Untitled Notes

HIIT improves:
- Glycemic control
- Insulin sensitivity
- Skeletal muscle oxidative capacity
HIIT reduces:
- HbA1c — comparable or superior to MICT
Practical takeaway: HIIT can meaningfully improve key glycemic and metabolic risk factors in Type II diabetes, with potential advantages over traditional moderate-intensity training in some domains

Primary site of glucose disposal is skeletal muscle
Exercise improves insulin sensitivity and glucose disposal
AMPK (adenosine monophosphate-activated protein kinase):
- Fuel-sensing enzyme
- Major insulin-independent glucose uptake regulator
- Activation promotes glucose transport, lipid and protein synthesis, and nutrient metabolism
- Remains transiently activated after exercise to regulate adaptations

HIIT increases mitochondrial capacity (e.g., citrate synthase activity, ETC complex content) after short high-intensity exposure (e.g., 90 ext{\% } \, \mathrm{HR}_{\max}, \ 2\ ext{weeks}).
HIIT elevates nuclear PGC-1α and total PGC-1α in skeletal muscle → increased mitochondrial biogenesis regulation

Acute HIIT improves postprandial glucose responses and reduces hyperglycemia burden in the short term

HIIT yields larger VO_2\max gains
HbA1c reductions are generally greater vs control; HIIT is not consistently superior to MICT for HbA1c
Protocol implications:
- Longer work intervals and higher training volumes tend to boost VO_2\max
- Shorter work intervals may optimize HbA1c reductions
- Age and BMI modulate responsiveness
Practical guidance: to maximize VO_2\max, use longer work intervals (LI) and higher volumes (HV) over longer training periods; elderly or higher BMI may experience attenuated gains

Cardiac structure: increased LV wall mass
Function improvements in:
- Systolic function (e.g., EF, SV)
- Diastolic function
- LV diastolic filling and reduced torsion observed
Cardiorespiratory fitness: HIIT yields increases in V{O}_2\text{peak}
Vascular function: endothelial function improves with HIIT

Exercise-induced glucose uptake is enhanced by muscular contractions (insulin-independent), especially with larger muscle recruitment
HIIT augments mitochondrial capacity, oxidative enzymes, and Ca(^{2+}) handling, contributing to improved peripheral insulin sensitivity and endurance
Cardiovascular adaptations (EDV, LV remodeling, EF/SV, diastolic function) underlie improved cardiorespiratory fitness and are linked to reduced mortality risk

Regular exercise improves glycemic control, insulin signaling, lipid metabolism; benefits extend to skeletal muscle, adipose tissue, liver, and pancreas
Acute metabolic benefits occur after individual sessions; sustained improvements require ongoing, long-term exercise

Practical protocol pointers:
- 1:1 work-to-rest ratio (i.e., \text{work}:\text{rest} = 1:1)
- Target intensity around a Borg RPE of 16\text{-}17
- Progressive adjustment of interval duration, intensity, and number
HIIT should be integrated with energy-restricted or other therapies and tailored to individual risk, fitness, and goals
Safety considerations: monitor hemodynamics and tolerance; adjust protocol based on progress and any side effects

HIIT offers robust glycemic and cardio-metabolic benefits in T2DM, with strong improvements in VO_2\max and cardiovascular health; glycemic outcomes are often on par with or better than MICT
Skeletal muscle adaptations (GLUT-4 upregulation, mitochondrial biogenesis, Ca(^{2+}) handling) underpin improved glucose regulation and insulin sensitivity

Use HIIT as an adjunct to overall lifestyle management, including diet and medication optimization
Prioritize functional, safe protocols and monitor hemodynamics and tolerance; adjust based on progress and side effects
Consider patient-specific factors (age, BMI, comorbidities) when selecting interval length, intensity, and total volume