak heart rate, chronotropic reserve and heart rate recovery at 30, 60, 90, and 120 seconds after the maximal incremental test with SB and placebo (n = 13).

Variable	SB	Placebo	p
CR (%)	86.45 ± 20.47	82.93 ± 17.63	0.13
Heart Rate
Peak	151.08 ± 20.77	147.92 ± 18.10	0.17
30 (s)	140.00 ± 19.39	134.77 ± 17.02	0.47
60 (s)	126.23 ± 18.03	117.77 ± 17.60	0.24
90 (s)	115.08 ± 20.25	105.08 ± 17.86	0.19
120 (s)	109.46 ± 19.59	99.15 ± 15.23	0.15

DISCUSSION

To the best of our knowledge, this is the first study to examine the acute effect of SB supplementation during a maximal incremental exercise test in individuals with T2DM. We hypothesized that acute SB intake would improve exercise performance and possibly influence biochemical and cardiovascular parameters. A significant increase in exercise test duration was observed in the SB condition. Additionally, acute SB supplementation did not yield additional benefits concerning the exercise-induced reduction in blood glucose, nor did it influence cardiovascular parameters. This absence of cardiovascular effects suggests that the ergogenic action of SB is primarily related to peripheral fatigue buffering rather than any acute cardiac or autonomic enhancement. These results suggest that while both exercise sessions were effective for glucose regulation, active SB supplementation may confer an additional benefit to exercise capacity in T2DM individuals, though the performance improvement was modest and did not translate into any acute cardiovascular changes. These findings warrant further investigation into future studies.

Physical Performance Analysis

Acid-base homeostasis during exercise is maintained by physicochemical buffers, which can be augmented by SB supplementation. Studies measuring pH during intense exercise have noted delayed intramuscular acidosis and improved performance with SB [¹⁸]. SB supplementation is most often studied in athletes due to its potential performance benefits [³⁴]; in contrast, it is rarely investigated in clinical populations such as T2DM. Therefore, our results are noteworthy in suggesting that SB supplementation can benefit physical performance in this population, although no improvements in cardiovascular responses were observed with acute SB intake. While we did not perform extensive laboratory tests to track biochemical changes from supplementation (e.g., blood pH, bicarbonate, or lactate levels were not measured), previous studies provide insight into the expected physiological effects. Stephens and coauthors (2002) [³⁵] reported a significant increase in plasma bicarbonate after ingesting 0.3 g/kg SB in a maximal cycling test. Similarly, Kumstát and coauthors (2018) [³⁶] found that blood pH, bicarbonate, and base excess rose significantly following 0.3 g/kg SB (p < 0.05) in competitive swimmers. Miranda and coauthors (2022) [³⁷] in a meta-analysis observed that SB supplementation significantly increased blood lactate levels (p = 0.006) in combat sport athletes, likely because SB facilitates H⁺ efflux from muscle to blood, thereby neutralizing acidity. This reduces intramuscular acidosis and allows glycolytic energy production to continue for longer [¹⁸,³³]. Additionally, Gurton and coauthors (2023) [³⁸] suggested that SB in solution form may be more effective than capsules, demonstrating ~2% better performance in repeated sprints and Yo-Yo IR2 tests when SB was ingested as a solution. These authors noted a greater decline in serum bicarbonate during maximal exercise with SB solution compared to capsules, which was the method used in our study. The biochemical changes reported in these prior studies likely underlie the performance improvement we observed, even though we did not directly measure them in our participants. Notably, the lack of any improvement in HR or BP in our study reinforces that the ergogenic benefit of SB is localized to buffering metabolic acidosis in muscles, without acute effects on cardiovascular function. In our study, the SB condition led to ~9.6% longer exercise duration than placebo. By comparison, a review by Carr and coauthors (2011) [²⁴] of 38 studies found a lower performance gain (~1.7% ± 2.0%) with a standard 0.3 g/kg SB dose in 1-minute sprint tests in athletes, indicating that our observed effect, though statistically significant, is within the range of reported variability. Carr and coauthors [²⁴] also observed a moderate correlation (r = 0.33) between performance gains and baseline bicarbonate levels, suggesting individual responsiveness to SB can vary. Acute vs chronic SB intake can produce different outcomes: for example, Durkalec-Michalski and coauthors (2020) [³⁹] found acute SB improved specific anaerobic performance in hockey players, whereas a chronic loading protocol did not yield additional benefits. In contrast, a meta-analysis by Lopes-Silva and coauthors (2019) [⁴⁰] noted that chronic SB intake (0.5 g/kg/day for 5 days) significantly improved Wingate test peak and mean power. Together, these comparisons highlight that our findings of a modest performance enhancement with acute SB are consistent with literature, but the magnitude of benefit can differ by protocol and population. Overall, the performance improvements we observed, while encouraging, were relatively marginal and came without changes in cardiovascular metrics, underscoring the targeted nature of SB effect.

Our results indicate that SB supplementation improved exercise performance, suggesting greater tolerance to high-intensity activity in individuals with T2DM. This aligns with previous studies highlighting the feasibility and benefits of high-intensity exercise in this population. For instance, Hwang and coauthors (2019) [²⁰] observed a significant increase in VO² peak (around 10% with high-intensity interval training - HIIT, and 8% with moderate-intensity continuous training - MICT) and exercise tolerance in older adults with T2DM after an 8-week intervention. Similarly, Støa and coauthors (2017) [¹⁹] reported a 21% increase in VO² max and a 0.58% (p < 0.001) absolute reduction in HbA1c in T2DM patients after 12 weeks of HIIT. In summary, while these studies demonstrate the long-term safety and efficacy of high-intensity exercise in T2DM, our acute findings reinforce that a single session of high-intensity exercise, complemented by an ergogenic aid like SB, can be safely performed by older adults with T2DM and may offer performance benefits. This suggests that integrating intensity strategies (with potential supplements) could optimize training outcomes in this population.

Blood Glucose

We observed significant reductions in capillary blood glucose in both SB and placebo trials (~15% decrease from preto post-exercise in each). In the SB condition, glucose changed from 151.31 ± 60.33 mg/dL to 127.85 ± 57.37 mg/dL (-15.5%, p = 0.002), and in the placebo condition from 155.85 ± 76.97 to 131.15 ± 79.78 mg/dL (-15.9%, p = 0.004). This underscores the role of acute exercise in glycemic control and metabolic health. Higher exercise intensity generally confers additional metabolic benefits [⁴¹]. Exercise exerts both acute and chronic effects on glucose uptake and inflammation, reducing blood glucose for up to 48 hours post-exercise and increasing glucose uptake up to 50-fold via insulin-dependent and independent pathways [⁷,⁴²]. In line with our results, Hiyane and coauthors (2008) [⁴²] showed in 10 middle-aged diabetics that blood glucose dropped significantly for up to 90 minutes after two exercise sessions at 90% and 110% of the anaerobic threshold. Similarly, a meta-analysis by Munan and coauthors (2020) [⁴³] (23 studies) found that a single exercise bout reduced 24-hour mean glucose by ~9 mg/dL (p < 0.001). Zhang and coauthors (2021) [⁴⁴] reported that in a HIIT intervention for T2DM, fasting, pre-exercise, and 11-hour post-exercise glucose levels were all significantly improved compared to controls. These findings confirm our observation of an immediate post-exercise reduction in glucose. In our study, SB did not produce an additional glucose-lowering beyond exercise alone, suggesting that the acute glycemic benefit was driven by exercise itself. It is plausible that the main influence of SB was on buffering capacity and fatigue delay, rather than direct metabolic effects on glucose disposal. Nonetheless, the acute reduction in post-exercise glucose is likely to persist in recovery [⁴²], and repeated regularly, this could contribute to better long-term glycemic control.

Cardiovascular Parameters

Chronotropic Incompetence evaluated by chronotropic reserve (CR) percentage, is the inability of heart rate (HR) to rise adequately with increased activity demand, and it affects exercise tolerance. Recent studies link CI with cardiovascular dysfunction in T2DM, associating it with higher risks of myocardial infarction, stroke, and sudden cardiac death [³,⁴]. In our results, mean CR was 86.45 ± 20.47% for SB and 82.93 ± 17.63% for placebo; the difference was not significant (p = 0.13). We observed that 5 of 13 participants (38.5%) under SB and 6 of 13 (46.2%) under placebo had CR values < 85%, indicative of CI, which could impair exercise performance. Hansen and coauthors (2014) [⁴⁵] found that individuals with T2DM had significantly lower chronotropic response index (CRI) and a higher prevalence of CI compared to healthy controls (42% vs. 6%). CI is a relevant cardiovascular risk marker in T2DM, though its causes are multifactorial and not fully understood. Evidence suggests that aerobic exercise can improve CI and related parameters. For example, Jin and coauthors (2017) [⁴⁶] reported that 12 weeks of aerobic training in T2DM patients with CI led to significant increases in maximum heart rate (13%), exercise time (24%), and peak VO₂ (26%). In our study, a single-session design is not sufficient to resolve CI, but it is noteworthy that a substantial portion of our sample met the CI criterion based on the 85% heart rate recovery (HRR) threshold.

HRR refers to the decline in HR immediately after exercise, reflecting reactivation of parasympathetic (vagal) tone and withdrawal of sympathetic drive. It is a non-invasive measure of autonomic function and an important indicator of cardiovascular health [⁴⁷]. In the first 30 seconds postexercise, the HR dropped by 18+ bpm in both SB (≈140 to 121 bpm) and placebo (≈135 to 119 bpm) conditions, which is above the threshold (18 bpm drop) considered normal; none of our participants had an abnormal (<18 bpm) 1-minute HRR. Additionally, no participant had a resting HR > 100 bpm. A resting tachycardia combined with reduced HRR is known to predict higher cardiovascular and mortality in T2DM [⁴]; encouragingly, our sample did not exhibit this high-risk profile. Several studies demonstrate a strong link between impaired HRR and increased health risks. Qiu and coauthors (2017) [⁴⁷] and Jae and coauthors (2016) [⁴⁸] both found that slower HRR and lower HR reserve significantly increase the risk of developing T2DM. Specifically, the poorest HRR was associated with a 1.66 times higher risk of T2DM, and the lowest quartile of HR reserve/recovery had a 2.7-fold higher risk. Conversely, each 1 bpm improvement in HR reserve or recovery was linked to a 2-3% reduction in T2DM risk. Delayed HRR after exercise is also tied to elevated risk of adverse cardiac events, including sudden cardiac death. Kurl and coauthors (2021) [⁴⁹] showed that lower HR reserve and slower HRR were associated with a significantly higher incidence of SCD, with each 1 bpm slower recovery increasing SCD risk by 1-2%. Vivekananthan and coauthors (2003) [⁵⁰] further emphasized this, indicating that impaired HRR independently predicts 6-year mortality in patients with coronary artery disease. These studies emphasize that improving HRR through interventions has prognostic importance. In our acute study, SB had no effect on HRR compared to placebo, which aligns with our finding that SB did not modulate autonomic or cardiovascular responses acutely. However, as SB enhanced exercise performance, and considering that improved fitness is associated with better autonomic regulation [⁴⁶], further research is warranted to explore whether repeated SB-assisted exercise sessions may contribute to long-term improvements in HRR.

Limitations

As with other clinical trials, this study has some inherent limitations. The sample size was relatively small, and no formal power calculation was conducted, which may have reduced sensitivity to minor effects, particularly in cardiovascular variables. Heterogeneity in clinical profiles of participants, including disease duration, comorbidities, fitness levels, and the use of antihypertensive medications that may alter autonomic responses, may have contributed to response variability. Intervention sessions were held on different days, which may introduce day-to-day variation, although pre-test conditions were standardized. Additionally, the absence of mechanistic biochemical assessments (e.g., blood gases, lactate) limits insights into the underlying physiological responses to SB. Finally, as an acute, single-dose study, the results may not reflect long-term adaptations. These factors underscore the need for further studies with larger samples and mechanistic evaluations to confirm and extend the present findings.

CONCLUSION

A significant increase in exercise test duration was observed with acute SB supplementation, suggesting that SB may have a beneficial effect on physical performance in middle-aged and older adults with T2DM. Although no significant differences were detected in cardiovascular parameters, both SB and placebo trials led to significant decreases in blood glucose, highlighting the positive impact of exercise itself. These findings indicate that strategies such as high-intensity exercise combined with an ergogenic aid like SB can be safe and may improve metabolic and performance outcomes in individuals with T2DM. However, as these results are preliminary and of limited translational value, further research with larger sample sizes and mechanistic evaluations is needed to confirm our findings and elucidate the underlying physiological mechanisms in this population.

• Funding:
  This study was financed in part by the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - Brasil (CAPES) - Finance Code 001.
• Institutional Review Board Statement:
  The study was conducted in accordance with the Declaration of Helsinki and approved by the Ethics Committee on Human Research at the State University of Ponta Grossa (UEPG) (Approval No. 62650422.9.0000.0105, October 10, 2022) for studies involving humans.
• Informed Consent Statement:
  Written informed consent has been obtained from the patient(s) to publish this paper.

Acknowledgments:

The authors would like to thank the Laboratory of Drug Development and Industrial Pharmacy for preparing the supplements used in this study, and the Laboratory of Physical Assessment and Health for providing the facilities and support necessary to conduct the research.

Use of Generative Artificial Intelligence

The authors declare that large language models and other generative artificial intelligence (AI) or AI-assisted technologies cannot be credited as authors and have not been listed as authors of this paper.

The authors declare that generative artificial intelligence (AI) or AI-assisted tools were used under full human supervision. The tool(s) and version(s) used, and their purpose, are described here: Google Gemini for text alignment. No confidential or sensitive data were uploaded to such tool(s), and all AI-assisted content was checked, corrected and approved by the authors, who take full responsibility for the integrity and originality of the manuscript.

Data Availability Statement:

Data are available on reasonable request for corresponding author.

REFERENCES

• ¹ International Diabetes Federation (IDF). IDF Diabetes Atlas, 10th ed. Brussels: International Diabetes Federation; 2021.
• ² Kanaley JA, Colberg SR, Corcoran MH, Malin SK, Rodriguez NR, Crespo CJ, et al. Exercise/physical activity in individuals with type 2 diabetes: a consensus statement from the American College of Sports Medicine. Med Sci Sports Exerc. 2022;54(2):353-68.
• ³ Keytsman C, Dendale P, Hansen D. Chronotropic incompetence during exercise in type 2 diabetes: aetiology, assessment methodology, prognostic impact and therapy. Sports Med. 2015;45(7):985-95.
• ⁴ Zafrir B, Shiran A, Haim M, Jaffe R, Halon DA, Lewis BS, et al. Resting heart rate and measures of effort-related cardiac autonomic dysfunction predict cardiovascular events in asymptomatic type 2 diabetes. Eur J Prev Cardiol. 2016;23(12):1298-306.
• ⁵ Tabachnikova V, Clarke S, Moran A, O'Donnell J, Howard P, Haykowsky MJ, et al. Heart rate response to exercise and recovery: independent prognostic measures in patients without known major cardiovascular disease. J Cardiopulm Rehabil Prev. 2022;42(3):E34-E41.
• ⁶ Nery C, Moraes SR, Novaes KA, Martins CO, Nascimento W, Leitão MB, et al. Effectiveness of resistance exercise compared to aerobic exercise without insulin therapy in patients with type 2 diabetes mellitus: a meta-analysis. Braz J Phys Ther. 2017;21(6):400-15.
• ⁷ American Diabetes Association Professional Practice Committee. Classification and diagnosis of diabetes: standards of medical care in diabetes-2022. Diabetes Care. 2022;45(Suppl 1):S17-S38.
• ⁸ Pereira WVC, Gomes TN, Miranda ER, Moreira SB, Negrão CE, Farah BQ, et al. Position of Brazilian Diabetes Society on exercise recommendations for people with type 1 and type 2 diabetes. Diabetol Metab Syndr. 2023;15(1):1-20.
• ⁹ Dhatariya KK, Glaser NS, Codner E, Umpierrez GE. Diabetic ketoacidosis. Nat Rev Dis Primers. 2020;6(1):40.
• ¹⁰ Pedersen BK, Saltin B. Exercise as medicine: evidence for prescribing exercise as therapy in 26 different chronic diseases. Scand J Med Sci Sports. 2015;25(Suppl 3):1-72.
• ¹¹ Janssen SM, Connelly DM. The effects of exercise interventions on physical function tests and glycemic control in adults with type 2 diabetes: a systematic review. J Bodyw Mov Ther. 2021;28:283-93.
• ¹² Gutch M, Razi SM, Kumar S, Gupta KK, Gupta A. Assessment of insulin sensitivity/resistance. Indian J Endocrinol Metab. 2015;19(1):160-4.
• ¹³ Pan B, Ge L, Xun Y, Wang Y, Wang Y, Lu Z. Exercise training modalities in patients with type 2 diabetes mellitus: a systematic review and network meta-analysis. Int J Behav Nutr Phys Act. 2018;15(1):1-14.
• ¹⁴ Heibel AB, Perim PHS, Oliveira LF, McNaughton LR, Saunders B. Time to optimize supplementation: modifying factors influencing the individual responses to extracellular buffering agents. Front Nutr. 2018;5:35.
• ¹⁵ Maughan RJ, Burke LM, Dvorak J, Larson-Meyer DE, Peeling P, Phillips SM, et al. IOC consensus statement: dietary supplements and the high-performance athlete. Int J Sport Nutr Exerc Metab. 2018;28(2):104-25.
• ¹⁶ Grgic J, Schoenfeld BJ, Davies TB, Lazinica B, Pedisic Z. Effects of sodium bicarbonate supplementation on muscular strength and endurance: a systematic review and meta-analysis. Sports Med. 2020;50(7):1361-75.
• ¹⁷ Calvo JL, Riera T, Suárez A, Hernández-González M, Peinado AB. Effect of sodium bicarbonate on energy metabolism during exercise: a systematic review and meta-analysis. J Int Soc Sports Nutr. 2021;18(1):1-17.
• ¹⁸ Grgic J, Mikulic P, Bishop DJ, Schoenfeld BJ, Pedisic Z. International Society of Sports Nutrition position stand: sodium bicarbonate and exercise performance. J Int Soc Sports Nutr. 2021;18(1):1-37.
• ¹⁹ Støa EM, Meling S, Nyhus L, Glenn NM, Helgerud J, Støren Ø. High-intensity interval training improves aerobic fitness and HbA1c among persons with type 2 diabetes. Eur J Appl Physiol. 2017;117(3):455-67.
• ²⁰ Hwang CL, Yoo JK, Kim HK, Hwang MH, Handberg EM, Petersen JW, et al. Effect of all-extremity high-intensity interval training vs. moderate-intensity continuous training on aerobic fitness in middle-aged and older adults with type 2 diabetes: a randomized controlled trial. Exp Gerontol. 2019;116:46-53.
• ²¹ Carr BM, Webster MJ, Boyd JC, Hudson GM, Scheett TP. Sodium bicarbonate supplementation improves hypertrophy-type resistance exercise performance. Eur J Appl Physiol. 2013;113(3):743-52.
• ²² Thomas C, Bishop DJ, Lambert K, Mercier J, Brooks GA. Effects of pre-exercise alkalosis on the decrease in VO₂ at the end of all-out exercise. Eur J Appl Physiol. 2016;116(1):85-95.
• ²³ Peinado AB, Holgado D, Luque-Casado A, Rojo-Tirado MA, Sanabria D, González C, et al. Effect of induced alkalosis on performance during a field-simulated BMX cycling competition. J Sci Med Sport. 2019;22(3):335-41.
• ²⁴ Carr J, Hopkins WG, Gore CJ. Effects of acute alkalosis and acidosis on performance. Sports Med. 2011;41(10):801-14.
• ²⁵ Price M, Moss P, Rance S. Effects of sodium bicarbonate ingestion on prolonged intermittent exercise. Med Sci Sports Exerc. 2003;35(8):1303-8.
• ²⁶ Green BG, Nachtigal D. Temperature affects human sweet taste via at least two mechanisms. Chem Senses. 2015;40(6):391-9.
• ²⁷ World Health Organization (WHO). WHO guidelines on drawing blood: best practices in phlebotomy [Diretrizes da OMS para a tiragem de sangue: boas práticas em flebotomia]. Geneva: World Health Organization; 2010. Available from: https://www.who.int/publications/i/item/9789241599221
  » https://www.who.int/publications/i/item/9789241599221
• ²⁸ Guedes DP. Practical manual for physical education assessment [Manual prático para avaliação em educação física]. Barueri: Manole; 2006.
• ²⁹ Puga GM, Lopes AL, Krinski K, Leguisamo CP, de Mello RB, Gaya A. Aerobic fitness evaluation during walking tests identifies the maximal lactate steady state. Sci World J. 2012;2012:769431.
• ³⁰ Tanaka H, Monahan KD, Seals DR. Age-predicted maximal heart rate revisited. J Am Coll Cardiol. 2001;37(1):153-6.
• ³¹ Borg GA. Psychophysical bases of perceived exertion. Med Sci Sports Exerc. 1982;14(5):377-81.
• ³² Brubaker PH, Kitzman DW. Chronotropic incompetence: causes, consequences, and management. Circulation. 2011;123(9):1010-20.
• ³³ Watanabe J, Thamilarasan M, Blackstone EH, Thomas JD, Lauer MS. Heart rate recovery immediately after treadmill exercise and left ventricular systolic dysfunction as predictors of mortality: the case of stress echocardiography. Circulation. 2001;104(16):1911-6.
• ³⁴ Kerksick CM, Wilborn CD, Roberts MD, Smith-Ryan AE, Kleiner SM, Jäger R, et al. ISSN exercise & sports nutrition review update: research & recommendations. J Int Soc Sports Nutr. 2018;15(1):38.
• ³⁵ Stephens TJ, McKenna MJ, Canny BJ, Snow RJ, McConell GK. Effect of sodium bicarbonate on muscle metabolism during intense endurance cycling. Med Sci Sports Exerc. 2002;34(4):614-21.
• ³⁶ Kumstát M, Dvořáková I, Malý T, Zahálka F. Does sodium citrate cause the same ergogenic effect as sodium bicarbonate on swimming performance? J Hum Kinet. 2018;65:89-98.
• ³⁷ Miranda WAS, Nunes RB, Lima-Silva AE, Bertuzzi R, Guglielmo LGA, Arins FB, et al. Can sodium bicarbonate supplementation improve combat sports performance? A systematic review and meta-analysis. Curr Nutr Rep. 2022;11(2):273-82.
• ³⁸ Gurton W, Wallace L, Tang J, Clark B, Cook C, Stokes KA. Sodium bicarbonate and time-to-exhaustion cycling performance: a retrospective analysis exploring the mediating role of expectation. Sports Med Open. 2023;9(1):65.
• ³⁹ Durkalec-Michalski K, Nowaczyk PM, Siedzik K. The influence of progressive-chronic and acute sodium bicarbonate supplementation on anaerobic power and specific performance in team sports: a randomized, double-blind, placebo-controlled crossover study. Nutr Metab (Lond). 2020;17:1-15.
• ⁴⁰ Lopes-Silva JP, Reale R, Franchini E. Acute and chronic effect of sodium bicarbonate ingestion on Wingate test performance: a systematic review and meta-analysis. J Sports Sci. 2019;37(7):762-71.
• ⁴¹ Harrington D, Henson J. Physical activity and exercise in the management of type 2 diabetes: where to start? Pract Diabetes. 2021;38(5):35-40b.
• ⁴² Hiyane WC, Silva TL, Silva CP, Costa GA, Souza ED. Blood glucose responses of type-2 diabetics during and after exercise performed at intensities above and below anaerobic threshold. Rev Bras Cineantropom Desempenho Hum. 2008;10(1):8-11.
• ⁴³ Munan M, Dranseikaite D, Goode R, Burns C, Lal S, Parkin T, et al. Acute and chronic effects of exercise on continuous glucose monitoring outcomes in type 2 diabetes: a meta-analysis. Front Endocrinol (Lausanne). 2020;11:495.
• ⁴⁴ Zhang QQ, Zhang MM, Zhao CJ, Zuo XY. Effects of acute exercise with different intensities on glycemic control in patients with type 2 diabetes mellitus. Acta Endocrinol (Buchar). 2021;17(2):212-8.
• ⁴⁵ Hansen D, Dendale P. Modifiable predictors of chronotropic incompetence in male patients with type 2 diabetes. J Cardiopulm Rehabil Prev. 2014;34(3):202-7.
• ⁴⁶ Jin L, Zhang J, Xu D, Zhou J, Wang T. Exercise training on chronotropic response and exercise capacity in patients with type 2 diabetes mellitus. Exp Ther Med. 2017;13(3):899-904.
• ⁴⁷ Qiu S, Wei Y, Huang Y, Zhou M, Yang C, Feng B. Attenuated heart rate recovery predicts risk of incident diabetes: insights from a meta-analysis. Diabet Med. 2017;34(12):1676-83.
• ⁴⁸ Jae SY, Lee H, Kim JH, Lee WJ, Park SY, Lee JH. Exercise heart rate reserve and recovery as predictors of incident type 2 diabetes. Am J Med. 2016;129(5):536.e7-536.e12.
• ⁴⁹ Kurl S, Laukkanen JA, Rauramaa R, Salonen JT, Lakka TA, Mäkikallio TH, et al. Exercise heart rate reserve and recovery as risk factors for sudden cardiac death. Prog Cardiovasc Dis. 2021;68:7-11.
• ⁵⁰ Vivekananthan DP, Blackstone EH, Pothier CE, Lauer MS. Heart rate recovery after exercise is a predictor of mortality, independent of the angiographic severity of coronary disease. J Am Coll Cardiol. 2003;42(5):831-8.

• Editor-in-Chief:
  Bill Jorge Costa

• Associate Editor:
  Bruno Pedroso

Publication Dates

• Publication in this collection
  03 Apr 2026
• Date of issue
  2026

History

• Received
  19 May 2025
• Accepted
  24 Sept 2025